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Crohn's Disease Forum » Books, Multimedia, Research & News » Etiology of inflammatory bowel disease: A unified hypothesis


 
11-18-2012, 05:30 PM   #61
Xiaofa Qin
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To my knowledge, the per capita data would be usually calculated as the amount (tons) of chemical used in a country divided by the population, rather than sampling. It seems the average amounts of antibiotics use in China was just calculated this way. Here is another link: http://en.uuuwell.com/article-246742-1.html. It states that China produces 210,000 tons of antibiotics annually, with 30,000 tons for export, and the remaining 180,000 tons left for domestic use. 180,000 tons antibiotics divided by 1.3 billion people equals to 138.46 gram per person. This heavy antibiotics use in China has a long history rather than just started in recent years. In fact, much more people in China have deeper belief in modern medicine rather than the traditional medicine like the herbs. In China, more than 60% of patients with mild flu symptoms are prescribed with antibiotics by the doctor, with the intention to prevent the development of bacteria infection. However, here in the US, antibiotics will be given to flu patients only after they indeed showed symptoms of bacteria infection.
11-18-2012, 06:44 PM   #62
wildbill_52280
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To my knowledge, the per capita data would be usually calculated as the amount (tons) of chemical used in a country divided by the population, rather than sampling. It seems the average amounts of antibiotics use in China was just calculated this way. Here is another link: http://en.uuuwell.com/article-246742-1.html. It states that China produces 210,000 tons of antibiotics annually, with 30,000 tons for export, and the remaining 180,000 tons left for domestic use. 180,000 tons antibiotics divided by 1.3 billion people equals to 138.46 gram per person. This heavy antibiotics use in China has a long history rather than just started in recent years. In fact, much more people in China have deeper belief in modern medicine rather than the traditional medicine like the herbs. In China, more than 60% of patients with mild flu symptoms are prescribed with antibiotics by the doctor, with the intention to prevent the development of bacteria infection. However, here in the US, antibiotics will be given to flu patients only after they indeed showed symptoms of bacteria infection.
i see what you are saying, by calculating it that way it tells us how much antibiotics are being consumed by the entire population of china. but it does not tell us what types of people are consuming it. a sampling bias would not exist in this method.

If these facts are true it may shed some doubt on the role of antibiotics, but doesnt seem like enough detailed information to come to any final conclusions.
the low rates of ibd were calculated over a time span of 50 years worth of data collection, without any hard data on chronological trends of antibiotic consumption, who is to say this trend in antibiotic consumption didnt just begin 5 years ago or even 2 years ago, which then wouldnt be reflected in the previous calculations for low rates, again leaving the possibility of low rates being explained by low antibiotic consumption. just not enough hard data yet.
11-19-2012, 10:13 PM   #63
Xiaofa Qin
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The positive link between antibiotics and IBD would likely be true, as it not only demonstrated in the nationwide study of Denmark (Hviid A, et al. Antibiotic use and inflammatory bowel diseases in childhood. Gut. 2011 Jan;60(1):49-54. http://www.ncbi.nlm.nih.gov/pubmed/20966024) but also in multiple other recent large-scale studies such as those in Finland (Virta L et al. Association of repeated exposure to antibiotics with the development of pediatric Crohn's disease—a nationwide, register-based finnish case-control study. Am J Epidemiol. 2012 Apr 15;175(8):775-84; http://www.ncbi.nlm.nih.gov/pubmed/22366379 ), UK (Kronman MP, et al. Antibiotic Exposure and IBD Development Among Children: A Population-Based Cohort Study. Pediatrics. 2012 Oct;130(4):e794-803. http://www.ncbi.nlm.nih.gov/pubmed/23008454), and Canada (Shaw SY, et al. Association between the use of antibiotics and new diagnoses of Crohn's disease and ulcerative colitis. Am J Gastroenterol. 2011 Dec; 106(12):2133-42. http://www.ncbi.nlm.nih.gov/pubmed/21912437). It just seems the existence of some other factors that make the effect of even such heavily used agents like antibiotics becomes trivial.
11-20-2012, 02:01 AM   #64
wildbill_52280
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The positive link between antibiotics and IBD would likely be true, It just seems the existence of some other factors that make the effect of even such heavily used agents like antibiotics becomes trivial.
i am in awe of its complexity, its a mind bender for sure. there is some order in this chaos, i like to focus on the most basic "hard" facts we have, the north south gradient and vitamin d theory, most apparent in north america. as well as what seems to be a spike after 1945 in rates, this is when antibiotics were on the market, but like you suggest some other factors seem to make antibiotics trivial, a small but good piece of the puzzle, if in fact there is a connection and there seems to be. but there was a spike in rates from about 1910 to 1930 so how could we explain that, that was before antibiotics. the best i could do here, is dietary influences processed manufactured food high in sugar low in fiber, but i believe its even more complex yet, then there comes the different types of bacteria that may be living down there, all these factors come into play for someone to develop crohns disease, it really may take the right combo of events, it could include ANY chemical that could reduce our defenses against bacterial invasion in a permanent way, such as damage to the microbiome, this would allow chronic infections/inflammation, even the relapsing remitting nature of the more mild and moderate cases suggest this a bit, some infective agent.

here is one of my new favorite studys on crohns that uses a new model of crohns disease, i come to realize the models we had before needed updating with all the new info we have in the disease, im glad someone(many) has done it, it could really advance our understanding, even though just its just a theoretical model.

http://www.plosone.org/article/info%...l.pone.0041594
11-25-2012, 07:52 PM   #65
Xiaofa Qin
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I totally agree that any assumption and hypothesis must be kept checked against the hard facts and only the facts have the power for the ultimate judgments.

As even the effects of antibiotics and smoking become trivial, there must be some more dominant factors for IBD. I suspected that saccharin might be just such a factor. Among the many other evidences, the unified hypothesis discussed here had also included a piece of information regarding the “pike” of IBD during 1910s and 1930s before the invention of antibiotics – it is suspected that the wide spread use of saccharin since World War I may have made a contribution. Again, this remains a hypothesis that needs stringent tests. I kept advocating checking out the possible link between saccharin and IBD just because saccharin consumption met many features of IBD and thus provided a simple explanation for many puzzles of IBD that most of the other suspected agents failed to explain.

