# lactulose breath test - confusion



## Guest (Oct 26, 2004)

i had a 2 hour lactulose breath test today. i thought i was getting tested for SIBO, but the technician who explained the entire procedure and why it was needed etc. told me this:---------a. when people take antibiotics sometimes it leads to bacteria overgrowth in the STOMACH.b. we are doing a test to see if that has happenedc. if it has we have some medicine that will clear it up for you so no worries this is easy to treat.----------------from reading this board i thought that:a. the test is for the small intestineb. antibiotics don't cause this - or atleast a major hospital wouldn't say thisc. its really hard to treat as its often caused by motility problems-------------------------but she told me:a. the small intestine is supposed to have bacteria in it just like the large intestine otherwise it could not break down food. i told her there are large contractions to sweep the bacteria out - but she said those happen everywhere in the digestive system b/c the whole thing contracts(not really understanding me)b. and that I spiked when the sugar went into my small intestine therefore i'm "normal".who is right? and am I normal?


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## Guest (Oct 26, 2004)

ok - i did my own research and she is dead wrong. she was thinking perhaps about tests using lactose or fructose, but this was lactulose and indeed measures for SIBO and rapid transit.also, since i spiked at the small intestine do i automatically quality for SIBO? or do i need to spike again at the large intestine? I only tested for 2 hours, so perhaps it didn't get there. Or maybe I spiked and she didn't tell me. so curious if you must spike twice for qualify for SIBO.


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## Guest (Oct 26, 2004)

ok - i did my own research and she is dead wrong. she was thinking perhaps about tests using lactose or fructose, but this was lactulose and indeed measures for SIBO and rapid transit.also, since i spiked at the small intestine do i automatically quality for SIBO? or do i need to spike again at the large intestine? I only tested for 2 hours, so perhaps it didn't get there. Or maybe I spiked and she didn't tell me. so curious if you must spike twice for qualify for SIBO.


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## skinny (Jul 27, 2002)

Joan, what do you mean by spiked? Did you hydrogen levels go above 20 ppm? Get a printout of your results and let us know. Also check out this graph. http://www-east.elsevier.com/ajg/issues/9512/ajg3368fla.htm skinny


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## skinny (Jul 27, 2002)

Joan, what do you mean by spiked? Did you hydrogen levels go above 20 ppm? Get a printout of your results and let us know. Also check out this graph. http://www-east.elsevier.com/ajg/issues/9512/ajg3368fla.htm skinny


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## flux (Dec 13, 1998)

> quote:a. the small intestine is supposed to have bacteria in it just like the large intestine otherwise it could not break down food.


As you learned, this is *false*.


> quote:i told her there are large contractions to sweep the bacteria out - but she said those happen everywhere in the digestive system b/c the whole thing contracts(not really understanding me)


Again, you are right. The contractions that sweep things out of the small intestine is Phase III of the MMC. The large intestine has its own MMCs, but they are generally independent of the small bowel.


> quote:b. and that I spiked when the sugar went into my small intestine therefore i'm "normal".


This is also wrong, but we have to see the results of your test and how much lactulose you took. It doesn't necessarily mean you have SIBO because the results could just mean rapid transit. Often the results are inconclusive. That particular paper referenced above had a lot of problems including how the test was performed.For example, to perform a proper test, you must have a light fiber/resistant starch free dinner and stop eating before midnight. And technically you should have mouthwash to eliminate false positive from the mouth. But even then the lactulose test is not the best test for this.


> quote:she was thinking perhaps about tests using lactose or fructose


Well, lactose and fructose ideally would not spike at all. They'd be absorbed.


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## flux (Dec 13, 1998)

> quote:a. the small intestine is supposed to have bacteria in it just like the large intestine otherwise it could not break down food.


As you learned, this is *false*.


> quote:i told her there are large contractions to sweep the bacteria out - but she said those happen everywhere in the digestive system b/c the whole thing contracts(not really understanding me)


Again, you are right. The contractions that sweep things out of the small intestine is Phase III of the MMC. The large intestine has its own MMCs, but they are generally independent of the small bowel.


> quote:b. and that I spiked when the sugar went into my small intestine therefore i'm "normal".


This is also wrong, but we have to see the results of your test and how much lactulose you took. It doesn't necessarily mean you have SIBO because the results could just mean rapid transit. Often the results are inconclusive. That particular paper referenced above had a lot of problems including how the test was performed.For example, to perform a proper test, you must have a light fiber/resistant starch free dinner and stop eating before midnight. And technically you should have mouthwash to eliminate false positive from the mouth. But even then the lactulose test is not the best test for this.


> quote:she was thinking perhaps about tests using lactose or fructose


Well, lactose and fructose ideally would not spike at all. They'd be absorbed.


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## Guest (Oct 26, 2004)

hi all - well i'm sort of guessing that even though she didn't understand how the tests work, she must be able to read them, and my levels probably didn't go above normal. but we'll see - i have to wait a month for the doctor to read the results.meanwhile today i'm eXTREMELY sick wiht lots of pressure in my chest. i woke up with major diarrhea and vomiting and i'm not sure why. wonder if it could be the lactulose and perhaps my transit is so slow that it took that long to go through my system. don't know


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## Guest (Oct 26, 2004)

hi all - well i'm sort of guessing that even though she didn't understand how the tests work, she must be able to read them, and my levels probably didn't go above normal. but we'll see - i have to wait a month for the doctor to read the results.meanwhile today i'm eXTREMELY sick wiht lots of pressure in my chest. i woke up with major diarrhea and vomiting and i'm not sure why. wonder if it could be the lactulose and perhaps my transit is so slow that it took that long to go through my system. don't know


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## bonniei (Jan 25, 2001)

skinny that is not the way the graph is supposed to look like. The graph in the link you posted was of the group average so it does not show double peaks.


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## bonniei (Jan 25, 2001)

skinny that is not the way the graph is supposed to look like. The graph in the link you posted was of the group average so it does not show double peaks.


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## Guest (Oct 27, 2004)

hi bonniei - can you guess why i'd still be so sick after that test? i'm throwing up and have gtreat pressure. had D this morning. also does Mirilax work the way lactulose does? - curious b/c some said ti was an indigestible sugar which is why it caused D. i had these same symtpoms when i took Mirilax.i feel so sad today - want to go home and give up. i don't want to live life like this anymore.


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## Guest (Oct 27, 2004)

hi bonniei - can you guess why i'd still be so sick after that test? i'm throwing up and have gtreat pressure. had D this morning. also does Mirilax work the way lactulose does? - curious b/c some said ti was an indigestible sugar which is why it caused D. i had these same symtpoms when i took Mirilax.i feel so sad today - want to go home and give up. i don't want to live life like this anymore.


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## bonniei (Jan 25, 2001)

Lactulose is known to cause gas and perhaps D because it is unabsorbable. So I would think your symptoms are consistent with that. I don't know how Miralax works.Please don't be sad. Affter all you are seeing an expert so keep persisting with him till you find the cause.I know a month seems too long to wait but really keep your mind absorbed with something else and the time will soon fly. You are so close to finding out the cause. Don't give up now.


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## bonniei (Jan 25, 2001)

Lactulose is known to cause gas and perhaps D because it is unabsorbable. So I would think your symptoms are consistent with that. I don't know how Miralax works.Please don't be sad. Affter all you are seeing an expert so keep persisting with him till you find the cause.I know a month seems too long to wait but really keep your mind absorbed with something else and the time will soon fly. You are so close to finding out the cause. Don't give up now.


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## echris (Jul 19, 2000)

joanofarc:When I had the same test, I had pretty bad D that evening and felt really crummy --- bloated and cramping. However, at the time I had the test, it was still kind of experimental so the GI docs weren't sure how to interpret it. My test appeared normal but they said that the total blowout that evening was not. I have not had a desire or a craving to repeat the test. Hopefully you will feel better tomorrow. I felt better the next day.


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## echris (Jul 19, 2000)

joanofarc:When I had the same test, I had pretty bad D that evening and felt really crummy --- bloated and cramping. However, at the time I had the test, it was still kind of experimental so the GI docs weren't sure how to interpret it. My test appeared normal but they said that the total blowout that evening was not. I have not had a desire or a craving to repeat the test. Hopefully you will feel better tomorrow. I felt better the next day.


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## Guest (Oct 27, 2004)

thank you all - thanks bonniei and echris, that makes me feel better. yes, i'd guess if you were having a blowout like this it would mean something. but doc already told me the ibser's are sensitive to non-absorbable sugars - so maybe thats all it means. i am still so sick - throwing up, pressure, lots of D - every 15 minutes for 10 hours now. And i'm at work! I just don't care anymore. I have to work, so.bonniei -i'll keep trudging along! thanks for the pick me up - i really need to hear these things.


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## Guest (Oct 27, 2004)

thank you all - thanks bonniei and echris, that makes me feel better. yes, i'd guess if you were having a blowout like this it would mean something. but doc already told me the ibser's are sensitive to non-absorbable sugars - so maybe thats all it means. i am still so sick - throwing up, pressure, lots of D - every 15 minutes for 10 hours now. And i'm at work! I just don't care anymore. I have to work, so.bonniei -i'll keep trudging along! thanks for the pick me up - i really need to hear these things.


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## SpAsMaN* (May 11, 2002)

Joan,watch out about the hospitals medicals staff,they think they knows everything but most of the time they put you in real troubles.







With little test,there is littles consequences, but when it comes to surgery,these guys can send you on the floor for years.Now,i feel it immediately when a doctornurse lie in my face.


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## SpAsMaN* (May 11, 2002)

Joan,watch out about the hospitals medicals staff,they think they knows everything but most of the time they put you in real troubles.







With little test,there is littles consequences, but when it comes to surgery,these guys can send you on the floor for years.Now,i feel it immediately when a doctornurse lie in my face.


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## eric (Jul 8, 1999)

FYIfor the testing infoGastrointestinal Motility Disorders The UNC Breath Testing Center There are 3 breath tests available at the UNC Breath Testing Center to help diagnose motility disorders. http://www.med.unc.edu/wrkunits/2depts/med...gidc/breath.htm Interesting to note."Hydrogen Breath Test:for bacterial overgrowth tests for bacteria in the small bowel. "Indications "diarrhea, abdominal bloating""Hydrogen Breath Test for lactose:intolerance tests for intolerance to milk."Indications "abdominal pain, abdominal bloating, diarrhea, nausea and/or vomiting"


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## eric (Jul 8, 1999)

FYIfor the testing infoGastrointestinal Motility Disorders The UNC Breath Testing Center There are 3 breath tests available at the UNC Breath Testing Center to help diagnose motility disorders. http://www.med.unc.edu/wrkunits/2depts/med...gidc/breath.htm Interesting to note."Hydrogen Breath Test:for bacterial overgrowth tests for bacteria in the small bowel. "Indications "diarrhea, abdominal bloating""Hydrogen Breath Test for lactose:intolerance tests for intolerance to milk."Indications "abdominal pain, abdominal bloating, diarrhea, nausea and/or vomiting"


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## SpAsMaN* (May 11, 2002)

I remember the day i had my colonoscopy,after it i start to work and felt so weak because i had NOTHING in my bowel.OF COURSE,nobody warn me about this possibility or to suggest a day off after a colono.


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## SpAsMaN* (May 11, 2002)

I remember the day i had my colonoscopy,after it i start to work and felt so weak because i had NOTHING in my bowel.OF COURSE,nobody warn me about this possibility or to suggest a day off after a colono.


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## skinny (Jul 27, 2002)

bonniei: What do you mean by double peak?eric:FYISmall intestinal bacterial overgrowth: a framework for understanding irritable bowel syndrome http://tinyurl.com/4u2uz skinny


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## skinny (Jul 27, 2002)

bonniei: What do you mean by double peak?eric:FYISmall intestinal bacterial overgrowth: a framework for understanding irritable bowel syndrome http://tinyurl.com/4u2uz skinny


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## eric (Jul 8, 1999)

I know about that Skinny. However, that abstract doesn't mean much without the whole paper. It was also just a search this doctor did on pubmed and medline for the words bloating for the framework.







You should read this one also. Although most of it is known, the authors layed it out well. http://www.pulsus.com/Gastro/18_10/andr_ed.htm but also a newer study. Part of all this is figureing out the differences in PI IBS and IBS in the general population.Elevated vasoactive intestinal peptide concentrations in patients with irritable bowel syndrome."In conclusion, no evidence of inflammation was detected in irritable bowel patients, but elevated vasoactive intestinal peptide concentrations were observed in both studies and might represent a potential diagnostic tool for irritable bowel syndrome."However, when you get down to it, much of this is also complex. And SIBO is also caused itself by abnormal motilityLactose Intolerance and Small Bowel Bacterial Overgrowth in IBS http://www.med.unc.edu/wrkunits/2depts/med...intolerance.pdf


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## eric (Jul 8, 1999)

I know about that Skinny. However, that abstract doesn't mean much without the whole paper. It was also just a search this doctor did on pubmed and medline for the words bloating for the framework.







You should read this one also. Although most of it is known, the authors layed it out well. http://www.pulsus.com/Gastro/18_10/andr_ed.htm but also a newer study. Part of all this is figureing out the differences in PI IBS and IBS in the general population.Elevated vasoactive intestinal peptide concentrations in patients with irritable bowel syndrome."In conclusion, no evidence of inflammation was detected in irritable bowel patients, but elevated vasoactive intestinal peptide concentrations were observed in both studies and might represent a potential diagnostic tool for irritable bowel syndrome."However, when you get down to it, much of this is also complex. And SIBO is also caused itself by abnormal motilityLactose Intolerance and Small Bowel Bacterial Overgrowth in IBS http://www.med.unc.edu/wrkunits/2depts/med...intolerance.pdf


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## bonniei (Jan 25, 2001)

There is supposed to be a double peak like this one. Click on the "Normal" album and then on the link SIBOoo1. http://photos.yahoo.com/bonniei2004 The first peak usually occurs around 60-80 mins after ingesting the lactulose. It indicates overgrowth in the small intestine. The second peak occurs later when the lactulose reaches the large intestine


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## bonniei (Jan 25, 2001)

There is supposed to be a double peak like this one. Click on the "Normal" album and then on the link SIBOoo1. http://photos.yahoo.com/bonniei2004 The first peak usually occurs around 60-80 mins after ingesting the lactulose. It indicates overgrowth in the small intestine. The second peak occurs later when the lactulose reaches the large intestine


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## Talissa (Apr 10, 2004)

Joanofarc, "this too shall pass"...really hope you're feeling better today. Eric, from the study you quote, " no evidence of inflammation was detected in irritable bowel patients"--I don't think they did biopsies...?This is too good. I posted this article yesterday in "news & abstracts", but it deserves to more than just Eric's link for this discussion...From this month's Canadian Journal of Gastroenterology(REALLY good article)~"...IBS therefore may begin as an inciting event injuring the bowel followed by an inability to down-regulate the subsequent inflammation. The reason for this ongoing inflammation is not clear, but interestingly, patients with IBS are less likely to have high-producer IL-10 gene alleles (40), similar to patients with inflammatory bowel disease. IL-10 plays a significant anti-inflammatory role; if IL-10 were produced in low levels, mild inflammation could persist......Other potential causes of continued low-level inflammation in the GI tract include food allergies and changes in bacterial microflora. Allergic reactions can evoke inflammatory cell infiltration in the GI tract (41), but the prevalence of food allergies in IBS is unclear (42). Gut microflora may be altered in patients with IBS (43); some findings suggest that IBS patients may have intestinal bacterial overgrowth (44) and increased colonic fermentation (45). ...Much remains unknown about the potential causes of IBS. There may not be a unifying hypothesis to link all the aspects of this diverse syndrome. Nevertheless, markers of low-grade inflammation, which were initially found in diarrhea-predominant and postinfectious cases of IBS, are increasingly being found in constipation-predominant patients as well. Thus, inflammation may figure as an underlying factor in visceral hypersensitivity in more cases of IBS than previously was suspected. These intriguing inroads may be the key to our understanding of the basis for the IBS and may yield exciting therapeutic possibilities." http://www.pulsus.com/Gastro/18_10/andr_ed.htm


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## Talissa (Apr 10, 2004)

Joanofarc, "this too shall pass"...really hope you're feeling better today. Eric, from the study you quote, " no evidence of inflammation was detected in irritable bowel patients"--I don't think they did biopsies...?This is too good. I posted this article yesterday in "news & abstracts", but it deserves to more than just Eric's link for this discussion...From this month's Canadian Journal of Gastroenterology(REALLY good article)~"...IBS therefore may begin as an inciting event injuring the bowel followed by an inability to down-regulate the subsequent inflammation. The reason for this ongoing inflammation is not clear, but interestingly, patients with IBS are less likely to have high-producer IL-10 gene alleles (40), similar to patients with inflammatory bowel disease. IL-10 plays a significant anti-inflammatory role; if IL-10 were produced in low levels, mild inflammation could persist......Other potential causes of continued low-level inflammation in the GI tract include food allergies and changes in bacterial microflora. Allergic reactions can evoke inflammatory cell infiltration in the GI tract (41), but the prevalence of food allergies in IBS is unclear (42). Gut microflora may be altered in patients with IBS (43); some findings suggest that IBS patients may have intestinal bacterial overgrowth (44) and increased colonic fermentation (45). ...Much remains unknown about the potential causes of IBS. There may not be a unifying hypothesis to link all the aspects of this diverse syndrome. Nevertheless, markers of low-grade inflammation, which were initially found in diarrhea-predominant and postinfectious cases of IBS, are increasingly being found in constipation-predominant patients as well. Thus, inflammation may figure as an underlying factor in visceral hypersensitivity in more cases of IBS than previously was suspected. These intriguing inroads may be the key to our understanding of the basis for the IBS and may yield exciting therapeutic possibilities." http://www.pulsus.com/Gastro/18_10/andr_ed.htm


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## Talissa (Apr 10, 2004)

I just got the pdf full article, ï¿½Elevated vasoactive intestinal peptide concentrations in patients with irritable bowel syndromeï¿½.They did do biopsies--from the rectum only and they admit this may not reflect the entire colon wall. They did 2 studies with 16 IBS patients--very small sample. They didnï¿½t find microscopic colitis(a form of IBD), which btw, differs from another study where out of 30 random IBS patients, 7 were found to have MC on biopsies: ( http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12891921 )Anyways, they said their study compared to another study were a 30% increase in mucosal inflammation was found in IBS patients. They called this ï¿½mild inflammation.ï¿½ They called it ï¿½nonsignificantï¿½ (bias? & not even a word reallyï¿½) Interestingly, they also found no difference in pain thresholds compared to controls.They concluded IBS was a hormonal problem(VIPs), nothing to do with inflammation. Who knows. But it was a VERY small study, with the researchers dismissing the inflammation they found. It sounds very biased. But I imagine many studies are when the researchers want a ctn outcome before the study begins...


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## Talissa (Apr 10, 2004)

I just got the pdf full article, ï¿½Elevated vasoactive intestinal peptide concentrations in patients with irritable bowel syndromeï¿½.They did do biopsies--from the rectum only and they admit this may not reflect the entire colon wall. They did 2 studies with 16 IBS patients--very small sample. They didnï¿½t find microscopic colitis(a form of IBD), which btw, differs from another study where out of 30 random IBS patients, 7 were found to have MC on biopsies: ( http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12891921 )Anyways, they said their study compared to another study were a 30% increase in mucosal inflammation was found in IBS patients. They called this ï¿½mild inflammation.ï¿½ They called it ï¿½nonsignificantï¿½ (bias? & not even a word reallyï¿½) Interestingly, they also found no difference in pain thresholds compared to controls.They concluded IBS was a hormonal problem(VIPs), nothing to do with inflammation. Who knows. But it was a VERY small study, with the researchers dismissing the inflammation they found. It sounds very biased. But I imagine many studies are when the researchers want a ctn outcome before the study begins...


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## skinny (Jul 27, 2002)

bonniei: That graph came out too small. What was it in reference to? Is this what normal people's (non IBS) graph typically look like?eric:


> quote:I know about that Skinny.However, that abstract doesn't mean much without the whole paper. It was also just a search this doctor did on pubmed and medline for the words bloating for the framework


Eric, what are you talking about? Henry Lin is a gastrointestinal motility specialist and associate professor of medicine in the Keck School of Medicine of USC. He's worked with Mark Pimentel and others on SIBO and motility disorders and published a few studies with them. "Just a search"? No, it's not just hacking away queries on medical databases. Lin has clinical experience in what he's writing about. It's interesting how you try to discredit him.


> quote:You should read this one also. Although most of it is known, the authors layed it out well. http://www.pulsus.com/Gastro/18_10/andr_ed.htm


I read it. Did you notice this at the end?"Much remains unknown about the potential causes of IBS. There may not be a unifying hypothesis to link all the aspects of this diverse syndrome. Nevertheless, markers of low-grade inflammation, which were initially found in diarrhea-predominant and postinfectious cases of IBS, are increasingly being found in constipation-predominant patients as well. Thus, inflammation may figure as an underlying factor in visceral hypersensitivity in more cases of IBS than previously was suspected."This is essentially the same thing Lin concludes except he is using SIBO as a framework. I believe that SIBO and inflammation are a subset of IBS.


> quote:Lactose Intolerance and Small Bowel Bacterial Overgrowth in IBS http://www.med.unc.edu/wrkunits/2depts/med...intolerance.pdf


This has some interesting critiques which is fine because these kinds of studies need to repeated over and refined with different variables.Here's another relevant abstract:Breath testing to evaluate lactose intolerance in irritable bowel syndrome correlates with lactulose testing and may not reflect true lactose malabsorption. http://tinyurl.com/5d24z skinny


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## skinny (Jul 27, 2002)

bonniei: That graph came out too small. What was it in reference to? Is this what normal people's (non IBS) graph typically look like?eric:


> quote:I know about that Skinny.However, that abstract doesn't mean much without the whole paper. It was also just a search this doctor did on pubmed and medline for the words bloating for the framework


Eric, what are you talking about? Henry Lin is a gastrointestinal motility specialist and associate professor of medicine in the Keck School of Medicine of USC. He's worked with Mark Pimentel and others on SIBO and motility disorders and published a few studies with them. "Just a search"? No, it's not just hacking away queries on medical databases. Lin has clinical experience in what he's writing about. It's interesting how you try to discredit him.


> quote:You should read this one also. Although most of it is known, the authors layed it out well. http://www.pulsus.com/Gastro/18_10/andr_ed.htm


I read it. Did you notice this at the end?"Much remains unknown about the potential causes of IBS. There may not be a unifying hypothesis to link all the aspects of this diverse syndrome. Nevertheless, markers of low-grade inflammation, which were initially found in diarrhea-predominant and postinfectious cases of IBS, are increasingly being found in constipation-predominant patients as well. Thus, inflammation may figure as an underlying factor in visceral hypersensitivity in more cases of IBS than previously was suspected."This is essentially the same thing Lin concludes except he is using SIBO as a framework. I believe that SIBO and inflammation are a subset of IBS.


> quote:Lactose Intolerance and Small Bowel Bacterial Overgrowth in IBS http://www.med.unc.edu/wrkunits/2depts/med...intolerance.pdf


This has some interesting critiques which is fine because these kinds of studies need to repeated over and refined with different variables.Here's another relevant abstract:Breath testing to evaluate lactose intolerance in irritable bowel syndrome correlates with lactulose testing and may not reflect true lactose malabsorption. http://tinyurl.com/5d24z skinny


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## eric (Jul 8, 1999)

Skinny, I don't want to take over the thread. But this author left a lot out and the study was only through searches from may 2004. Small intestinal bacterial overgrowth: a framework for understanding irritable bowel syndrome."EVIDENCE ACQUISITION: Ovid MEDLINE was searched through May 2004 for relevant English-language articles beginning with those related to bloating, gas, and IBS. Bibliographies of pertinent articles and books were also scanned for additional suitable citations."and only for those relevant to bloating gas and IBS. This seems biased somewhat to me anyway.Also how do you explain the part about altered motilty causing SIBO? What causes the altered motility to cause sibo in the first place? Why have they moved from just altered motilty as an explanation for IBS, because it did not explain everything to MOTILITY, VISCERAL HYPERSENSITIVITY, and BRAIN-GUT AXIS dysregulation?www.med.unc.edu/medicine/fgidc/ historyfunctionaldisorders.pdfYou should also read this really important article in the newest "Digestivehealth matters" from the IFFGD, do you get those?This article, "Viceral Sensations and Brain Gut Mechansims" from DR Mayer at UCLA. I think you might find it highly enlightening.


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## eric (Jul 8, 1999)

Skinny, I don't want to take over the thread. But this author left a lot out and the study was only through searches from may 2004. Small intestinal bacterial overgrowth: a framework for understanding irritable bowel syndrome."EVIDENCE ACQUISITION: Ovid MEDLINE was searched through May 2004 for relevant English-language articles beginning with those related to bloating, gas, and IBS. Bibliographies of pertinent articles and books were also scanned for additional suitable citations."and only for those relevant to bloating gas and IBS. This seems biased somewhat to me anyway.Also how do you explain the part about altered motilty causing SIBO? What causes the altered motility to cause sibo in the first place? Why have they moved from just altered motilty as an explanation for IBS, because it did not explain everything to MOTILITY, VISCERAL HYPERSENSITIVITY, and BRAIN-GUT AXIS dysregulation?www.med.unc.edu/medicine/fgidc/ historyfunctionaldisorders.pdfYou should also read this really important article in the newest "Digestivehealth matters" from the IFFGD, do you get those?This article, "Viceral Sensations and Brain Gut Mechansims" from DR Mayer at UCLA. I think you might find it highly enlightening.


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## eric (Jul 8, 1999)

I talked to an author of the VIP study. They are certainly not bias and lead investigators in IBS, as a matter of fact they are less biased then the majority of researchers, because there focus is on the BIG PICTURE of IBS and not more narrowally focused research. The VIP study was a somewhat older study just published now. Second study to find elavated VIP, yet that does not in anyway explain the big picture, either, just an observation. They only looked at inflammation in the outer bowel layer (epithelium) which seems to be working normally and did not find inflammation in that small study in those IBSers. Inflammation has been found mainly in PI IBS, in deeper tissues of the bowel wall, but some evidence in some subgroups, of inflammation in d and c and d/c patinets, mainly mast cells. Mast cells can be inflammed by chronic stressors without a pathogen also. It is hard to study inner layers of the bowel wall because it may cause infection or other issues in the study subjects and is very invasive. Larger studies are still needed. At this point inflammation has not been found in all IBSers. IT is also believed just to contribute to the problem. I personally thought it might even contribute to getting IBS, by these procedures and mucking with the bowel wall.There is still the problem of inflammation not being a biological marker in ALL of IBS, because it does not always cause pain a must for an IBS diagnoses. IT seems to contribute to it in some IBS patients, specifically PI IBSers and some evidence in subgroups of IBSers.There can be inflammation in the digestive tract with no pain. That is a fact. It is a must for the diagnoses of IBS to have pain or discomfort.Aspirin, can even cause gi inflammation without pain. Some people with UC have higher viceral pain thresholds then IBS and have inflammation and all people with celiac have inflammation and not all of them have pain.The pimental studies have not been replicated by other investigators, in fact researchers have had a hard time replicating them. The research on IBS has lead to different subgroups with different mechanisms and cellular changes causing different symptoms, leading to altered bowel motility and viceral hypersensitivity and brain gut axis dysregulation.This paper is consistent with these aspects.Simmering innards: Does irritable bowel syndrome have an immunological basis?and modern research still understands IBS as,"The cause of IBS is yet to be determined. However, modern research understands IBS as a disorder of increased reactivity of the bowel, visceral hypersensitivity and dysfunction of the brain-gut axis. There are subgroups being defined as well, including post-infectious IBS which can lead to IBS symptoms. Other work using brain imaging shows that the pain regulation center of the brain (cingulate cortex) can be impaired, as well as good evidence for there being abnormalities in motility which can at least in part explain the diarrhea and constipation. So finding a specific "cause" of IBS has grown out of general interest in place of understanding physiological subgroups that may become amenable to more specific treatments. Hope that helps.Doug " http://www.ibshealth.com/ibs_foods_2.htm


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## eric (Jul 8, 1999)

I talked to an author of the VIP study. They are certainly not bias and lead investigators in IBS, as a matter of fact they are less biased then the majority of researchers, because there focus is on the BIG PICTURE of IBS and not more narrowally focused research. The VIP study was a somewhat older study just published now. Second study to find elavated VIP, yet that does not in anyway explain the big picture, either, just an observation. They only looked at inflammation in the outer bowel layer (epithelium) which seems to be working normally and did not find inflammation in that small study in those IBSers. Inflammation has been found mainly in PI IBS, in deeper tissues of the bowel wall, but some evidence in some subgroups, of inflammation in d and c and d/c patinets, mainly mast cells. Mast cells can be inflammed by chronic stressors without a pathogen also. It is hard to study inner layers of the bowel wall because it may cause infection or other issues in the study subjects and is very invasive. Larger studies are still needed. At this point inflammation has not been found in all IBSers. IT is also believed just to contribute to the problem. I personally thought it might even contribute to getting IBS, by these procedures and mucking with the bowel wall.There is still the problem of inflammation not being a biological marker in ALL of IBS, because it does not always cause pain a must for an IBS diagnoses. IT seems to contribute to it in some IBS patients, specifically PI IBSers and some evidence in subgroups of IBSers.There can be inflammation in the digestive tract with no pain. That is a fact. It is a must for the diagnoses of IBS to have pain or discomfort.Aspirin, can even cause gi inflammation without pain. Some people with UC have higher viceral pain thresholds then IBS and have inflammation and all people with celiac have inflammation and not all of them have pain.The pimental studies have not been replicated by other investigators, in fact researchers have had a hard time replicating them. The research on IBS has lead to different subgroups with different mechanisms and cellular changes causing different symptoms, leading to altered bowel motility and viceral hypersensitivity and brain gut axis dysregulation.This paper is consistent with these aspects.Simmering innards: Does irritable bowel syndrome have an immunological basis?and modern research still understands IBS as,"The cause of IBS is yet to be determined. However, modern research understands IBS as a disorder of increased reactivity of the bowel, visceral hypersensitivity and dysfunction of the brain-gut axis. There are subgroups being defined as well, including post-infectious IBS which can lead to IBS symptoms. Other work using brain imaging shows that the pain regulation center of the brain (cingulate cortex) can be impaired, as well as good evidence for there being abnormalities in motility which can at least in part explain the diarrhea and constipation. So finding a specific "cause" of IBS has grown out of general interest in place of understanding physiological subgroups that may become amenable to more specific treatments. Hope that helps.Doug " http://www.ibshealth.com/ibs_foods_2.htm


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## eric (Jul 8, 1999)

Joann, didn't mean to hijack this thread, my applogies and I hope your feeling better now.


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## eric (Jul 8, 1999)

Joann, didn't mean to hijack this thread, my applogies and I hope your feeling better now.


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## Talissa (Apr 10, 2004)

Hey Eric, that's cool you talked to one of the study's authors! Still think there was bias, but whatever. Lin has bias too... And you're right, the paper Lin wrote re: bacterial overgrowth published in JAMA is an editorial based on his and others' research. I bought it for $12(not bad). From his research Lin believes altered motility is a RESULT of SIBO, not the cause. Others disagree with him.Lin's research though is unique, because its solely funded by some extremely wealthy family, not an Rx company hidden away......but more research is needed...BEEP...this is a recording...







Joan/Susan--WHERE ARE YOU!? Hope you post soon, ya nut. We're all going to start worrying abt you and the stress is going to cause us all flares, and it'll be all YOUR fault!







Write soon, Love, T-


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## Talissa (Apr 10, 2004)

Hey Eric, that's cool you talked to one of the study's authors! Still think there was bias, but whatever. Lin has bias too... And you're right, the paper Lin wrote re: bacterial overgrowth published in JAMA is an editorial based on his and others' research. I bought it for $12(not bad). From his research Lin believes altered motility is a RESULT of SIBO, not the cause. Others disagree with him.Lin's research though is unique, because its solely funded by some extremely wealthy family, not an Rx company hidden away......but more research is needed...BEEP...this is a recording...







Joan/Susan--WHERE ARE YOU!? Hope you post soon, ya nut. We're all going to start worrying abt you and the stress is going to cause us all flares, and it'll be all YOUR fault!







Write soon, Love, T-


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## bonniei (Jan 25, 2001)

Hi skinny I don't know if you can download it and then enlarge it. And I hope you did click on SIBOoo1. If you mean you can't read the units and the caption, this is the graph of a person showing SIBO. Idon't think IBS or nonIBS matters so much in a graph On the x-axis the units are 10 mins apart and thogh the marked ones are 20 mins apart.The units on the y-axis are 5 ppm apart The graph is flat for the first 40 mins at 0 ppm.The first peak is around 60 mins at a little over 15 ppm. The first valley is at 90 mins at about 12 ppm. After that there is a peak, a valley, a peak, a valley and a peak (which are really considered as one peak because the valleysare not substantial) and then it proceeds to fall gradually to about 11ppm at 350 mins into the test. So this second peak which is made up of 3 valleys and 2 peaks , has all the three peaks over 20 ppm ad the valleys between 17 and 19 ppm. Hope that helps.If I can find the pic again I'll try enlarging it while scanning it and then upload it.