The north south gradient seems one of the many features of IBD, as shown in many, despite not all, of studies. Again, the latitude would be just an affecting factor rather than a sufficient important causative factor, as IBD in countries like Russia remained very low. This north-south gradient had used to be explained by the likely more hygiene condition (low bacteria in the environment), but recently the notion of sunshine/vitamin D become more popular. I feel the hygiene theory fits better with more other facts such as the emergence of IBD in modern society along with the improved sanitary condition, the positive link between IBD and antibiotics, etc.

Thanks wildbill_52280 for sharing the article (Craven M, et al. Inflammation drives dysbiosis and bacterial invasion in murine models of ileal Crohn's disease. PLoS One. 2012;7(7):e41594. http://www.plosone.org/article/info%...l.pone.0041594). I read trough this paper and feel it a very interesting study. It is just a little bit of regret that the feces was flushed out (with 10 ml PBS) and missed the important information as how the inflammation changed the microbiota inside the luminal content, which would be the place where the dysbiosis seen in IBD patients originated. Thus this paper actually reflected the change of the bacteria in the collected gut tissue after flush, which may make the dysbiosis seemingly more dramatic. The main bacteria in the gut of mice are Firmicutes (see Figure 2 of this linked paper: http://www.sciencedirect.com/science...92867406001929). Thus the predominately Firmicutes found in the normal animals would be just reflected this fact. However, according to the study by Johansson ME et al (The inner of the two Muc2 mucin-dependent mucus layers in colon is devoid of bacteria. Proc Natl Acad Sci U S A. 2008 Sep 30;105(39):15064-9. http://www.ncbi.nlm.nih.gov/pubmed/18806221), under normal condition, these gut bacteria are actually separated from the gut tissue through the adhesive mucus layer. Thus the measured bacteria in the normal animals would be just those within the feces or loose mucus that left behind after the flush. In contrast, with the depletion of goblet cells (thus the mucus) after the inflammation, the bacteria in animals treated with Toxoplasma gondii or high dose indomethacin would be mainly those capable of infiltrating into the gut tissue and then readily growing in this totally different new environment. The invasive E. coli would just be such a kind of bacteria. Thus a key question of this dysbiosis would be how the invasive E. coli get into the tissue. I believe the breaking down of the gut barrier would be the critical factor. Here I would like to give a simple example. I think the dysbiosis seen in this study would be somehow like an infection of the skin after a cut. There are many kinds of bacteria on our skin (http://en.wikipedia.org/wiki/Skin_flora). If we take a piece of this normal skin to analyze, the bacteria would reflect this diverse skin flora. But these bacteria are actually on the surface of the skin mixed with the dead skin cells, rather than inside the tissue. After a wound, the skin became easily got infected. The bigger the wound, the more likely and the more severe would be the infection, no matter how the wound was caused, either by cut, scrape, scratch, bite by a dog or cat, or burn. Although there are many kinds of bacteria on the skin, the most common skin infection has been Staphylococcus and Streptococcus that only make up a tiny portion of skin flora. Most of the many kinds of bacteria on skin can never grow and thus make an infection inside the wounds. In fact, many of the skin bacteria have never been able to be cultured by us. The infection would also be affected by the genetic background. Those with immune defects would likely result in more severe infection, more Staphylococcus or Streptococcus being detected in the tissue, thus a more severe inflammation and “dysbiosis”.

Actually, here lies the fundamental difference between my vision of the cause of IBD versus the main stream of thoughts. I suspected that the inflammation in IBD would be by nature just as simple as the infection of the skin after a cut. The skin is protected by a layer of dead skin cells, while the gut is protected mainly by the mucus layer secreted by the goblet cells. The skin could be cut by a knife, while the mucus layer may be broken down by the digestive proteases that became poorly inactivated due to a reduction in gut bacteria. I believe that the infection and inflammation are more determined by the tightness of the barrier rather than the absolute amount of bacteria in the surrounding environment and suspect the inflammation in IBD would be just a natural secondary reaction to the infiltrated bacterial and other harmful luminal components through the damaged gut barrier, while the main stream of thoughts in IBD kept wondering what caused the accumulation of inflammatory cells in the gut, why there is an enhanced immune response in the gut despite of the reduction in gut bacteria along with the improved hygiene, how the immune tolerance was lost, why some bacteria like the invasive E. coli become present in gut tissue, etc, and constructed a lot of sophisticated fascinating hypotheses and theories about that.
11-25-2012, 08:24 PM   #66
mf15
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Xiaofa Qin: I also have been trying to figure out the spikes in UC starting in the 1910/20/30 era. It could be anything such as Wession oil/corn oil first sold 1899,Crisco 1911,use of excess nitrate fertilizer,to chlorination of water,cold chain,lack of fermented food in the diet, or many others. Part of the spike in the USA may even have been due to immigration from Eastern Europe. As far as saccharin goes I never ate any to my knowledge and my UC started in 1980.
We of course know that bacteria play an important role,since some can be put into UC remission from Fecal Transplant. Lack of vitamin K2 in the diet may play a role since it is necessary for certain bacteria to grow including MAP,but others also need it.
UC might also be a disease of oxidation,where hydrogen peroxide is not quenched fast enough. Another possible is lack of Bromine in the diet,low taurine,the taurine bromine complex is a potent killer of bacteria,as is the TAUCl.
Please keep up the good work.
Old Mike
11-25-2012, 10:22 PM   #67
Xiaofa Qin
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Thanks Old Mike for the comments. Yes, there are numerous possibilities. Hope one day people can still figure out the fundamental cause(s) and mechanism(s) of IBD.
11-26-2012, 01:37 AM   #68
wildbill_52280
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As even the effects of antibiotics and smoking become trivial, there must be some more dominant factors for IBD. I suspected that saccharin might be just such a factor. Among the many other evidences, the unified hypothesis discussed here had also included a piece of information regarding the “spike” of IBD during 1910s and 1930s before the invention of antibiotics – it is suspected that the wide spread use of saccharin since World War I may have made a contribution. Again, this remains a hypothesis that needs stringent tests. I kept advocating checking out the possible link between saccharin and IBD just because saccharin consumption met many features of IBD and thus provided a simple explanation for many puzzles of IBD that most of the other suspected agents failed to explain.
i am now interested in looking more into the possible role of saccharin as contributing factor in ibd. just from a few minutes of casual research i learned that during world war 1 there was reportedly a shortage in sugar, which may have motivated the popularization of saccharin, the increase of rates during this time period is associated with the reported popularization of saccharin, so i see the possibility may exist.

The north south gradient seems one of the many features of IBD, as shown in many, despite not all, of studies. Again, the latitude would be just an affecting factor rather than a sufficient important causative factor, as IBD in countries like Russia remained very low. This north-south gradient had used to be explained by the likely more hygiene condition (low bacteria in the environment), but recently the notion of sunshine/vitamin D become more popular. I feel the hygiene theory fits better with more other facts such as the emergence of IBD in modern society along with the improved sanitary condition, the positive link between IBD and antibiotics, etc.
the details on russia are interesting.
im not to sharp on what the hygiene theory exactly is,although i have heard the term, but from recent reading it is proposed that from lack of exposure to pathogens at an early age this may lead to abnormal immune responses later in life. i remember a study done on mice where they exposed them to different antibiotics and examined the intestinal flora changes, in an attempt to simulate similar conditions of dosing for humans, and there were certain population of bacteria that became extinct in the intestine, but the researchers then observed when the mice were reintroduced to the non antibiotic exposed mice, that mice would eat the feces of other mice, and then the flora would renormalize itself to pre-antibiotic conditions. If this actually translates to real life, our fear of human feces seems to be a detriment to our health rather then a benefit, but i suppose our attitudes towards feces cannot be simplified this easily, in an all good or all bad dichotomy.



Thus a key question of this dysbiosis would be how the invasive E. coli get into the tissue. I believe the breaking down of the gut barrier would be the critical factor. Here I would like to give a simple example. I think the dysbiosis seen in this study would be somehow like an infection of the skin after a cut. There are many kinds of bacteria on our skin (http://en.wikipedia.org/wiki/Skin_flora). If we take a piece of this normal skin to analyze, the bacteria would reflect this diverse skin flora. But these bacteria are actually on the surface of the skin mixed with the dead skin cells, rather than inside the tissue. After a wound, the skin became easily got infected. The bigger the wound, the more likely and the more severe would be the infection, no matter how the wound was caused, either by cut, scrape, scratch, bite by a dog or cat, or burn. Although there are many kinds of bacteria on the skin, the most common skin infection has been Staphylococcus and Streptococcus that only make up a tiny portion of skin flora. Most of the many kinds of bacteria on skin can never grow and thus make an infection inside the wounds. In fact, many of the skin bacteria have never been able to be cultured by us. The infection would also be affected by the genetic background. Those with immune defects would likely result in more severe infection, more Staphylococcus or Streptococcus being detected in the tissue, thus a more severe inflammation and “dysbiosis”.

Actually, here lies the fundamental difference between my vision of the cause of IBD versus the main stream of thoughts. I suspected that the inflammation in IBD would be by nature just as simple as the infection of the skin after a cut. The skin is protected by a layer of dead skin cells, while the gut is protected mainly by the mucus layer secreted by the goblet cells. The skin could be cut by a knife, while the mucus layer may be broken down by the digestive proteases that became poorly inactivated due to a reduction in gut bacteria. I believe that the infection and inflammation are more determined by the tightness of the barrier rather than the absolute amount of bacteria in the surrounding environment and suspect the inflammation in IBD would be just a natural secondary reaction to the infiltrated bacterial and other harmful luminal components through the damaged gut barrier, while the main stream of thoughts in IBD kept wondering what caused the accumulation of inflammatory cells in the gut, why there is an enhanced immune response in the gut despite of the reduction in gut bacteria along with the improved hygiene, how the immune tolerance was lost, why some bacteria like the invasive E. coli become present in gut tissue, etc, and constructed a lot of sophisticated fascinating hypotheses and theories about that.
interesting idea with the wound analogy, i have not read much about wounds on the skin and how bacteria behave in that environment, so its hard to comment. but if ibd is a wound similar to the skin, how would we explain it not resolving itself ,permanantly all on its own, also like a wound?
we likely could be wounded by material from hard/sharp food components as well, but something so simple doesnt seem to be responsible for ibd, those small wounds likely heal very fast and occur frequently without our awareness.

but the question, how does the bacteria get in the wound is an interesting one, it reminds of the concept of intracellular bacteria, and i wondered, if the gut is covered in a protective layer of bacteria, of what importance is an intracellular pathogen at all? it seems it would have get past all the mucus and good flora, how would a pathogen be able to do that? if genetic defects of intracellular bacterial clearance play a large role, its seems that these genetic defects are another trivial detail in the events that are responsible for crohns, seemingly leading back to the gi flora.
im not suggesting that a pathogen alone is responsible for all the inflammation, as there are experiments the seem to show just food particles may lead to inflammation when coming in contact with a compromised intestinal wall.
11-26-2012, 02:52 AM   #69
PlutoCronie
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The most obvious possible indicator of environmental stressors having been the instigator of my CD is that prior to having moved to the Upper Midwest, USA, I have never had any serious digestive issues. Between going from one of the best drinking water sources in the nation, to water which has been problematic, to the lack of sunshine exposure, to possible dangerous insecticides even in organic foods, here, I can take my pick of what caused my CD. Also, emotional stress itself. I agree that artificial sweeteners can not be declared the primary culprit, for the reasons cited by other posters.
__________________
Diagnosed with Crohn's Colitis in May 2011

Alternative Healing Regimen:
High Alkaline Diet; Alkaline Water; Herbal teas, especially Kombucha and Detox, for nutrition and inflammation; weekly internal cleansing (coffee) and internal probiotics/anti-inflammatory supplements, esp, Glucosamine; naturopathic and holistic lifestyle approach; color and music Tx.
Was initially diagnosed by a Gastroenterologist, but
currently only under the care of a GP due to lack of medical insurance.

Last edited by PlutoCronie; 11-27-2012 at 01:07 AM.
11-26-2012, 08:19 PM   #70
kiny
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The invasive E. coli would just be such a kind of bacteria. Thus a key question of this dysbiosis would be how the invasive E. coli get into the tissue. I believe the breaking down of the gut barrier would be the critical factor.
Invasive E. Coli is not an innocent bystander or secondary effect for me.

OmpC immunoglobulin tests are positive years before there is any damage to the intestine, the OmpC reaction is a reaction against the E Coli cell wall.

http://www.ncbi.nlm.nih.gov/pubmed/22842615

Serological markers predict inflammatory bowel disease years before the diagnosis.

"anti-OmpC were most accurate in predicting incident CD"

Before dysbiosis, before lesions, before they are diagnosed with crohn's disease they have OmpC immunoglobulin markers.


Increased OmpC reactions are associated with LF82 AIEC.