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## bonniei (Jan 25, 2001)

Hi skinny I don't know if you can download it and then enlarge it. And I hope you did click on SIBOoo1. If you mean you can't read the units and the caption, this is the graph of a person showing SIBO. Idon't think IBS or nonIBS matters so much in a graph On the x-axis the units are 10 mins apart and thogh the marked ones are 20 mins apart.The units on the y-axis are 5 ppm apart The graph is flat for the first 40 mins at 0 ppm.The first peak is around 60 mins at a little over 15 ppm. The first valley is at 90 mins at about 12 ppm. After that there is a peak, a valley, a peak, a valley and a peak (which are really considered as one peak because the valleysare not substantial) and then it proceeds to fall gradually to about 11ppm at 350 mins into the test. So this second peak which is made up of 3 valleys and 2 peaks , has all the three peaks over 20 ppm ad the valleys between 17 and 19 ppm. Hope that helps.If I can find the pic again I'll try enlarging it while scanning it and then upload it.


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## eric (Jul 8, 1999)

If you email me Talissa for the VIP study I will send it to you. I guarantee you also there not bias. They have nothing to be bias about. They are also already world leading researchers in their fields. More importantly they actually care and want to learn and find out more about IBS. They were also just awarded an NIH award for"$4.3 million over a five-year period to establish a Gastrointestinal Biopsychosocial Research Center focused on the causes and treatment of functional gastrointestinal (GI) disorders." http://www.ibsgroup.org/ubb/ultimatebb.php...c;f=10;t=000991 I have been talking to them for over three years now on a regular basis.


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## eric (Jul 8, 1999)

If you email me Talissa for the VIP study I will send it to you. I guarantee you also there not bias. They have nothing to be bias about. They are also already world leading researchers in their fields. More importantly they actually care and want to learn and find out more about IBS. They were also just awarded an NIH award for"$4.3 million over a five-year period to establish a Gastrointestinal Biopsychosocial Research Center focused on the causes and treatment of functional gastrointestinal (GI) disorders." http://www.ibsgroup.org/ubb/ultimatebb.php...c;f=10;t=000991 I have been talking to them for over three years now on a regular basis.


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## Talissa (Apr 10, 2004)

> quote:I have been talking to them for over three years now on a regular basis.


Well I guess I sure stepped in it, didn't I...







As I said earlier, I read the report this am, Eric, but thanks for offering--could have saved me the $25!I'm sure they've done much to help us IBSr's... But with all due respect, if they aren't biased, how could they find what they term "mild inflammation" in the IBS patients--known as low grade inflammation to others--but then in the abstract, they write "we found no inflammation".And is a study with 16 people something to hang your hat on? And a rectum sample only? Come on. And then they reference a study where occult colitis was found in IBS(with inc'd IL-1), but instead of saying may be its because the biopsies were actually from the colon wall, they infer maybe its because the IBS patients live in Canada.Seriously, it doesn't sound biased to you? With ZERO ill-intent, Tal


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## Talissa (Apr 10, 2004)

> quote:I have been talking to them for over three years now on a regular basis.


Well I guess I sure stepped in it, didn't I...







As I said earlier, I read the report this am, Eric, but thanks for offering--could have saved me the $25!I'm sure they've done much to help us IBSr's... But with all due respect, if they aren't biased, how could they find what they term "mild inflammation" in the IBS patients--known as low grade inflammation to others--but then in the abstract, they write "we found no inflammation".And is a study with 16 people something to hang your hat on? And a rectum sample only? Come on. And then they reference a study where occult colitis was found in IBS(with inc'd IL-1), but instead of saying may be its because the biopsies were actually from the colon wall, they infer maybe its because the IBS patients live in Canada.Seriously, it doesn't sound biased to you? With ZERO ill-intent, Tal


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## eric (Jul 8, 1999)

Tal, there were nine authors to the study.These are peer reviewed abstracts.No offence but these abstracts are hard to interpret like the experts here who know what they are talking about.Read this doctors biography. This is just one of them. I can say again I guarantee they are not biased, they are a recgonized leading center in the US for one, and also train visiting physcians from all over the world for another and if you look at the majority of IBS abstracts most of these doctors are referenced or asked to comment on new IBS research. William E. Whitehead, PhDCodirector of the UNC center for functional gi and motility disorders.Prior to that he was"Prior to coming to UNC, Dr. Whitehead was at Johns Hopkins School of Medicine for 15 years, where he was chief of the Gastrointestinal Physiology Laboratory at the Bayview Medical Center. He also headed a research program on vomiting disorders, irritable bowel syndrome (IBS), and incontinence."You don't get to be "chief of the Gastrointestinal Physiology Laboratory at the Bayview Medical Center." unless you know what your doing and talking about. For one he is one of the worlds authorities on constipation.But read the rest of his whole bio. and he is only one of the nine authors of the study. http://www.med.unc.edu/wrkunits/2depts/med...dc/whitehed.htm Read Drossman bio, the other Co-Director of the UNC Center.Douglas A. Drossman, MD http://www.med.unc.edu/wrkunits/2depts/med...dc/drossman.htm Just between these two they have published more then 700 books and that is just part of their careers and who they are in all this research.Drossman is "Chair of the Executive Committee (since 1989) and President (since 2003) of the Rome Foundation Editor of Rome II: The Functional Gastrointestinal Disorders, 2nd edition; senior editor for Rome III to be published in 2006 "Read the list of "Collaborating Investigators and Clinicians" http://www.med.unc.edu/wrkunits/2depts/med...ectr_collab.htm and also download their newsletter here which I would read if I were you, because it is state of the art on all this and its free, you won't regret it.Digest Newsletter http://www.med.unc.edu/wrkunits/2depts/med...n_materials.htm Two centers in the US have gotten major funding right now from the NIH for a total of over 8 million dollars in IBS research and other research in functional disorders and disease, UCLA a brand new state of the art center. UCLA/CURE Neuroenteric Disease Program."The grant has significant implications for a better understanding of such common gastrointestinal disorders as irritable bowel syndrome, Functional dyspepsia and common urological disorders such as irritable bladder syndrome ("interstitial cystitis"). In addition, a major research focus is on neurobiological mechanisms underlying the greater vulnerability of women to develop some of these disorders.The center grant involves investigators and consultants from four different institutions: UCLA, VAGLAHS, Ohio State University and University of Pittsburgh who are interacting closely to accomplish the principal goals of the proposed studies. "and the NEW UNC grant.These centers which already had connections, are setting up new and better collaborations for research and connecting the different centers electronically and starting a huge database and research from around the world. They recieved these grants because of their recognized world excellence in the fields.I say this, because they are out to help us all. I would hope and think we should be careful about the ones that really do care and really aren't biased and try to understand who is who in all this and the research. Tal, I can tell you also, if you ever met them, I think you would be very impressed at what they know and how nice and down to earth they really are and why they care.Drossman wrote this a while ago to, you ought to read that as well. It was in Gastroenterology.Medicine Has Become http://www.ibsgroup.org/cgi-local/ubbcgi/u...c&f=10&t=001004


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## eric (Jul 8, 1999)

Tal, there were nine authors to the study.These are peer reviewed abstracts.No offence but these abstracts are hard to interpret like the experts here who know what they are talking about.Read this doctors biography. This is just one of them. I can say again I guarantee they are not biased, they are a recgonized leading center in the US for one, and also train visiting physcians from all over the world for another and if you look at the majority of IBS abstracts most of these doctors are referenced or asked to comment on new IBS research. William E. Whitehead, PhDCodirector of the UNC center for functional gi and motility disorders.Prior to that he was"Prior to coming to UNC, Dr. Whitehead was at Johns Hopkins School of Medicine for 15 years, where he was chief of the Gastrointestinal Physiology Laboratory at the Bayview Medical Center. He also headed a research program on vomiting disorders, irritable bowel syndrome (IBS), and incontinence."You don't get to be "chief of the Gastrointestinal Physiology Laboratory at the Bayview Medical Center." unless you know what your doing and talking about. For one he is one of the worlds authorities on constipation.But read the rest of his whole bio. and he is only one of the nine authors of the study. http://www.med.unc.edu/wrkunits/2depts/med...dc/whitehed.htm Read Drossman bio, the other Co-Director of the UNC Center.Douglas A. Drossman, MD http://www.med.unc.edu/wrkunits/2depts/med...dc/drossman.htm Just between these two they have published more then 700 books and that is just part of their careers and who they are in all this research.Drossman is "Chair of the Executive Committee (since 1989) and President (since 2003) of the Rome Foundation Editor of Rome II: The Functional Gastrointestinal Disorders, 2nd edition; senior editor for Rome III to be published in 2006 "Read the list of "Collaborating Investigators and Clinicians" http://www.med.unc.edu/wrkunits/2depts/med...ectr_collab.htm and also download their newsletter here which I would read if I were you, because it is state of the art on all this and its free, you won't regret it.Digest Newsletter http://www.med.unc.edu/wrkunits/2depts/med...n_materials.htm Two centers in the US have gotten major funding right now from the NIH for a total of over 8 million dollars in IBS research and other research in functional disorders and disease, UCLA a brand new state of the art center. UCLA/CURE Neuroenteric Disease Program."The grant has significant implications for a better understanding of such common gastrointestinal disorders as irritable bowel syndrome, Functional dyspepsia and common urological disorders such as irritable bladder syndrome ("interstitial cystitis"). In addition, a major research focus is on neurobiological mechanisms underlying the greater vulnerability of women to develop some of these disorders.The center grant involves investigators and consultants from four different institutions: UCLA, VAGLAHS, Ohio State University and University of Pittsburgh who are interacting closely to accomplish the principal goals of the proposed studies. "and the NEW UNC grant.These centers which already had connections, are setting up new and better collaborations for research and connecting the different centers electronically and starting a huge database and research from around the world. They recieved these grants because of their recognized world excellence in the fields.I say this, because they are out to help us all. I would hope and think we should be careful about the ones that really do care and really aren't biased and try to understand who is who in all this and the research. Tal, I can tell you also, if you ever met them, I think you would be very impressed at what they know and how nice and down to earth they really are and why they care.Drossman wrote this a while ago to, you ought to read that as well. It was in Gastroenterology.Medicine Has Become http://www.ibsgroup.org/cgi-local/ubbcgi/u...c&f=10&t=001004


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## skinny (Jul 27, 2002)

bonniei: It's ok, you don't have to rescan the graph.eric:


> quote:and only for those relevant to bloating gas and IBS. This seems biased somewhat to me anyway.


Of course it's biased.


> quote:Also how do you explain the part about altered motilty causing SIBO? What causes the altered motility to cause sibo in the first place? Why have they moved from just altered motilty as an explanation for IBS, because it did not explain everything to MOTILITY, VISCERAL HYPERSENSITIVITY, and BRAIN-GUT AXIS dysregulation?


It can happen vice versa - SIBO causing the altered motility. In Pimentel's studies some of his patients that had SIBO eradicated also had normal bowel motility. For most of them this was temporary lasting a month or so, but then there are cases where the IBS was cured [or in remission if you will].I don't have explanations for every case because simply I don't know, but thanks to Pimentel, Lin, and others we are getting a better understanding of IBS.


> quote:There is still the problem of inflammation not being a biological marker in ALL of IBS, because it does not always cause pain a must for an IBS diagnoses. IT seems to contribute to it in some IBS patients, specifically PI IBSers and some evidence in subgroups of IBSers.There can be inflammation in the digestive tract with no pain. That is a fact. It is a must for the diagnoses of IBS to have pain or discomfort.


Eric, you mentioned a few times that your IBS is in remission (although you mentioned a couple times your symptoms are 90% better which doesn't make sense to me). If you have no pain or discomfort, does that mean you no longer have IBS? Oh wait you are going by the Rome II diagnostic criteria. So what? That definition could change in the future. Pain and discomfort are subjective words.


> quote:The pimental studies have not been replicated by other investigators, in fact researchers have had a hard time replicating them.


Tell me Eric: What other GI researchers have attempted to replicate the SIBO studies? Drossman, any of the other UNC experts? Before we talk about having a hard time replicating the studies, I have to see some evidence that an attempt has been made. I may be wrong, but I see zero effort on the UNC researchers to replicate the studies.Isn't it funny how none of the researchers who made ground breaking discoveries in SIBO are on the Rome committee? That seems really biased to me.skinnyedit: minor spelling correction


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## skinny (Jul 27, 2002)

bonniei: It's ok, you don't have to rescan the graph.eric:


> quote:and only for those relevant to bloating gas and IBS. This seems biased somewhat to me anyway.


Of course it's biased.


> quote:Also how do you explain the part about altered motilty causing SIBO? What causes the altered motility to cause sibo in the first place? Why have they moved from just altered motilty as an explanation for IBS, because it did not explain everything to MOTILITY, VISCERAL HYPERSENSITIVITY, and BRAIN-GUT AXIS dysregulation?


It can happen vice versa - SIBO causing the altered motility. In Pimentel's studies some of his patients that had SIBO eradicated also had normal bowel motility. For most of them this was temporary lasting a month or so, but then there are cases where the IBS was cured [or in remission if you will].I don't have explanations for every case because simply I don't know, but thanks to Pimentel, Lin, and others we are getting a better understanding of IBS.


> quote:There is still the problem of inflammation not being a biological marker in ALL of IBS, because it does not always cause pain a must for an IBS diagnoses. IT seems to contribute to it in some IBS patients, specifically PI IBSers and some evidence in subgroups of IBSers.There can be inflammation in the digestive tract with no pain. That is a fact. It is a must for the diagnoses of IBS to have pain or discomfort.


Eric, you mentioned a few times that your IBS is in remission (although you mentioned a couple times your symptoms are 90% better which doesn't make sense to me). If you have no pain or discomfort, does that mean you no longer have IBS? Oh wait you are going by the Rome II diagnostic criteria. So what? That definition could change in the future. Pain and discomfort are subjective words.


> quote:The pimental studies have not been replicated by other investigators, in fact researchers have had a hard time replicating them.


Tell me Eric: What other GI researchers have attempted to replicate the SIBO studies? Drossman, any of the other UNC experts? Before we talk about having a hard time replicating the studies, I have to see some evidence that an attempt has been made. I may be wrong, but I see zero effort on the UNC researchers to replicate the studies.Isn't it funny how none of the researchers who made ground breaking discoveries in SIBO are on the Rome committee? That seems really biased to me.skinnyedit: minor spelling correction


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## Talissa (Apr 10, 2004)

Okay Susan, now I'm sorta kinda worried abt you. Hope all's well and you check in soon...Skinny, Great points. Esp the part abt the pain, as mine is gone now, but I still have IBS...not acc to current "Rome" though...will have to see if that changes also in Rome III.Found this awhile back...Drossman 2004:"The "Organification" of Functional GI Disorders""I recently attended an international meeting that focused on potential new mechanisms to help understand the functional gastrointestinal (GI) disorders. It was exciting to hear experts address new concepts on how: 1) mucosal inflammation could alter neurotransmitter, ion channel, or nerve growth factor activity and early gene expression, all of which might influence motility and visceral sensation;..." http://www.med.unc.edu/medicine/fgidc/organification.htm Of course then he goes on and sounds just like Eric, or better stated, Eric sounds just like him...Just interesting that he acknowledges the role mucosal inflammation can have in IBS. And this inflammation can be caused by gut flora dysbiosis as stated in the above canadian j gastroenterology article posted above...One day Drossman may even utter...bacterial overgrowth!!!Stranger things have happened...


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## Talissa (Apr 10, 2004)

Okay Susan, now I'm sorta kinda worried abt you. Hope all's well and you check in soon...Skinny, Great points. Esp the part abt the pain, as mine is gone now, but I still have IBS...not acc to current "Rome" though...will have to see if that changes also in Rome III.Found this awhile back...Drossman 2004:"The "Organification" of Functional GI Disorders""I recently attended an international meeting that focused on potential new mechanisms to help understand the functional gastrointestinal (GI) disorders. It was exciting to hear experts address new concepts on how: 1) mucosal inflammation could alter neurotransmitter, ion channel, or nerve growth factor activity and early gene expression, all of which might influence motility and visceral sensation;..." http://www.med.unc.edu/medicine/fgidc/organification.htm Of course then he goes on and sounds just like Eric, or better stated, Eric sounds just like him...Just interesting that he acknowledges the role mucosal inflammation can have in IBS. And this inflammation can be caused by gut flora dysbiosis as stated in the above canadian j gastroenterology article posted above...One day Drossman may even utter...bacterial overgrowth!!!Stranger things have happened...


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## SpAsMaN* (May 11, 2002)

Skinny,i'm a big beleiver in the altered motility theory as a cause of IBS.With a normal peristaltic,most of us would be:


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## SpAsMaN* (May 11, 2002)

Skinny,i'm a big beleiver in the altered motility theory as a cause of IBS.With a normal peristaltic,most of us would be:


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## skinny (Jul 27, 2002)

> quote:Okay Susan, now I'm sorta kinda worried abt you. Hope all's well and you check in soon...


Hey hope you are doing well too. It's pretty odd that you'd have a bad reaction to the lactulose. My test was for 90 minutes, and I didn't get a spike until the 90 min mark (it was nearly 20 ppm). Please try to get a copy of your test results and let us know what your graph looked like.Talissa:


> quote:Skinny, Great points. Esp the part abt the pain, as mine is gone now, but I still have IBS...not acc to current "Rome" though...will have to see if that changes also in Rome III.


Well to me it seems like there is a monopoly of what IBS is going to be defined as. It seems like Drossman is the head honcho on this and decides who gets who gets to go on the committee. I'm going to be very skeptical of the new Rome III if it doesn't incorporate significant findings in IBS research.


> quote:Of course then he goes on and sounds just like Eric, or better stated, Eric sounds just like him...Just interesting that he acknowledges the role mucosal inflammation can have in IBS. And this inflammation can be caused by gut flora dysbiosis as stated in the above canadian j gastroenterology article posted above...


Ya know I was thinking the same thing. Eric sounds a lot like Drossman, and it's probably because he's a friend. I understand how influential mentors can be and how hard it can be to criticize your own friends. However the way science works is that criticism is a good thing even among your own peers (but maybe not to their egos







) I believe there is a tendency to agree on issues when you are closely associated with someone.


> quote:One day Drossman may even utter...bacterial overgrowth!!!Stranger things have happened...


You wanna see something strange?







I just checked the link that Eric provided: http://www.med.unc.edu/wrkunits/2depts/med...n_materials.htm There is what appears to be an update to Drossman's bacterial overgrowth (August 2004?)New version: http://www.med.unc.edu/wrkunits/2depts/med...ibs_08_2004.pdf compare this with the older version which is still online (but not as a linked page)Old version: http://www.med.unc.edu/wrkunits/2depts/med...rowthandibs.htm If you read both versions carefully, there are some noticeable edits that look like an attempt to cover up some tracks.New version: It botches up the reference to Pimentel's study. The old version references the 2000 study and the new version references the 2003 study by actually talking about the 2000 study.The new version didn't update the limitations of the study except at point 2 where it acknowledges that the study is a double blind placebo controlled study. The old version criticized that it wasn't (which was true for the 2000 study).Here are Pimentel's two antibiotic/SIBO studies:Eradication of Small Intestinal Bacterial Overgrowth Reduces Symptoms of Irritable Bowel Syndrome (2000) http://www-east.elsevier.com/ajg/issues/9512/ajg3368fla.htm Normalization of lactulose breath testing correlates with symptom improvement in irritable bowel syndrome: a double-blind, randomized, placebo-controlled study. (2003) http://www.ncbi.nlm.nih.gov/entrez/query.f...2&dopt=Abstract Ah things that make you wanna go Hmmmm...


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## skinny (Jul 27, 2002)

> quote:Okay Susan, now I'm sorta kinda worried abt you. Hope all's well and you check in soon...


Hey hope you are doing well too. It's pretty odd that you'd have a bad reaction to the lactulose. My test was for 90 minutes, and I didn't get a spike until the 90 min mark (it was nearly 20 ppm). Please try to get a copy of your test results and let us know what your graph looked like.Talissa:


> quote:Skinny, Great points. Esp the part abt the pain, as mine is gone now, but I still have IBS...not acc to current "Rome" though...will have to see if that changes also in Rome III.


Well to me it seems like there is a monopoly of what IBS is going to be defined as. It seems like Drossman is the head honcho on this and decides who gets who gets to go on the committee. I'm going to be very skeptical of the new Rome III if it doesn't incorporate significant findings in IBS research.


> quote:Of course then he goes on and sounds just like Eric, or better stated, Eric sounds just like him...Just interesting that he acknowledges the role mucosal inflammation can have in IBS. And this inflammation can be caused by gut flora dysbiosis as stated in the above canadian j gastroenterology article posted above...


Ya know I was thinking the same thing. Eric sounds a lot like Drossman, and it's probably because he's a friend. I understand how influential mentors can be and how hard it can be to criticize your own friends. However the way science works is that criticism is a good thing even among your own peers (but maybe not to their egos







) I believe there is a tendency to agree on issues when you are closely associated with someone.


> quote:One day Drossman may even utter...bacterial overgrowth!!!Stranger things have happened...


You wanna see something strange?







I just checked the link that Eric provided: http://www.med.unc.edu/wrkunits/2depts/med...n_materials.htm There is what appears to be an update to Drossman's bacterial overgrowth (August 2004?)New version: http://www.med.unc.edu/wrkunits/2depts/med...ibs_08_2004.pdf compare this with the older version which is still online (but not as a linked page)Old version: http://www.med.unc.edu/wrkunits/2depts/med...rowthandibs.htm If you read both versions carefully, there are some noticeable edits that look like an attempt to cover up some tracks.New version: It botches up the reference to Pimentel's study. The old version references the 2000 study and the new version references the 2003 study by actually talking about the 2000 study.The new version didn't update the limitations of the study except at point 2 where it acknowledges that the study is a double blind placebo controlled study. The old version criticized that it wasn't (which was true for the 2000 study).Here are Pimentel's two antibiotic/SIBO studies:Eradication of Small Intestinal Bacterial Overgrowth Reduces Symptoms of Irritable Bowel Syndrome (2000) http://www-east.elsevier.com/ajg/issues/9512/ajg3368fla.htm Normalization of lactulose breath testing correlates with symptom improvement in irritable bowel syndrome: a double-blind, randomized, placebo-controlled study. (2003) http://www.ncbi.nlm.nih.gov/entrez/query.f...2&dopt=Abstract Ah things that make you wanna go Hmmmm...


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## flux (Dec 13, 1998)

> quote:What other GI researchers have attempted to replicate the SIBO studies? Drossman, any of the other UNC experts?


Because nobody knows how to do it right. Breath testing is fraught with unreliability. So any replicated studies would end up telling us that breath testing is fraught with unreliability. That problem could perhaps be solved by jamming tubes down people's throats to obtain real cultures, but that would only tell us about gastric and duodenal BO and not anything deeper.Even if we really did find this, we have the question of figuring whether there is non-incidental connection between it and what we call IBS. This isn't easy either because the treatments for BO are fraught with unreliability as well.(This is, of course, not to say that further study should be being done. )


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## flux (Dec 13, 1998)

> quote:What other GI researchers have attempted to replicate the SIBO studies? Drossman, any of the other UNC experts?


Because nobody knows how to do it right. Breath testing is fraught with unreliability. So any replicated studies would end up telling us that breath testing is fraught with unreliability. That problem could perhaps be solved by jamming tubes down people's throats to obtain real cultures, but that would only tell us about gastric and duodenal BO and not anything deeper.Even if we really did find this, we have the question of figuring whether there is non-incidental connection between it and what we call IBS. This isn't easy either because the treatments for BO are fraught with unreliability as well.(This is, of course, not to say that further study should be being done. )


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## Guest (Oct 28, 2004)

hi everyone-i'm here. no worries







just recovering today - still getting D, but no longer throwing up. the D and extra movement is actually helping me get rid of the gas (coming from the juice I've been drinknig,i guess)and the fact that i'm not eating ... i actually feel better than i normally do. my stomach is quite flat for once.this also happened after getting a very bad flu where i was vomiting and had D for 2 days straight. both times about every 15 minutes for hours on end. i think that is consistent with ibs - that we have a stronger reaction perhaps. anyway, after that i was feeling great for a day until i started eating and then it came right back within a few hours.well i ,for one, tried the anti-inflammatory medicine route and it did not help with my symptoms (except for bladder urgency), but that does not mean its not helping others. my current regular gi doc who is pretty up on current ibs theories (however i doubt his intelligence sometimes) is really pursuing this low-grade inflammation thing. also he told me that the motility specialist i am seeing is doing research on low-grade inflammation as causal to ibs symptoms i guess. so they are taking this seriously. eric i agree with you sometimes b/c clearly the brain plays a role, but sometimes i think we need to think about how the body is influencing the brain more. i hear a lot about brain-gut axis but when people say that they mean BRAIN-gut axis (in that order) and they aren't really thinking the other way around. that is the only real bias i see with what you talk about. in other words what if there is an organic reason why the brain continues to react the way it does. also, i think many with ibs actually have other things going on. seems like if your digestive system is in trouble of course you are going to have pain, gas, bloating, D or C. a number of things could cause that and most of us with ibs are sent home after a sigmoidoscopy if we even get that. we take things that never help our symptoms yet the docs don't care. and we don't die of this. so there is not much incentive to fix the system right now. and i DO think the system of thinking about this is very faulty or in its infancy b/c otherwise they have an inkling as to how to treat us. so thats that.i'll try to get my graph. they sent it to my doc (the motility specialist $900/hour dude) to view and get back to me in a MONTH!. so i'll see if they'll send it to me - for a fee of course. i feel like we could all just figure it out here.ps. i've always been interested in the fact tha a lot of IBSer's have extra nerve endings. i think its interesting that some think inflammation could cause this and that could influence peristalsis and sensitivity. that makes perfect sense to me! why hasn't the Extra Nerve Endings issue meant anything to anyone before????pps. i also think its dangerous to not question people just b/c they are experts. brilliant people get stuck in patterns of thinking all the time. the whole reason the US does better than Japan with new technologies is b/c there is free thinking here and one can question and fail as much as you want. i think that philosophy applies to everything. so could be someone with a totally different approach makes major waves in IBS understanding. you never know.


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## Guest (Oct 28, 2004)

hi everyone-i'm here. no worries







just recovering today - still getting D, but no longer throwing up. the D and extra movement is actually helping me get rid of the gas (coming from the juice I've been drinknig,i guess)and the fact that i'm not eating ... i actually feel better than i normally do. my stomach is quite flat for once.this also happened after getting a very bad flu where i was vomiting and had D for 2 days straight. both times about every 15 minutes for hours on end. i think that is consistent with ibs - that we have a stronger reaction perhaps. anyway, after that i was feeling great for a day until i started eating and then it came right back within a few hours.well i ,for one, tried the anti-inflammatory medicine route and it did not help with my symptoms (except for bladder urgency), but that does not mean its not helping others. my current regular gi doc who is pretty up on current ibs theories (however i doubt his intelligence sometimes) is really pursuing this low-grade inflammation thing. also he told me that the motility specialist i am seeing is doing research on low-grade inflammation as causal to ibs symptoms i guess. so they are taking this seriously. eric i agree with you sometimes b/c clearly the brain plays a role, but sometimes i think we need to think about how the body is influencing the brain more. i hear a lot about brain-gut axis but when people say that they mean BRAIN-gut axis (in that order) and they aren't really thinking the other way around. that is the only real bias i see with what you talk about. in other words what if there is an organic reason why the brain continues to react the way it does. also, i think many with ibs actually have other things going on. seems like if your digestive system is in trouble of course you are going to have pain, gas, bloating, D or C. a number of things could cause that and most of us with ibs are sent home after a sigmoidoscopy if we even get that. we take things that never help our symptoms yet the docs don't care. and we don't die of this. so there is not much incentive to fix the system right now. and i DO think the system of thinking about this is very faulty or in its infancy b/c otherwise they have an inkling as to how to treat us. so thats that.i'll try to get my graph. they sent it to my doc (the motility specialist $900/hour dude) to view and get back to me in a MONTH!. so i'll see if they'll send it to me - for a fee of course. i feel like we could all just figure it out here.ps. i've always been interested in the fact tha a lot of IBSer's have extra nerve endings. i think its interesting that some think inflammation could cause this and that could influence peristalsis and sensitivity. that makes perfect sense to me! why hasn't the Extra Nerve Endings issue meant anything to anyone before????pps. i also think its dangerous to not question people just b/c they are experts. brilliant people get stuck in patterns of thinking all the time. the whole reason the US does better than Japan with new technologies is b/c there is free thinking here and one can question and fail as much as you want. i think that philosophy applies to everything. so could be someone with a totally different approach makes major waves in IBS understanding. you never know.


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## Talissa (Apr 10, 2004)

Hey Susan! Glad you're back, feeling better, and lucid as ever...great commentary.














(You too skinny)


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## Talissa (Apr 10, 2004)

Hey Susan! Glad you're back, feeling better, and lucid as ever...great commentary.














(You too skinny)


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## flux (Dec 13, 1998)

> quote: the whole reason the US does better than Japan with new technologies


Huh?


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## flux (Dec 13, 1998)

> quote: the whole reason the US does better than Japan with new technologies


Huh?


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## eric (Jul 8, 1999)

Joan, glad you feeling better. Hopefully you will be able to eat again soon.On the brain gut axis you mention, IBS is already a brain gut axis dysregulation, regardless of the cause. But there is just as much research going on in looking at gut mechanisms as there is brain impairment, more actually on gut abnormalities then brain, because within the last five years they are just starting to use newer tecnologies to understand it all. The brain is usally listed first, because its the top of the order and the head huncho, no pun intended. It is not a competition between the two, its a bidirectional communication between the two, the "gut brain and the Brain. Or the Central nervous system and the enteric nervous system. The enteric nervous system is the brain in the gut. Although it can run autonomically it is still under the influence of the brain. The brain controls gut activity in various ways, including sensation, muscle activity, and also emotional and behavioral reactions to gut activity. The influence of the brain on the gut is very powerful as well as the gut influnces the brain, but divided between several different influences.The brain can trigger symptoms and the gut can trigger symptoms, that is really the important take home message. Basic Principles -- Brain-Gut http://www.iffgd.org/symposium2003report.html Skinny there are others studying Sibo and IBS and have been for a while now.Dr Drossman, in no way has to "cover his tracks." LOL He was responding more to a newer study where this time they did the study right, whereas the first time it was blown out of purportion, by the investigator and the media. He writes with much more caution to what he is writing about.If you look at this link, there are comments about it, but not the full text. http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=11151884 It is a controversial topic in IBS.even now Pimental is more careful in calling IBS, SIBO. With words like "association." And "In conclusion, phase III is reduced in subjects with IBS and SIBO." Two different problems, sibo and IBS?The UNC only see's ten percent of their patients with SIBO?I will also say look at all these studies. Pimental has a few IBS studies, done recently on sibo and IBS. But it seems all the rest of this are being ignored. Look at all the pages and the sheer volume of studies and problems. They can already in part explain altered motility in IBS. But IBS is not just a motility problem. I will give you another Carl Sagan quote,"Extrodinary claims, require extrodinary proof."


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## eric (Jul 8, 1999)

Joan, glad you feeling better. Hopefully you will be able to eat again soon.On the brain gut axis you mention, IBS is already a brain gut axis dysregulation, regardless of the cause. But there is just as much research going on in looking at gut mechanisms as there is brain impairment, more actually on gut abnormalities then brain, because within the last five years they are just starting to use newer tecnologies to understand it all. The brain is usally listed first, because its the top of the order and the head huncho, no pun intended. It is not a competition between the two, its a bidirectional communication between the two, the "gut brain and the Brain. Or the Central nervous system and the enteric nervous system. The enteric nervous system is the brain in the gut. Although it can run autonomically it is still under the influence of the brain. The brain controls gut activity in various ways, including sensation, muscle activity, and also emotional and behavioral reactions to gut activity. The influence of the brain on the gut is very powerful as well as the gut influnces the brain, but divided between several different influences.The brain can trigger symptoms and the gut can trigger symptoms, that is really the important take home message. Basic Principles -- Brain-Gut http://www.iffgd.org/symposium2003report.html Skinny there are others studying Sibo and IBS and have been for a while now.Dr Drossman, in no way has to "cover his tracks." LOL He was responding more to a newer study where this time they did the study right, whereas the first time it was blown out of purportion, by the investigator and the media. He writes with much more caution to what he is writing about.If you look at this link, there are comments about it, but not the full text. http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=11151884 It is a controversial topic in IBS.even now Pimental is more careful in calling IBS, SIBO. With words like "association." And "In conclusion, phase III is reduced in subjects with IBS and SIBO." Two different problems, sibo and IBS?The UNC only see's ten percent of their patients with SIBO?I will also say look at all these studies. Pimental has a few IBS studies, done recently on sibo and IBS. But it seems all the rest of this are being ignored. Look at all the pages and the sheer volume of studies and problems. They can already in part explain altered motility in IBS. But IBS is not just a motility problem. I will give you another Carl Sagan quote,"Extrodinary claims, require extrodinary proof."


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## eric (Jul 8, 1999)

Forgot the link.There are gut problems here, genetic problems here, brain problems here in the systems effected and impairments, altered stress ciruit problems here, serotonin problems here, psycological problems and associations here, mast cells, serotonin cells and all kinds of things. http://www.docguide.com/news/content.nsf/A...52568880078C249 Two big players in the gut and IBS are serotonin-containing entero-endocrine cells ... EC, and mast cells. The mast cells are one of the cells they see inflammed in IBS, espcially PI IBS, but also some newer research in IBS.Here is a mast cell, which is already connected to bladder issues in IBS, can be set off by food sensitivites and allergies and also can be degrandulated by chronic stress with out a pathogen, because it is an end point to the HPA axis (the body stress circuit, which also helps fight infection, hence the link to PI IBS) and mast cells embedded in the deep tissue of the gut. http://www.chronicprostatitis.com/mastcells.html This shows a normal and degrandulating cell.