"High osmolarity induced a significant increase in the ability of LF82 bacteria to interact with Intestine-407 cells, which correlates with increased OmpC expression"

http://www.ncbi.nlm.nih.gov/pubmed/17367388


Not only that, LF82 is found in the place of inflammation and not in the place of the skip lesion and they directly stimulate the immune response. They are not innocent secondary bystanders, they are causative.

Last edited by kiny; 11-26-2012 at 08:47 PM.
11-27-2012, 10:17 PM   #71
Xiaofa Qin
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Thanks wildbill_52280, PlutoCronie and kiny for the comments. Following is my personal thoughts and opinion.

As for why the inflammation in IBD became persistent rather than resolved quickly as a wound on a skin, there are several reasons I can think of: 1) the inflammation of the gut would also result in the reduction (depletion) of the goblet cells and thus the mucus production, which tends to generate a vicious circle that make it difficult to restore the full function; 2) the persistent existence of high level of digestive proteases (thus the cut). The disturbance of gut bacteria and impaired inactivation of digestive proteases can not only be caused by dietary chemicals and antibiotics but also drugs like sulphasalazine, one of the most important medication used for the treatment of IBD (http://www.ncbi.nlm.nih.gov/pubmed/7801055 ); 3) the consistent existence of large amounts of bacteria in the gut may also facilitate the persistent infection and inflammation.

I am not saying invasive E. coli is an innocent bystander. As stated in my paper, I believe once getting into the tissue any bacteria would become the enemy of our body, no matter they are the foe or friends before the entry. Actually, I have expected that antibiotics should be more effective than they currently appeared to be, and suspect that the impaired inactivation of digestive proteases may be a factor confounded its real efficacy (Qin X. Impaired inactivation of digestive proteases: a factor that may have confounded the efficacy of antibiotics aimed at reducing the exposure to luminal bacteria and their components. Am J Gastroenterol. 2008 Nov;103(11):2955-6. http://www.ncbi.nlm.nih.gov/pubmed/19032485 ).

However, I indeed believe the appearance of invasive E. coli and other bacteria inside the tissue are largely secondary to the damage of the gut barrier. An increase in intestinal permeability had been observed not only in patients long before their diagnosis, but also in the healthy relatives and more importantly their spouse that may never develop into IBD (Söderholm JD, et al. Different intestinal permeability patterns in relatives and spouses of patients with Crohn's disease: an inherited defect in mucosal defence? Gut. 1999 Jan;44(1):96-100. http://www.ncbi.nlm.nih.gov/pubmed/9862833) and (Breslin NP, et al. Intestinal permeability is increased in a proportion of spouses of patients with Crohn's disease. Am J Gastroenterol. 2001 Oct;96(10):2934-8. http://www.ncbi.nlm.nih.gov/pubmed/11693329). Their gut may appear very normal without any lesion, but they already have the problem in gut barrier function, which could probably be caused by the thinner in the mucus layer due to increased degradation by the poorly inactivated digestive proteases. As we know, ASCAs (the anti-Saccharomyces cerevisiae mannan antibodies) are actually much common than antibodies against Escherichia coli outer membrane porin C (OmpC) and flagellin CBir1, despite Saccharomyces cerevisiae are not invasive, adhesive, and not that “invincible”. Probably, before the defect in gut barrier is big enough to let large amount of whole bacteria sneak in, some debris of these bacteria, either those habited in gut lumen like E. coli or from the brewed foods like Saccharomyces cerevisiae, had already permeate into the tissue and generated some immune response. Interestingly, although ASCAs are the most commonly seen in Crohn’s patients, people hardly regard Saccharomyces cerevisiae as harmful. In my opinion, Saccharomyces cerevisiae might not be that innocent. The infiltration of the components of Saccharomyces cerevisiae would also result in some immune reaction. I wonder some of the beneficial effect of the so-called special carbohydrate diet may attribute to the exclusion of foods enriched with Saccharomyces cerevisiae such as bread, beers, etc.
11-27-2012, 11:13 PM   #72
wildbill_52280
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Interestingly, although ASCAs are the most commonly seen in Crohn’s patients, people hardly regard Saccharomyces cerevisiae as harmful. In my opinion, Saccharomyces cerevisiae might not be that innocent. The infiltration of the components of Saccharomyces cerevisiae would also result in some immune reaction. I wonder some of the beneficial effect of the so-called special carbohydrate diet may attribute to the exclusion of foods enriched with Saccharomyces cerevisiae such as bread, beers, etc.
in my experiance, this IS one way that the SCD diet is helpful, i utilize many of the concepts of the SCD to manage/improve my symptoms, so i never come into contact with this yeast, unless its on purpose, and this is how i determined the specific knowledge of how my body reacts to saccharomyces cerevisiae, when i changed from a source of wheat made without the yeast, to when i was making my own bread, which to rise i needed to add the yeast. going strictly from one wheat source with no yeast, to the bread i made with the yeast i saw more issues, mucus maldigestion etc. that was when i learned how my body reacted to yeast.

currently i consume 700 calories of wheat daily with no major issues.
11-28-2012, 06:47 AM   #73
kiny
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thanks for the reply Xiaofa Qin, you're one of the few researches who came here to openly discuss their paper, it's appreciated
11-28-2012, 05:08 PM   #74
PlutoCronie
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Regarding wheat, I do much better without any wheat products, but when I want pasta, I try to stay with the veggie macoroni, made from powered beet and spinach. I would like to get off of wheat enitrely.
11-28-2012, 11:13 PM   #75
Xiaofa Qin
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Thanks wildbill_52280 and PlutoCronie for sharing the experience and info, and thanks kiny for the kind praise. I also appreciate the many people having interest in this hypothesis and shared their opinion. As I described in earlier post, I found the possible link between saccharin and IBD just by chance. My feeling regarding the importance of this link also up and down many times. The dramatic decrease in IBD in Monroe County in later 1970s made me feel saccharin might be an important causative factor, because not much factors may explain such a decrease. Later, reports of the high incidence of IBD in Canada where the use of saccharin had been under strict control since later 1970s made me feel saccharin could not be that important. Then, the recent finding that sucralose, the new sweetener first approved in Canada in 1991, may be linked to IBD thorough a similar mechanism as saccharin made me regain some confidence in the original saccharin and protease hypothesis. Definitely, there would be some other dietary chemicals or other factors also linked to IBD one way or another. Hope one day we can get a clear picture of these risk factors and get rid of IBD from modern society.
11-29-2012, 01:36 AM   #76
wildbill_52280
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Xiaofa Qin,

ill have to say i have lost some of my mental sharpness for the past week or so, despite that, i tried to keep up with some of our conversations. having said that, if you recall the study i posted in this thread a few posts back about a new model of crohns disease utilizing t gondii to induce ileal inflammation, the study below is one reason why i like this model, due to the real possibility that t gondii may somehow be involved in IBD, I was just curious if you were aware of this study and of this possibility. I dont imply this study below proves very much about anything except for the facts that are reported/supposedly found. although the researchers propose some of their own interpretations of these facts, i suppose to me, i wonder what finding MAP or t gondii in ibd/crohns could imply about the disease. i read that not only map is an intracellular replicatiing organism but supposedly so is T gondii, and some intracellularlly replicate successfully by manipulating the inflammatory response and enhancing it on purpose, they seem to be able to proliferate in susceptible hosts that may already have some degree of inflammation, but enhance this inflammation to successfully replicate, via tnf-alpha, and supposedly this is how tnf-alpha inhibitors can induce a remission. to lower tnf-alpha production, this lowers inflammation perhaps, by limiting the growth of some organism. and the relapsing remitting nature of ibd/crohns, may simply be the reintroduction of a new opportunistic organism to start the whole process over again. but this is one of the main processess of ibd, i do not imply that i believe this is some sort of complete model for the disease, just one of the main processes that may occur.

Ann N Y Acad Sci. 2009 Sep;1173:640-8.
Infectious serologies and autoantibodies in inflammatory bowel disease: insinuations at a true pathogenic role.
Lidar M, Langevitz P, Barzilai O, Ram M, Porat-Katz BS, Bizzaro N, Tonutti E, Maieron R, Chowers Y, Bar-Meir S, Shoenfeld Y.
Source
Center for Autoimmune Disease, Rheumatology Unit, Sheba Medical Center, Tel Hashomer, Israel.
Abstract
The aim of this study was to reevaluate the role of infection in inflammatory bowel disease (IBD). Sera from 119 patients with IBD [80 with Crohn's disease (CD); 39 with ulcerative colitis] and 98 healthy controls were assessed using the Bio-Rad BioPlex 2200 for the presence of Toxoplasma gondii, cytomegalovirus, Epstein-Barr virus, Treponema pallidum, and Saccharomyces cerevisiae. Hepatitis B virus, hepatitis C virus (HCV), and anti-Helicobacter pylori antibodies were assessed by ELISA. In addition, sera were tested for a panel of antibodies associated with thrombophilia as well as various autoantibodies. Titers of antibodies toward HCV and T. gondii, and S. cerevisiae were higher in IBD patients than in controls, while the H. pylori autoantibodies were less prevalent among the patient population. Several thrombophilia-associated antibodies were more common in CD patients, and a single patient had a thromboembolic event. Our results show an excess of anti-HCV and anti-T. gondii antibodies among patients with IBD compared to healthy controls. Whereas the former may be the result of immunosuppression from the inflammatory disease itself or from the medications used to treat it, the latter association suggests that T. gondii is involved in the etiopathogenesis of IBD, and especially CD, in humans, as has been shown in the murine model. However, our findings also reiterate the positive association between CD and anti-S. cerevisiae antibodies as well as the negative association with H. pylori infections. These, in turn, lend indirect support to the "hygiene hypothesis" in IBD as well as the newly proposed role of commensal bacteria in the initiation of the disease process.
11-29-2012, 09:36 PM   #77
Xiaofa Qin
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Thanks wildbill_52280 for the interest in my opinion. Frankly, I have not read much on the possible link between Toxoplasma gondii and IBD. According to Wikipedia (http://en.wikipedia.org/wiki/Toxoplasma_gondii), “the rates of positive sero-prevalence in women at child-bearing age between 1990 and 2000 were 58% in Central European countries, 51–72% in several Latin-American countries and 54–77% in West African countries”, with only 11–28% in cold climate areas such as Scandinavian countries where IBD is very high. I do not know how Toxoplasma gondii infection would fit into the temporal and geographical features of IBD. As we know, it has been well documented that TNF-alpha is a pivotal factor for inflammation. The anti-TNF-alpha antibody had also been effectively used for other inflammatory diseases like rheumatoid arthritis, ankylosing spondylitis and psoriasis. The notion that efficacy of this kind of drugs primarily attributed to their inhibition on Toxoplasma gondii or other bacteria inside the macrophages seems a very odd interpretation. It also seems not true that macrophage can be easily disabled by bacteria like Toxoplasma gondii and let the bacteria hide deep inside them to launch a vehement attack to the host. In contrast, monocytes/macrophages are the valiant fighters that played a vital role in defending the body against Toxoplasma gondii. Some defects in these cells will result in extensive intestinal necrosis and rapid death of the animal. Here are several research articles by Dunay IR et al on this:

1. Gr1(+) inflammatory monocytes are required for mucosal resistance to the pathogen Toxoplasma gondii. Immunity. 2008 Aug 15;29(2):306-17. http://www.ncbi.nlm.nih.gov/pubmed/18691912

2. Inflammatory monocytes but not neutrophils are necessary to control infection with Toxoplasma gondii in mice. Infect Immun. 2010 Apr;78(4):1564-70. http://www.ncbi.nlm.nih.gov/pubmed/20145099

3. Monocytes mediate mucosal immunity to Toxoplasma gondii. Curr Opin Immunol. 2010 Aug;22(4):461-6. http://www.ncbi.nlm.nih.gov/pubmed/20537517
11-30-2012, 01:29 AM   #78
wildbill_52280
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Thanks wildbill_52280 for the interest in my opinion. Frankly, I have not read much on the possible link between Toxoplasma gondii and IBD. According to Wikipedia (http://en.wikipedia.org/wiki/Toxoplasma_gondii), “the rates of positive sero-prevalence in women at child-bearing age between 1990 and 2000 were 58% in Central European countries, 51–72% in several Latin-American countries and 54–77% in West African countries”, with only 11–28% in cold climate areas such as Scandinavian countries where IBD is very high. I do not know how Toxoplasma gondii infection would fit into the temporal and geographical features of IBD. As we know, it has been well documented that TNF-alpha is a pivotal factor for inflammation. The anti-TNF-alpha antibody had also been effectively used for other inflammatory diseases like rheumatoid arthritis, ankylosing spondylitis and psoriasis. The notion that efficacy of this kind of drugs primarily attributed to their inhibition on Toxoplasma gondii or other bacteria inside the macrophages seems a very odd interpretation. It also seems not true that macrophage can be easily disabled by bacteria like Toxoplasma gondii and let the bacteria hide deep inside them to launch a vehement attack to the host. In contrast, monocytes/macrophages are the valiant fighters that played a vital role in defending the body against Toxoplasma gondii. Some defects in these cells will result in extensive intestinal necrosis and rapid death of the animal. Here are several research articles by Dunay IR et al on this:

1. Gr1(+) inflammatory monocytes are required for mucosal resistance to the pathogen Toxoplasma gondii. Immunity. 2008 Aug 15;29(2):306-17. http://www.ncbi.nlm.nih.gov/pubmed/18691912

2. Inflammatory monocytes but not neutrophils are necessary to control infection with Toxoplasma gondii in mice. Infect Immun. 2010 Apr;78(4):1564-70. http://www.ncbi.nlm.nih.gov/pubmed/20145099

3. Monocytes mediate mucosal immunity to Toxoplasma gondii. Curr Opin Immunol. 2010 Aug;22(4):461-6. http://www.ncbi.nlm.nih.gov/pubmed/20537517
Xiaofa Qin,

Here is a study(abstract) that talks about these concepts, but it is regarding Adherent Invasive E. Coli, and not t. gondii or MAP. I now realize it sounds strange for a bacteria/organism to be living within a cell that is supposed to be destroying it, but this is what is being reported, i certainly do not make up the rules of the universe.

http://www.nature.com/labinvest/jour...t2011156a.html
11-30-2012, 07:46 AM   #79
mf15
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Can't forget Zonulin and what interferes with it.
Controls tight junctions in the small intestine,too much and you get celiac disease,wheat and others
cause the problem. Seems to act only in small intestine,but knockout mice get inflammed colons

from upregulated zonulin in the small intestine.

Here is some info read down.

One thing to remember is if your small intestine is leaking then all kinds of stuff can pass through.

Old Mike

http://physrev.physiology.org/content/91/1/151.long



http://gut.bmj.com/content/58/1/41.full.pdf+html



Seems I might want to make my sourdough with vsl3.

Regular old sourdough may also do it,makes me wonder before bakers yeast breads were naturally fermented,the sourdough starter contains both bacteria and yeast.
Seems to tie in with your observations Wild Bill.
There seems a possibility that the use of bakers yeast in breads,as
opposed to sour fermentation might be part of the problem.Early 20th centruy.

"Commercially produced yeast first appeared in the United States in the 1860s. Charles and Maximillian Fleischmann, immigrants from Austria-Hungary, with the financial backing of James Gaff, patented and sold standardized cakes of compressed yeast...produced in their factory in Cincinati. By the early twentieth century, factory-produced yeast was widely available. Cookbook recipes began specifying that commercial yeast be added directly to bread dough in sufficient quantities to leaven it in less than two hours. Bread changed in texture, becoming lighter and softer, and its flavor turned blander..."
---Oxford Encylopedia of Food and Drink in America, Andrew F. Smith [Oxford University Press:New York], Volume 2, 2004 (p. 652

http://thefooddoc.blogspot.com/2007/...own-toxic.html
11-30-2012, 09:14 PM   #80
PlutoCronie
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Looking back to when my CD symptoms first began, I realize it was relatively soon after I had finished a course of antibiotics for upper respiratory illness. In fact, for about 5 years preceding the CD symptoms I had been on all kinds of antibiotics, as well as anti-inflammation Rx. I am not concluding that this alone is what caused my CD because there had been other substantial stressors present at the time, but I would not rule out that my digestive system had been seriously compromised by these Rx antibiotics/anti-inflammatory Rx.
12-02-2012, 01:52 PM   #81
Xiaofa Qin
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Thanks wildbill_52280, Old Mike and PlutoCronie for sharing the info.

I read through the article provided by wildbill_52280 (http://www.nature.com/labinvest/jour...t2011156a.html). I found it a very interesting study with fascinating conclusions. However, I was confused with the statement that “the amount of TNF-α released by infected macrophages is correlated with the load of intramacrophagic AIEC bacteria and their intracellular replication. TNF-α secretion was not related to the number of bacteria entering host cells because when the number of bacteria internalized in macrophage was decreased by blocking lipid raft-dependent and clathrin-coated pits-dependent endocytosis, the amount of TNF-α secreted by infected macrophages was not modified”. As per my understanding, the load of AIEC bacteria inside the cell and thus the amount of bacteria available for intracellular replication would be ultimately determined by how much bacteria got entered the cell. The similar TNF-α production with or without the blockage of bacteria entering would suggest the TNF-α production seemed more likely depending on interaction of the bacteria and macrophages at the surface rather than inside the macrophages. This notion would also be more in accordance with the current knowledge that TNF-α production can be greatly stimulated by lipopolysaccharides (LPS) (http://en.wikipedia.org/wiki/Tumor_n...s_factor-alpha), the major component of the outer membrane of Gram-negative bacteria like E. coli (http://en.wikipedia.org/wiki/Lipopolysaccharide), through its binding with Toll-like receptor 4 (TLR 4) (http://en.wikipedia.org/wiki/TLR_4) on the surface of cells like macrophages and the activation of the related pathways. It does not need the bacteria to be alive and replicating. The LPS could be the purified agents or those from the debris of the dead bacteria. In fact, the feces contains large amounts of LPS with more than 1 mg/g. LPS is also called as endotoxin, and a dose of 1 µg/kg injected into the blood would be enough to induce shock in humans. The amount of endotoxin possessed by gut bacteria can cause the death of the host thousands times over. Thus, it is the effectiveness of gut barrier rather than the amount of these harmful components in the lumen determined the safety of the body.

Thanks Old Mike for sharing the info on Zonulin. It is indeed a very interesting molecule and it further demonstrated the importance of gut barrier in some diseases.