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## eric (Jul 8, 1999)

Forgot the link.There are gut problems here, genetic problems here, brain problems here in the systems effected and impairments, altered stress ciruit problems here, serotonin problems here, psycological problems and associations here, mast cells, serotonin cells and all kinds of things. http://www.docguide.com/news/content.nsf/A...52568880078C249 Two big players in the gut and IBS are serotonin-containing entero-endocrine cells ... EC, and mast cells. The mast cells are one of the cells they see inflammed in IBS, espcially PI IBS, but also some newer research in IBS.Here is a mast cell, which is already connected to bladder issues in IBS, can be set off by food sensitivites and allergies and also can be degrandulated by chronic stress with out a pathogen, because it is an end point to the HPA axis (the body stress circuit, which also helps fight infection, hence the link to PI IBS) and mast cells embedded in the deep tissue of the gut. http://www.chronicprostatitis.com/mastcells.html This shows a normal and degrandulating cell.


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## eric (Jul 8, 1999)

On the brain gut axis.regardless of the cause, do you think IBS in itself can cause emotional upset?"If you suffer from frequent emotional distress -- perhaps because of extreme stress, depression, or anxiety -- the unrelenting flood of adrenaline and CRF will take a toll on your digestive system. For one thing, the hormones can make the cells in the stomach and intestines extra-sensitive to pain. As a result, normal contractions and movements can become excruciating. The new signals can also disrupt the motion of the intestines, causing bouts of constipation or diarrhea." http://www.ahealthyme.com/topic/mindbodygu...AETVTWCYSYZSFEQ Where does the adrenaline come from?The Hypothalamic-Pituitary Adrenal (HPA) Axis .What cells does it effect in the gut. Mast cells.


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## eric (Jul 8, 1999)

On the brain gut axis.regardless of the cause, do you think IBS in itself can cause emotional upset?"If you suffer from frequent emotional distress -- perhaps because of extreme stress, depression, or anxiety -- the unrelenting flood of adrenaline and CRF will take a toll on your digestive system. For one thing, the hormones can make the cells in the stomach and intestines extra-sensitive to pain. As a result, normal contractions and movements can become excruciating. The new signals can also disrupt the motion of the intestines, causing bouts of constipation or diarrhea." http://www.ahealthyme.com/topic/mindbodygu...AETVTWCYSYZSFEQ Where does the adrenaline come from?The Hypothalamic-Pituitary Adrenal (HPA) Axis .What cells does it effect in the gut. Mast cells.


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## Guest (Oct 28, 2004)

yes i definitely think ibs in itself can definitely cause emotional upset as well as any chronic disease. they should measure people brain chemicals when they have a simple cold b/c most folks i know get pretty good depression just from that. am i missing something? confused!


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## Guest (Oct 28, 2004)

yes i definitely think ibs in itself can definitely cause emotional upset as well as any chronic disease. they should measure people brain chemicals when they have a simple cold b/c most folks i know get pretty good depression just from that. am i missing something? confused!


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## jools41 (Jan 8, 2004)

i have never heard of this breath test let alone never been offered it.i wonder why this is?


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## jools41 (Jan 8, 2004)

i have never heard of this breath test let alone never been offered it.i wonder why this is?


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## Guest (Oct 29, 2004)

good question jools. its taken me 13 years to get offered this.


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## Guest (Oct 29, 2004)

good question jools. its taken me 13 years to get offered this.


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## flux (Dec 13, 1998)

> quote:i have never heard of this breath test let alone never been offered it.i wonder why this is?


It's more popular in pediatric GI than adult.


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## flux (Dec 13, 1998)

> quote:i have never heard of this breath test let alone never been offered it.i wonder why this is?


It's more popular in pediatric GI than adult.


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## skinny (Jul 27, 2002)

> quote:Skinny there are others studying Sibo and IBS and have been for a while now.


Who? Where? You said that researchers had a hard time replicating the studies.


> quoter Drossman, in no way has to "cover his tracks." LOL He was responding more to a newer study where this time they did the study right, whereas the first time it was blown out of purportion, by the investigator and the media.He writes with much more caution to what he is writing about.


Look Eric don't be silly. Drossman is the chair of Rome and one of the top researchers in IBS. He botched up the references and still has misinformation about the studies on the updated page. I would have a hard time believing that this was a typo or errors due to ignorance. If he writes more cautiously, it's not to be more forthcoming about his errors.A *real* scientist would admit to their errors and correct them appropriately.


> quote:If you look at this link, there are comments about it, but not the full text. http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=11151884


What about it? Sure at the time Drossman made good critiques on the earlier study, but interesting enough the updated study had about the same results.


> quote:It is a controversial topic in IBS.even now Pimental is more careful in calling IBS, SIBO. With words like "association." And"In conclusion, phase III is reduced in subjects with IBS and SIBO." Two different problems, sibo and IBS?


Eric if you are going to quote something, put a reference to it. The point of conducting studies in groups of people is to find correlations. A strong correlation does not always equate to causation. When repeated studies are done to refine different variables and the results show a strong correlation, then it's pretty safe to say there is a cause. So yeah you have to use words like "association". BTW SIBO symptoms and IBS symptoms are identical - pain/discomfort, altered bowel motility, and bloating.


> quote:The UNC only see's ten percent of their patients with SIBO?


Huh? I don't know what you are talking about.


> quote:I will also say look at all these studies. Pimental has a few IBS studies, done recently on sibo and IBS. But it seems all the rest of this are being ignored. Look at all the pages and the sheer volume of studies and problems. They can already in part explain altered motility in IBS. But IBS is not just a motility problem.


Pimentel focuses on certain areas. His profile is here:


> quote: Mark Pimentel, MD, FRCPC, is the Director of the Gastrointestinal Motility Laboratory at Cedars-Sinai Medical Center. Dr. Pimentel also serves as Assistant Professor in Residence for the University of California, Los Angeles (UCLA), School of Medicine.Board certified in internal medicine and gastroenterology, Dr. Pimentel has been awarded various investigator-driven grants related to gastrointestinal motility. His primary research interests involve irritable bowel syndrome and its relationship to small intestinal motility and bacterial overgrowth. Other interests include gastric motility in diabetes. http://www.csmc.edu/5930.html


Not all GI researchers can be experts in all aspects of the field. If something is being ignored, it sure looks like it in the Rome committees. There are no SIBO experts there. Hmmm.


> quote:I will give you another Carl Sagan quote,"Extrodinary claims, require extrodinary proof."


Philosopher David Hume coined the phrase, but Sagan popularized it. BTW, you didn't answer this question, so I'll ask it again:If you have no pain or discomfort, does that mean you no longer have IBS?skinny


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## skinny (Jul 27, 2002)

> quote:Skinny there are others studying Sibo and IBS and have been for a while now.


Who? Where? You said that researchers had a hard time replicating the studies.


> quoter Drossman, in no way has to "cover his tracks." LOL He was responding more to a newer study where this time they did the study right, whereas the first time it was blown out of purportion, by the investigator and the media.He writes with much more caution to what he is writing about.


Look Eric don't be silly. Drossman is the chair of Rome and one of the top researchers in IBS. He botched up the references and still has misinformation about the studies on the updated page. I would have a hard time believing that this was a typo or errors due to ignorance. If he writes more cautiously, it's not to be more forthcoming about his errors.A *real* scientist would admit to their errors and correct them appropriately.


> quote:If you look at this link, there are comments about it, but not the full text. http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=11151884


What about it? Sure at the time Drossman made good critiques on the earlier study, but interesting enough the updated study had about the same results.


> quote:It is a controversial topic in IBS.even now Pimental is more careful in calling IBS, SIBO. With words like "association." And"In conclusion, phase III is reduced in subjects with IBS and SIBO." Two different problems, sibo and IBS?


Eric if you are going to quote something, put a reference to it. The point of conducting studies in groups of people is to find correlations. A strong correlation does not always equate to causation. When repeated studies are done to refine different variables and the results show a strong correlation, then it's pretty safe to say there is a cause. So yeah you have to use words like "association". BTW SIBO symptoms and IBS symptoms are identical - pain/discomfort, altered bowel motility, and bloating.


> quote:The UNC only see's ten percent of their patients with SIBO?


Huh? I don't know what you are talking about.


> quote:I will also say look at all these studies. Pimental has a few IBS studies, done recently on sibo and IBS. But it seems all the rest of this are being ignored. Look at all the pages and the sheer volume of studies and problems. They can already in part explain altered motility in IBS. But IBS is not just a motility problem.


Pimentel focuses on certain areas. His profile is here:


> quote: Mark Pimentel, MD, FRCPC, is the Director of the Gastrointestinal Motility Laboratory at Cedars-Sinai Medical Center. Dr. Pimentel also serves as Assistant Professor in Residence for the University of California, Los Angeles (UCLA), School of Medicine.Board certified in internal medicine and gastroenterology, Dr. Pimentel has been awarded various investigator-driven grants related to gastrointestinal motility. His primary research interests involve irritable bowel syndrome and its relationship to small intestinal motility and bacterial overgrowth. Other interests include gastric motility in diabetes. http://www.csmc.edu/5930.html


Not all GI researchers can be experts in all aspects of the field. If something is being ignored, it sure looks like it in the Rome committees. There are no SIBO experts there. Hmmm.


> quote:I will give you another Carl Sagan quote,"Extrodinary claims, require extrodinary proof."


Philosopher David Hume coined the phrase, but Sagan popularized it. BTW, you didn't answer this question, so I'll ask it again:If you have no pain or discomfort, does that mean you no longer have IBS?skinny


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## Jhouston (Nov 9, 2003)

Anyone know what the inflammatory markers are? Joann


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## Jhouston (Nov 9, 2003)

Anyone know what the inflammatory markers are? Joann


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## eric (Jul 8, 1999)

Skinny, I will come back and address all your concerns and answer your questions.But first, Irritable Bowel Syndrome - An Evidence-Based Approach to DiagnosisPosted 06/21/2004 B.D. Cash; W.D. Chey "The potential role of small intestinal bacterial overgrowth (SIBO) as an aetiology for IBS symptoms has been highlighted by two recent publications.36,37 Pimentel et al.36 performed lactulose hydrogen breath testing in 202 patients fulfilling the Rome I criteria referred for evaluation of possible SIBO. Seventy-eight percent (157/202) had breath test results that were consistent with SIBO and were treated with a 10-day course of antibiotics. Forty-seven of these patients (29.9%) were restudied 7-10 days after completion of the antibiotics and SIBO eradication was achieved in 25 (53.2%). Twelve patients (48%) with SIBO eradication did not meet the Rome I criteria when their symptoms were reassessed (interpreted as improvement), while only four patients (18.2%) with persistent SIBO failed to meet the Rome I criteria after treatment. While intriguing, a number of methodological limitations of the study by Pimental et al., including potential selection bias, the absence of a gold standard for the diagnosis of SIBO, the use of an unusual antibiotic to treat SIBO, short study duration and incomplete follow-up data for the majority of enrolled patients, limits the conclusions that can be drawn regarding the role of SIBO in patients with suspected IBS.The same group of investigators subsequently reported the results of a double-blind randomized placebo-controlled trial evaluating the effects of therapy for SIBO upon IBS symptoms.37 The prevalence of SIBO in patients with IBS in this study was 84%, similar to the 78% rate observed in the previous trial, and significantly greater than the 20% prevalence rate observed in healthy controls. Seven days after completion of neomycin or placebo, patients returned for symptom assessment and lactulose breath testing. IBS patients who were successfully treated for their SIBO based upon normalization of breath test results reported significantly greater improvement in IBS symptoms than patients with a persistently abnormal breath test result. There are no data evaluating the long-term effects and durability of antibiotic therapy in patients with IBS and SIBO. Further studies to address this highly controversial area are eagerly awaited.Summary of the use of breath tests for the diagnosis of IBS: Current best evidence does not support the routine use of breath tests for lactose intolerance or SIBO to exclude organic gastrointestinal disease in patients who present with typical IBS symptoms without alarm features. http://www.medscape.com/viewarticle/481182_3


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## eric (Jul 8, 1999)

Skinny, I will come back and address all your concerns and answer your questions.But first, Irritable Bowel Syndrome - An Evidence-Based Approach to DiagnosisPosted 06/21/2004 B.D. Cash; W.D. Chey "The potential role of small intestinal bacterial overgrowth (SIBO) as an aetiology for IBS symptoms has been highlighted by two recent publications.36,37 Pimentel et al.36 performed lactulose hydrogen breath testing in 202 patients fulfilling the Rome I criteria referred for evaluation of possible SIBO. Seventy-eight percent (157/202) had breath test results that were consistent with SIBO and were treated with a 10-day course of antibiotics. Forty-seven of these patients (29.9%) were restudied 7-10 days after completion of the antibiotics and SIBO eradication was achieved in 25 (53.2%). Twelve patients (48%) with SIBO eradication did not meet the Rome I criteria when their symptoms were reassessed (interpreted as improvement), while only four patients (18.2%) with persistent SIBO failed to meet the Rome I criteria after treatment. While intriguing, a number of methodological limitations of the study by Pimental et al., including potential selection bias, the absence of a gold standard for the diagnosis of SIBO, the use of an unusual antibiotic to treat SIBO, short study duration and incomplete follow-up data for the majority of enrolled patients, limits the conclusions that can be drawn regarding the role of SIBO in patients with suspected IBS.The same group of investigators subsequently reported the results of a double-blind randomized placebo-controlled trial evaluating the effects of therapy for SIBO upon IBS symptoms.37 The prevalence of SIBO in patients with IBS in this study was 84%, similar to the 78% rate observed in the previous trial, and significantly greater than the 20% prevalence rate observed in healthy controls. Seven days after completion of neomycin or placebo, patients returned for symptom assessment and lactulose breath testing. IBS patients who were successfully treated for their SIBO based upon normalization of breath test results reported significantly greater improvement in IBS symptoms than patients with a persistently abnormal breath test result. There are no data evaluating the long-term effects and durability of antibiotic therapy in patients with IBS and SIBO. Further studies to address this highly controversial area are eagerly awaited.Summary of the use of breath tests for the diagnosis of IBS: Current best evidence does not support the routine use of breath tests for lactose intolerance or SIBO to exclude organic gastrointestinal disease in patients who present with typical IBS symptoms without alarm features. http://www.medscape.com/viewarticle/481182_3


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## eric (Jul 8, 1999)

Jhouston http://www.pulsus.com/Gastro/18_10/andr_ed.htm


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## eric (Jul 8, 1999)

Jhouston http://www.pulsus.com/Gastro/18_10/andr_ed.htm


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## Jhouston (Nov 9, 2003)

Thanks, hmmm Great Smokeys lab does a test for inflamation,think it is Calprotectin (neitrophils)and Eosinophil protein X. These are GS's inflamatory markers through stool analysis. I suppose the markers from study above is only by biopsy. Joann


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## Jhouston (Nov 9, 2003)

Thanks, hmmm Great Smokeys lab does a test for inflamation,think it is Calprotectin (neitrophils)and Eosinophil protein X. These are GS's inflamatory markers through stool analysis. I suppose the markers from study above is only by biopsy. Joann


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## eric (Jul 8, 1999)

Skinny have forgotten you and will respond as soon as I have a little more time.Yes, Jhouston, and the biopsies can sometimes cause infection as they take them from deep in the bowel wall tissues. IT is an invasive procedure. In IBS there are different kind of inflammation then say IBD conditions also.You might also want to read this."The pathophysiology of irritable bowel syndrome.Schwetz I, Bradesi S, Mayer EA.Center of Neurovisceral Sciences and Women's Health (CNS),, Division of Digestive Diseases and Brain Research Institute, Department of Medicine, Los Angeles, CA, USA.Recent studies have provided evidence to suggest a possible role for mucosal immune activation in the pathophysiology of irritable bowel syndrome (IBS). On the other hand, novel findings using functional brain-imaging techniques support the concept that altered perception of visceral stimuli plays a key role in IBS symptom generation. These seemingly contradictory findings have revived the discussion about the relative contribution of peripheral versus central mechanisms in the symptom generation of IBS. In this review, we will provide evidence for the hypothesis that, in the absence of changes in visceral perception and alterations in endogenous pain modulation systems, chronic inflammatory mucosal changes in the gut are not a plausible mechanism to explain the presence of chronic abdominal pain, a clinical hallmark of IBS."However, its in PDF format so you may need adobe reader. http://www.minervamedica.it/index2.t?show=R10Y2004N05A0419 Click on the full text at the bottom of the page.


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## eric (Jul 8, 1999)

Skinny have forgotten you and will respond as soon as I have a little more time.Yes, Jhouston, and the biopsies can sometimes cause infection as they take them from deep in the bowel wall tissues. IT is an invasive procedure. In IBS there are different kind of inflammation then say IBD conditions also.You might also want to read this."The pathophysiology of irritable bowel syndrome.Schwetz I, Bradesi S, Mayer EA.Center of Neurovisceral Sciences and Women's Health (CNS),, Division of Digestive Diseases and Brain Research Institute, Department of Medicine, Los Angeles, CA, USA.Recent studies have provided evidence to suggest a possible role for mucosal immune activation in the pathophysiology of irritable bowel syndrome (IBS). On the other hand, novel findings using functional brain-imaging techniques support the concept that altered perception of visceral stimuli plays a key role in IBS symptom generation. These seemingly contradictory findings have revived the discussion about the relative contribution of peripheral versus central mechanisms in the symptom generation of IBS. In this review, we will provide evidence for the hypothesis that, in the absence of changes in visceral perception and alterations in endogenous pain modulation systems, chronic inflammatory mucosal changes in the gut are not a plausible mechanism to explain the presence of chronic abdominal pain, a clinical hallmark of IBS."However, its in PDF format so you may need adobe reader. http://www.minervamedica.it/index2.t?show=R10Y2004N05A0419 Click on the full text at the bottom of the page.


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## Jhouston (Nov 9, 2003)

Eric, From all I have read on bb it is my opinion that I do not have bonafide IBS even though gastro dxed IBS. Chronic abdominal pain is a hallmark of IBS! so how many of us do not have Chronic pain. maybe once in awhile? or how about If I do this = pain but if I don't no pain. like eating a certain food or drink. and if GSDL is correct in diagnostic inflamatory markers to dx IBD then I may have low level inflamation that was not detected on colonoscopy since my tests results showed eosinophil protein x high but not Calprotectin. Both of those are markers for IBD by GSDL. confusing... Joann


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## Jhouston (Nov 9, 2003)

Eric, From all I have read on bb it is my opinion that I do not have bonafide IBS even though gastro dxed IBS. Chronic abdominal pain is a hallmark of IBS! so how many of us do not have Chronic pain. maybe once in awhile? or how about If I do this = pain but if I don't no pain. like eating a certain food or drink. and if GSDL is correct in diagnostic inflamatory markers to dx IBD then I may have low level inflamation that was not detected on colonoscopy since my tests results showed eosinophil protein x high but not Calprotectin. Both of those are markers for IBD by GSDL. confusing... Joann


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## Guest (Oct 30, 2004)

personally i don't think pain should be part of the ibs criteria. there is a huge difference between pain (sharp) and what a lot of us feel which is more like pressure and involves our stomach muslces reacting to being stretched etc - plus i have a lot of afferent sensations in other parts of my body that have nothign to do with pain or discomfort - but seem to be triggered by my bowel/abdomen area. plus i had major D for a whole year before developing bloating sensations and for sure i had ibs at that point too -- if indeed that is what i have now.do these experts know much? i don't know.


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## Guest (Oct 30, 2004)

personally i don't think pain should be part of the ibs criteria. there is a huge difference between pain (sharp) and what a lot of us feel which is more like pressure and involves our stomach muslces reacting to being stretched etc - plus i have a lot of afferent sensations in other parts of my body that have nothign to do with pain or discomfort - but seem to be triggered by my bowel/abdomen area. plus i had major D for a whole year before developing bloating sensations and for sure i had ibs at that point too -- if indeed that is what i have now.do these experts know much? i don't know.


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## Jhouston (Nov 9, 2003)

Joan, I'm with you on this. A lot of what you post is VERY similar to my experience. My son said to me yesterday "your belly". sometimes I look in the mirror and I look 5 months pregnant. I also have that feeling like I am being stretched and chest and other parts of body not quite right. sometimes it feels like the muscles of abdomen are not fully functioning. Joann


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## Jhouston (Nov 9, 2003)

Joan, I'm with you on this. A lot of what you post is VERY similar to my experience. My son said to me yesterday "your belly". sometimes I look in the mirror and I look 5 months pregnant. I also have that feeling like I am being stretched and chest and other parts of body not quite right. sometimes it feels like the muscles of abdomen are not fully functioning. Joann


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## eric (Jul 8, 1999)

First, I would not get diagnosed with IBS really from a primary care doctor, but by a gastroenterologist, and then I would ask them if they are using the Rome Criteria ll criteria for the diagnoses. Pain or discomfort is a must, but IBS is diagnoed with a SPECIFIC cluster of symptoms, minus allarm features. This is very important. Also the type and kind of pain in the diagnoses is important, as well as other things that are not needed for the diagnoses but contribute to them, for example, symptoms that awake you at nght are rare, the sensation of incomplete evacuation. There is also alternating IBS, d and c. Also many functional disorders overlap, dyspepsia for example cn over lap with IBS commonly, an upper functional gi disorder, with bloating. There is also functional d, with no pain, functional c with no pain, functioanl chronic abdominal pain, with no d or c etc.Jhouston, there are many things that can cause minor inflammation, if you have C, some people have diver for example, but others who take Nasids amy and even some foods can aggravate the gi tract, and a person should be tested by a gastroenterologist if they have celiac or microscopic colitus. If there are any alarm features with a person, they may require a more diteiled differential workup. This may also depend on age to an extent as well.Bloating also is not well understood and may yet be another problem comorbid with IBS as well as part of IBS itself. In IBS the muscles in the abdomen are not fully functioning. Many people with IBS complain of bloating and distension, more as the day progresses then when they first wake up. More because of abdominal muscles reacting later in the day. This combined with viceral hypersensitivity can be a problem. When there is no visable distension it may be more a viceral hypersensivity issues and when there is visable distension, it maybe more of a muscle related issue.alsoAbdominal PainMedical Author: Dennis Lee, M.D. Medical Editor: Jay W.Marks, M.D. What is abdominal pain? What causes abdominal pain? How is the cause of abdominal pain diagnosed? Special problem in irritable bowel syndrome (IBS) of diagnosing the cause of abdominal pain Why can diagnosis of the cause of abdominal pain be difficult? How can I help my doctor to determine the cause of my abdominal pain? Abdominal Pain At A Glance http://www.medicinenet.com/abdominal_pain/article.htm


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## eric (Jul 8, 1999)

First, I would not get diagnosed with IBS really from a primary care doctor, but by a gastroenterologist, and then I would ask them if they are using the Rome Criteria ll criteria for the diagnoses. Pain or discomfort is a must, but IBS is diagnoed with a SPECIFIC cluster of symptoms, minus allarm features. This is very important. Also the type and kind of pain in the diagnoses is important, as well as other things that are not needed for the diagnoses but contribute to them, for example, symptoms that awake you at nght are rare, the sensation of incomplete evacuation. There is also alternating IBS, d and c. Also many functional disorders overlap, dyspepsia for example cn over lap with IBS commonly, an upper functional gi disorder, with bloating. There is also functional d, with no pain, functional c with no pain, functioanl chronic abdominal pain, with no d or c etc.Jhouston, there are many things that can cause minor inflammation, if you have C, some people have diver for example, but others who take Nasids amy and even some foods can aggravate the gi tract, and a person should be tested by a gastroenterologist if they have celiac or microscopic colitus. If there are any alarm features with a person, they may require a more diteiled differential workup. This may also depend on age to an extent as well.Bloating also is not well understood and may yet be another problem comorbid with IBS as well as part of IBS itself. In IBS the muscles in the abdomen are not fully functioning. Many people with IBS complain of bloating and distension, more as the day progresses then when they first wake up. More because of abdominal muscles reacting later in the day. This combined with viceral hypersensitivity can be a problem. When there is no visable distension it may be more a viceral hypersensivity issues and when there is visable distension, it maybe more of a muscle related issue.alsoAbdominal PainMedical Author: Dennis Lee, M.D. Medical Editor: Jay W.Marks, M.D. What is abdominal pain? What causes abdominal pain? How is the cause of abdominal pain diagnosed? Special problem in irritable bowel syndrome (IBS) of diagnosing the cause of abdominal pain Why can diagnosis of the cause of abdominal pain be difficult? How can I help my doctor to determine the cause of my abdominal pain? Abdominal Pain At A Glance http://www.medicinenet.com/abdominal_pain/article.htm


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## eric (Jul 8, 1999)

Skinny, I will answer this first. before the HT I had four severe pain attacks a week Sometimes twice a day. IT was also out of control, it controled me, but now I can control it most of the time. I had to use the bathroom some days ten times and then sometimes would switch to more C. I had incomplete evacuation, and back problems from it and a long list of IBS related symptoms. After the HT I improved about 80 percent and have improved further to about 90 percent over the last four years after treatment. I know for sure I had classic IBS pain predominate and alternating IBS. I even basically know how I got it. I have continued to improve as well. Am I "cured" no but would say yes I am in remission and maybe someday not have any symptoms hopefully. What I am also not now, is suicidal from it either. It was like Japense water torture day in and day out for thirty three years. I will still repond more to some other issues here as well.


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## eric (Jul 8, 1999)

Skinny, I will answer this first. before the HT I had four severe pain attacks a week Sometimes twice a day. IT was also out of control, it controled me, but now I can control it most of the time. I had to use the bathroom some days ten times and then sometimes would switch to more C. I had incomplete evacuation, and back problems from it and a long list of IBS related symptoms. After the HT I improved about 80 percent and have improved further to about 90 percent over the last four years after treatment. I know for sure I had classic IBS pain predominate and alternating IBS. I even basically know how I got it. I have continued to improve as well. Am I "cured" no but would say yes I am in remission and maybe someday not have any symptoms hopefully. What I am also not now, is suicidal from it either. It was like Japense water torture day in and day out for thirty three years. I will still repond more to some other issues here as well.


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## Guest (Nov 1, 2004)

what makes doctors think that a person wouldn't have ibs like symptoms if they actually had organic disease. that is what i don't understand. the rhome criteria might identify ibs patients, but doesn't it also identify a bunch of other people too?jhouston i totally understand.


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## Guest (Nov 1, 2004)

what makes doctors think that a person wouldn't have ibs like symptoms if they actually had organic disease. that is what i don't understand. the rhome criteria might identify ibs patients, but doesn't it also identify a bunch of other people too?jhouston i totally understand.


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## Jhouston (Nov 9, 2003)

I have an "Irritable Bowel" without the syndrome







Joann I Never take nsaids. I had colonoscopy, Upper endoscopy. maybe I need to do colonoscopy again. I am scared they will find something Bad! I hate to use the "S" word.....spasms is what I think ...muscular spasms. which can be due to Stress. the other "S" word







Stress in that my gut is stressed by something and I )mind, spirit) is stressed by my gut and outside influences. Take the path of least resistance...no irritating food, do ht or meditate etc, find out if there is anything in the gut that shouldn't be there and irradicate it. prescribed by a wise, not so old woman ..ME Joann


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## Jhouston (Nov 9, 2003)

I have an "Irritable Bowel" without the syndrome







Joann I Never take nsaids. I had colonoscopy, Upper endoscopy. maybe I need to do colonoscopy again. I am scared they will find something Bad! I hate to use the "S" word.....spasms is what I think ...muscular spasms. which can be due to Stress. the other "S" word







Stress in that my gut is stressed by something and I )mind, spirit) is stressed by my gut and outside influences. Take the path of least resistance...no irritating food, do ht or meditate etc, find out if there is anything in the gut that shouldn't be there and irradicate it. prescribed by a wise, not so old woman ..ME Joann


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## eric (Jul 8, 1999)

Skinny, don't know where you think Dr D is "covering his tracks"?He also has tons of researchers who peer review his work as well as work with them all and you can see how much the IBS communitiy fully respects his and his coworkers work.I am actually surprized to seean almost serious contempt for him. To bad you have never meet him and found out how nice and knowledgable he really is in FBD's and how much he really cares and is trying to help all FBD people. His work is by no means the only work I research with IBS, there are top people in their fileds doing the research. DR Wood, DR Ester Sternberg, Dr Gershon, Dr Whitehead, Dr Mayer, and many more all highly respected in their fields and bring a lot to the table, many world recgonized experts sharing information.The links to the other researchers are there, just not the full text.Sometimes too narrow a focus is not a great thing to the bigger picture, unless its all incorporated?Many doctors including the UNC know about SIBO, if you go look at the new 6 annual IFFGD symposium, you will see its part of the program. http://www.iffgd.org/images/FGID_brochure2005.pdf IN order to get to top you have to work your way there.On the quote and reference I figured you read it since it is one of Pimentals studies. http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12498278 Bacterial Overgrowth Syndrome http://www.emedicine.com/med/topic198.htm Small Bowel Bacterial Overgrowth is a Common Cause of Chronic Diarrhea http://www.medscape.com/viewarticle/483735?src=search I also just find it odd, I have never seen Dr Pimental talk about all the problems in IBS, I have never seen anything written by him on PI IBS or serotonin, or brain impairments and all the other research done over the years. Or how he fully explains serotonin dysregulation, how SIBO causes nerve hypersensitivity, alterations in motility the d/c c and c/d or the role of genetics the sensation of incomplete evacuation, rectal hypersensitvity and a host of other issues.


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## eric (Jul 8, 1999)

Skinny, don't know where you think Dr D is "covering his tracks"?He also has tons of researchers who peer review his work as well as work with them all and you can see how much the IBS communitiy fully respects his and his coworkers work.I am actually surprized to seean almost serious contempt for him. To bad you have never meet him and found out how nice and knowledgable he really is in FBD's and how much he really cares and is trying to help all FBD people. His work is by no means the only work I research with IBS, there are top people in their fileds doing the research. DR Wood, DR Ester Sternberg, Dr Gershon, Dr Whitehead, Dr Mayer, and many more all highly respected in their fields and bring a lot to the table, many world recgonized experts sharing information.The links to the other researchers are there, just not the full text.Sometimes too narrow a focus is not a great thing to the bigger picture, unless its all incorporated?Many doctors including the UNC know about SIBO, if you go look at the new 6 annual IFFGD symposium, you will see its part of the program. http://www.iffgd.org/images/FGID_brochure2005.pdf IN order to get to top you have to work your way there.On the quote and reference I figured you read it since it is one of Pimentals studies. http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=12498278 Bacterial Overgrowth Syndrome http://www.emedicine.com/med/topic198.htm Small Bowel Bacterial Overgrowth is a Common Cause of Chronic Diarrhea http://www.medscape.com/viewarticle/483735?src=search I also just find it odd, I have never seen Dr Pimental talk about all the problems in IBS, I have never seen anything written by him on PI IBS or serotonin, or brain impairments and all the other research done over the years. Or how he fully explains serotonin dysregulation, how SIBO causes nerve hypersensitivity, alterations in motility the d/c c and c/d or the role of genetics the sensation of incomplete evacuation, rectal hypersensitvity and a host of other issues.


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## skinny (Jul 27, 2002)

> quote:Skinny, don't know where you think Dr D is "covering his tracks"?


Eric, did you read my post a page back? I posted it very clearly. I'll do it again since you seem to have trouble following me. Please read the following carefully.New version: http://www.med.unc.edu/wrkunits/2depts/med...ibs_08_2004.pdf compare this with the older version which is still online (but not as a linked page)Old version: http://www.med.unc.edu/wrkunits/2depts/med...rowthandibs.htm Drossman's new version jumbles Pimentel's 2000 and 2003 study. The 2000 study was an intent to treat study with several antibiotics used. The 2003 study was a double blind placebo controlled study with a single antibiotic.If you read the new version, you'll see where Drossman has some glaring errors on that pdf file.1) He references the 2003 study as "Eradication of Small Intestinal Bacterial Overgrowth Reduces Symptoms of IBS". This is incorrect. That is the title of the 2000 study.2) He rehashes his objections that have been refuted in the 2003 study. They only place where there is an edit is where he acknowledges it was a double blind placebo controlled study.If you compare both versions of his bacterial overgrowth articles, it looks like he was trying to hide his errors.









> quote:He also has tons of researchers who peer review his work as well as work with them all and you can see how much the IBS communitiy fully respects his and his coworkers work.


I read his profile and looks like he's very accomplished in the field. I'm not knocking him on his track record. If he has researchers who peer review his work, how come they didn't catch these errors? I find that to be very strange.


> quote:I am actually surprized to seean almost serious contempt for him. To bad you have never meet him and found out how nice and knowledgable he really is in FBD's and how much he really cares and is trying to help all FBD people.