Thanks PlutoCronie for sharing the antibiotics story. According to the multiple large-scale studies as listed in the previous post (#66 in this thread), the series use of antibiotics could be definitely one of the most important causative factors. You see, the cause of IBD might not be so complex that is beyond our ability to trace.
12-02-2012, 06:01 PM   #82
wildbill_52280
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, I was confused with the statement that “the amount of TNF-α released by infected macrophages is correlated with the load of intramacrophagic AIEC bacteria and their intracellular replication. TNF-α secretion was not related to the number of bacteria entering host cells because when the number of bacteria internalized in macrophage was decreased by blocking lipid raft-dependent and clathrin-coated pits-dependent endocytosis, the amount of TNF-α secreted by infected macrophages was not modified”. As per my understanding, the load of AIEC bacteria inside the cell and thus the amount of bacteria available for intracellular replication would be ultimately determined by how much bacteria got entered the cell. The similar TNF-α production with or without the blockage of bacteria entering would suggest the TNF-α production seemed more likely depending on interaction of the bacteria and macrophages at the surface rather than inside the macrophages. This notion would also be more in accordance with the current knowledge that TNF-α production can be greatly stimulated by lipopolysaccharides (LPS) (http://en.wikipedia.org/wiki/Tumor_n...s_factor-alpha), the major component of the outer membrane of Gram-negative bacteria like E. coli (http://en.wikipedia.org/wiki/Lipopolysaccharide), through its binding with Toll-like receptor 4 (TLR 4) (http://en.wikipedia.org/wiki/TLR_4) on the surface of cells like macrophages and the activation of the related pathways. It does not need the bacteria to be alive and replicating. The LPS could be the purified agents or those from the debris of the dead bacteria.
You have a good point, it might not be entirely clear whether intracellular AIEC are manipulating the macrophage from the inside to produce more tnf-alpha, since tnf-alpha did not seem to reduce when the bacteria were blocked from entering the cell. I believe that is what i said before and was a mistake, the authors dont seem to be claiming that aeic is manipulating the production of tnf from the inside of the cell. but the important part is that they #1 AEIC can live inside the macrophage #2 somehow use tnf-alpha production to replicate intracellularly #3 replication can be influenced by reducing production or enhancing supply of tnf-a.

"Interestingly, dose-dependent increases in the number of intracellular AIEC LF82 bacteria were observed when infected macrophages were stimulated with exogenous TNF-α, and neutralization of TNF-α secreted by AIEC-infected macrophages using anti-TNF-α antibodies induced a significant decrease in the number of intramacrophagic bacteria. These results indicate that AIEC bacteria use TNF-α as a Trojan horse to ensure their intracellular replication because replication of AIEC bacteria within macrophages induces the release of TNF-α, which in turn increases the intramacrophagic replication of AIEC. Neutralizing TNF-α secreted by infected macrophages may represent an effective strategy to control AIEC intracellular replication."

so i think at least in the abstract they are saying, despite the observation that suggests the amount of tnf-alpha secretion is not dependant upon the bacteria entering the cell, when they supply more tnf-a, the bacteria replication enhances, and when they inhibit tnf-a, they decrease, therefore their intracellular replication is somehow dependant upon tnf-a secretion, but not upon entering the cell.
12-02-2012, 10:22 PM   #83
Xiaofa Qin
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Thanks wildbill_52280 for sharing the analysis and thoughts regarding this paper ((http://www.nature.com/labinvest/jour...t2011156a.html). Actually, this paper you provided has made me read more on adherent and invasive Escherichia coli (AIEC) and related research in recent couple of days. These are really good studies. However, frankly, it also raised me a big concern regarding the crucial methodology used in these studies that I have hesitated to discuss in the previous post. As described in the paper (here is a link to a freely assessable article with detailed description on the methods: http://www.ncbi.nlm.nih.gov/pmc/arti...df/0770-04.pdf), the replication of AIEC was determined by the Gentamicin protection assay (http://en.wikipedia.org/wiki/Gentami...otection_assay). Basically, the bacteria and the macrophages were first incubated together for a period of time, and then the bacteria outside the macrophages were washed away. After that the cells were incubated for long periods with a media containing 20 µg/ml gentamicin to prevent the growth of bacteria outside the cell. At the wikepedia site regarding this assay, it clearly stated that “As for bacteria, only species susceptible to gentamicin can be assayed.” However, I am afraid of that 20 µg/ml of gentamicin used in these studies might be not enough ot have really completely prevented the growth of some resistant strains of AIEC. According to a study by Mawer SL and Greenwood D. (Specific and non-specific resistance to aminoglycosides in Escherichia coli. J Clin Pathol. 1978 Jan;31(1):12-5. http://www.ncbi.nlm.nih.gov/pmc/arti...00171-0020.pdf), the minimum antibacterial concentration (MAC) of gentamicin for a regular Escherichia coli K12 (the type of E. coli used in many AIEC studies as the non-adherent and non-invasive control) strain J53 was 4 µg/ml. However, the MAC increased to 32 µg/ml once the bacteria got the R factor RS28. Interestingly, presence of the antibiotics just caused a delay in the rapid growth phase. Once the lag phase was overcome, the bacteria replicated just as fast as in the absence of antibiotics. Study had shown that multidrug (including gentamicin) resistance is common in Escherichia coli from patients with Crohn's disease (Dogan B, et al. Multidrug resistance is common in Escherichia coli associated with ileal Crohn's disease. Inflamm Bowel Dis. 2012 Apr 16. [Epub ahead of print]. http://www.ncbi.nlm.nih.gov/pubmed/22508665). Some researchers on AIEC study indeed found some strains of E. coli were resistant to gentamicin and they changed the antibiotics to 100 µg/ml kanamycin instead (Martinez-Medina M, et al. Adherent-invasive Escherichia coli phenotype displayed by intestinal pathogenic E. coli strains from cats, dogs, and swine. Appl Environ Microbiol. 2011 Aug 15;77(16):5813-7. http://www.ncbi.nlm.nih.gov/pmc/arti...df/zam5813.pdf). If the guess that 20 µg/ml gentamicin would be not enough to completely inhibit the growth of bacteria would be true, all the puzzles regarding the results could be easily explained: the TNF-α production is not related to the number of bacteria got entered into the cell, as this production would actually just determined by the amount of bacteria survived and became flourished in the culture media; the exogenous TNF-α will increase while the anti TNF-α antibody would decrease the amount of bacteria inside the cells as the phagocytosis of the macrophage could be greatly enhanced by TNF-α (Hess DJ, et al. Escherichia coli and TNF-alpha modulate macrophage phagocytosis of Candida glabrata. J Surg Res. 2009 Aug;155(2):217-24. http://www.ncbi.nlm.nih.gov/pubmed/19482303). TNF-α has not served as an accomplice that helped the replication of bacteria inside the cell; rather TNF-α served as a signal that mobilized the macrophages to fight. I believe this scenario would make more sense. Thus the more bacteria grown in the media, the more production of the TNF-α, the more active of the macrophages, and the more bacteria could be found inside the cell. If this would be true, at least some of the bacteria we saw inside the cells would be virtually actively captured by the macrophages to destroy. This guess does not mean to dispute the conclusion that AIEC can get inside and replicate within the macrophages and other cells just like some pathogenic strains of Shigella, Salmonella, Mycobacterium, and Listeria did, but it does suggest we may have overestimated the capability of AIEC living inside the cell and underestimate the capacity of macrophages against the bacteria. With the limited info available, this is just a guess. However, these studies should indeed have included the measurements of the amount of bacteria and the level of LPS in the media and demonstrated as the results in the paper, as this is a critical issue in this kind of studies.