Dr. Douglas Drossman is considered "world authority in the field of functional GI disorders" according to his profile. For someone to hold that title, I would hold that person to a *very high* standard. And BTW, in science there are no _authorities_.I'll repost Carl Sagan's Baloney Detection Kit since these are good scientific guidelines to follow:
Wherever possible there must be independent confirmation of the facts
Encourage substantive debate on the evidence by knowledgeable proponents of all points of view.
Arguments from authority carry little weight (in science there are no "authorities").
Spin more than one hypothesis - don't simply run with the first idea that caught your fancy.
Try not to get overly attached to a hypothesis just because it's yours.
Quantify, wherever possible.
If there is a chain of argument every link in the chain must work.
"Occam's razor" - if there are two hypothesis that explain the data equally well choose the simpler.
Ask whether the hypothesis can, at least in principle, be falsified (shown to be false by some unambiguous test). In other words, it is testable? Can others duplicate the experiment and get the same result?Additional issues are:
Conduct control experiments - especially "double blind" experiments where the person taking measurements is not aware of the test and control subjects.
Check for confounding factors - separate the variables._adapted from Carl Sagan's Baloney Detection Kit in the book Demon Haunted World_



> quote:Sometimes too narrow a focus is not a great thing to the bigger picture, unless its all incorporated?


That's why you need experts from all focuses to come together and butt heads together to debate it. Why are there no SIBO experts on the Rome committee? Do you have any clue?


> quote:Many doctors including the UNC know about SIBO, if you go look at the new 6 annual IFFGD symposium, you will see its part of the program. http://www.iffgd.org/images/FGID_brochure2005.pdf IN order to get to top you have to work your way there.


The only thing I could find about it wasifferential Diagnosis and Tests to Exclude Other Disease ï¿½ What is the evidence for their value? Brooks D. Cash, MD...Breath Studies for Bacterial OvergrowthI'm not familiar with his work, but it doesn't look like he's done any SIBO studies. It would be better to hear it from someone who has clinical experience in this because the research may be misconstrued.


> quote:Bacterial Overgrowth Syndrome http://www.emedicine.com/med/topic198.htm


"Last Updated: November 8, 2001" Sorry this is not up to date with the latest research. Please be aware of this.


> quote:Small Bowel Bacterial Overgrowth is a Common Cause of Chronic Diarrhea http://www.medscape.com/viewarticle/483735?src=search


I couldn't access the study without registering, but I found the abstract here:Small Bowel Bacterial Overgrowth is a Common Cause of Chronic Diarrhea (August 2004) http://tinyurl.com/5egwn "Conclusion: Small bowel bacterial overgrowth is a common (33ï¿½67%) cause of chronic diarrhea."It was good that they used C-d-xylose breath/lactulose test alone and combination, but it was too bad they didn't check for symptoms associated with IBS.


> quote:I also just find it odd, I have never seen Dr Pimental talk about all the problems in IBS, I have never seen anything written by him on PI IBS or serotonin, or brain impairments and all the other research done over the years. Or how he fully explains serotonin dysregulation, how SIBO causes nerve hypersensitivity, alterations in motility the d/c c and c/d or the role of genetics the sensation of incomplete evacuation, rectal hypersensitvity and a host of other issues.


Look I don't know the guy or what his position about IBS is, but you have to admit he's doing some important work that needs to be taken more seriously by other GI researchers.Additional reading:Uninvited Guests: The Impact of Small Intestinal Bacterial Overgrowth on Nutritional Statusby Oren Zaidel and Henry C. Lin http://www.healthsystem.virginia.edu/inter...idelArticle.pdf skinny


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## skinny (Jul 27, 2002)

> quote:Skinny, don't know where you think Dr D is "covering his tracks"?


Eric, did you read my post a page back? I posted it very clearly. I'll do it again since you seem to have trouble following me. Please read the following carefully.New version: http://www.med.unc.edu/wrkunits/2depts/med...ibs_08_2004.pdf compare this with the older version which is still online (but not as a linked page)Old version: http://www.med.unc.edu/wrkunits/2depts/med...rowthandibs.htm Drossman's new version jumbles Pimentel's 2000 and 2003 study. The 2000 study was an intent to treat study with several antibiotics used. The 2003 study was a double blind placebo controlled study with a single antibiotic.If you read the new version, you'll see where Drossman has some glaring errors on that pdf file.1) He references the 2003 study as "Eradication of Small Intestinal Bacterial Overgrowth Reduces Symptoms of IBS". This is incorrect. That is the title of the 2000 study.2) He rehashes his objections that have been refuted in the 2003 study. They only place where there is an edit is where he acknowledges it was a double blind placebo controlled study.If you compare both versions of his bacterial overgrowth articles, it looks like he was trying to hide his errors.









> quote:He also has tons of researchers who peer review his work as well as work with them all and you can see how much the IBS communitiy fully respects his and his coworkers work.


I read his profile and looks like he's very accomplished in the field. I'm not knocking him on his track record. If he has researchers who peer review his work, how come they didn't catch these errors? I find that to be very strange.


> quote:I am actually surprized to seean almost serious contempt for him. To bad you have never meet him and found out how nice and knowledgable he really is in FBD's and how much he really cares and is trying to help all FBD people.


Dr. Douglas Drossman is considered "world authority in the field of functional GI disorders" according to his profile. For someone to hold that title, I would hold that person to a *very high* standard. And BTW, in science there are no _authorities_.I'll repost Carl Sagan's Baloney Detection Kit since these are good scientific guidelines to follow:
Wherever possible there must be independent confirmation of the facts
Encourage substantive debate on the evidence by knowledgeable proponents of all points of view.
Arguments from authority carry little weight (in science there are no "authorities").
Spin more than one hypothesis - don't simply run with the first idea that caught your fancy.
Try not to get overly attached to a hypothesis just because it's yours.
Quantify, wherever possible.
If there is a chain of argument every link in the chain must work.
"Occam's razor" - if there are two hypothesis that explain the data equally well choose the simpler.
Ask whether the hypothesis can, at least in principle, be falsified (shown to be false by some unambiguous test). In other words, it is testable? Can others duplicate the experiment and get the same result?Additional issues are:
Conduct control experiments - especially "double blind" experiments where the person taking measurements is not aware of the test and control subjects.
Check for confounding factors - separate the variables._adapted from Carl Sagan's Baloney Detection Kit in the book Demon Haunted World_



> quote:Sometimes too narrow a focus is not a great thing to the bigger picture, unless its all incorporated?


That's why you need experts from all focuses to come together and butt heads together to debate it. Why are there no SIBO experts on the Rome committee? Do you have any clue?


> quote:Many doctors including the UNC know about SIBO, if you go look at the new 6 annual IFFGD symposium, you will see its part of the program. http://www.iffgd.org/images/FGID_brochure2005.pdf IN order to get to top you have to work your way there.


The only thing I could find about it wasifferential Diagnosis and Tests to Exclude Other Disease ï¿½ What is the evidence for their value? Brooks D. Cash, MD...Breath Studies for Bacterial OvergrowthI'm not familiar with his work, but it doesn't look like he's done any SIBO studies. It would be better to hear it from someone who has clinical experience in this because the research may be misconstrued.


> quote:Bacterial Overgrowth Syndrome http://www.emedicine.com/med/topic198.htm


"Last Updated: November 8, 2001" Sorry this is not up to date with the latest research. Please be aware of this.


> quote:Small Bowel Bacterial Overgrowth is a Common Cause of Chronic Diarrhea http://www.medscape.com/viewarticle/483735?src=search


I couldn't access the study without registering, but I found the abstract here:Small Bowel Bacterial Overgrowth is a Common Cause of Chronic Diarrhea (August 2004) http://tinyurl.com/5egwn "Conclusion: Small bowel bacterial overgrowth is a common (33ï¿½67%) cause of chronic diarrhea."It was good that they used C-d-xylose breath/lactulose test alone and combination, but it was too bad they didn't check for symptoms associated with IBS.


> quote:I also just find it odd, I have never seen Dr Pimental talk about all the problems in IBS, I have never seen anything written by him on PI IBS or serotonin, or brain impairments and all the other research done over the years. Or how he fully explains serotonin dysregulation, how SIBO causes nerve hypersensitivity, alterations in motility the d/c c and c/d or the role of genetics the sensation of incomplete evacuation, rectal hypersensitvity and a host of other issues.


Look I don't know the guy or what his position about IBS is, but you have to admit he's doing some important work that needs to be taken more seriously by other GI researchers.Additional reading:Uninvited Guests: The Impact of Small Intestinal Bacterial Overgrowth on Nutritional Statusby Oren Zaidel and Henry C. Lin http://www.healthsystem.virginia.edu/inter...idelArticle.pdf skinny


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## flux (Dec 13, 1998)

> quoterossman's new version jumbles Pimentel's 2000 and 2003 study.


Not exactly....


> quote:1) He references the 2003 study as "Eradication of Small Intestinal Bacterial Overgrowth Reduces Symptoms of IBS". This is incorrect. That is the title of the 2000 study.


It looks to me that he is referencing the 2000 study. It's the year that is wrong.


> quote:2) He rehashes his objections that have been refuted in the 2003 study. They only place where there is an edit is where he acknowledges it was a double blind placebo controlled study.


I think it is the initial hash. The edit is odd because on the web it says


> quote:This is not a placebo-controlled double-blinded study.


but the pdf says


> quote:The reported study was also is a placebo-controlled double-blinded study


I think that line was intending to say The reported study was also *not* a placebo-controlled double-blinded study.That the wording is slightly different from what's on the web suggests to me that the PDF and the online article are the *same article* at different stages of editing.


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## flux (Dec 13, 1998)

> quoterossman's new version jumbles Pimentel's 2000 and 2003 study.


Not exactly....


> quote:1) He references the 2003 study as "Eradication of Small Intestinal Bacterial Overgrowth Reduces Symptoms of IBS". This is incorrect. That is the title of the 2000 study.


It looks to me that he is referencing the 2000 study. It's the year that is wrong.


> quote:2) He rehashes his objections that have been refuted in the 2003 study. They only place where there is an edit is where he acknowledges it was a double blind placebo controlled study.


I think it is the initial hash. The edit is odd because on the web it says


> quote:This is not a placebo-controlled double-blinded study.


but the pdf says


> quote:The reported study was also is a placebo-controlled double-blinded study


I think that line was intending to say The reported study was also *not* a placebo-controlled double-blinded study.That the wording is slightly different from what's on the web suggests to me that the PDF and the online article are the *same article* at different stages of editing.


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## eric (Jul 8, 1999)

Skinny, there is an upcoming UNC chat Nov 9.I know DR whitehead will be there and maybe Dr Drossman. I know Dr Whitehead wrote on the SIBO and IBS issues as well as Dr Drossman.IBS PublicationsAnother look at bacteria and IBSBy Douglas A. Drossman, M.D. http://www.aboutibs.org/Publications/bacteria.html IBS PublicationsAnother look at bacteria and IBSIs IBS a Bacterial Infection?By: William E. Whitehead, Ph.D., Professor of Medicine and Co-Director, University of North Carolina Center for Functional GI and Motility Disorders http://www.aboutibs.org/Publications/bacteria2.html Why not go to the free chat and see about asking them the questions on it all? They have been doing these free chats for a couple years now and they are very informative and you get to ask them personally.


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## eric (Jul 8, 1999)

Skinny, there is an upcoming UNC chat Nov 9.I know DR whitehead will be there and maybe Dr Drossman. I know Dr Whitehead wrote on the SIBO and IBS issues as well as Dr Drossman.IBS PublicationsAnother look at bacteria and IBSBy Douglas A. Drossman, M.D. http://www.aboutibs.org/Publications/bacteria.html IBS PublicationsAnother look at bacteria and IBSIs IBS a Bacterial Infection?By: William E. Whitehead, Ph.D., Professor of Medicine and Co-Director, University of North Carolina Center for Functional GI and Motility Disorders http://www.aboutibs.org/Publications/bacteria2.html Why not go to the free chat and see about asking them the questions on it all? They have been doing these free chats for a couple years now and they are very informative and you get to ask them personally.


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## skinny (Jul 27, 2002)

Eric: You haven't addressed my concern regarding the Drossman bacterial articles. I am a little surprised since you like to tackle some complex issues in IBS research, but what I'm talking about is something that could be understood on a high school reading level. By now I think it's the fourth time I confronted you on this issue and you keep on evading it.


> quote:Skinny, there is an upcoming UNC chat Nov 9. I know DR whitehead will be there and maybe Dr Drossman. I know Dr Whitehead wrote on the SIBO and IBS issues as well as Dr Drossman.


I don't like chats due to the limitations of the protocol, but it's a good way to get some quick answers. Can you connect via an IRC client?


> quote:IBS PublicationsAnother look at bacteria and IBSBy Douglas A. Drossman, M.D. http://www.aboutibs.org/Publications/bacteria.html IBS PublicationsAnother look at bacteria and IBSIs IBS a Bacterial Infection?By: William E. Whitehead, Ph.D., Professor of Medicine and Co-Director, University of North Carolina Center for Functional GI and Motility Disorders http://www.aboutibs.org/Publications/bacteria2.html


*sigh* How many times do I have to tell you this is not up to date?


> quote:Why not go to the free chat and see about asking them the questions on it all? They have been doing these free chats for a couple years now and they are very informative and you get to ask them personally.


I wouldn't mind chatting, but the topic doesn't look relevant to my questions. I've got a better idea. Since you seem unable or unwilling to answer my concerns, forward the BB thread link to Drossman/Whitehead and see if you can get a response and post it by proxy. How does that sound?skinny


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## skinny (Jul 27, 2002)

Eric: You haven't addressed my concern regarding the Drossman bacterial articles. I am a little surprised since you like to tackle some complex issues in IBS research, but what I'm talking about is something that could be understood on a high school reading level. By now I think it's the fourth time I confronted you on this issue and you keep on evading it.


> quote:Skinny, there is an upcoming UNC chat Nov 9. I know DR whitehead will be there and maybe Dr Drossman. I know Dr Whitehead wrote on the SIBO and IBS issues as well as Dr Drossman.


I don't like chats due to the limitations of the protocol, but it's a good way to get some quick answers. Can you connect via an IRC client?


> quote:IBS PublicationsAnother look at bacteria and IBSBy Douglas A. Drossman, M.D. http://www.aboutibs.org/Publications/bacteria.html IBS PublicationsAnother look at bacteria and IBSIs IBS a Bacterial Infection?By: William E. Whitehead, Ph.D., Professor of Medicine and Co-Director, University of North Carolina Center for Functional GI and Motility Disorders http://www.aboutibs.org/Publications/bacteria2.html


*sigh* How many times do I have to tell you this is not up to date?


> quote:Why not go to the free chat and see about asking them the questions on it all? They have been doing these free chats for a couple years now and they are very informative and you get to ask them personally.


I wouldn't mind chatting, but the topic doesn't look relevant to my questions. I've got a better idea. Since you seem unable or unwilling to answer my concerns, forward the BB thread link to Drossman/Whitehead and see if you can get a response and post it by proxy. How does that sound?skinny


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## flux (Dec 13, 1998)

> quote:I don't like chats due to the limitations of the protocol


Huh?


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## flux (Dec 13, 1998)

> quote:I don't like chats due to the limitations of the protocol


Huh?


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## eric (Jul 8, 1999)

I was pointing out the different authors. I am also not worried like you are about anyone covering there tracks. I think you should be more worried about the problem from the orginal Dr Pimental study and its total bias in the media and was not corrected by Dr Pimental before being published.And as far as them not being a part of the international rome experts, its probably because they have not worked their way up there to be recognized in their field yet.However, like I said go to the chat. If you have never been to one and its been going on for two years now, why not try one and ask them yourself about the bacteria and IBS issues? They will be forthcoming and honest with you on it. They will not post to the bb. The only one who has done that is Dr Palsson on the HT forum. These doctors will not get invovled in disputes on a public IBS bb.I do like to tackle complex issues in IBS research, which is why I don't understand how so much evidence from Lin and Pimental seems to disregard a huge body of other IBS research and only promote SIBO and IBS, whith basically new information from all the previous IBS research or ongoing IBS research. No one calls sibo IBS or IBS SIBO. This will be real news when all of the centers, and I can tell you right now, they all know about sibo, get the same results as Pimental. Because something is not adding up for sure in my book on it all. It is my understanding right now, SIBO is caused by a functional motlity problem. But IBS is not just a functional motility problem, because it cannot be explained by the observations on it as just abnormal motility alone. But rather abnormal motility, viceral hypersensitivity and altered brain gut axis dysfunction.It is up to Pimental or Lin, to prove otherwise and to also prove the mechanisms that SIBO can cause to lead to d and C and D/C and viceral hyprsensitvity and areas of the brain that they know are impaired. As well as the gentics in IBS and how PI IBS can lead to IBS and many many unanswered questions in regards to sibo and IBS. I just never see Pimental or LIn talk about any of this? I bet also in part because both sibo and IBS have motility problems as issues, they maybe commonly found together perhaps, more then in the general population. I also know people with sibo, but they did not have IBS? As everyone is saying future studies are needed.Did you ever read this Skinny."Not sure if this would work for everyone...it is a link to the journal and the abstract there is in italian, but the .pdf link on the bottom gives me the whole article in English.K." http://www.minervamedica.it/index2.t?show=R10Y2004N05A0419 Do you know who Dr Mayer is in IBS research?There is also this, do you know who Dr Gershon in general research on gut functioning and in IBS research?Review article: serotonin receptors and transporters - roles in normal and abnormal gastrointestinal motility.Gershon MD.Department of Anatomy & Cell Biology, Columbia University, New York, NY, USA.Summary The gut is the only organ that can display reflexes and integrative neuronal activity even when isolated from the central nervous system. This activity can be triggered by luminal stimuli that are detected by nerves via epithelial intermediation. Epithelial enterochromaffin cells act as sensory transducers that activate the mucosal processes of both intrinsic and extrinsic primary afferent neurones through their release of 5-hydroxytryptamine (5-HT). Intrinsic primary afferent neurones are present in both the submucosal and myenteric plexuses. Peristaltic and secretory reflexes are initiated by submucosal intrinsic primary afferent neurones, which are stimulated by 5-HT acting at 5-HT(1P) receptors. 5-HT acting at 5-HT(4) receptors enhances the release of transmitters from their terminals and from other terminals in prokinetic reflex pathways. Signalling to the central nervous system is predominantly 5-HT(3) mediated, although serotonergic transmission within the enteric nervous system and the activation of myenteric intrinsic primary afferent neurones are also 5-HT(3) mediated. The differential distribution of 5-HT receptor subtypes makes it possible to use 5-HT(3) antagonists and 5-HT(4) agonists to treat intestinal discomfort and motility. 5-HT(3) antagonists alleviate the nausea and vomiting associated with cancer chemotherapy and the discomfort from the bowel in irritable bowel syndrome; however, because 5-HT-mediated fast neurotransmission within the enteric nervous system and the stimulation of mucosal processes of myenteric intrinsic primary afferent neurones are 5-HT(3) mediated, 5-HT(3) antagonists tend to be constipating and should be used only when pre-existing constipation is not a significant component of the problem to be treated. In contrast, 5-HT(4) agonists, such as tegaserod, are safe and effective in the treatment of irritable bowel syndrome with constipation and chronic constipation. They do not stimulate nociceptive extrinsic nerves nor initiate peristaltic and secretory reflexes. Instead, they rely on natural stimuli to activate reflexes, which they strengthen by enhancing the release of transmitters in prokinetic pathways. Finally, when all the signalling by 5-HT is over, its action is terminated by uptake into enterocytes or neurones, which is mediated by the serotonin reuptake transporter. In inflammation, serotonergic signalling is specifically diminished in the mucosa. Transcripts encoding tryptophan hydroxylase-1 and serotonin reuptake transporter are both markedly decreased. Successive potentiation of 5-HT and/or desensitization of its receptor could account for the symptoms seen in diarrhoea-predominant and constipation-predominant irritable bowel syndrome, respectively. Symptoms associated with the down-regulation of the serotonin reuptake transporter in the human mucosa in irritable bowel syndrome are similar to the symptoms associated with the knockout of the serotonin reuptake transporter in mice. The observation that molecular defects occur in the human gut in irritable bowel syndrome strengthens the hand of those seeking to legitimize the disease. At least it is not 'all in your head'. The bowel contributes.PMID: 15521849


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## eric (Jul 8, 1999)

I was pointing out the different authors. I am also not worried like you are about anyone covering there tracks. I think you should be more worried about the problem from the orginal Dr Pimental study and its total bias in the media and was not corrected by Dr Pimental before being published.And as far as them not being a part of the international rome experts, its probably because they have not worked their way up there to be recognized in their field yet.However, like I said go to the chat. If you have never been to one and its been going on for two years now, why not try one and ask them yourself about the bacteria and IBS issues? They will be forthcoming and honest with you on it. They will not post to the bb. The only one who has done that is Dr Palsson on the HT forum. These doctors will not get invovled in disputes on a public IBS bb.I do like to tackle complex issues in IBS research, which is why I don't understand how so much evidence from Lin and Pimental seems to disregard a huge body of other IBS research and only promote SIBO and IBS, whith basically new information from all the previous IBS research or ongoing IBS research. No one calls sibo IBS or IBS SIBO. This will be real news when all of the centers, and I can tell you right now, they all know about sibo, get the same results as Pimental. Because something is not adding up for sure in my book on it all. It is my understanding right now, SIBO is caused by a functional motlity problem. But IBS is not just a functional motility problem, because it cannot be explained by the observations on it as just abnormal motility alone. But rather abnormal motility, viceral hypersensitivity and altered brain gut axis dysfunction.It is up to Pimental or Lin, to prove otherwise and to also prove the mechanisms that SIBO can cause to lead to d and C and D/C and viceral hyprsensitvity and areas of the brain that they know are impaired. As well as the gentics in IBS and how PI IBS can lead to IBS and many many unanswered questions in regards to sibo and IBS. I just never see Pimental or LIn talk about any of this? I bet also in part because both sibo and IBS have motility problems as issues, they maybe commonly found together perhaps, more then in the general population. I also know people with sibo, but they did not have IBS? As everyone is saying future studies are needed.Did you ever read this Skinny."Not sure if this would work for everyone...it is a link to the journal and the abstract there is in italian, but the .pdf link on the bottom gives me the whole article in English.K." http://www.minervamedica.it/index2.t?show=R10Y2004N05A0419 Do you know who Dr Mayer is in IBS research?There is also this, do you know who Dr Gershon in general research on gut functioning and in IBS research?Review article: serotonin receptors and transporters - roles in normal and abnormal gastrointestinal motility.Gershon MD.Department of Anatomy & Cell Biology, Columbia University, New York, NY, USA.Summary The gut is the only organ that can display reflexes and integrative neuronal activity even when isolated from the central nervous system. This activity can be triggered by luminal stimuli that are detected by nerves via epithelial intermediation. Epithelial enterochromaffin cells act as sensory transducers that activate the mucosal processes of both intrinsic and extrinsic primary afferent neurones through their release of 5-hydroxytryptamine (5-HT). Intrinsic primary afferent neurones are present in both the submucosal and myenteric plexuses. Peristaltic and secretory reflexes are initiated by submucosal intrinsic primary afferent neurones, which are stimulated by 5-HT acting at 5-HT(1P) receptors. 5-HT acting at 5-HT(4) receptors enhances the release of transmitters from their terminals and from other terminals in prokinetic reflex pathways. Signalling to the central nervous system is predominantly 5-HT(3) mediated, although serotonergic transmission within the enteric nervous system and the activation of myenteric intrinsic primary afferent neurones are also 5-HT(3) mediated. The differential distribution of 5-HT receptor subtypes makes it possible to use 5-HT(3) antagonists and 5-HT(4) agonists to treat intestinal discomfort and motility. 5-HT(3) antagonists alleviate the nausea and vomiting associated with cancer chemotherapy and the discomfort from the bowel in irritable bowel syndrome; however, because 5-HT-mediated fast neurotransmission within the enteric nervous system and the stimulation of mucosal processes of myenteric intrinsic primary afferent neurones are 5-HT(3) mediated, 5-HT(3) antagonists tend to be constipating and should be used only when pre-existing constipation is not a significant component of the problem to be treated. In contrast, 5-HT(4) agonists, such as tegaserod, are safe and effective in the treatment of irritable bowel syndrome with constipation and chronic constipation. They do not stimulate nociceptive extrinsic nerves nor initiate peristaltic and secretory reflexes. Instead, they rely on natural stimuli to activate reflexes, which they strengthen by enhancing the release of transmitters in prokinetic pathways. Finally, when all the signalling by 5-HT is over, its action is terminated by uptake into enterocytes or neurones, which is mediated by the serotonin reuptake transporter. In inflammation, serotonergic signalling is specifically diminished in the mucosa. Transcripts encoding tryptophan hydroxylase-1 and serotonin reuptake transporter are both markedly decreased. Successive potentiation of 5-HT and/or desensitization of its receptor could account for the symptoms seen in diarrhoea-predominant and constipation-predominant irritable bowel syndrome, respectively. Symptoms associated with the down-regulation of the serotonin reuptake transporter in the human mucosa in irritable bowel syndrome are similar to the symptoms associated with the knockout of the serotonin reuptake transporter in mice. The observation that molecular defects occur in the human gut in irritable bowel syndrome strengthens the hand of those seeking to legitimize the disease. At least it is not 'all in your head'. The bowel contributes.PMID: 15521849


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## skinny (Jul 27, 2002)

> quote:I was pointing out the different authors. I am also not worried like you are about anyone covering there tracks. I think you should be more worried about the problem from the orginal Dr Pimental study and its total bias in the media and was not corrected by Dr Pimental before being published.


Eric you are really dense. Yes the original study had biases, but these became a non-issue in the second study except for selecting patients who were suspected for SIBO. So you are really bringing up an non-issue. I'm sure Pimentel saw all the criticisms with the first study, so that prompted him to conduct a better one. And now he's doing it again with another non-absorbable antibiotic similar to neomycin sulfate. What is needed is independent confirmation from other researchers.BTW, it is spelled Piment*e*l.


> quote:And as far as them not being a part of the international rome experts, its probably because they have not worked their way up there to be recognized in their field yet.


Oh I'd say they worked themselves up there, but not taken seriously by other researchers.


> quote:However, like I said go to the chat. If you have never been to one and its been going on for two years now, why not try one and ask them yourself about the bacteria and IBS issues? They will be forthcoming and honest with you on it. They will not post to the bb. The only one who has done that is Dr Palsson on the HT forum. These doctors will not get invovled in disputes on a public IBS bb.


I asked you to post their response by proxy not telling them to get on here. I thought you were in the loop with Drossman. I do not like chat rooms because you can't be verbose with all the information you are trying to present. So I'll pass. This is an open forum which is well suited for this kind of discussion.


> quote:I do like to tackle complex issues in IBS research, which is why I don't understand how so much evidence from Lin and Pimental seems to disregard a huge body of other IBS research and only promote SIBO and IBS, whith basically new information from all the previous IBS research or ongoing IBS research. No one calls sibo IBS or IBS SIBO. This will be real news when all of the centers, and I can tell you right now, they all know about sibo, get the same results as Pimental.


You claimed that other researchers had a hard time replicated the SIBO results, yet you didn't come up with one study that attempted to do it. And don't tell me about this one:Small Bowel Bacterial Overgrowth is a Common Cause of Chronic Diarrhea (August 2004) http://tinyurl.com/5egwn ...that didn't even find out if they had IBS symptoms or select constipation prone subjects. Pimentel did check for all of that.So where is a study that replicated the Pimentel SIBO studies?


> quote:Because something is not adding up for sure in my book on it all. It is my understanding right now, SIBO is caused by a functional motlity problem. But IBS is not just a functional motility problem, because it cannot be explained by the observations on it as just abnormal motility alone. But rather abnormal motility, viceral hypersensitivity and altered brain gut axis dysfunction.


SIBO symptoms are IBS symptoms. I'm sure SIBO doesn't explain all IBS cases simply because they don't have it. So what? Why not be different subgroups of IBS: SIBO, inflammation, and brain-gut dysfunction, or whatever else. After all IBS is defined by the *symptoms.*


> quote:It is up to Pimental or Lin, to prove otherwise and to also prove the mechanisms that SIBO can cause to lead to d and C and D/C and viceral hyprsensitvity and areas of the brain that they know are impaired.


So you are telling me that in order to have IBS you have to have a brain-gut dysfunction? Where is the evidence this happens for all IBS cases? So what: it could be secondary cause. It could be a combination of brain-gut dysfunction causing the SIBO and when it is wiped out, it returns because the brain-gut interaction is causing the bacteria to reflux. All these hypotheses need to be researched and ironed out.


> quote:As well as the gentics in IBS and how PI IBS can lead to IBS and many many unanswered questions in regards to sibo and IBS. I just never see Pimental or LIn talk about any of this?


I haven't either, but like I said - different researchers have focuses. That's why you need them to get them all together to debate theories.


> quoteid you ever read this Skinny.


No I haven't. I not familiar with Mayer or Gershon all that much. But I'm not going to read the stuff you link unless you are willing to read the information I present you.So before I move on, I need to get some straightforward answers from you:1) Did you read and compare both Drossman articles on bacterial overgrowth that I linked to?2) If so, did you find any errors in the updated Drossman article (the pdf file)?Just answer these questions and I'll move on from here. That should be simple enough for you.skinny


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## skinny (Jul 27, 2002)

> quote:I was pointing out the different authors. I am also not worried like you are about anyone covering there tracks. I think you should be more worried about the problem from the orginal Dr Pimental study and its total bias in the media and was not corrected by Dr Pimental before being published.


Eric you are really dense. Yes the original study had biases, but these became a non-issue in the second study except for selecting patients who were suspected for SIBO. So you are really bringing up an non-issue. I'm sure Pimentel saw all the criticisms with the first study, so that prompted him to conduct a better one. And now he's doing it again with another non-absorbable antibiotic similar to neomycin sulfate. What is needed is independent confirmation from other researchers.BTW, it is spelled Piment*e*l.


> quote:And as far as them not being a part of the international rome experts, its probably because they have not worked their way up there to be recognized in their field yet.


Oh I'd say they worked themselves up there, but not taken seriously by other researchers.


> quote:However, like I said go to the chat. If you have never been to one and its been going on for two years now, why not try one and ask them yourself about the bacteria and IBS issues? They will be forthcoming and honest with you on it. They will not post to the bb. The only one who has done that is Dr Palsson on the HT forum. These doctors will not get invovled in disputes on a public IBS bb.


I asked you to post their response by proxy not telling them to get on here. I thought you were in the loop with Drossman. I do not like chat rooms because you can't be verbose with all the information you are trying to present. So I'll pass. This is an open forum which is well suited for this kind of discussion.


> quote:I do like to tackle complex issues in IBS research, which is why I don't understand how so much evidence from Lin and Pimental seems to disregard a huge body of other IBS research and only promote SIBO and IBS, whith basically new information from all the previous IBS research or ongoing IBS research. No one calls sibo IBS or IBS SIBO. This will be real news when all of the centers, and I can tell you right now, they all know about sibo, get the same results as Pimental.


You claimed that other researchers had a hard time replicated the SIBO results, yet you didn't come up with one study that attempted to do it. And don't tell me about this one:Small Bowel Bacterial Overgrowth is a Common Cause of Chronic Diarrhea (August 2004) http://tinyurl.com/5egwn ...that didn't even find out if they had IBS symptoms or select constipation prone subjects. Pimentel did check for all of that.So where is a study that replicated the Pimentel SIBO studies?


> quote:Because something is not adding up for sure in my book on it all. It is my understanding right now, SIBO is caused by a functional motlity problem. But IBS is not just a functional motility problem, because it cannot be explained by the observations on it as just abnormal motility alone. But rather abnormal motility, viceral hypersensitivity and altered brain gut axis dysfunction.


SIBO symptoms are IBS symptoms. I'm sure SIBO doesn't explain all IBS cases simply because they don't have it. So what? Why not be different subgroups of IBS: SIBO, inflammation, and brain-gut dysfunction, or whatever else. After all IBS is defined by the *symptoms.*


> quote:It is up to Pimental or Lin, to prove otherwise and to also prove the mechanisms that SIBO can cause to lead to d and C and D/C and viceral hyprsensitvity and areas of the brain that they know are impaired.


So you are telling me that in order to have IBS you have to have a brain-gut dysfunction? Where is the evidence this happens for all IBS cases? So what: it could be secondary cause. It could be a combination of brain-gut dysfunction causing the SIBO and when it is wiped out, it returns because the brain-gut interaction is causing the bacteria to reflux. All these hypotheses need to be researched and ironed out.


> quote:As well as the gentics in IBS and how PI IBS can lead to IBS and many many unanswered questions in regards to sibo and IBS. I just never see Pimental or LIn talk about any of this?


I haven't either, but like I said - different researchers have focuses. That's why you need them to get them all together to debate theories.


> quoteid you ever read this Skinny.


No I haven't. I not familiar with Mayer or Gershon all that much. But I'm not going to read the stuff you link unless you are willing to read the information I present you.So before I move on, I need to get some straightforward answers from you:1) Did you read and compare both Drossman articles on bacterial overgrowth that I linked to?2) If so, did you find any errors in the updated Drossman article (the pdf file)?Just answer these questions and I'll move on from here. That should be simple enough for you.skinny


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## flux (Dec 13, 1998)

> quote:Why not be different subgroups of IBS: SIBO, inflammation, and brain-gut dysfunction, or whatever else. After all IBS is defined by the symptoms.


If you read this carefully, you will see that you answered your own question.


> quote:You claimed that other researchers had a hard time replicated the SIBO results, yet you didn't come up with one study that attempted to do it.


Where would find "attempts"?


> quote: I'm not going to read the stuff you link unless you are willing to read the information I present you


Logic?


> quote:2) If so, did you find any errors in the updated Drossman article (the pdf file)?


This is a red herring.


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## flux (Dec 13, 1998)

> quote:Why not be different subgroups of IBS: SIBO, inflammation, and brain-gut dysfunction, or whatever else. After all IBS is defined by the symptoms.


If you read this carefully, you will see that you answered your own question.


> quote:You claimed that other researchers had a hard time replicated the SIBO results, yet you didn't come up with one study that attempted to do it.


Where would find "attempts"?


> quote: I'm not going to read the stuff you link unless you are willing to read the information I present you


Logic?


> quote:2) If so, did you find any errors in the updated Drossman article (the pdf file)?


This is a red herring.


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## eric (Jul 8, 1999)

I don't think calling me dense is so ice Skinny.I also know that someone else edits a lot of the writings from these doctors to the public.I do see what your talking about, but don't view it as seriously as you seem too.Independent confirmation has not been acheived yet. They don't publish until that happens. It is also more on the intial researchers to prove the factors and the connections. That has not been fully done yet. These researchers have a very specific interest in sibo. Like I said I have seen nothing written my them connecting all the dots yet either to the huge body of previous research done on IBS, but not just IBS functional disorders in general which can and do greatly over lap. SIBO also usally causes symptoms an hour to an hour and a half after eating and then usally abdominal pain, bloating, and diarrhea. I don't thing this explains alternators or constipation for one either and they already have good reasons for that happening and why already in IBS. Plus you have to match all the symptoms, such as the sensation of incomplete evaucation and rectal sensitivity etc.From what I have read the second study had problems as well?Going back to the first.This did not make me happy personally."Some journalists (and possibly the author) addressed the findings of this study in a very dramatic fashion: ". . . 'This is really exciting because it points to the cause of the disease. Treatments for IBS to this point have been directed at symptoms, not any cause,' said Dr. Mark Pimental." (Reuters 12/13/00) However, even when findings come from a well-designed study, the investigators are obliged to monitor and temper what is put into print. Otherwise, media coverage itself can bias decisions of physicians, patients, or regulators."He was already using the cause word before it was even figured all out? What gives with that really.Maybe this helps explain your next point"And as far as them not being a part of the international rome experts, its probably because they have not worked their way up there to be recognized in their field yet.--------------------------------------------------------------------------------Oh I'd say they worked themselves up there, but not taken seriously by other researchers."personally at the end of the day, I don't believe they are high enough up there yet. You have to work your way up there as a doctor, it isn't just a matter of what you point out, but also of credentials and much more then that in the bigger picture. All IBS researchers also know about them and their studies.You have a lot of excuses not to just pop into the chat and ask a question, but they aren't good enough in my book. Just join and ask, who knows you might learn quite a few things in general in IBS while our there. One of the authors will be there for sure. IT is also extremely good of them to do these public forums for the general public for free and to help educate IBSers and help answer their questions. That is in my book extremely helpful. Not many places to that or not many doctors. Were taking some extremly busy researchers.I have pointed out other researchers and sibo and IBS, but the full texts are not online, just the comments in gastroenterology magazine. For that you might have to go to the library. But they won't publish until they have something worth while to publish."SIBO symptoms are IBS symptoms"No there not really, they can mimick SOME symptoms, but not all, that is a big part of the problem here. In order to get that also, you have to sudy indepth rome symptoms and callsifications and even types of pain and things doctors learn in school.There are already different sub groups of IBS, all leading to altered motility, viceral hypersensivity and brain gut axis dysfunction.Dr Mayer is head of the "UCLA Center for Neurovisceral Sciences & Women's Health "The other really big center studying parts of IBS like the UNC who both were awarded a total of 8 million dollars by the NIH.Dr Gershon, is one of the biggest doctors in gastroenterology. A world expert and pioneer in how the gut woks and specifically in how serotonin makes the gut work.This is why a narrow focus can be a problem. "Dr. Gershon's earliest work involved investigations of the function of serotonin in the bowel, but it soon also came to involve studies of the cellular and molecular basis of intrinsic reflex control and ontogeny of the ENS. Dr. Gershon's work has been vital in the rediscovery of the unique ability of the enteric nervous system (ENS) to function independently of CNS input, and he has become the acknowledged world leader in research in enteric neuronal development."We actually have some MAJOR experts in many fields helping with IBS.GershonDrossmanWhiteheadEsther Sternberg, MDChief, Section on Neuroendocrine Immunology and BehaviorDirector, Molecular, Cellular and Behavioral Integrative Neuroscience ProgramNational Institute of Mental Health, National Institute of HealthA pioneer in the field of neural-immune interactions, Dr. Sternberg will present the scientific evidence proving molecular, neuroanatomical and hormonal links between the brain and immune system and will discuss the role that disruptions of such links play in inflammatory/autoimmune disease. and many many more.Pimentel hs two studies out on sibo and IBS. The first flawed, the second questionable it would seem.The combined studies from the above authors are in the thousands in many fields, neurogastroenterology, immunology, gastroenterology, neurology and a whole lot more and hundreds if not more in IBS and functional gastro disorders.


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## eric (Jul 8, 1999)

I don't think calling me dense is so ice Skinny.I also know that someone else edits a lot of the writings from these doctors to the public.I do see what your talking about, but don't view it as seriously as you seem too.Independent confirmation has not been acheived yet. They don't publish until that happens. It is also more on the intial researchers to prove the factors and the connections. That has not been fully done yet. These researchers have a very specific interest in sibo. Like I said I have seen nothing written my them connecting all the dots yet either to the huge body of previous research done on IBS, but not just IBS functional disorders in general which can and do greatly over lap. SIBO also usally causes symptoms an hour to an hour and a half after eating and then usally abdominal pain, bloating, and diarrhea. I don't thing this explains alternators or constipation for one either and they already have good reasons for that happening and why already in IBS. Plus you have to match all the symptoms, such as the sensation of incomplete evaucation and rectal sensitivity etc.From what I have read the second study had problems as well?Going back to the first.This did not make me happy personally."Some journalists (and possibly the author) addressed the findings of this study in a very dramatic fashion: ". . . 'This is really exciting because it points to the cause of the disease. Treatments for IBS to this point have been directed at symptoms, not any cause,' said Dr. Mark Pimental." (Reuters 12/13/00) However, even when findings come from a well-designed study, the investigators are obliged to monitor and temper what is put into print. Otherwise, media coverage itself can bias decisions of physicians, patients, or regulators."He was already using the cause word before it was even figured all out? What gives with that really.Maybe this helps explain your next point"And as far as them not being a part of the international rome experts, its probably because they have not worked their way up there to be recognized in their field yet.--------------------------------------------------------------------------------Oh I'd say they worked themselves up there, but not taken seriously by other researchers."personally at the end of the day, I don't believe they are high enough up there yet. You have to work your way up there as a doctor, it isn't just a matter of what you point out, but also of credentials and much more then that in the bigger picture. All IBS researchers also know about them and their studies.You have a lot of excuses not to just pop into the chat and ask a question, but they aren't good enough in my book. Just join and ask, who knows you might learn quite a few things in general in IBS while our there. One of the authors will be there for sure. IT is also extremely good of them to do these public forums for the general public for free and to help educate IBSers and help answer their questions. That is in my book extremely helpful. Not many places to that or not many doctors. Were taking some extremly busy researchers.I have pointed out other researchers and sibo and IBS, but the full texts are not online, just the comments in gastroenterology magazine. For that you might have to go to the library. But they won't publish until they have something worth while to publish."SIBO symptoms are IBS symptoms"No there not really, they can mimick SOME symptoms, but not all, that is a big part of the problem here. In order to get that also, you have to sudy indepth rome symptoms and callsifications and even types of pain and things doctors learn in school.There are already different sub groups of IBS, all leading to altered motility, viceral hypersensivity and brain gut axis dysfunction.Dr Mayer is head of the "UCLA Center for Neurovisceral Sciences & Women's Health "The other really big center studying parts of IBS like the UNC who both were awarded a total of 8 million dollars by the NIH.Dr Gershon, is one of the biggest doctors in gastroenterology. A world expert and pioneer in how the gut woks and specifically in how serotonin makes the gut work.This is why a narrow focus can be a problem. "Dr. Gershon's earliest work involved investigations of the function of serotonin in the bowel, but it soon also came to involve studies of the cellular and molecular basis of intrinsic reflex control and ontogeny of the ENS. Dr. Gershon's work has been vital in the rediscovery of the unique ability of the enteric nervous system (ENS) to function independently of CNS input, and he has become the acknowledged world leader in research in enteric neuronal development."We actually have some MAJOR experts in many fields helping with IBS.GershonDrossmanWhiteheadEsther Sternberg, MDChief, Section on Neuroendocrine Immunology and BehaviorDirector, Molecular, Cellular and Behavioral Integrative Neuroscience ProgramNational Institute of Mental Health, National Institute of HealthA pioneer in the field of neural-immune interactions, Dr. Sternberg will present the scientific evidence proving molecular, neuroanatomical and hormonal links between the brain and immune system and will discuss the role that disruptions of such links play in inflammatory/autoimmune disease. and many many more.Pimentel hs two studies out on sibo and IBS. The first flawed, the second questionable it would seem.The combined studies from the above authors are in the thousands in many fields, neurogastroenterology, immunology, gastroenterology, neurology and a whole lot more and hundreds if not more in IBS and functional gastro disorders.


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## eric (Jul 8, 1999)

forgot the link http://www.conference-cast.com/ibs/GUIs/bios.cfm I also pointed this out to you before. Its not that know ones knows anything about sibo and IBS. This was also from 2000. As you can see its complex.LACTOSE INTOLERANCE AND SMALL BOWEL BACTERIAL OVERGROWTH http://www.ibsgroup.org/cgi-local/ubbcgi/u...c&f=10&t=001018


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## eric (Jul 8, 1999)

forgot the link http://www.conference-cast.com/ibs/GUIs/bios.cfm I also pointed this out to you before. Its not that know ones knows anything about sibo and IBS. This was also from 2000. As you can see its complex.LACTOSE INTOLERANCE AND SMALL BOWEL BACTERIAL OVERGROWTH http://www.ibsgroup.org/cgi-local/ubbcgi/u...c&f=10&t=001018


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## Talissa (Apr 10, 2004)

Worth reading...The Truth About the Drug Companies: How They Deceive Us and What to Do About It"...Angell, "during her two decades at [the New England Journal of Medicine] had a front-row seat on the growing corruption of the pharmaceutical industry." Perhaps, but since leaving the Journal, she's gone behind the curtains of Big Pharma, Big University, and Big Faculty......Angell reminds us of the increasingly cozy relationships between big industry and the faculties of universities....Angell's examples of the large consulting fees paid by industry to individual faculty members and to NIH scientists and directors are astounding." http://content.nejm.org/cgi/content/full/351/15/1580


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## Talissa (Apr 10, 2004)

Worth reading...The Truth About the Drug Companies: How They Deceive Us and What to Do About It"...Angell, "during her two decades at [the New England Journal of Medicine] had a front-row seat on the growing corruption of the pharmaceutical industry." Perhaps, but since leaving the Journal, she's gone behind the curtains of Big Pharma, Big University, and Big Faculty......Angell reminds us of the increasingly cozy relationships between big industry and the faculties of universities....Angell's examples of the large consulting fees paid by industry to individual faculty members and to NIH scientists and directors are astounding." http://content.nejm.org/cgi/content/full/351/15/1580


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## Talissa (Apr 10, 2004)

If Dr Drossman is at that chat, maybe you can ask him what his "consultant" fees are for the ELEVEN pharmaceutical co's which currently use him as a "consultant"?


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## Talissa (Apr 10, 2004)

If Dr Drossman is at that chat, maybe you can ask him what his "consultant" fees are for the ELEVEN pharmaceutical co's which currently use him as a "consultant"?


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## eric (Jul 8, 1999)