Last edited by Xiaofa Qin; 12-03-2012 at 08:03 AM.
12-03-2012, 09:46 AM   #84
kiny
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TNF-α has not served as an accomplice that helped the replication of bacteria inside the cell; rather TNF-α served as a signal that mobilized the macrophages to fight. I believe this scenario would make more sense. Thus the more bacteria grown in the media, the more production of the TNF-α, the more active of the macrophages, and the more bacteria could be found inside the cell. If this would be true, at least some of the bacteria we saw inside the cells would be virtually actively captured by the macrophages to destroy.
Thank you. In 2006 someone wrote this, and I have remembered it for 6 years because of the last line in their interpretation.

http://www.ncbi.nlm.nih.gov/pubmed/16503465

"Local inflammatory reaction to inoculation with E coli was attenuated, as quantified by changes in bloodflow (ileal disease 50%, n=6, p=0.01; colonic disease 77%, n=6, p=0.0003). This response was mediated by nitric oxide in controls, was increased by sildenafil in patients, and was not related to CARD15 genotype.

INTERPRETATION:

In Crohn's disease, a constitutionally weak immune response predisposes to accumulation of intestinal contents that breach the mucosal barrier of the bowel wall, resulting in granuloma formation and chronic inflammation. Polymorphisms in CARD15 do not underlie this phenotype, but incapacitate the NOD2 pathway that can compensate for impairment of innate inflammation. Current treatment of secondary chronic inflammation might exaggerate the underlying lesion and promote chronic disease."

Last edited by kiny; 12-03-2012 at 10:02 AM.
12-03-2012, 09:38 PM   #85
Xiaofa Qin
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Thanks kiny for sharing this interesting article.
01-12-2013, 12:18 AM   #86
Xiaofa Qin
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I started a discussion last month at several IBD-related LinkedIn groups including the European Crohn's and Colitis Organisation ECCO, CCFA (Crohn's & Colitis Foundation of America), IBD - Crohn's disease & Ulcerative Colitis – CCF, and IBD Research Foundation, entitled “We should put a little bit more effort to find out the cause of inflammatory bowel disease”, in hoping to generate some in-depth discussion on the cause and etiology of IBD among the IBD professionals. It turned out only Mr. Michael Seres, a patient with Crohn’s disease, and two other non-IBD professionals gave some response. I had also submitted an abstract to the 2012 Advances in Inflammatory Bowel Diseases: Crohn's and Colitis Foundation's Clinical and Research Conference and the 8th European Crohn's and Colitis Organisation Congress of Inflammatory Bowel Diseases 2013, in hoping to have the chance exchanging information, evidences and views with IBD professions regarding the etiology of IBD, but the abstract was rejected by both of the conferences. I believe everybody knew a big problem in IBD is we still do not know its cause. However, it seems hardly any people who had the resource really had the urge and interest in finding out the cause of the remarkable increase in IBD.
01-12-2013, 12:32 AM   #87
Moe.
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One day they'll get it and suffer.
It there kids will get it and they'll suffer.

Round n round it goes.
The cause the reason?
No one knows!

I can complain and whinge and whine
Or I can sit here and make a nursery rhyme.

Sorry off topic.
01-12-2013, 01:55 AM   #88
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Your research is very interesting Xiaofa Qin, thank you! We allow you to translate it into French?
01-12-2013, 01:59 AM   #89
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We also note and believe there is not a single cause but different causes; several environmental interactions (mainly chemicals including junkfood, etc. sweeteners, additives, excipients, pharmaceutical, etc. overuse of antibiotics. stress, acidity, acidosis = inflammation) these environmental interactions inducing an imbalance in the homeostasis of the body, causing an imbalance within the microbiota, microbiota where there have not a single bacterium as seen, but interactions between several bacteria, yeasts, fungi, or ... as primary reason an imbalance of the microbiota .... The first main food microorganisms is sugars then nutrients... This is clearly a cascade of causes which leads to symptoms of IBD, different gradients, different sub-groups based on micro-organisms involved ... diagnoses (often late) based mainly on the findings of lesions, lesions are a result. Search for a single cause, we think it's like trying to make a snowman in summer heatwave...
01-12-2013, 02:30 AM   #90
wildbill_52280
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I started a discussion last month at several IBD-related LinkedIn groups including the European Crohn's and Colitis Organisation ECCO, CCFA (Crohn's & Colitis Foundation of America), IBD - Crohn's disease & Ulcerative Colitis – CCF, and IBD Research Foundation, entitled “We should put a little bit more effort to find out the cause of inflammatory bowel disease”, in hoping to generate some in-depth discussion on the cause and etiology of IBD among the IBD professionals. It turned out only Mr. Michael Seres, a patient with Crohn’s disease, and two other non-IBD professionals gave some response. I had also submitted an abstract to the 2012 Advances in Inflammatory Bowel Diseases: Crohn's and Colitis Foundation's Clinical and Research Conference and the 8th European Crohn's and Colitis Organisation Congress of Inflammatory Bowel Diseases 2013, in hoping to have the chance exchanging information, evidences and views with IBD professions regarding the etiology of IBD, but the abstract was rejected by both of the conferences. I believe everybody knew a big problem in IBD is we still do not know its cause. However, it seems hardly any people who had the resource really had the urge and interest in finding out the cause of the remarkable increase in IBD.
Thanks for keeping us updated.

I also wonder why it has taken so long for any interest in fecal transplants for IBD when Thomas J Borody had his experiments published in i think 2003, that was ten years ago, and it is probably the most promising treatment out there. ill admit, we only just finished the microbiome project and know little about the intestinal flora and what can be considered healthy to choose the correct donor, that was one thing that may have been holding some people back from interest. but i have found 3 studys last year that will be completed this year, so thats promising.
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