CURRICULUM VITAEDouglas Arnold Drossman, M.D.Co-Director, UNC Center for Functional GI and Motility DisordersOffice:1110 Bioinformatics BuildingChapel Hill, NC 27599-7080 Born March 20, 1946, Brooklyn, New YorkMarried, 1970, Deborah Ducoff (1946)Children: David Samuel (1974)Daniel Robert (1977)EDUCATION:Academic Diploma, Honors, Jamaica H.S., Jamaica, New York, 1962B.A., Cum Laude, Hofstra University, Hempstead, New York, 1966M.D., Albert Einstein College of Medicine, Bronx, New York, 1970POSTGRADUATE TRAINING:Medical InternshipUniversity of North Carolina - 7/70-6/71North Carolina Memorial HospitalChapel Hill, North CarolinaL. G. Welt, M.D., Chairman, Department of MedicineJunior Medical ResidencyUniversity of North Carolina 7/71-6/72North Carolina Memorial HospitalChapel Hill, North CarolinaH. Fallon, M.D., Acting Chairman, Department of MedicineSenior Associate Medical Resident and Teaching Assistant in MedicineNew York University - Bellevue Medical Center 7/72-6/73New York, New YorkSaul Farber, M.D., Chairman, Department of MedicineInstructor and Fellow in Medicine and Psychiatry (Psychosomatic Medicine)University of Rochester Medical Center 7/75-6/76Rochester, New YorkGeorge L. Engel, M.D., Chairman, Medical-Psychiatric Liaison GroupDROSSMAN 2Fellow in GastroenterologyDivision of Digestive Diseases and Nutrition 7/76-6/78Department of Medicine, University of North Carolinaat Chapel Hill - North Carolina Memorial HospitalChapel Hill, North CarolinaDon W. Powell, M.D., ChiefMILITARY SERVICE:Major, United States Air Force Medical Corps 8/73-7/75Chief of Internal MedicineUSAF Hospital, Bergstrom AFB, TexasEMPLOYMENT HISTORYrofessor of Medicine and Psychiatry 7/90School of MedicineUniversity of North Carolina at Chapel HillMarschall S. Runge, M.D., Chair, Department of MedicineR. Goldin, M.D., Chair, Department of PsychiatryAssociate Professor of Medicine and Psychiatry 7/83Assistant Professor of Medicine and Psychiatry 7/78Instructor, Department of Medicine 7/77Clinical Instructor 11/76-10/77School of NursingUniversity of North Carolina at Chapel HillNurse Practitioner ProgramCERTIFICATION:Internal Medicine, June, 1973Gastroenterology, October, 1979LICENSURE:North Carolina August 1976Texas January 1974New York January 1971DROSSMAN 3PROFESSIONAL SOCIETIES:Member, American Psychosomatic Society 1977Councillor 1985-19881990-1992Secretary/Treasurer 1992-1995President-Elect 1995-1996President 1996-1997Fellow, American College of Physicians 1978Member, Durham-Orange County Medical Society 1978Member, American Federation for Clinical Research 1979Member, American Gastroenterological Association 1980Member, American Society for Gastrointestinal Endoscopy 1982Member, Southern Society for Clinical Investigation 1986Member, Academy of Behavioral Medicine Research 1986Fellow, American College of Gastroenterology 1989Fellow, American Academy on Physician and Patient 1992PROFESSIONAL SERVICE:EDITORIAL APPOINTMENTS:a. Editorial BoardsASTBehavioral Medicine Abstracts 1985-1991Stress Medicine 1985-1992Current Concepts in Gastroenterology 1986-1990Inflammatory Bowel Disease 1994-1998CURRENTJournal of Clinical Gastroenterology 1986-Merck Manual, Gastroenterology Editor 1987-15th (1987) 16th (1992), and 17th (1999) editionsMerck Manual of Medical Information, Home Edition, Gastroenterology Editor 1997 ï¿½1st (1997) and 2nd (2003) editionsMind-Body Medicine 1993-Psychosomatic Medicine 1997-Gastroenterology 1998-Medscape Gastroenterology 1999Participate-Newsletter of the International Foundation for 2000-Functional Gastrointestinal DisordersRomanian Journal of Gastroenterology 2000-International Journal of Functional Syndromes 2001-b. Editor:Functional Brain-Gut Research Group Newsletter 1990-Participate-Newsletter of the International Foundation for 2000-Functional Gastrointestinal Disorders (Senior Associate Editor)DROSSMAN 4c. Associate Editor:Gastroenterology 2001-d. Ad hoc reviewer for:Annals of Internal Medicine 1978-Gastroenterology 1978-General Hospital Psychiatry 1979-Archives of Internal Medicine 1981 -American Journal of Psychiatry 1981 -American Journal of Digestive Diseases 1981 -American Journal of Gastroenterology 1982 -Psychosomatics 1983 -Digestive Diseases and Sciences 1983 -Journal of the Amer. Medical Assoc. 1984 -Journal of General Internal Medicine 1985 -Journal of Clinical Gastroenterology 1985 -Health Psychology 1989 -Gut 1990 -Western Journal of Medicine 1991 -New England Journal of Medicine 1992 -ADVISORY BOARDS:Health Digest (Whittle communications) 1986-1992The Partnership for Quality Living (CCFA and Kabi Pharmacia, Inc.) 1993-1994Merck Manual (GI Section Editor, 1994-) 1988-UCLA Center for Functional Bowel Disorders and Abdominal Pain 1992-International Foundation for Functional Gastrointestinal Disorders 1992-Center for the Advancement of Health 1995-Olestra Surveillance Advisory Council 1996-ABC News 1997-Medscape Gastroenterology 1999-Glaxo Wellcome 2000-Intestinal Disease Foundation, Pittsburgh, PA 2000-Novartis 2000-UCLA Mind-Body Collaborative Research Center 2001-National Womenï¿½s Health Resource Center 2001-GlaxoSmithKline Risk Management Program Advisory Panel 2002-PHARMACEUTIC CONSULTATION (SELECTED-ACTIVE):Glaxo-Smith KlineProcter & GambleSolvayAstra-ZenecaNovartisEMD - MerckForest LaboratoriesLilly PharmaceuticalsWellspring PharmaceuticalsSanofi~SynthelaboEisai Co., Ltd.DROSSMAN 5GRANTS AND AWARDSGRANTS AND AWARDS: FEDERAL1. The Irritable Bowel Syndrome: Characterizing the Patient. Principal Investigator (35%), 4/l/83 -3/3l/86, #ROlAM29934, National Institutes of Health (NIADDK), $345,l36.2. Abuse/Psychosocial Factors in Patients with GI Disorders. Principal Investigator (40%), 9/1/91 -8/31/95, #RO1MH46959, National Institutes of Health (NIMH), $844,476.3. Multicenter Trial of Functional Bowel Disorders. Principal Investigator (40%), 9/30/95 - 8/31/00,#RO1DK49334, National Institutes of Health (DK), $2,969,913 First year award, $622,572.4. Multicenter Trial of Functional Bowel Disorders. Principal Investigator (40%), 9/01/00 - 8/31/02,#RO1DK49334, National Institutes of Health (NIDDK), $877,621 First year award, $1,544,471 2-yearextension of previous award.5. Psychophysiology of Irritable Bowel Syndrome. Co-Investigator (20%) with William E. Whitehead,PhD, Principal Investigator. 12/1/97- 11/30/02 National Institutes of Health (NIDDK), $840,402 FirstYear Award, $124,367. (Bridge funds, $92,889 awarded for 7/1/97-11/30/97)6. Gastrointestinal Biopsychosocial Research Center at UNC. Response to RFA OB-03-004.7/01/04 ï¿½ 6/30/09; R24 DK067674Co-Principal Investigator (20%) with William Whitehead, Co-Principal Investigator (20%). National Institutes of Health (NIDDK) First year award $993,453($682,089 direct), and full-term 5-year award, $4,953,824 ($3,401,217 direct).GRANTS AND AWARDS: FOUNDATIONSAWARDED1. Medical Liaison Development Fund, funded by S. S. Zlinkoff Foundation, 1979, $5,500; Renewal1980, $6,500.2. Health related quality of life in patients with IBD. Pilot study. Core Center for Diarrheal Diseases(CCDD), UNC. Principal Investigator, 4/1/86-8/31/86, $10,000.3. Mail Survey of Health Related Quality of Life in IBD. National Foundation for Ileitis and Colitis,New York, N.Y. Principal Investigator, 7/1/87-12/31/88, $5,000.4. Planning Grant: Health Related Quality of Life in an Israeli IBD Population. Co-Investigatorwith Dr. Ami Sperber, Bersheva Medical Center, Jerusalem, Israel, 3/15/93-12/31/93, $6,000.5. Clinical and Physiological Characteristics of Functional Distal Esophageal Disorders.Multinational Working Teams to Develop Diagnostic Criteria for Functional GastrointestinalDisorders. Co-Investigator with Dr. Yehuda Ringel MD, Principal Investigator 1/1/99-12/31/99,$29,970.6. ACG Institute 2002 Clinical Scholar Award. American College of Gastroenterology. 07/02-07/03,$15,000.7. United States-Israel Binational Science Foundation Proposal: ï¿½Is Gynecological SurgeryAssociated with Subsequent Development of IBS and Other Painful Disorders.ï¿½ Co-Investigatorwith Ami Sperber MD, Principal Investigator. 9/2002-06/2006, $219,977. US component, $71,427.8. APS Presidentï¿½s Award. American Psychosomatic Society. 03/2003, $1,000.DROSSMAN 69. Does Education Improve Outcome in Patients with Irritable Bowel Syndrome? American Collegeof Gastroenterology. Co-Investigator with Albena Halpert MD, and Charlene Prather, MD, PrincipalInvestigators. 07/01/02-06/30/03, $35,000.10. American College of Gastroenterology Clinical Scholar Award. American College ofGastroenterology 7/1/03 ï¿½ 6/30/04. $15,000.11. The Epidemiology of Functional Gastrointestinal Disorders in Latin America: A PopulationbasedStudy. Co-Investigator with Principal Investigator, Loreto Cortes, MD, Rodolfo Peï¿½a, MD, andDouglas Morgan, MD, Rome III Committees, 7/1/03 ï¿½ 6/30/04, $30,000.GRANTS AND AWARDS: PHARMACEUTICAL1. Smith, Kline and Beckman award for study of the irritable bowel syndrome. 1982, $7,500.2. A Pilot Evaluation of BW942C in the Treatment of IBS. Burroughs Wellcome Co. Inc., ResearchTriangle Park, N.C. Principal Investigator, 12/84-12/85, $32,400.3. A Parallel Study of Buspirone in the Treatment of IBS. Bristol-Myers Pharmaceutical Group,Evansville, Ind. Principal Investigator, 4/1/88-4/30/90, $50,500.4. Gift for personal research activities. Sandoz Pharmaceuticals, 12/90, $5,000.5. The Prevalence of Functional Gastrointestinal Disorders in a Randomized National Sample.Procter & Gamble Co. Inc. Principal Investigator, 3/1/90-12/31/90, $15,000.6. Study of Subgroups of Irritable Bowel Syndrome in a Randomized National Sample. Procter &Gamble Co. Inc. Principal Investigator, 1/1/91-9/30/91. $12,000.7. A Parallel Study to Determine the Efficacy of Librax for Treatment of Irritable BowelSyndrome. Hoffmann La Roche Co.8. Survey of Illness Severity in Functional Bowel Disorders. Glaxo Corporation. 3/19/93, $9,860.9. Development of a Quality of Life Instrument for Irritable Bowel Syndrome. SandozCorporation. 1/1/95-9/1/95, $50,000.10. An Investigative Survey to Determine Optimal Methods for Measuring Clinical Endpoints inPatients with Irritable Bowel Syndrome. Smith Kline Beecham. 4/1/95-8/1/95, $45,000.11. Multicenter Trial of Fedotozine in Treatment of Irritable Bowel Syndrome. Glaxo Corp. 1/1/95-4/30/95, $52,000.12. A Double-Blind Study to Compare the Efficacy and Safety of SB-207266-A with Placebo inPatients with Irritable Bowel Syndrome. Smith Kline Beecham. 8/1/96-7/31/97, $65,000.13. A Multicenter, Double-blind, Placebo Controlled, Parallel Group Dose-response Study ofControlled Release Darifenacin in Treatment of IBS. Pfizer Corp. 1/1/97-12/31/97, $56,175.14. Multicenter Trial of Alosetron In Treatment of IBS. Glaxo-Wellcome. 1/1/98-12/31/98, $22,850.DROSSMAN 715. A Double-Blind, Randomized, Placebo-Controlled Phase II Clinical Trial of OPC 12759(Rebamipide) for the Treatment of Non-Ulcer Dyspepsia in Patients with/without HelicobacterPylori. Otsuka. 4/1/98-12/31/98, $148,860.16. An 8-Week Randomized, Double-Blind, Placebo-Controlled Study to Evaluate the Efficacy andSafety of Alosetron (GR68755) 1 Mg BID in the Treatment of Anxiety in Females with IrritableBowel Syndrome. Glaxo-Wellcome. 7/1/97-6/30/98, $93,574.50.17. A Double-Blind, Placebo-Controlled Dose Ranging Study to Compare the Efficacy and Safety ofThree Doses of SB-207266-A (20mg, 5mg and 1 mg od) with Placebo Over 12 weeks in theTreatment of Irritable Bowel Syndrome. SmithKline Beecham. 7/27/98-7/26/99, $52,864.18. A 12-Month Randomized, Double Blind, Placebo-Controlled Study to Evaluate the Quality ofLife and Safety Associated with the Long-Term Use of Alosetron (GR68755) in Subjects withIrritable Bowel Syndrome. GlaxoWellcome. 5/15/98-12/31/99, $40,212.19. A Single-Blind, Placebo Controlled Continuation Study to Investigate the Safety of SB-207266-A. SmithKline Beecham. 9/1/98-12/22/98, $72,800.20. A 12-week, randomized, double-blind, placebo-controlled, study of Alosetron (GR68755) in malesubjects with alternating diarrhea/constipation irritable bowel syndrome. ICON Protocol#S3B20023. 3/15/00-12/15/00, $21,000.21. A 12 week randomized, double-blind, placebo-controlled study of Alosetron (GR68755) infemale subjects with alternating diarrhea/constipation irritable bowel syndrome. ICON Protocol#S3B20013. 3/15/00-12/15/00, $21,000.22. A dose-ranging safety and efficacy study of the effect of Recombinant-Methionyl HumanNeurotrophin-3 (NT-3) on bowel function in patients with constipation. Regeneron Pharmaceuticals,Inc. 5/15/00-5/14/01, $52,570.23. A study to evaluate the safety and efficacy of TAK-637 (30 mg BID, 60 mg BID and 120 mg BID)versus placebo in subjects with irritable bowel syndrome. TAP Holdings-Phoenix International.Protocol TAK-637-99-201. 7/20/00-7/19/01, $41,030.24. A randomized, double-blind, placebo-controlled multicenter study to assess the efficacy, safetyand tolerability of tegaserod 2 mg bid and 6 mg bid given orally vs. placebo in patients withchronic constipation CHTF919 E 2302. Novartis Pharmaceuticals Corporation. 9/1/01-9/1/02,$45,860.25. A 12-Week, Randomized, Double-Blind, Placebo-Controlled, Fixed-Dose, Parallel Group,Multicenter Study of The Safety and Efficacy of Dexloxiglumide 200 MG B.I.D. and 200 MGT.I.D. in Female Patients with Constipation-Predominant Irritable Bowel Syndrome DEX-MD-01A. Forest Laboratories/ICON. 02/20/02-6/17/03, $99,070.26. An Open-Label Extension of Study DEX-MD-01A to Investigate the Long-Term Safety andEfficacy of Dexloxiglumide 200 MG T.I.D. in Female Patients with Constipation-PredominantIrritable Bowel Syndrome DEX-MD-01B. Forest Laboratories/ICON. 2/20/02-11/14/03, $49,940.27. An Open-Label Extension of Study Dex-MD-01B and Dex-MD-02B To Investigate the Long-Term Safety and Efficacy of Dexloxiglumide 200 MG T.I.D. In Female Patients withConstipation-Predominant Irritable Bowel Syndrome. Principal Investigator with Christine Dalton,PA-C. Forest Laboratories, Inc. Protocol DEX-MD-10. Project period- 02/13/03-11/14/03. $14,000.DROSSMAN 828. A Double-Blind, Placebo-Controlled, Randomized, Multicenter Study to Investigate the Safetyand Efficacy of 2 mg TID of Cilansetron Over 12 Weeks Followed by a 4-Week RandomizedTreatment Period in Diarrhea-Predominant Irritable Bowel Syndrome Subjects. PrincipalInvestigator with Christine Dalton, PA-C. Solvay Pharmaceuticals, Inc./Quintiles, Inc. ProtocolS2413011. 06/20/02-10/20/03. $34,716.29. An Eight-Week, Randomized, Double-Blind, Placebo-Controlled, Dose-Ranging Study toEvaluate Efficacy and Safety of SB 223412 in Subjects with Irritable Bowel Syndrome. PrincipalInvestigator with Christine Dalton, PA-C. GlaxoSmithKline. Protocol SB223412. 7/30/02 ï¿½ 7/29/03.$37,084.30. A Multi-Center, Double-Blind, Randomized, Placebo-Controlled, Phase III Study of the Efficacyand Safety or Oral RU-0211 for the Treatment of Occasional Constipation. Principal Investigatorwith Christine Dalton, PA-C. Sucampo Pharmaceuticals. Protocol SPI 0211SC0232. Project period ï¿½2/13/03-10/14/03. $43,200.31. A Twelve-Week Randomized, Double-Blind, Placebo-Controlled, Parallel Group Study to Assesthe Safety and Efficacy of 0.5 mg QD, 1 mg QD, and 1 mg BID of Alosetron in Female Subjectswith Severe Diarrhea Predominant IBS Who Have Failed Conventional Therapy. PrincipalInvestigator with Christine Dalton, PA-C. GlaxoSmithKline. Protocol S3B30040 Project period09/15/03-09/14/04. $31,73932. A 12-Week, Double-Blind, Randomized Study of the Safety and Efficacy of Oral SPI-0211 inSubjects with Constipation-Predominant Irritable Bowel Syndrome. Principal Investigator withChristine Dalton, PA-C. Sucampo Pharmaceuticals. Protocol SPI 0211 SC0221. Project period ï¿½06/01/03-12/31/04. $40,000.33. Clinical and Physiological Differences Among Sub-groups of IBS: A comparison of IBS withConstipation, IBS with Diarrhea and Mixed/Alternators. Principal Investigator. NovartisPharmaceuticals, Project Period - 9/30/03 ï¿½ 12/31/04. $249,199.34. A Multicenter, Double-Blind, Placebo-Controlled Efficacy and Safety Study of Low-DoseNaltrexone HCl (PTI-901) in Female Patients with Irritable Bowel Syndrome. PrincipalInvestigator with Christine Dalton, PA-C. Pain Therapeutics. Protocol PTI-901-NB, 1/15/-1/14/05,$43,297.35. A Multicenter, Double-Blind, Placebo-Controlled Efficacy and Safety Study of Low-DoseNaltrexone HCl (PTI-901) in Male Patients with Irritable Bowel Syndrome. PrincipalInvestigator with Christine Dalton, PA-C. Pain Therapeutics Protocol PTI-901-NC 1/15/04-1/14/05,$42,999.GRANTS AND AWARDS: UNIVERSITY OF NORTH CAROLINA1. Junior Faculty Development Award. University of North Carolina $3,000, 1981.2. Jefferson-Pilot Fellowship in Academic Medicine. University of North Carolina, $8,000, 1981-85.3. TEAM Mini-Grant for the Development of a Natural Language Inquiry Computerized PatientSimulation. University of North Carolina, 4/7/88, $4,000.4. Dept. of Medicine Award for study of Health Related Quality of Life in IBD. University of NorthCarolina, 2/1/89, $3,500.5. Kenan Professor-Sabbatical. University of North Carolina, 2002-2003, $56,000.DROSSMAN 96. Division of Gastroenterology and Hepatology Eugene M. Bozymski Award in Endoscopy,presented by the GI fellows, 6/19/04, $500COMMITTEES (Research, Service, Education)EPARTMENT OF MEDICINE:Internship Selection Committee 1977 -Housestaff-Faculty Committee 1980 - 1984Chairman, Selection Committee, Mack Lipkin Sr. Visiting Professorship 1983 -MEDICAL SCHOOL:Committee for Curriculum Review III. Subcommittee on Transition from 1981-1983the Basic Sciences to the Medical SciencesHealth Promotion/Disease Prevention Steering Comm. 1983Residency Student Advisor 1991-UNC Medical Practice and the Community (MPAC); Content Subcommittee 1995NATIONAL:American Gastroenterological Association (AGA)Council on Nerve-Gut Interactions 198l-1986Program Selection Committee Member - Clinical 1985-1986Program Selection Chairman-Functional Nerve/Gut 1990-1992Education and Training Committee 1993-1996GLC Curriculum Task Force on Motility 1994-1995, 2001Chair, Abstract Selection, Functional GI Disorders 1998Abstract Selection Committee, Functional GI Disorders 1999Clinical Teaching Project 1994-2002Nominating Committee 1998Abstract Selection Committee: Pharmacological Treatment of 2000FGID (#87)Co-Chair, Motility & Nerve-Gut Interactions Section 2001-2003Chair, Motility & Nerve-Gut Interactions Section 2003-2005American Psychosomatic SocietyCouncil Member 1985-19881990-19921986 Meeting Program Committee 1985-1986Chairman, Membership Committee 1988-19921992 50th Anniversary Program Committee 1991-1992Secretary/Treasurer 1992-1995Finance Committee 1992-Liaison Committee 1993-Long Range Planning Committee 1993-1994 Program Committee 1993-1994President-Elect 1995-1996President 1996-1997American College of Gastroenterology (ACG)Abstract Selection Committee - Small bowel 1992Chairman, Ad Hoc Committee on Doctor/Patient Relations 1992-1994DROSSMAN 10Patient Care Committee (Co-Chair 1995-1997) 1995-Functional/Brain-Gut Research Group of AGA (FBGRG) 1989-Chair 1989-1994Newsletter Editor 1989-American College of Physicians (ACP)MKSAP IX Program Committee (Gastroenterology) 1989-1991American Digestive Disease SocietySelection Committee: Research Investigator Award of Brain-gut Hormones 1987American Academy on Physician and PatientCharter Fellow and Faculty Coordinator 1988-Crohn's and Colitis Foundation of America (CCFA)IBD Forum Planning Committee 1991-1996Patient Education Committee 1994-National Institutes of Health (NIH)Planning Committee:"IBS: State of the-Art and Research Objectives" Symposium 1992Program Coordinator:"1st Int'l Symposium on Functional Gastrointestinal Disorders" 1995American Digestive Health FoundationChair, Digestive Health Initiative on Functional GI Disorders 1999-2001INTERNATIONAL:Rome FoundationTo Develop Guidelines for Diagnosis of Irritable Bowel Syndrome 1986-1988Chair, Rome I Coordinating Committee 1989-1994Chair, Rome II Coordinating Committee 1995-2000Chair, Rome III Coordinating Committee 2000-2006President, Rome Foundation 2004-International Foundation for Functional GI Disorders 1992-Advisory Board 1993-Board of Trustees 1995-Chair, Scientific Advisory Committee 1995-Chair, 1st International Symposium 1995Chair, 2nd International Symposium 1997Chair, 3rd International Symposium 1999Chair, 4th International Symposium 2001Chair, 5th International Symposium 2003Chair 6th International Symposium 2005Chair, IFFGD Research Award Committee 2003, 2005DROSSMAN 11International Scientific Committees:Chair, Functional/Brain-Gut Research Group of AGA 1989-1994Newsletter Editor 1990-Scientific Secretariat, Italian-International Postgraduate Program in Motility 1990-1992Rome, ItalyScientific Committee - International Symposium on Neurogastroenterology 1995Rome, ItalySymposium Chair, First Int'l Symposium on Functional GI Disorders 1995Rome, ItalyScientific Committee - International Symposium on the Pelvic Floor, 1997-1998Montreal, CanadaScientific Committee - International Symposium on Chronic GI Disorders 1998Lake Maggiore, ItalyISIS- International Society for the Investigation of Stress, 1998Melbourne, AustraliaIntï¿½l. Society Committee, Biopsychosocial Approach to FBD, 2000Brain-Gut 2000 Congress, Toulouse, FranceIntï¿½l. Scientific Advisory Board, 16th International Congress of 2001Psychosomatic Medicine (ICPM), Gothenburg, Sweden 2001Intï¿½l Scientific Advisory Board, European Congress of Psychosomatic 2004Research, Berlin, GermanyIntï¿½l Scientific Committee, ANEMGI-Onlus (Associazione per la 2005NeuroGastroenterologia e la Motilitï¿½ Gastrointestinale, Rome, ItalyIntï¿½l Advisory Committee, 18th World Congress on Psychosomatic 2005Medicine, Kobe, JapanADMINISTRATIVE ACTIVITIES, SCHOOL OF MEDICINE:Co-Director, Medical-Psychiatric Liaison Program, Faculty-Resident 1977-1990Study GroupAd Hoc Member, Consultation-Liaison Division, Dept. of Psychiatry 1978-Jerry Finkel, MD, DirectorAssociate Medical Director: Carolina Fitness Program 1988-1991Co-Director, UNC Center for Functional GI and Motility Disorders 1994-MISC. HONORS AND AWARDS:1. Who's Who in American Colleges and Universities 1965-19662. NFIC Tar Heel Research Council Award, Inflammatory Bowel Disease 19903. "Best Doctors in America" Woodward/White Publ., Inc.1992-19951998-19992001-20022003-20044. "Best Doctors in America - Southeast Region" 1996-19975. Who's Who in the South and Southwest; 22-25th Edit. 1992-19986. Amer. Psychosomatic Society Visiting Scholar Award 19947. Who's Who in the World; 12th Edition 1995-19968. Intl. Who's Who in Medicine; 2nd Edition 1995-19969. Who's Who in American Education; Fifth and Sixth Editions 1996-200510. Who's Who in Medicine and Healthcarea. 1st Edition 1997-1998DROSSMAN 12b. 2nd Edition 1999-2000c. 4th Edition 2002-200311. Cercle Andrï¿½ Lambling, May 1998 199812. Janssen Award for Clinical Research in Digestive Diseases 199913. Functional Brain-Gut Research Group Research Scientist Award 200114. ï¿½Americaï¿½s Top Doctorsï¿½-2nd edition, Castle Connolly Medical Ltd. 200215. ACG Clinical Scholar Award 2002-200316. APS Presidentï¿½s Award. American Psychosomatic Society 200317. Whoï¿½s Who in Americaa. 58th Edition 2004b. 59th Edition 200518. American Gastroenterological Association Distinguished Educator Award 2004DROSSMAN 13BIBLIOGRAPHY:ARTICLES IN REFEREED JOURNALS:1. Gardner DL, Quagliata F, Drossman D, Kalish M and Schimmer B. Attempted prevention ofarteriolar lesions in accelerated rat hypertension by immunosuppression. BRITISH JOURNAL OFEXPERIMENTAL PATHOLOGY 51:242-252, l970.2. Drossman DA, Powell DW, Sessions JT Jr. The irritable bowel syndrome. GASTROENTEROL73:8ll-822, 1977.3. Drossman DA. Can the primary care physician be better trained in the psychosocial dimensions ofpatient care? INTERNATIONAL JOURNAL OF PSYCHIATRY IN MEDICINE 8:169-184, 1978.4. Drossman DA. The problem patient. Evaluation and care of medical patients with psychosocialdisturbances. ANNALS OF INTERNAL MEDICINE 88:366-372, 1978.5. Goldsmith JC, Drossman DA, Blatt PM. Hemobilia complicating warfarin therapy. SOUTHERNMEDICAL JOURNAL 72:748-750, 1979.6. Drossman DA, Heizer WD, Ontjes DA. Anorexia nervosa. GASTROENTEROL 77:1115-1131,1979.7. Kinard HB III, Powell DW, Sandler RS, Callahan WT, Lapis JL, Levinson SL, Jones JD, DrossmanDA, Jackson AL. A current approach to upper gastrointestinal bleeding. JOURNAL OF CLINICALGASTROENTEROL 3:231-240, 1981.8. Levinson SL, Powell DW, Callahan WT, Jones JD, Kinard HB III, Jackson AL, Lapis JL, DrossmanDA. A current approach to rectal bleeding. JOURNAL OF CLINICAL GASTROENTEROL 3(SUPPL. 1):9-16, 1981.9. Greganti MA, Drossman DA, Rogers JF. The role of the attending physician. ARCHIVES OFINTERNAL MEDICINE 142:698-699, 1982.10. Drossman DA, Sandler RS, McKee DC, Lovitz AJ. Bowel patterns among subjects not seeking healthcare: Use of a questionnaire to identify a population with bowel dysfunction. GASTROENTEROL83:529-534, l982.11. Drossman DA. Patients with psychogenic abdominal pain: Six years' observation in the medicalsetting. AMERICAN JOURNAL OF PSYCHIATRY l39:l549-l557, l982.12. Sandler RS, Drossman DA, Nathan HP, McKee DC. Symptom complaints and health care seekingbehavior in subjects with bowel dysfunction. GASTROENTEROL 87:314-318, 1984.13. Steckman M, Drossman DA, Lesesne HR. Hepatobiliary disease that precedes ulcerative colitis. JCLIN GASTROENTEROL 6:425-428, 198414. Haggerty JJ Jr., Drossman DA. Use of psychotropic drugs in patients with peptic ulcer disease.PSYCHOSOMATICS 26:277-285,1985.15. Drossman DA. Is the cotton-topped tamarin a model for behavioral research? DIG DIS SCI 30:24s-27s, 1985.16. Drossman DA. Psychosocial aspects of inflammatory bowel disease. STRESS MEDICINE 2:119-128, 1986.DROSSMAN 1417. Drossman DA, Sandler RS, Broom CM, McKee DC. Urgency and fecal soiling in people with boweldysfunction. DIG DIS SCI 31:1221-1225, 198618. Lowman BC, Drossman DA, Cramer EM, McKee DC. Recollection of childhood events in adultswith irritable bowel syndrome. J CLIN GASTROENTEROL 9:324-330, 1987.19. Sandler RS, Drossman DA. Bowel Habits in Young Adults Not Seeking Health Care. DIG DIS SCI32:841-845, 1987.20. Mitchell CM, Drossman DA. The irritable bowel syndrome: Understanding and treating abiopsychosocial illness disorder. ANN BEHAV MED 9:13-18, 1987.21. Drossman DA, McKee DC, Sandler RS, Mitchell CM, Lowman BC, Burger AL, Cramer EM.Psychosocial factors in the irritable bowel syndrome: A multivariate study of patients and nonpatientswith IBS. GASTROENTEROL 95:701-708, 1988.22. Drossman DA, Patrick DL, Mitchell CM, Zagami EA, Appelbaum MI. Health related quality of life ininflammatory bowel disease: Functional status and patient worries and concerns. DIG DIS SCI34:1379-1386, 1989.23. Thompson WG, Dotevall G, Drossman DA, Heaton KW, Kruis W. Irritable bowel syndrome:Guidelines for the diagnosis. GASTROENTEROLOGY INTERNATIONAL 2:92-95, 198924. Garrett JW, Drossman DA. Health status in inflammatory bowel disease: Biologic and behavioralconsiderations. GASTROENTEROL 99:90-96, 1990.25. Drossman DA, Leserman J, Nachman G, Li Z, Gluck H, Toomey TC Mitchell CM. Sexual andphysical abuse among women with functional or organic gastrointestinal disorders. ANN INTERNMED 113:828-833, 1990.26. Drossman DA, Thompson WG, Talley NJ, Funch-Jensen P, Janssens J, Whitehead WE. Identificationof subgroups of functional gastrointestinal disorders. GASTROENTEROLOGY INTERNATIONAL3:159-172, 199027. Friedman CP, France CL, Drossman DA. A randomized comparison of alternative formats for clinicalsimulations. MEDICAL DECISION MAKING 11:265-272, 1991.28. Drossman DA. Illness behaviour in the irritable bowel syndrome. GASTROENTEROLOGYINTERNATIONAL 4:77-81, 1991.29. Drossman DA, Leserman J, Mitchell CM, Li Z, Zagami EA, Patrick DL. Health status and health careuse in persons with inflammatory bowel disease: A national sample. DIG DIS SCI 36: 1746-1755,1991.30. Drossman DA, Leserman J, Li Z, Mitchell CM, Zagami EA, Patrick DL. The Rating Form of IBDPatient Concerns: A new measure of health status. PSYCHOSOM MED 53:701-712, 1991.31. Drossman DA, Thompson WG: Irritable Bowel Syndrome: Review and a graduated multi-componenttreatment approach. ANN INTERN MED 116:1009-1016, 1992.32. Drossman DA, Li Z, Patrick DL. Ulcerative Colitis and Crohn's Disease health status scales forresearch and clinical practice. J CLIN GASTROENTEROLOGY 15:104-112, 199233. Drossman DA. Psychosocial factors in functional dyspepsia. EUR J GASTROENTEROL HEPATOL4:602-607, 1992.DROSSMAN 1534. Thompson WG, Creed F, Drossman DA, Heaton KW, Mazzacca G. Functional bowel disorders andfunctional abdominal pain. GASTROENTEROLOGY INTERNATIONAL 5:75-91, 1992.35. Pisetsky I, Keram E, Drossman DA. Building a Psychiatric-Medical Liaison: Observations of theProcess. PSYCHIATR MED 10:149-163, 1992.36. Gwyther RE, Bentz EJ, Drossman DA, Berolzheimer N. Validity of the family APGAR in patientswith irritable bowel syndrome. CLINICAL RESEARCH AND METHODS 25:21-25, 1993.37. Novack DH, Volk G, Drossman DA, Lipkin M Jr. Medical Interviewing and Interpersonal SkillsTeaching in U.S. Medical Schools: Progress, Problems and Promise. JAMA 269:2101-2105, 1993.38. Cassileth BR, Drossman DA. Psychosocial factors in gastrointestinal illness. PSYCHOTHERPSYCHOSOM, 59:131-143, 1993.39. Drossman DA, Li Z, Andruzzi E, Temple R, Talley NJ, Thompson WG, Whitehead WE, Janssens J,Funch-Jensen P, Corazziari E, Richter JE, Koch GG. US Householder survey of functional GIdisorders: Prevalence, Sociodemography and Health Impact. DIG DIS SCI 38:1569-1580, 1993.40. Talley NJ, Nyren O, Drossman DA, Heaton KW, Veldhuyzen van Zanten SJO, Koch MM, RansohoffDF. The irritable bowel syndrome: Toward optimal design of treatment trials.GASTROENEROLOGY INTERNATIONAL 4: 189-211, 1993.41. Lydiard RB, Greenwald S, Weissman MM, Johnson J, Drossman DA, Ballenger JC. Panic disorderand gastrointestinal symptoms: Findings from the NIMH Epidemiologic Catchment Area Project. AMJ PSYCHIATRY 151: 64-70, 1994.42. Drossman DA. Irritable bowel syndrome: The role of psychosocial factors. STRESS MEDICINE10:49-55, 199443. Drossman DA. Struggling with the "Controlling" patient. AM J GASTROENTEROL 89:1441-1446,1994.44. Drossman DA. The irritable bowel syndrome. THE GASTROENTEROLOGIST 2:315-326, 1994.45. Drossman DA. Sexual and physical abuse and gastrointestinal illness. SCAND JGASTROENTEROL, 208 (SUPPL.):90-96, 1995.46. Leserman J, Drossman DA, Li Z, Toomey TC, Nachman G. The reliability and validity of a sexualand physical abuse history questionnaire in female patients with gastrointestinal disorders.BEHAVIORAL MEDICINE 21:141-150, 1995.47. Drossman DA, Li Z, Toner BB, Diamant NE, Creed FH, Thompson DG, Read NW, Babbs C, BarreiroM, Bank L, Whitehead WE, Schuster MM, Guthrie EA. Functional bowel disorders: A multinationalcomparison of health status, and development of an illness severity index. DIG DIS SCI 40:986-995,1995.48. Zuckerman MJ, Guerra LG, Drossman DA, Foland JA, Gavin GG. Comparison of bowel patterns inHispanics and non-Hispanic Whites. DIG DIS SCI 40:1763-1769, 1995.49. Drossman DA, Creed FH, Fava GA, Olden KW, Patrick DL, Toner BB, Whitehead WE. Psychosocialaspects of the functional gastrointestinal disorders. GASTROENTEROLOGY INTERNATIONAL8:47-90, 1995.DROSSMAN 1650. Drossman DA. Diagnosing and treating patients with refractory functional gastrointestinal disorders.ANN INTERN MED 123:688-697, 1995.51. Drossman DA, Talley NJ, Olden KW, Leserman J, Barreiro MA. Sexual and physical abuse andgastrointestinal illness: Review and recommendations. ANN INTERN MED 123:782-794, 1995.52. Drossman DA, Brandt LJ, Sears C, Li Z, Nat J, Bozymski EM. A preliminary study of patients'concerns related to GI endoscopy. AMER J GASTROENTEROL 91:287-291, 1996.53. Zuckerman MJ, Guerra LG, Drossman DA, Foland JA, Gavin GG. Health care seeking behaviorsrelated to bowel complaints: Hispanic versus non-Hispanic Whites. DIG DIS SCI 41:77-82, 1996.54. Leserman J, Drossman DA, Li Z, Toomey TC, Nachman G, Glogau L. Sexual and physical abusehistory in gastroenterology practice: How types of abuse impact health status. PSYCHOSOMATICMEDICINE 58:4-15, 1996.55. Ouyang A, Camilleri M, Drossman DA, Kahrilas PJ, Reynolds JC, Richter JE, Shaker R. Task forceon training in motility, diverticular disease, and functional illnesses. GASTROENTEROL 110:1274-1276, 1996.56. Whitehead WE, Drossman DA. Biofeedback for disorders of elimination: Fecal incontinence andpelvic floor dyssynergia. PROFESSIONAL PSYCHOLOGY: RESEARCH AND PRACTICE27:234-240, 1996.57. Drossman DA, Li Z, Leserman J, Toomey TC, Hu YJB. Health status by GI diagnosis and abusehistory. GASTROENTEROLOGY 110:999-1007, 1996.58. Drossman DA. Chronic functional abdominal pain. AMER J GASTROENTEROL 91:2270-2281,1996.59. Drossman DA. The role of psychosocial factors in gastrointestinal illness. SCAND JGASTROENTEROL, 31 (SUPPL. 221):1-4, 1996.60. Leserman J, Li Z, Drossman DA, Toomey TC, Nachman G, Glogau L. Impact of sexual and physicalabuse dimensions on health status: Development of an abuse severity measure. PSYCHOSOMATICMEDICINE 59:152-160, 1997.61. Drossman DA. Irritable bowel syndrome and sexual/physical abuse history. EUR JGASTROENTEROL HEPATOL 9:327-330, 1997.62. Drossman DA, Whitehead WE, Camilleri, M. Irritable bowel syndrome: A technical review forpractice guideline development. GASTROENTEROL 112:2120-2137, 1997.63. Drossman DA, Whitehead WE, Camilleri M. Medical position statement: Irritable bowel syndrome.GASTROENTEROL 112:2118-2119, 1997.64. Drossman DA. Psychosocial sound bites: Exercises in the patient-doctor relationship. AMER JGASTROENTEROL 92:1418-1423, 1997.65. Provenzale D, Shearin M, Phillips-Bute B, Drossman DA, Li Z, Tillinger W, Schmitt C, Bollinger R,Koruda M. Health-related quality of life after ileoanal pull-through: Evaluation and assessment ofnew health status measures. GASTROENTEROL 113:7-14, 1997DROSSMAN 1766. Drossman DA. Importance of the psyche in heartburn and dyspepsia. ALIMENT PHARMACOLTHER, 11(SUPPL. 2):57-67, 1997.67. Leserman J, Li Z, Drossman DA, Hu JB. Selected symptoms associated with sexual and physicalabuse history: The impact on subsequent health care visits. PSYCHOLOGICAL MEDICINE 28:417-425, 1998.68. Patrick DL, Drossman DA, Frederick IO, DiCesare J, Puder KL. Quality of life in persons withirritable bowel syndrome: Development of a new measure. DIG DIS SCI 43:400-411, 1998.69. Leserman J, Li Z, Hu YJB, Drossman DA. How multiple types of stressors impact on health.PSYCHOSOMATIC MEDICINE 60:175-181, 1998.70. Drossman DA. Presidential Address: Gastrointestinal illness and the Biopsychosocial model.PSYCHOSOMATIC MEDICINE 60:258-267, 1998.71. Drossman DA. Review Article: An integrated approach to the irritable bowel syndrome. ALIMENTPHARM THER 13(4) (SUPPL. 2):3-14, 1999.72. Camilleri M, Mayer EA, Drossman DA, Heath A, Dukes GE, McSorley D, Kong S, Mangel AW,Northcutt AR. Improvement in pain and bowel function in female irritable bowel syndrome patientswith alosetron, a 5HT3 receptor antagonist. ALIMENT PHARM THER, 13:1149-1159, 1999.73. Russo MW, Gaynes BN, Drossman DA. A national survey of practice patterns of gastroenterologistswith comparison to the past two decades. J CLIN GASTROENTEROLOGY 29(339):343, 1999.74. Drossman DA. The functional gastrointestinal disorders and the Rome II process. GUT 45(SUPPL.II):II1-II5, 1999.75. Drossman DA, Creed FH, Olden KW, Svedlund J, Toner BB, Whitehead WE. Psychosocial aspectsof the functional gastrointestinal disorders. GUT 45(SUPPL. II):II25-II30, 1999.76. Thompson WG, Longstreth GF, Drossman DA, Heaton KW, Irvine EJ, Mï¿½ller-Lissner SA.Functional Bowel Disorders and Functional Abdominal Pain. GUT 45(SUPPL. II):II43-II47, 1999.77. Drossman DA. Do psychosocial factors define symptom severity and patient status in Irritable BowelSyndrome? AMER J MEDICINE Mayer EA, Dent J (eds). 107 SUPPL. 5A (No.8), pp 41S-50S. 1999.78. Casati J, Toner BB, C de Rooy E, Drossman DA, Maunder RG. Concerns of Patients withInflammatory Bowel Disease: A Review of Emerging Themes. DIG DIS SCIENCES 45(1):26-31,2000.79. Drossman DA, Patrick DL, Whitehead WE, Toner BB, Diamant NE, Hu YJB, Jia H, Bangdiwala SI.Further validation of the IBS-QOL: A disease specific quality of life questionnaire. AMER JGASTROENTEROLOGY 95(4):999-1007, 2000.80. Drossman DA, Whitehead WE, Toner BB, Diamant N, Hu YJB, Bangdiwala SI, Jia H. Whatdetermines severity among patients with painful functional bowel disorders? AMER JGASTROENTEROLOGY 95(4):974-980, 2000.81. Drossman DA, Li Z, Leserman J, Keefe FJ, Hu YJ, Toomey TC. Effects of coping on health outcomeamong female patients with gastrointestinal disorders. PSYCHOSOMATIC MEDICINE 62:309-317,2000.82. Ringel Y, Sperber A, Drossman DA. Irritable Bowel Syndrome. ANN REV MED 52:319-338, 2001.DROSSMAN 1883. Waldstein SR, Neumann SA, Drossman DA, Novack DH. Teaching psychosomatic (biopsychosocial)medicine in United States medical schools: Survey findings. PSYCHOSOMATIC MEDICINE63:335-343, 2001.84. Levenstein S, Li Z, Almer S, Barbosa A, Marquis P, Moser G, Sperber A, Toner B, Drossman DA.Cross-cultural variation in disease-related concerns among patients with inflammatory bowel disease.AM J GASTROENTEROL 96(6):1822-1830, 2001.85. Ringel Y, Dalton CB, Brandt LJ, Hu Y, Jia H, Bangdiwala S, Drossman DA. FlexibleSigmoidoscopy: The Patientsï¿½ Perception. GASTROINTESTINAL ENDOSCOPY 55(3): 315-320,2002.86. Drossman DA, Ringel Y. Irritable Bowel Syndrome: Classification and Conceptualization.JOURNAL OF CLINICAL GASTROENTEROLOGY 35 (1) Suppl: S7-S10, 2002.87. Gibbs-Gallagher N; Palsson OS; Levy RL; Meyer K; Drossman DA; Whitehead WE. Selective recallof gastrointestinal-sensation words: Evidence for a cognitive-behavioral contribution to irritable bowelsyndrome. AM J GASTROENTEROL 96 (4): 1133-1138, 2001.88. Ringel Y, Drossman DA. Functional chest pain of presumed esophageal origin. ARCHIVES OFINTERNAL MEDICINE 162 (3): 365-366, 2002.89. Drossman DA; Camilleri M; Mayer E; Whitehead WE. Irritable bowel syndrome: A technical reviewfor practice guideline development. GASTROENTEROL, 123 (6): 2108-2131, 2002.90. Drossman DA, Camilleri M; Mayer E; Whitehead WE. Medical position statement: Irritable bowelsyndrome. GASTROENTEROL, 123 (6): 2105-2107, 2002.91. Longstreth GF, Drossman DA. New developments in the diagnosis and treatment of Irritable BowelSyndrome, CURRENT GASTRO REPORTS, 4 (5): 427-434, 2002.92. Chey WD, Olden K, Carter E, Boyle J, Drossman D, Chang L. Utility of the Rome I and Rome IIcriteria for IBS in US women. AM J GASTROENTEROL, 97 (11): 2803-2811, 2002.93. Drossman DA, Ringel Y, Vogt B, Leserman J, Lin W, Smith JK, Whitehead B. Alterations of brainactivity associated with resolution of emotional distress and pain in a case of severe IBS.GASTROENTEROL, 124: 754-761, 2003.94. Ringel Y, Drossman DA, Turkington TG, Hawk TC, Bradshaw B, Coleman RE, Whitehead WE.Regional brain activation in response to rectal distension in patients with irritable bowel syndrome andthe effect of a history of abuse. DIGESTIVE DISEASE SCIENCE Sep;48(9):1774-81, 2003.95. Muller-Lissner S, Koch G, Talley NJ, Drossman D, Rueegg P, Dunger-Baldauf C, Lefkowitz M.Subjectï¿½s Global Assessment of Relief: An appropriate method to assess the impact of treatment onirritable bowel syndrome-related symptoms in clinical trials. JOURNAL OF CLINICALEPIDEMIOLOGY 56: 310-316, 2003.96. Parkman HP, Rao SS, Reynolds JC, Schiller LR, Wald A, Miner PB, Lahr C, Wald A, Lembo AJ,Drossman DA, Waltzman L, Stambler N, Cedarbaum JM. Neurotrophin-3 improves functionalconstipation. AM J GASTROENTEROL 98:1338-1347, 2003.97. Drossman DA, Toner BB, Whitehead WE, Diamant NE, Dalton CB, Duncan S et al. Cognitive-Behavioral Therapy vs. Education and Desipramine vs. Placebo for Moderate to Severe FunctionalBowel Disorders. GASTROENTEROL, 125: 19-31, 2003.DROSSMAN 1998. Dalton CB, Drossman DA, Hathaway JM, Bangdiwala SI Perceptions of physicians and patients withorganic and functional GI disorders. JOURNAL OF CLINICAL GASTROENTEROLOGY ANDHEPATOLOGY 2(2):121-126,2004.99. Ringel Y, Whitehead WE, Toner BB, Diamant NE, Hu Y, Jia H ,Bangdiwala SI, Drossman DA.Sexual and Physical Abuse are Not Associated with Rectal Hypersensitivity in Patients with IrritableBowel Syndrome, GUT 53: 845-849, 2004.100. Drossman, DA, Functional Abdominal Pain Syndrome, JOURNAL OF CLINICALGASTROENTEROLOGY AND HEPATOLOGY, 2:353-365, 2004.101. Halpert, A, Drossman, DA. Biopsychosocial Issues in Irritable Bowel Syndrome. Mental Fitness, InPress, 2004.102. Drossman DA. What Does the Future Hold for IBS and the Functional GI Disorders. J CLINICALGASTROENTEROLOGY, in press, 2004103. Halpert AD, Dalton CB, Diamant N, Toner B, Hu Y, Morris C, Bangdiwala S, Whitehead W,Drossman D. Clinical Response to Tricyclic Antidepressants in Functional Bowel Disorders is NotRelated to Dosage. American Journal of Gastroenterology, In Press, 2004104. Whitehead WE, Levy RL, Von Korff M, Feld A, Palsson O, Turner M, Drossman DA. Usual medicalcare for irritable bowel syndrome. Alimentary Pharmacology and Therapeutics, In Press 2004.NON-REFEREED ARTICLES:1. Drossman DA, Powell DW, Sessions JT Jr. The irritable bowel syndrome: a challenge for thephysician. CURRENT CONCEPTS IN GASTROENTEROLOGY 3:4-7, 1978.2. Drossman DA. Irritable bowel: Flexibility is the key to proper management. MODERN MEDICINE48:26-31, 1980.3. Sandler RS, Drossman DA. A conservative approach to the diagnosis of irritable bowel syndrome.IM - INTERNAL MEDICINE FOR THE SPECIALIST 2:39-47, 1981.4. Drossman DA. Consultation: Abdominal pain: How far do you go in the workup? MODERNMEDICINE 50:217-222, 1982.5. Drossman DA. Psychogenic chest pain. CHEST PAIN 8(3):l-7, l982.6. Drossman DA. Psychosocial aspects of the irritable bowel syndrome. SURVEY OF DIGESTIVEDISEASES l(l): l30-l35, l983.7. Drossman DA, Lowman BC. Irritable bowel syndrome: Epidemiology, diagnosis and treatment.GASTROENTEROLOGICAL CLINICS OF NORTH AMERICA 14:559-574, 1985.8. Drossman DA. The patient with chronic undiagnosed abdominal pain. HOSP PRACTICE21(11A):22-29, 1986.9. Drossman DA. Depression and the gastrointestinal disorders. CLIN ADVANCES IN THETREATMENT OF DEPRESSION 1:8-11, 1987.DROSSMAN 2010. Buccini R, Drossman DA. Chronic Idiopathic Abdominal Pain. CURRENT CONCEPTS INGASTROENTEROLOGY 12:3-11, 1988.11. Drossman DA. Irritable Bowel Syndrome. HOSPITAL PRACTICE 3(9):119-133, 198812. Drossman DA. Irritable Bowel Syndrome. AMERICAN FAMILY PHYSICIAN 39:159-164, 198913. Drossman DA, Weiss T, Rahe RH. Who are we? The American Psychosomatic Society MembershipSurvey. PSYCHOSOMATIC MEDICINE 51:648-651, 198914. Brannan DP, Drossman DA. Irritable Bowel Syndrome: Recognition and Management. HOSPITALMEDICINE 26:93-99, 1990.15. Brannan DP, Drossman DA. Towards a newer understanding of Irritable Bowel Syndrome.CONTEMPORARY INTERNAL MEDICINE Sep.:73-91 1991.16. Drossman DA. The link between early abuse and GI disorders in women. EMERGENCYMEDICINE 24(6):171-175, 199217. Drossman DA. Psychosocial factors in inflammatory bowel disease. PRACTICALGASTROENTEROLOGY 16(5):24N-24U, 1992.18. Drossman DA, Sandler RS, Sartor RB. Our new president: Don W. Powell, M.D.GASTROENTEROL 104:1249-1251, 1993.19. Drossman DA. Measuring quality of life in inflammatory bowel disease.PHARMACOECONOMICS 6:578-580, 1994.20. Fullwood AP, Drossman DA. The relationship of psychiatric illness with gastrointestinal disease.ANN REV MED 46:483-496, 1995.21. Leserman J, Toomey TC, Drossman DA. Medical consequences of sexual and physical abuse inwomen. HUMANE MEDICINE 11:23-28, 1995.22. Talal AH, Drossman DA. Psychosocial Factors in Inflammatory bowel disease. GASTROENTEROLCLIN N AMER 24:699-716, 1995.23. Drossman DA. Irritable Bowel Syndrome. GASTROINTESTINAL DISEASES TODAY 4:9-18,1995.24. Drossman DA. Life stresses and effects on ulcerative colitis (Commentary on paper by Levenstein etal.: "Psychological Stress and Disease Activity in Ulcerative Colitis. INFLAMMATORY BOWELDISEASES 1:86-87, 1995.25. Cerda JJ, Drossman DA, Scherl EJ. Effective, compassionate management of IBS. PATIENT CARE30:131-144, 1996.26. Almounajed G, Drossman DA. Newer aspects of the irritable bowel syndrome. PRIMARY CARE:CLINICS IN OFFICE PRACTICE 23:477-495, 1996.27. Drossman DA. The functional gastrointestinal disorders: Introduction SEMINARS INGASTROINTESTINAL DISEASES 7:1-3, 1996.DROSSMAN 2128. Dalton CB, Drossman DA. Diagnosing and treating irritable bowel syndrome. ADVANCE forPHYSICIAN ASSISTANTS 10:11-14, 1996.29. Dalton CB, Drossman DA. Diagnosis and Treatment of Irritable Bowel Syndrome. AM FAMPHYSICIAN 55:875-880, 1997.30. Drossman DA. Irritable bowel syndrome: Guidelines for Canadian family physicians. Position paperSYCHOSOCIAL INFLUENCES, 1997.31. Dalton CB, Drossman DA. Diagnosis and treatment of irritable bowel syndrome. DRUGS OFTODAY 34(7): 585-592, 1998.32. Cerda J, Drossman DA, Richter J. Reflux, abdominal pain, diarrhea. PATIENT CARE, April 15,1999. Whitehead WE, Gibbs NA, Li Z, Drossman DA: Is functional dyspepsia just a subset of theirritable bowel syndrome?. BAILLIERES CLINICAL GASTROENTEROLOGY 12:443-461, 1998.33. Gaynes B, Drossman DA. The role of the mental health professional in the assessment andmanagement of Irritable Bowel Syndrome. CNS SPECTRUMS 4(4):19-30, 1999.


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CURRICULUM VITAEDouglas Arnold Drossman, M.D.Co-Director, UNC Center for Functional GI and Motility DisordersOffice:1110 Bioinformatics BuildingChapel Hill, NC 27599-7080 Born March 20, 1946, Brooklyn, New YorkMarried, 1970, Deborah Ducoff (1946)Children: David Samuel (1974)Daniel Robert (1977)EDUCATION:Academic Diploma, Honors, Jamaica H.S., Jamaica, New York, 1962B.A., Cum Laude, Hofstra University, Hempstead, New York, 1966M.D., Albert Einstein College of Medicine, Bronx, New York, 1970POSTGRADUATE TRAINING:Medical InternshipUniversity of North Carolina - 7/70-6/71North Carolina Memorial HospitalChapel Hill, North CarolinaL. G. Welt, M.D., Chairman, Department of MedicineJunior Medical ResidencyUniversity of North Carolina 7/71-6/72North Carolina Memorial HospitalChapel Hill, North CarolinaH. Fallon, M.D., Acting Chairman, Department of MedicineSenior Associate Medical Resident and Teaching Assistant in MedicineNew York University - Bellevue Medical Center 7/72-6/73New York, New YorkSaul Farber, M.D., Chairman, Department of MedicineInstructor and Fellow in Medicine and Psychiatry (Psychosomatic Medicine)University of Rochester Medical Center 7/75-6/76Rochester, New YorkGeorge L. Engel, M.D., Chairman, Medical-Psychiatric Liaison GroupDROSSMAN 2Fellow in GastroenterologyDivision of Digestive Diseases and Nutrition 7/76-6/78Department of Medicine, University of North Carolinaat Chapel Hill - North Carolina Memorial HospitalChapel Hill, North CarolinaDon W. Powell, M.D., ChiefMILITARY SERVICE:Major, United States Air Force Medical Corps 8/73-7/75Chief of Internal MedicineUSAF Hospital, Bergstrom AFB, TexasEMPLOYMENT HISTORYrofessor of Medicine and Psychiatry 7/90School of MedicineUniversity of North Carolina at Chapel HillMarschall S. Runge, M.D., Chair, Department of MedicineR. Goldin, M.D., Chair, Department of PsychiatryAssociate Professor of Medicine and Psychiatry 7/83Assistant Professor of Medicine and Psychiatry 7/78Instructor, Department of Medicine 7/77Clinical Instructor 11/76-10/77School of NursingUniversity of North Carolina at Chapel HillNurse Practitioner ProgramCERTIFICATION:Internal Medicine, June, 1973Gastroenterology, October, 1979LICENSURE:North Carolina August 1976Texas January 1974New York January 1971DROSSMAN 3PROFESSIONAL SOCIETIES:Member, American Psychosomatic Society 1977Councillor 1985-19881990-1992Secretary/Treasurer 1992-1995President-Elect 1995-1996President 1996-1997Fellow, American College of Physicians 1978Member, Durham-Orange County Medical Society 1978Member, American Federation for Clinical Research 1979Member, American Gastroenterological Association 1980Member, American Society for Gastrointestinal Endoscopy 1982Member, Southern Society for Clinical Investigation 1986Member, Academy of Behavioral Medicine Research 1986Fellow, American College of Gastroenterology 1989Fellow, American Academy on Physician and Patient 1992PROFESSIONAL SERVICE:EDITORIAL APPOINTMENTS:a. Editorial BoardsASTBehavioral Medicine Abstracts 1985-1991Stress Medicine 1985-1992Current Concepts in Gastroenterology 1986-1990Inflammatory Bowel Disease 1994-1998CURRENTJournal of Clinical Gastroenterology 1986-Merck Manual, Gastroenterology Editor 1987-15th (1987) 16th (1992), and 17th (1999) editionsMerck Manual of Medical Information, Home Edition, Gastroenterology Editor 1997 ï¿½1st (1997) and 2nd (2003) editionsMind-Body Medicine 1993-Psychosomatic Medicine 1997-Gastroenterology 1998-Medscape Gastroenterology 1999Participate-Newsletter of the International Foundation for 2000-Functional Gastrointestinal DisordersRomanian Journal of Gastroenterology 2000-International Journal of Functional Syndromes 2001-b. Editor:Functional Brain-Gut Research Group Newsletter 1990-Participate-Newsletter of the International Foundation for 2000-Functional Gastrointestinal Disorders (Senior Associate Editor)DROSSMAN 4c. Associate Editor:Gastroenterology 2001-d. Ad hoc reviewer for:Annals of Internal Medicine 1978-Gastroenterology 1978-General Hospital Psychiatry 1979-Archives of Internal Medicine 1981 -American Journal of Psychiatry 1981 -American Journal of Digestive Diseases 1981 -American Journal of Gastroenterology 1982 -Psychosomatics 1983 -Digestive Diseases and Sciences 1983 -Journal of the Amer. Medical Assoc. 1984 -Journal of General Internal Medicine 1985 -Journal of Clinical Gastroenterology 1985 -Health Psychology 1989 -Gut 1990 -Western Journal of Medicine 1991 -New England Journal of Medicine 1992 -ADVISORY BOARDS:Health Digest (Whittle communications) 1986-1992The Partnership for Quality Living (CCFA and Kabi Pharmacia, Inc.) 1993-1994Merck Manual (GI Section Editor, 1994-) 1988-UCLA Center for Functional Bowel Disorders and Abdominal Pain 1992-International Foundation for Functional Gastrointestinal Disorders 1992-Center for the Advancement of Health 1995-Olestra Surveillance Advisory Council 1996-ABC News 1997-Medscape Gastroenterology 1999-Glaxo Wellcome 2000-Intestinal Disease Foundation, Pittsburgh, PA 2000-Novartis 2000-UCLA Mind-Body Collaborative Research Center 2001-National Womenï¿½s Health Resource Center 2001-GlaxoSmithKline Risk Management Program Advisory Panel 2002-PHARMACEUTIC CONSULTATION (SELECTED-ACTIVE):Glaxo-Smith KlineProcter & GambleSolvayAstra-ZenecaNovartisEMD - MerckForest LaboratoriesLilly PharmaceuticalsWellspring PharmaceuticalsSanofi~SynthelaboEisai Co., Ltd.DROSSMAN 5GRANTS AND AWARDSGRANTS AND AWARDS: FEDERAL1. The Irritable Bowel Syndrome: Characterizing the Patient. Principal Investigator (35%), 4/l/83 -3/3l/86, #ROlAM29934, National Institutes of Health (NIADDK), $345,l36.2. Abuse/Psychosocial Factors in Patients with GI Disorders. Principal Investigator (40%), 9/1/91 -8/31/95, #RO1MH46959, National Institutes of Health (NIMH), $844,476.3. Multicenter Trial of Functional Bowel Disorders. Principal Investigator (40%), 9/30/95 - 8/31/00,#RO1DK49334, National Institutes of Health (DK), $2,969,913 First year award, $622,572.4. Multicenter Trial of Functional Bowel Disorders. Principal Investigator (40%), 9/01/00 - 8/31/02,#RO1DK49334, National Institutes of Health (NIDDK), $877,621 First year award, $1,544,471 2-yearextension of previous award.5. Psychophysiology of Irritable Bowel Syndrome. Co-Investigator (20%) with William E. Whitehead,PhD, Principal Investigator. 12/1/97- 11/30/02 National Institutes of Health (NIDDK), $840,402 FirstYear Award, $124,367. (Bridge funds, $92,889 awarded for 7/1/97-11/30/97)6. Gastrointestinal Biopsychosocial Research Center at UNC. Response to RFA OB-03-004.7/01/04 ï¿½ 6/30/09; R24 DK067674Co-Principal Investigator (20%) with William Whitehead, Co-Principal Investigator (20%). National Institutes of Health (NIDDK) First year award $993,453($682,089 direct), and full-term 5-year award, $4,953,824 ($3,401,217 direct).GRANTS AND AWARDS: FOUNDATIONSAWARDED1. Medical Liaison Development Fund, funded by S. S. Zlinkoff Foundation, 1979, $5,500; Renewal1980, $6,500.2. Health related quality of life in patients with IBD. Pilot study. Core Center for Diarrheal Diseases(CCDD), UNC. Principal Investigator, 4/1/86-8/31/86, $10,000.3. Mail Survey of Health Related Quality of Life in IBD. National Foundation for Ileitis and Colitis,New York, N.Y. Principal Investigator, 7/1/87-12/31/88, $5,000.4. Planning Grant: Health Related Quality of Life in an Israeli IBD Population. Co-Investigatorwith Dr. Ami Sperber, Bersheva Medical Center, Jerusalem, Israel, 3/15/93-12/31/93, $6,000.5. Clinical and Physiological Characteristics of Functional Distal Esophageal Disorders.Multinational Working Teams to Develop Diagnostic Criteria for Functional GastrointestinalDisorders. Co-Investigator with Dr. Yehuda Ringel MD, Principal Investigator 1/1/99-12/31/99,$29,970.6. ACG Institute 2002 Clinical Scholar Award. American College of Gastroenterology. 07/02-07/03,$15,000.7. United States-Israel Binational Science Foundation Proposal: ï¿½Is Gynecological SurgeryAssociated with Subsequent Development of IBS and Other Painful Disorders.ï¿½ Co-Investigatorwith Ami Sperber MD, Principal Investigator. 9/2002-06/2006, $219,977. US component, $71,427.8. APS Presidentï¿½s Award. American Psychosomatic Society. 03/2003, $1,000.DROSSMAN 69. Does Education Improve Outcome in Patients with Irritable Bowel Syndrome? American Collegeof Gastroenterology. Co-Investigator with Albena Halpert MD, and Charlene Prather, MD, PrincipalInvestigators. 07/01/02-06/30/03, $35,000.10. American College of Gastroenterology Clinical Scholar Award. American College ofGastroenterology 7/1/03 ï¿½ 6/30/04. $15,000.11. The Epidemiology of Functional Gastrointestinal Disorders in Latin America: A PopulationbasedStudy. Co-Investigator with Principal Investigator, Loreto Cortes, MD, Rodolfo Peï¿½a, MD, andDouglas Morgan, MD, Rome III Committees, 7/1/03 ï¿½ 6/30/04, $30,000.GRANTS AND AWARDS: PHARMACEUTICAL1. Smith, Kline and Beckman award for study of the irritable bowel syndrome. 1982, $7,500.2. A Pilot Evaluation of BW942C in the Treatment of IBS. Burroughs Wellcome Co. Inc., ResearchTriangle Park, N.C. Principal Investigator, 12/84-12/85, $32,400.3. A Parallel Study of Buspirone in the Treatment of IBS. Bristol-Myers Pharmaceutical Group,Evansville, Ind. Principal Investigator, 4/1/88-4/30/90, $50,500.4. Gift for personal research activities. Sandoz Pharmaceuticals, 12/90, $5,000.5. The Prevalence of Functional Gastrointestinal Disorders in a Randomized National Sample.Procter & Gamble Co. Inc. Principal Investigator, 3/1/90-12/31/90, $15,000.6. Study of Subgroups of Irritable Bowel Syndrome in a Randomized National Sample. Procter &Gamble Co. Inc. Principal Investigator, 1/1/91-9/30/91. $12,000.7. A Parallel Study to Determine the Efficacy of Librax for Treatment of Irritable BowelSyndrome. Hoffmann La Roche Co.8. Survey of Illness Severity in Functional Bowel Disorders. Glaxo Corporation. 3/19/93, $9,860.9. Development of a Quality of Life Instrument for Irritable Bowel Syndrome. SandozCorporation. 1/1/95-9/1/95, $50,000.10. An Investigative Survey to Determine Optimal Methods for Measuring Clinical Endpoints inPatients with Irritable Bowel Syndrome. Smith Kline Beecham. 4/1/95-8/1/95, $45,000.11. Multicenter Trial of Fedotozine in Treatment of Irritable Bowel Syndrome. Glaxo Corp. 1/1/95-4/30/95, $52,000.12. A Double-Blind Study to Compare the Efficacy and Safety of SB-207266-A with Placebo inPatients with Irritable Bowel Syndrome. Smith Kline Beecham. 8/1/96-7/31/97, $65,000.13. A Multicenter, Double-blind, Placebo Controlled, Parallel Group Dose-response Study ofControlled Release Darifenacin in Treatment of IBS. Pfizer Corp. 1/1/97-12/31/97, $56,175.14. Multicenter Trial of Alosetron In Treatment of IBS. Glaxo-Wellcome. 1/1/98-12/31/98, $22,850.DROSSMAN 715. A Double-Blind, Randomized, Placebo-Controlled Phase II Clinical Trial of OPC 12759(Rebamipide) for the Treatment of Non-Ulcer Dyspepsia in Patients with/without HelicobacterPylori. Otsuka. 4/1/98-12/31/98, $148,860.16. An 8-Week Randomized, Double-Blind, Placebo-Controlled Study to Evaluate the Efficacy andSafety of Alosetron (GR68755) 1 Mg BID in the Treatment of Anxiety in Females with IrritableBowel Syndrome. Glaxo-Wellcome. 7/1/97-6/30/98, $93,574.50.17. A Double-Blind, Placebo-Controlled Dose Ranging Study to Compare the Efficacy and Safety ofThree Doses of SB-207266-A (20mg, 5mg and 1 mg od) with Placebo Over 12 weeks in theTreatment of Irritable Bowel Syndrome. SmithKline Beecham. 7/27/98-7/26/99, $52,864.18. A 12-Month Randomized, Double Blind, Placebo-Controlled Study to Evaluate the Quality ofLife and Safety Associated with the Long-Term Use of Alosetron (GR68755) in Subjects withIrritable Bowel Syndrome. GlaxoWellcome. 5/15/98-12/31/99, $40,212.19. A Single-Blind, Placebo Controlled Continuation Study to Investigate the Safety of SB-207266-A. SmithKline Beecham. 9/1/98-12/22/98, $72,800.20. A 12-week, randomized, double-blind, placebo-controlled, study of Alosetron (GR68755) in malesubjects with alternating diarrhea/constipation irritable bowel syndrome. ICON Protocol#S3B20023. 3/15/00-12/15/00, $21,000.21. A 12 week randomized, double-blind, placebo-controlled study of Alosetron (GR68755) infemale subjects with alternating diarrhea/constipation irritable bowel syndrome. ICON Protocol#S3B20013. 3/15/00-12/15/00, $21,000.22. A dose-ranging safety and efficacy study of the effect of Recombinant-Methionyl HumanNeurotrophin-3 (NT-3) on bowel function in patients with constipation. Regeneron Pharmaceuticals,Inc. 5/15/00-5/14/01, $52,570.23. A study to evaluate the safety and efficacy of TAK-637 (30 mg BID, 60 mg BID and 120 mg BID)versus placebo in subjects with irritable bowel syndrome. TAP Holdings-Phoenix International.Protocol TAK-637-99-201. 7/20/00-7/19/01, $41,030.24. A randomized, double-blind, placebo-controlled multicenter study to assess the efficacy, safetyand tolerability of tegaserod 2 mg bid and 6 mg bid given orally vs. placebo in patients withchronic constipation CHTF919 E 2302. Novartis Pharmaceuticals Corporation. 9/1/01-9/1/02,$45,860.25. A 12-Week, Randomized, Double-Blind, Placebo-Controlled, Fixed-Dose, Parallel Group,Multicenter Study of The Safety and Efficacy of Dexloxiglumide 200 MG B.I.D. and 200 MGT.I.D. in Female Patients with Constipation-Predominant Irritable Bowel Syndrome DEX-MD-01A. Forest Laboratories/ICON. 02/20/02-6/17/03, $99,070.26. An Open-Label Extension of Study DEX-MD-01A to Investigate the Long-Term Safety andEfficacy of Dexloxiglumide 200 MG T.I.D. in Female Patients with Constipation-PredominantIrritable Bowel Syndrome DEX-MD-01B. Forest Laboratories/ICON. 2/20/02-11/14/03, $49,940.27. An Open-Label Extension of Study Dex-MD-01B and Dex-MD-02B To Investigate the Long-Term Safety and Efficacy of Dexloxiglumide 200 MG T.I.D. In Female Patients withConstipation-Predominant Irritable Bowel Syndrome. Principal Investigator with Christine Dalton,PA-C. Forest Laboratories, Inc. Protocol DEX-MD-10. Project period- 02/13/03-11/14/03. $14,000.DROSSMAN 828. A Double-Blind, Placebo-Controlled, Randomized, Multicenter Study to Investigate the Safetyand Efficacy of 2 mg TID of Cilansetron Over 12 Weeks Followed by a 4-Week RandomizedTreatment Period in Diarrhea-Predominant Irritable Bowel Syndrome Subjects. PrincipalInvestigator with Christine Dalton, PA-C. Solvay Pharmaceuticals, Inc./Quintiles, Inc. ProtocolS2413011. 06/20/02-10/20/03. $34,716.29. An Eight-Week, Randomized, Double-Blind, Placebo-Controlled, Dose-Ranging Study toEvaluate Efficacy and Safety of SB 223412 in Subjects with Irritable Bowel Syndrome. PrincipalInvestigator with Christine Dalton, PA-C. GlaxoSmithKline. Protocol SB223412. 7/30/02 ï¿½ 7/29/03.$37,084.30. A Multi-Center, Double-Blind, Randomized, Placebo-Controlled, Phase III Study of the Efficacyand Safety or Oral RU-0211 for the Treatment of Occasional Constipation. Principal Investigatorwith Christine Dalton, PA-C. Sucampo Pharmaceuticals. Protocol SPI 0211SC0232. Project period ï¿½2/13/03-10/14/03. $43,200.31. A Twelve-Week Randomized, Double-Blind, Placebo-Controlled, Parallel Group Study to Assesthe Safety and Efficacy of 0.5 mg QD, 1 mg QD, and 1 mg BID of Alosetron in Female Subjectswith Severe Diarrhea Predominant IBS Who Have Failed Conventional Therapy. PrincipalInvestigator with Christine Dalton, PA-C. GlaxoSmithKline. Protocol S3B30040 Project period09/15/03-09/14/04. $31,73932. A 12-Week, Double-Blind, Randomized Study of the Safety and Efficacy of Oral SPI-0211 inSubjects with Constipation-Predominant Irritable Bowel Syndrome. Principal Investigator withChristine Dalton, PA-C. Sucampo Pharmaceuticals. Protocol SPI 0211 SC0221. Project period ï¿½06/01/03-12/31/04. $40,000.33. Clinical and Physiological Differences Among Sub-groups of IBS: A comparison of IBS withConstipation, IBS with Diarrhea and Mixed/Alternators. Principal Investigator. NovartisPharmaceuticals, Project Period - 9/30/03 ï¿½ 12/31/04. $249,199.34. A Multicenter, Double-Blind, Placebo-Controlled Efficacy and Safety Study of Low-DoseNaltrexone HCl (PTI-901) in Female Patients with Irritable Bowel Syndrome. PrincipalInvestigator with Christine Dalton, PA-C. Pain Therapeutics. Protocol PTI-901-NB, 1/15/-1/14/05,$43,297.35. A Multicenter, Double-Blind, Placebo-Controlled Efficacy and Safety Study of Low-DoseNaltrexone HCl (PTI-901) in Male Patients with Irritable Bowel Syndrome. PrincipalInvestigator with Christine Dalton, PA-C. Pain Therapeutics Protocol PTI-901-NC 1/15/04-1/14/05,$42,999.GRANTS AND AWARDS: UNIVERSITY OF NORTH CAROLINA1. Junior Faculty Development Award. University of North Carolina $3,000, 1981.2. Jefferson-Pilot Fellowship in Academic Medicine. University of North Carolina, $8,000, 1981-85.3. TEAM Mini-Grant for the Development of a Natural Language Inquiry Computerized PatientSimulation. University of North Carolina, 4/7/88, $4,000.4. Dept. of Medicine Award for study of Health Related Quality of Life in IBD. University of NorthCarolina, 2/1/89, $3,500.5. Kenan Professor-Sabbatical. University of North Carolina, 2002-2003, $56,000.DROSSMAN 96. Division of Gastroenterology and Hepatology Eugene M. Bozymski Award in Endoscopy,presented by the GI fellows, 6/19/04, $500COMMITTEES (Research, Service, Education)EPARTMENT OF MEDICINE:Internship Selection Committee 1977 -Housestaff-Faculty Committee 1980 - 1984Chairman, Selection Committee, Mack Lipkin Sr. Visiting Professorship 1983 -MEDICAL SCHOOL:Committee for Curriculum Review III. Subcommittee on Transition from 1981-1983the Basic Sciences to the Medical SciencesHealth Promotion/Disease Prevention Steering Comm. 1983Residency Student Advisor 1991-UNC Medical Practice and the Community (MPAC); Content Subcommittee 1995NATIONAL:American Gastroenterological Association (AGA)Council on Nerve-Gut Interactions 198l-1986Program Selection Committee Member - Clinical 1985-1986Program Selection Chairman-Functional Nerve/Gut 1990-1992Education and Training Committee 1993-1996GLC Curriculum Task Force on Motility 1994-1995, 2001Chair, Abstract Selection, Functional GI Disorders 1998Abstract Selection Committee, Functional GI Disorders 1999Clinical Teaching Project 1994-2002Nominating Committee 1998Abstract Selection Committee: Pharmacological Treatment of 2000FGID (#87)Co-Chair, Motility & Nerve-Gut Interactions Section 2001-2003Chair, Motility & Nerve-Gut Interactions Section 2003-2005American Psychosomatic SocietyCouncil Member 1985-19881990-19921986 Meeting Program Committee 1985-1986Chairman, Membership Committee 1988-19921992 50th Anniversary Program Committee 1991-1992Secretary/Treasurer 1992-1995Finance Committee 1992-Liaison Committee 1993-Long Range Planning Committee 1993-1994 Program Committee 1993-1994President-Elect 1995-1996President 1996-1997American College of Gastroenterology (ACG)Abstract Selection Committee - Small bowel 1992Chairman, Ad Hoc Committee on Doctor/Patient Relations 1992-1994DROSSMAN 10Patient Care Committee (Co-Chair 1995-1997) 1995-Functional/Brain-Gut Research Group of AGA (FBGRG) 1989-Chair 1989-1994Newsletter Editor 1989-American College of Physicians (ACP)MKSAP IX Program Committee (Gastroenterology) 1989-1991American Digestive Disease SocietySelection Committee: Research Investigator Award of Brain-gut Hormones 1987American Academy on Physician and PatientCharter Fellow and Faculty Coordinator 1988-Crohn's and Colitis Foundation of America (CCFA)IBD Forum Planning Committee 1991-1996Patient Education Committee 1994-National Institutes of Health (NIH)Planning Committee:"IBS: State of the-Art and Research Objectives" Symposium 1992Program Coordinator:"1st Int'l Symposium on Functional Gastrointestinal Disorders" 1995American Digestive Health FoundationChair, Digestive Health Initiative on Functional GI Disorders 1999-2001INTERNATIONAL:Rome FoundationTo Develop Guidelines for Diagnosis of Irritable Bowel Syndrome 1986-1988Chair, Rome I Coordinating Committee 1989-1994Chair, Rome II Coordinating Committee 1995-2000Chair, Rome III Coordinating Committee 2000-2006President, Rome Foundation 2004-International Foundation for Functional GI Disorders 1992-Advisory Board 1993-Board of Trustees 1995-Chair, Scientific Advisory Committee 1995-Chair, 1st International Symposium 1995Chair, 2nd International Symposium 1997Chair, 3rd International Symposium 1999Chair, 4th International Symposium 2001Chair, 5th International Symposium 2003Chair 6th International Symposium 2005Chair, IFFGD Research Award Committee 2003, 2005DROSSMAN 11International Scientific Committees:Chair, Functional/Brain-Gut Research Group of AGA 1989-1994Newsletter Editor 1990-Scientific Secretariat, Italian-International Postgraduate Program in Motility 1990-1992Rome, ItalyScientific Committee - International Symposium on Neurogastroenterology 1995Rome, ItalySymposium Chair, First Int'l Symposium on Functional GI Disorders 1995Rome, ItalyScientific Committee - International Symposium on the Pelvic Floor, 1997-1998Montreal, CanadaScientific Committee - International Symposium on Chronic GI Disorders 1998Lake Maggiore, ItalyISIS- International Society for the Investigation of Stress, 1998Melbourne, AustraliaIntï¿½l. Society Committee, Biopsychosocial Approach to FBD, 2000Brain-Gut 2000 Congress, Toulouse, FranceIntï¿½l. Scientific Advisory Board, 16th International Congress of 2001Psychosomatic Medicine (ICPM), Gothenburg, Sweden 2001Intï¿½l Scientific Advisory Board, European Congress of Psychosomatic 2004Research, Berlin, GermanyIntï¿½l Scientific Committee, ANEMGI-Onlus (Associazione per la 2005NeuroGastroenterologia e la Motilitï¿½ Gastrointestinale, Rome, ItalyIntï¿½l Advisory Committee, 18th World Congress on Psychosomatic 2005Medicine, Kobe, JapanADMINISTRATIVE ACTIVITIES, SCHOOL OF MEDICINE:Co-Director, Medical-Psychiatric Liaison Program, Faculty-Resident 1977-1990Study GroupAd Hoc Member, Consultation-Liaison Division, Dept. of Psychiatry 1978-Jerry Finkel, MD, DirectorAssociate Medical Director: Carolina Fitness Program 1988-1991Co-Director, UNC Center for Functional GI and Motility Disorders 1994-MISC. HONORS AND AWARDS:1. Who's Who in American Colleges and Universities 1965-19662. NFIC Tar Heel Research Council Award, Inflammatory Bowel Disease 19903. "Best Doctors in America" Woodward/White Publ., Inc.1992-19951998-19992001-20022003-20044. "Best Doctors in America - Southeast Region" 1996-19975. Who's Who in the South and Southwest; 22-25th Edit. 1992-19986. Amer. Psychosomatic Society Visiting Scholar Award 19947. Who's Who in the World; 12th Edition 1995-19968. Intl. Who's Who in Medicine; 2nd Edition 1995-19969. Who's Who in American Education; Fifth and Sixth Editions 1996-200510. Who's Who in Medicine and Healthcarea. 1st Edition 1997-1998DROSSMAN 12b. 2nd Edition 1999-2000c. 4th Edition 2002-200311. Cercle Andrï¿½ Lambling, May 1998 199812. Janssen Award for Clinical Research in Digestive Diseases 199913. Functional Brain-Gut Research Group Research Scientist Award 200114. ï¿½Americaï¿½s Top Doctorsï¿½-2nd edition, Castle Connolly Medical Ltd. 200215. ACG Clinical Scholar Award 2002-200316. APS Presidentï¿½s Award. American Psychosomatic Society 200317. Whoï¿½s Who in Americaa. 58th Edition 2004b. 59th Edition 200518. American Gastroenterological Association Distinguished Educator Award 2004DROSSMAN 13BIBLIOGRAPHY:ARTICLES IN REFEREED JOURNALS:1. Gardner DL, Quagliata F, Drossman D, Kalish M and Schimmer B. Attempted prevention ofarteriolar lesions in accelerated rat hypertension by immunosuppression. BRITISH JOURNAL OFEXPERIMENTAL PATHOLOGY 51:242-252, l970.2. Drossman DA, Powell DW, Sessions JT Jr. The irritable bowel syndrome. GASTROENTEROL73:8ll-822, 1977.3. Drossman DA. Can the primary care physician be better trained in the psychosocial dimensions ofpatient care? INTERNATIONAL JOURNAL OF PSYCHIATRY IN MEDICINE 8:169-184, 1978.4. Drossman DA. The problem patient. Evaluation and care of medical patients with psychosocialdisturbances. ANNALS OF INTERNAL MEDICINE 88:366-372, 1978.5. Goldsmith JC, Drossman DA, Blatt PM. Hemobilia complicating warfarin therapy. SOUTHERNMEDICAL JOURNAL 72:748-750, 1979.6. Drossman DA, Heizer WD, Ontjes DA. Anorexia nervosa. GASTROENTEROL 77:1115-1131,1979.7. Kinard HB III, Powell DW, Sandler RS, Callahan WT, Lapis JL, Levinson SL, Jones JD, DrossmanDA, Jackson AL. A current approach to upper gastrointestinal bleeding. JOURNAL OF CLINICALGASTROENTEROL 3:231-240, 1981.8. Levinson SL, Powell DW, Callahan WT, Jones JD, Kinard HB III, Jackson AL, Lapis JL, DrossmanDA. A current approach to rectal bleeding. JOURNAL OF CLINICAL GASTROENTEROL 3(SUPPL. 1):9-16, 1981.9. Greganti MA, Drossman DA, Rogers JF. The role of the attending physician. ARCHIVES OFINTERNAL MEDICINE 142:698-699, 1982.10. Drossman DA, Sandler RS, McKee DC, Lovitz AJ. Bowel patterns among subjects not seeking healthcare: Use of a questionnaire to identify a population with bowel dysfunction. GASTROENTEROL83:529-534, l982.11. Drossman DA. Patients with psychogenic abdominal pain: Six years' observation in the medicalsetting. AMERICAN JOURNAL OF PSYCHIATRY l39:l549-l557, l982.12. Sandler RS, Drossman DA, Nathan HP, McKee DC. Symptom complaints and health care seekingbehavior in subjects with bowel dysfunction. GASTROENTEROL 87:314-318, 1984.13. Steckman M, Drossman DA, Lesesne HR. Hepatobiliary disease that precedes ulcerative colitis. JCLIN GASTROENTEROL 6:425-428, 198414. Haggerty JJ Jr., Drossman DA. Use of psychotropic drugs in patients with peptic ulcer disease.PSYCHOSOMATICS 26:277-285,1985.15. Drossman DA. Is the cotton-topped tamarin a model for behavioral research? DIG DIS SCI 30:24s-27s, 1985.16. Drossman DA. Psychosocial aspects of inflammatory bowel disease. STRESS MEDICINE 2:119-128, 1986.DROSSMAN 1417. Drossman DA, Sandler RS, Broom CM, McKee DC. Urgency and fecal soiling in people with boweldysfunction. DIG DIS SCI 31:1221-1225, 198618. Lowman BC, Drossman DA, Cramer EM, McKee DC. Recollection of childhood events in adultswith irritable bowel syndrome. J CLIN GASTROENTEROL 9:324-330, 1987.19. Sandler RS, Drossman DA. Bowel Habits in Young Adults Not Seeking Health Care. DIG DIS SCI32:841-845, 1987.20. Mitchell CM, Drossman DA. The irritable bowel syndrome: Understanding and treating abiopsychosocial illness disorder. ANN BEHAV MED 9:13-18, 1987.21. Drossman DA, McKee DC, Sandler RS, Mitchell CM, Lowman BC, Burger AL, Cramer EM.Psychosocial factors in the irritable bowel syndrome: A multivariate study of patients and nonpatientswith IBS. GASTROENTEROL 95:701-708, 1988.22. Drossman DA, Patrick DL, Mitchell CM, Zagami EA, Appelbaum MI. Health related quality of life ininflammatory bowel disease: Functional status and patient worries and concerns. DIG DIS SCI34:1379-1386, 1989.23. Thompson WG, Dotevall G, Drossman DA, Heaton KW, Kruis W. Irritable bowel syndrome:Guidelines for the diagnosis. GASTROENTEROLOGY INTERNATIONAL 2:92-95, 198924. Garrett JW, Drossman DA. Health status in inflammatory bowel disease: Biologic and behavioralconsiderations. GASTROENTEROL 99:90-96, 1990.25. Drossman DA, Leserman J, Nachman G, Li Z, Gluck H, Toomey TC Mitchell CM. Sexual andphysical abuse among women with functional or organic gastrointestinal disorders. ANN INTERNMED 113:828-833, 1990.26. Drossman DA, Thompson WG, Talley NJ, Funch-Jensen P, Janssens J, Whitehead WE. Identificationof subgroups of functional gastrointestinal disorders. GASTROENTEROLOGY INTERNATIONAL3:159-172, 199027. Friedman CP, France CL, Drossman DA. A randomized comparison of alternative formats for clinicalsimulations. MEDICAL DECISION MAKING 11:265-272, 1991.28. Drossman DA. Illness behaviour in the irritable bowel syndrome. GASTROENTEROLOGYINTERNATIONAL 4:77-81, 1991.29. Drossman DA, Leserman J, Mitchell CM, Li Z, Zagami EA, Patrick DL. Health status and health careuse in persons with inflammatory bowel disease: A national sample. DIG DIS SCI 36: 1746-1755,1991.30. Drossman DA, Leserman J, Li Z, Mitchell CM, Zagami EA, Patrick DL. The Rating Form of IBDPatient Concerns: A new measure of health status. PSYCHOSOM MED 53:701-712, 1991.31. Drossman DA, Thompson WG: Irritable Bowel Syndrome: Review and a graduated multi-componenttreatment approach. ANN INTERN MED 116:1009-1016, 1992.32. Drossman DA, Li Z, Patrick DL. Ulcerative Colitis and Crohn's Disease health status scales forresearch and clinical practice. J CLIN GASTROENTEROLOGY 15:104-112, 199233. Drossman DA. Psychosocial factors in functional dyspepsia. EUR J GASTROENTEROL HEPATOL4:602-607, 1992.DROSSMAN 1534. Thompson WG, Creed F, Drossman DA, Heaton KW, Mazzacca G. Functional bowel disorders andfunctional abdominal pain. GASTROENTEROLOGY INTERNATIONAL 5:75-91, 1992.35. Pisetsky I, Keram E, Drossman DA. Building a Psychiatric-Medical Liaison: Observations of theProcess. PSYCHIATR MED 10:149-163, 1992.36. Gwyther RE, Bentz EJ, Drossman DA, Berolzheimer N. Validity of the family APGAR in patientswith irritable bowel syndrome. CLINICAL RESEARCH AND METHODS 25:21-25, 1993.37. Novack DH, Volk G, Drossman DA, Lipkin M Jr. Medical Interviewing and Interpersonal SkillsTeaching in U.S. Medical Schools: Progress, Problems and Promise. JAMA 269:2101-2105, 1993.38. Cassileth BR, Drossman DA. Psychosocial factors in gastrointestinal illness. PSYCHOTHERPSYCHOSOM, 59:131-143, 1993.39. Drossman DA, Li Z, Andruzzi E, Temple R, Talley NJ, Thompson WG, Whitehead WE, Janssens J,Funch-Jensen P, Corazziari E, Richter JE, Koch GG. US Householder survey of functional GIdisorders: Prevalence, Sociodemography and Health Impact. DIG DIS SCI 38:1569-1580, 1993.40. Talley NJ, Nyren O, Drossman DA, Heaton KW, Veldhuyzen van Zanten SJO, Koch MM, RansohoffDF. The irritable bowel syndrome: Toward optimal design of treatment trials.GASTROENEROLOGY INTERNATIONAL 4: 189-211, 1993.41. Lydiard RB, Greenwald S, Weissman MM, Johnson J, Drossman DA, Ballenger JC. Panic disorderand gastrointestinal symptoms: Findings from the NIMH Epidemiologic Catchment Area Project. AMJ PSYCHIATRY 151: 64-70, 1994.42. Drossman DA. Irritable bowel syndrome: The role of psychosocial factors. STRESS MEDICINE10:49-55, 199443. Drossman DA. Struggling with the "Controlling" patient. AM J GASTROENTEROL 89:1441-1446,1994.44. Drossman DA. The irritable bowel syndrome. THE GASTROENTEROLOGIST 2:315-326, 1994.45. Drossman DA. Sexual and physical abuse and gastrointestinal illness. SCAND JGASTROENTEROL, 208 (SUPPL.):90-96, 1995.46. Leserman J, Drossman DA, Li Z, Toomey TC, Nachman G. The reliability and validity of a sexualand physical abuse history questionnaire in female patients with gastrointestinal disorders.BEHAVIORAL MEDICINE 21:141-150, 1995.47. Drossman DA, Li Z, Toner BB, Diamant NE, Creed FH, Thompson DG, Read NW, Babbs C, BarreiroM, Bank L, Whitehead WE, Schuster MM, Guthrie EA. Functional bowel disorders: A multinationalcomparison of health status, and development of an illness severity index. DIG DIS SCI 40:986-995,1995.48. Zuckerman MJ, Guerra LG, Drossman DA, Foland JA, Gavin GG. Comparison of bowel patterns inHispanics and non-Hispanic Whites. DIG DIS SCI 40:1763-1769, 1995.49. Drossman DA, Creed FH, Fava GA, Olden KW, Patrick DL, Toner BB, Whitehead WE. Psychosocialaspects of the functional gastrointestinal disorders. GASTROENTEROLOGY INTERNATIONAL8:47-90, 1995.DROSSMAN 1650. Drossman DA. Diagnosing and treating patients with refractory functional gastrointestinal disorders.ANN INTERN MED 123:688-697, 1995.51. Drossman DA, Talley NJ, Olden KW, Leserman J, Barreiro MA. Sexual and physical abuse andgastrointestinal illness: Review and recommendations. ANN INTERN MED 123:782-794, 1995.52. Drossman DA, Brandt LJ, Sears C, Li Z, Nat J, Bozymski EM. A preliminary study of patients'concerns related to GI endoscopy. AMER J GASTROENTEROL 91:287-291, 1996.53. Zuckerman MJ, Guerra LG, Drossman DA, Foland JA, Gavin GG. Health care seeking behaviorsrelated to bowel complaints: Hispanic versus non-Hispanic Whites. DIG DIS SCI 41:77-82, 1996.54. Leserman J, Drossman DA, Li Z, Toomey TC, Nachman G, Glogau L. Sexual and physical abusehistory in gastroenterology practice: How types of abuse impact health status. PSYCHOSOMATICMEDICINE 58:4-15, 1996.55. Ouyang A, Camilleri M, Drossman DA, Kahrilas PJ, Reynolds JC, Richter JE, Shaker R. Task forceon training in motility, diverticular disease, and functional illnesses. GASTROENTEROL 110:1274-1276, 1996.56. Whitehead WE, Drossman DA. Biofeedback for disorders of elimination: Fecal incontinence andpelvic floor dyssynergia. PROFESSIONAL PSYCHOLOGY: RESEARCH AND PRACTICE27:234-240, 1996.57. Drossman DA, Li Z, Leserman J, Toomey TC, Hu YJB. Health status by GI diagnosis and abusehistory. GASTROENTEROLOGY 110:999-1007, 1996.58. Drossman DA. Chronic functional abdominal pain. AMER J GASTROENTEROL 91:2270-2281,1996.59. Drossman DA. The role of psychosocial factors in gastrointestinal illness. SCAND JGASTROENTEROL, 31 (SUPPL. 221):1-4, 1996.60. Leserman J, Li Z, Drossman DA, Toomey TC, Nachman G, Glogau L. Impact of sexual and physicalabuse dimensions on health status: Development of an abuse severity measure. PSYCHOSOMATICMEDICINE 59:152-160, 1997.61. Drossman DA. Irritable bowel syndrome and sexual/physical abuse history. EUR JGASTROENTEROL HEPATOL 9:327-330, 1997.62. Drossman DA, Whitehead WE, Camilleri, M. Irritable bowel syndrome: A technical review forpractice guideline development. GASTROENTEROL 112:2120-2137, 1997.63. Drossman DA, Whitehead WE, Camilleri M. Medical position statement: Irritable bowel syndrome.GASTROENTEROL 112:2118-2119, 1997.64. Drossman DA. Psychosocial sound bites: Exercises in the patient-doctor relationship. AMER JGASTROENTEROL 92:1418-1423, 1997.65. Provenzale D, Shearin M, Phillips-Bute B, Drossman DA, Li Z, Tillinger W, Schmitt C, Bollinger R,Koruda M. Health-related quality of life after ileoanal pull-through: Evaluation and assessment ofnew health status measures. GASTROENTEROL 113:7-14, 1997DROSSMAN 1766. Drossman DA. Importance of the psyche in heartburn and dyspepsia. ALIMENT PHARMACOLTHER, 11(SUPPL. 2):57-67, 1997.67. Leserman J, Li Z, Drossman DA, Hu JB. Selected symptoms associated with sexual and physicalabuse history: The impact on subsequent health care visits. PSYCHOLOGICAL MEDICINE 28:417-425, 1998.68. Patrick DL, Drossman DA, Frederick IO, DiCesare J, Puder KL. Quality of life in persons withirritable bowel syndrome: Development of a new measure. DIG DIS SCI 43:400-411, 1998.69. Leserman J, Li Z, Hu YJB, Drossman DA. How multiple types of stressors impact on health.PSYCHOSOMATIC MEDICINE 60:175-181, 1998.70. Drossman DA. Presidential Address: Gastrointestinal illness and the Biopsychosocial model.PSYCHOSOMATIC MEDICINE 60:258-267, 1998.71. Drossman DA. Review Article: An integrated approach to the irritable bowel syndrome. ALIMENTPHARM THER 13(4) (SUPPL. 2):3-14, 1999.72. Camilleri M, Mayer EA, Drossman DA, Heath A, Dukes GE, McSorley D, Kong S, Mangel AW,Northcutt AR. Improvement in pain and bowel function in female irritable bowel syndrome patientswith alosetron, a 5HT3 receptor antagonist. ALIMENT PHARM THER, 13:1149-1159, 1999.73. Russo MW, Gaynes BN, Drossman DA. A national survey of practice patterns of gastroenterologistswith comparison to the past two decades. J CLIN GASTROENTEROLOGY 29(339):343, 1999.74. Drossman DA. The functional gastrointestinal disorders and the Rome II process. GUT 45(SUPPL.II):II1-II5, 1999.75. Drossman DA, Creed FH, Olden KW, Svedlund J, Toner BB, Whitehead WE. Psychosocial aspectsof the functional gastrointestinal disorders. GUT 45(SUPPL. II):II25-II30, 1999.76. Thompson WG, Longstreth GF, Drossman DA, Heaton KW, Irvine EJ, Mï¿½ller-Lissner SA.Functional Bowel Disorders and Functional Abdominal Pain. GUT 45(SUPPL. II):II43-II47, 1999.77. Drossman DA. Do psychosocial factors define symptom severity and patient status in Irritable BowelSyndrome? AMER J MEDICINE Mayer EA, Dent J (eds). 107 SUPPL. 5A (No.8), pp 41S-50S. 1999.78. Casati J, Toner BB, C de Rooy E, Drossman DA, Maunder RG. Concerns of Patients withInflammatory Bowel Disease: A Review of Emerging Themes. DIG DIS SCIENCES 45(1):26-31,2000.79. Drossman DA, Patrick DL, Whitehead WE, Toner BB, Diamant NE, Hu YJB, Jia H, Bangdiwala SI.Further validation of the IBS-QOL: A disease specific quality of life questionnaire. AMER JGASTROENTEROLOGY 95(4):999-1007, 2000.80. Drossman DA, Whitehead WE, Toner BB, Diamant N, Hu YJB, Bangdiwala SI, Jia H. Whatdetermines severity among patients with painful functional bowel disorders? AMER JGASTROENTEROLOGY 95(4):974-980, 2000.81. Drossman DA, Li Z, Leserman J, Keefe FJ, Hu YJ, Toomey TC. Effects of coping on health outcomeamong female patients with gastrointestinal disorders. PSYCHOSOMATIC MEDICINE 62:309-317,2000.82. Ringel Y, Sperber A, Drossman DA. Irritable Bowel Syndrome. ANN REV MED 52:319-338, 2001.DROSSMAN 1883. Waldstein SR, Neumann SA, Drossman DA, Novack DH. Teaching psychosomatic (biopsychosocial)medicine in United States medical schools: Survey findings. PSYCHOSOMATIC MEDICINE63:335-343, 2001.84. Levenstein S, Li Z, Almer S, Barbosa A, Marquis P, Moser G, Sperber A, Toner B, Drossman DA.Cross-cultural variation in disease-related concerns among patients with inflammatory bowel disease.AM J GASTROENTEROL 96(6):1822-1830, 2001.85. Ringel Y, Dalton CB, Brandt LJ, Hu Y, Jia H, Bangdiwala S, Drossman DA. FlexibleSigmoidoscopy: The Patientsï¿½ Perception. GASTROINTESTINAL ENDOSCOPY 55(3): 315-320,2002.86. Drossman DA, Ringel Y. Irritable Bowel Syndrome: Classification and Conceptualization.JOURNAL OF CLINICAL GASTROENTEROLOGY 35 (1) Suppl: S7-S10, 2002.87. Gibbs-Gallagher N; Palsson OS; Levy RL; Meyer K; Drossman DA; Whitehead WE. Selective recallof gastrointestinal-sensation words: Evidence for a cognitive-behavioral contribution to irritable bowelsyndrome. AM J GASTROENTEROL 96 (4): 1133-1138, 2001.88. Ringel Y, Drossman DA. Functional chest pain of presumed esophageal origin. ARCHIVES OFINTERNAL MEDICINE 162 (3): 365-366, 2002.89. Drossman DA; Camilleri M; Mayer E; Whitehead WE. Irritable bowel syndrome: A technical reviewfor practice guideline development. GASTROENTEROL, 123 (6): 2108-2131, 2002.90. Drossman DA, Camilleri M; Mayer E; Whitehead WE. Medical position statement: Irritable bowelsyndrome. GASTROENTEROL, 123 (6): 2105-2107, 2002.91. Longstreth GF, Drossman DA. New developments in the diagnosis and treatment of Irritable BowelSyndrome, CURRENT GASTRO REPORTS, 4 (5): 427-434, 2002.92. Chey WD, Olden K, Carter E, Boyle J, Drossman D, Chang L. Utility of the Rome I and Rome IIcriteria for IBS in US women. AM J GASTROENTEROL, 97 (11): 2803-2811, 2002.93. Drossman DA, Ringel Y, Vogt B, Leserman J, Lin W, Smith JK, Whitehead B. Alterations of brainactivity associated with resolution of emotional distress and pain in a case of severe IBS.GASTROENTEROL, 124: 754-761, 2003.94. Ringel Y, Drossman DA, Turkington TG, Hawk TC, Bradshaw B, Coleman RE, Whitehead WE.Regional brain activation in response to rectal distension in patients with irritable bowel syndrome andthe effect of a history of abuse. DIGESTIVE DISEASE SCIENCE Sep;48(9):1774-81, 2003.95. Muller-Lissner S, Koch G, Talley NJ, Drossman D, Rueegg P, Dunger-Baldauf C, Lefkowitz M.Subjectï¿½s Global Assessment of Relief: An appropriate method to assess the impact of treatment onirritable bowel syndrome-related symptoms in clinical trials. JOURNAL OF CLINICALEPIDEMIOLOGY 56: 310-316, 2003.96. Parkman HP, Rao SS, Reynolds JC, Schiller LR, Wald A, Miner PB, Lahr C, Wald A, Lembo AJ,Drossman DA, Waltzman L, Stambler N, Cedarbaum JM. Neurotrophin-3 improves functionalconstipation. AM J GASTROENTEROL 98:1338-1347, 2003.97. Drossman DA, Toner BB, Whitehead WE, Diamant NE, Dalton CB, Duncan S et al. Cognitive-Behavioral Therapy vs. Education and Desipramine vs. Placebo for Moderate to Severe FunctionalBowel Disorders. GASTROENTEROL, 125: 19-31, 2003.DROSSMAN 1998. Dalton CB, Drossman DA, Hathaway JM, Bangdiwala SI Perceptions of physicians and patients withorganic and functional GI disorders. JOURNAL OF CLINICAL GASTROENTEROLOGY ANDHEPATOLOGY 2(2):121-126,2004.99. Ringel Y, Whitehead WE, Toner BB, Diamant NE, Hu Y, Jia H ,Bangdiwala SI, Drossman DA.Sexual and Physical Abuse are Not Associated with Rectal Hypersensitivity in Patients with IrritableBowel Syndrome, GUT 53: 845-849, 2004.100. Drossman, DA, Functional Abdominal Pain Syndrome, JOURNAL OF CLINICALGASTROENTEROLOGY AND HEPATOLOGY, 2:353-365, 2004.101. Halpert, A, Drossman, DA. Biopsychosocial Issues in Irritable Bowel Syndrome. Mental Fitness, InPress, 2004.102. Drossman DA. What Does the Future Hold for IBS and the Functional GI Disorders. J CLINICALGASTROENTEROLOGY, in press, 2004103. Halpert AD, Dalton CB, Diamant N, Toner B, Hu Y, Morris C, Bangdiwala S, Whitehead W,Drossman D. Clinical Response to Tricyclic Antidepressants in Functional Bowel Disorders is NotRelated to Dosage. American Journal of Gastroenterology, In Press, 2004104. Whitehead WE, Levy RL, Von Korff M, Feld A, Palsson O, Turner M, Drossman DA. Usual medicalcare for irritable bowel syndrome. Alimentary Pharmacology and Therapeutics, In Press 2004.NON-REFEREED ARTICLES:1. Drossman DA, Powell DW, Sessions JT Jr. The irritable bowel syndrome: a challenge for thephysician. CURRENT CONCEPTS IN GASTROENTEROLOGY 3:4-7, 1978.2. Drossman DA. Irritable bowel: Flexibility is the key to proper management. MODERN MEDICINE48:26-31, 1980.3. Sandler RS, Drossman DA. A conservative approach to the diagnosis of irritable bowel syndrome.IM - INTERNAL MEDICINE FOR THE SPECIALIST 2:39-47, 1981.4. Drossman DA. Consultation: Abdominal pain: How far do you go in the workup? MODERNMEDICINE 50:217-222, 1982.5. Drossman DA. Psychogenic chest pain. CHEST PAIN 8(3):l-7, l982.6. Drossman DA. Psychosocial aspects of the irritable bowel syndrome. SURVEY OF DIGESTIVEDISEASES l(l): l30-l35, l983.7. Drossman DA, Lowman BC. Irritable bowel syndrome: Epidemiology, diagnosis and treatment.GASTROENTEROLOGICAL CLINICS OF NORTH AMERICA 14:559-574, 1985.8. Drossman DA. The patient with chronic undiagnosed abdominal pain. HOSP PRACTICE21(11A):22-29, 1986.9. Drossman DA. Depression and the gastrointestinal disorders. CLIN ADVANCES IN THETREATMENT OF DEPRESSION 1:8-11, 1987.DROSSMAN 2010. Buccini R, Drossman DA. Chronic Idiopathic Abdominal Pain. CURRENT CONCEPTS INGASTROENTEROLOGY 12:3-11, 1988.11. Drossman DA. Irritable Bowel Syndrome. HOSPITAL PRACTICE 3(9):119-133, 198812. Drossman DA. Irritable Bowel Syndrome. AMERICAN FAMILY PHYSICIAN 39:159-164, 198913. Drossman DA, Weiss T, Rahe RH. Who are we? The American Psychosomatic Society MembershipSurvey. PSYCHOSOMATIC MEDICINE 51:648-651, 198914. Brannan DP, Drossman DA. Irritable Bowel Syndrome: Recognition and Management. HOSPITALMEDICINE 26:93-99, 1990.15. Brannan DP, Drossman DA. Towards a newer understanding of Irritable Bowel Syndrome.CONTEMPORARY INTERNAL MEDICINE Sep.:73-91 1991.16. Drossman DA. The link between early abuse and GI disorders in women. EMERGENCYMEDICINE 24(6):171-175, 199217. Drossman DA. Psychosocial factors in inflammatory bowel disease. PRACTICALGASTROENTEROLOGY 16(5):24N-24U, 1992.18. Drossman DA, Sandler RS, Sartor RB. Our new president: Don W. Powell, M.D.GASTROENTEROL 104:1249-1251, 1993.19. Drossman DA. Measuring quality of life in inflammatory bowel disease.PHARMACOECONOMICS 6:578-580, 1994.20. Fullwood AP, Drossman DA. The relationship of psychiatric illness with gastrointestinal disease.ANN REV MED 46:483-496, 1995.21. Leserman J, Toomey TC, Drossman DA. Medical consequences of sexual and physical abuse inwomen. HUMANE MEDICINE 11:23-28, 1995.22. Talal AH, Drossman DA. Psychosocial Factors in Inflammatory bowel disease. GASTROENTEROLCLIN N AMER 24:699-716, 1995.23. Drossman DA. Irritable Bowel Syndrome. GASTROINTESTINAL DISEASES TODAY 4:9-18,1995.24. Drossman DA. Life stresses and effects on ulcerative colitis (Commentary on paper by Levenstein etal.: "Psychological Stress and Disease Activity in Ulcerative Colitis. INFLAMMATORY BOWELDISEASES 1:86-87, 1995.25. Cerda JJ, Drossman DA, Scherl EJ. Effective, compassionate management of IBS. PATIENT CARE30:131-144, 1996.26. Almounajed G, Drossman DA. Newer aspects of the irritable bowel syndrome. PRIMARY CARE:CLINICS IN OFFICE PRACTICE 23:477-495, 1996.27. Drossman DA. The functional gastrointestinal disorders: Introduction SEMINARS INGASTROINTESTINAL DISEASES 7:1-3, 1996.DROSSMAN 2128. Dalton CB, Drossman DA. Diagnosing and treating irritable bowel syndrome. ADVANCE forPHYSICIAN ASSISTANTS 10:11-14, 1996.29. Dalton CB, Drossman DA. Diagnosis and Treatment of Irritable Bowel Syndrome. AM FAMPHYSICIAN 55:875-880, 1997.30. Drossman DA. Irritable bowel syndrome: Guidelines for Canadian family physicians. Position paperSYCHOSOCIAL INFLUENCES, 1997.31. Dalton CB, Drossman DA. Diagnosis and treatment of irritable bowel syndrome. DRUGS OFTODAY 34(7): 585-592, 1998.32. Cerda J, Drossman DA, Richter J. Reflux, abdominal pain, diarrhea. PATIENT CARE, April 15,1999. Whitehead WE, Gibbs NA, Li Z, Drossman DA: Is functional dyspepsia just a subset of theirritable bowel syndrome?. BAILLIERES CLINICAL GASTROENTEROLOGY 12:443-461, 1998.33. Gaynes B, Drossman DA. The role of the mental health professional in the assessment andmanagement of Irritable Bowel Syndrome. CNS SPECTRUMS 4(4):19-30, 1999.


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## eric (Jul 8, 1999)

DOUGLAS A. DROSSMANAssociate EditorGastroenterologyMedicine Has Become aBusiness, But What Isthe Cost?I have seen a great deal of changes inthe practice of medicine. I grew upin the 50s and 60s, when MarcusWelby and James Kildare were rolemodels for physicians. At that time, aphysician would sit at the bedside,hold hands, take a pulse, and talk tofamiliesï¿½and the patients expected it.Some would say this had healingvalue. Others would now argue thatthere really was not much more to do.There were no ultrasound or computedtomography studies, endoscopywas only beginning, and treatmentswere limited. During medical schoolin the 1960s, emphasis was placed onthe medical history, the physical examination,and the clinical decisionmaking.The greatest respect went tothe clinician/teachers. They couldelicit on rounds that a patient with anobscure patchy pneumonia was a birdfancier, or identify that the new admissiondeveloped unexplained chestpain on the 1-year anniversary of theparentï¿½s death from a myocardial infarction.They could not only auscultateparadoxical splitting of S2, butalso could draw the cardiac cycle andexplain the physiology.Later during residency and fellowship,rounds were rich with discussionson the pathophysiology of diarrheawith inpatients staying ford-xylose tests or 72-hour stool fat collections.We learned how to managegastrointestinal bleeding, often to endoscopeand identify the bleeding sitebefore sending the patient to arteriographyor surgery. The gastrointestinalfellows would see patients in clinicwith attending supervision and wouldï¿½followï¿½ them over several years untilthey said goodbye when leaving forpractice. For those staying in academicmedicine, the goal was to emulatethe highly respected ï¿½triplethreatsï¿½: effective clinicians and educatorswho could also secure NationalInstitutes of Health grants (when thepayline approached 50%) and evenchair a gastrointestinal division or departmentof medicine.So much has changed. The remarkablegrowth of medical knowledgeand technology has relegated much ofthese time-honored ï¿½doctorisms,ï¿½such as the physical examination, bedsideteaching, or even continuity ofcare to the archives. Clinicians nowmust learn to interpret ultrasonography,or computed tomography, imagesand the physical examination cursorilyscreens for more definitive tests.In many ways, we believe we aresmarter, more efficient, and more capableof saving lives.But are we at risk of throwing outthe baby with the bathwater? Thewell-executed history and physical examinationnot only permits the mostvalid acquisition of clinical informationbut also facilitates the physicianpatientrelationship and has therapeuticvalue. Bedside teaching enables aprocess of learning between teacher,student, and patient that brings to focusthe patient and illness rather thanthe disease alone. Continuity of careprovides a longitudinal dimension inwhich a physician can truly ï¿½knowï¿½the patient, and, in the process, provideongoing knowledge, guidance,and hope. These are human values relatingto the process of medicine thatwe as physicians must retain in ourpursuit of new technical skills.How is medicine now practicedcompared with 30ï¿½40 years ago? Thepatient care seen on television has becomean allegory; it has moved fromthe bedside to the emergency roomwhere 3-camera fast takes and multiplesound bites show the speed andquick thinking of health care teamsthat move from one patient to another.With regard to the day-to-dayactivities in teaching centers, medicalattendings are discouraged fromteaching on work rounds because itinterferes with team efficiency and autonomy.The training of completephysical examinations has been supplantedby regional examinationsbased on the patientï¿½s chief complaint,and technology is becomingthe ï¿½gold standardï¿½ of diagnosis. Oneday on rounds, an intern presenting apatient with congestive cardiomyopathynoted the large neck veins andcardiac findings and reported a normalabdominal examination. The attending,eager to teach, showed the verylarge liver that was missed, only tohear the intern sheepishly ask the residentif he should get an ultrasound toconfirm that it truly was enlarged.Residents do ï¿½shift workï¿½ on theiradmission days, and the night floats,who cover until the early morning, arenot around the next day when questionsare asked about why a procedurewas scheduled. On admission days,the ward team greets each new patientas a group, where 10ï¿½15 minutesare spent at the bedside while oneperson takes the history (ï¿½why are youhere now?ï¿½) and 3 stethoscopes simultaneouslyauscult the chest. Then allretire to the computers to ï¿½cut andpasteï¿½ the past medical and social historytemplates. Patients, confusedabout who is really their doctor, oftenlink up with the medical student, theone who comes back after ï¿½lightningï¿½rounds to see if there are any morequestions.What has led to such changes? Anew factor is affecting health care inways that would never have been anticipated:medicine has become a business.This has occurred because ofhefty drug costs, decreasing reimbursementsfrom insurance companiesand Medicare/Medicaid, increasingregulatory burdens, the loss ofcross-subsidization to cover the uninsured,and the need to treat a largernumber and proportion of uninsuredpatients requiring more specializedand costly services. This fiscal aspecthas so permeated medical practiceand patient care that, to younger physicians,it goes unnoticed. In the realworld of medicine, speed and effi-GASTROENTEROLOGY 2004;126:952ï¿½953ciency using modern technology arethe priorities, because the cost ofhealth care and the very salaries of thehealth care personnel depend on it.The effects are profound. Physiciansare now ï¿½providers,ï¿½ guided bycase managers who decide on thelength of ï¿½clientï¿½ hospital stays, andprofessionals in business suits, notwhite coats, determine health carepolicy. Responsibility for patient careis now diffused among multiple providerswith no single person willing orable to assume final responsibility forthe patient. As a result, when decisionsare made, the patient becomesconfused and feels caught in the middle.It is no wonder that malpracticelitigations and the use of alternativemedicine have grown so dramatically.Within gastroenterology, we aremoving toward being an imaging specialty,in which patients may soonhave direct access to procedures,thereby bypassing clinical decisionmaking, as is occurring with communitycomputed tomography studies. Infact, endoscopy, the investigative andtherapeutic tool of the gastroenterologist,has become an annuity for thesurvival of academic programs andclinical practices, and the greatest respectgoes to those who endoscopethe most and the fastest.However, the cost is greatest at theacademic institutions where our physicians,teachers, and investigators ofthe future are being trained. Departmentchairs, who would like to bevalued for holding Chief of Servicerounds to show clarity in thinking tothe house staff, or for mentoring theirfaculty, are now also judged by theirability to balance the budget and todevelop a top-notch market plan forapproval by the Dean. Division chiefswho seek to promote and support thecareers of their members reluctantlyare compelled to request ï¿½bottomlineï¿½ funding sources from faculty toaccount to the department for theirtime if or when their grants run out.Recruitment strategies have shiftedfrom identifying young faculty withhopeful career paths to capturingthose either already funded, or whoare willing to work 4 days a weekdoing clinical service. For faculty,teaching is an uncompensated luxurythat fits between writing grants andsupporting oneself through clinicalservice. Furthermore, the time allottedfor teaching is compressed with theloss of formal teaching rounds, reducedtime for clinic visits, and increasednumbers of consultations. Ineffect, the value of teaching, mentoring,and caring for patients has beensupplanted by the need for each physicianand their departments in academicsor in practice to become fiscallyindependent.It is understandable, desirable, andinevitable that health care must be ef-ficient, and, in the least, financiallyneutral. However, I am concernedthat we are losing our sense of professionalismif we substitute rather thanintegrate financial management forthe time-honored values that distinguishus as physicians and educators:to develop an effective physician-patientrelationship, to mentor trainees,to establish camaraderie in peer associations,and to feel gratified in theprocess. The deeply engrained physicianethic of doing what you do forthe benefit of the patient and of teachingyoung physicians is becoming subsumedto the need to earn moremoney, often for third-party payers,and to get out on time. Technology,instead of being a resource that addsto our experience and wisdom, is believedto be sufficient for clinical decision-making. Yet, unguided technologycoupled with the speed andvolume of the workload actually increasescosts and risk to patients. Conversely,our ability to obtain criticalinformation directly from the patientwith whom we develop a relationshipreduces malpractice and improves patientsatisfaction, adherence to treatment,and even the outcome. Thesetimeless skills, if not transferred to ourstudents, will be lost.Are there solutions? There are anumber of possibilities. I believe thatwe must reward scholarly cliniciansand teachers by having the learninginstitutions, third-party payers whobenefit from these clinicians, and Congressshow their support financially.There needs to be a reallocation ofinstitutional overhead expenses, a taxto third-party payers, and, possibly, acongressional mandate to provide directeducational funds. The continuationof good educational skills must befostered. Accrediting agencies such asthe Accreditation Council for GraduateMedical Education and the LiaisonCommittee on Medical Educationcould set standards for quality assurancein teaching with more attentionpaid to basic clinical skills, evidencebasedmedicine, clinical reasoning, theuse of the biopsychosocial interview,and the cost-effective use of diagnostictests. Continuing medical educationcredits must be required in these areas.Certifying boards such as theAmerican Board of Internal Medicineand the American Board of MedicalSpecialties should call for demonstrationof these competencies for recertification.At the medical school level,deans could allocate specific fundingfor skilled teachers and reward their accomplishmentswith bonuses and promotions.Private foundations shouldsupport more fellowships and sabbaticalsfor clinician teachers. The Instituteof Medicine and other nationallyprestigious groups could influence thethinking of health care leaders by issuingappropriate directives. Ultimately,by fostering the development of educatorsand role models, we will reducecosts and improve quality of care. Isthere time to work out the solutions?Our profession and society dependon it.DOUGLAS A. DROSSMAN


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## eric (Jul 8, 1999)

DOUGLAS A. DROSSMANAssociate EditorGastroenterologyMedicine Has Become aBusiness, But What Isthe Cost?I have seen a great deal of changes inthe practice of medicine. I grew upin the 50s and 60s, when MarcusWelby and James Kildare were rolemodels for physicians. At that time, aphysician would sit at the bedside,hold hands, take a pulse, and talk tofamiliesï¿½and the patients expected it.Some would say this had healingvalue. Others would now argue thatthere really was not much more to do.There were no ultrasound or computedtomography studies, endoscopywas only beginning, and treatmentswere limited. During medical schoolin the 1960s, emphasis was placed onthe medical history, the physical examination,and the clinical decisionmaking.The greatest respect went tothe clinician/teachers. They couldelicit on rounds that a patient with anobscure patchy pneumonia was a birdfancier, or identify that the new admissiondeveloped unexplained chestpain on the 1-year anniversary of theparentï¿½s death from a myocardial infarction.They could not only auscultateparadoxical splitting of S2, butalso could draw the cardiac cycle andexplain the physiology.Later during residency and fellowship,rounds were rich with discussionson the pathophysiology of diarrheawith inpatients staying ford-xylose tests or 72-hour stool fat collections.We learned how to managegastrointestinal bleeding, often to endoscopeand identify the bleeding sitebefore sending the patient to arteriographyor surgery. The gastrointestinalfellows would see patients in clinicwith attending supervision and wouldï¿½followï¿½ them over several years untilthey said goodbye when leaving forpractice. For those staying in academicmedicine, the goal was to emulatethe highly respected ï¿½triplethreatsï¿½: effective clinicians and educatorswho could also secure NationalInstitutes of Health grants (when thepayline approached 50%) and evenchair a gastrointestinal division or departmentof medicine.So much has changed. The remarkablegrowth of medical knowledgeand technology has relegated much ofthese time-honored ï¿½doctorisms,ï¿½such as the physical examination, bedsideteaching, or even continuity ofcare to the archives. Clinicians nowmust learn to interpret ultrasonography,or computed tomography, imagesand the physical examination cursorilyscreens for more definitive tests.In many ways, we believe we aresmarter, more efficient, and more capableof saving lives.But are we at risk of throwing outthe baby with the bathwater? Thewell-executed history and physical examinationnot only permits the mostvalid acquisition of clinical informationbut also facilitates the physicianpatientrelationship and has therapeuticvalue. Bedside teaching enables aprocess of learning between teacher,student, and patient that brings to focusthe patient and illness rather thanthe disease alone. Continuity of careprovides a longitudinal dimension inwhich a physician can truly ï¿½knowï¿½the patient, and, in the process, provideongoing knowledge, guidance,and hope. These are human values relatingto the process of medicine thatwe as physicians must retain in ourpursuit of new technical skills.How is medicine now practicedcompared with 30ï¿½40 years ago? Thepatient care seen on television has becomean allegory; it has moved fromthe bedside to the emergency roomwhere 3-camera fast takes and multiplesound bites show the speed andquick thinking of health care teamsthat move from one patient to another.With regard to the day-to-dayactivities in teaching centers, medicalattendings are discouraged fromteaching on work rounds because itinterferes with team efficiency and autonomy.The training of completephysical examinations has been supplantedby regional examinationsbased on the patientï¿½s chief complaint,and technology is becomingthe ï¿½gold standardï¿½ of diagnosis. Oneday on rounds, an intern presenting apatient with congestive cardiomyopathynoted the large neck veins andcardiac findings and reported a normalabdominal examination. The attending,eager to teach, showed the verylarge liver that was missed, only tohear the intern sheepishly ask the residentif he should get an ultrasound toconfirm that it truly was enlarged.Residents do ï¿½shift workï¿½ on theiradmission days, and the night floats,who cover until the early morning, arenot around the next day when questionsare asked about why a procedurewas scheduled. On admission days,the ward team greets each new patientas a group, where 10ï¿½15 minutesare spent at the bedside while oneperson takes the history (ï¿½why are youhere now?ï¿½) and 3 stethoscopes simultaneouslyauscult the chest. Then allretire to the computers to ï¿½cut andpasteï¿½ the past medical and social historytemplates. Patients, confusedabout who is really their doctor, oftenlink up with the medical student, theone who comes back after ï¿½lightningï¿½rounds to see if there are any morequestions.What has led to such changes? Anew factor is affecting health care inways that would never have been anticipated:medicine has become a business.This has occurred because ofhefty drug costs, decreasing reimbursementsfrom insurance companiesand Medicare/Medicaid, increasingregulatory burdens, the loss ofcross-subsidization to cover the uninsured,and the need to treat a largernumber and proportion of uninsuredpatients requiring more specializedand costly services. This fiscal aspecthas so permeated medical practiceand patient care that, to younger physicians,it goes unnoticed. In the realworld of medicine, speed and effi-GASTROENTEROLOGY 2004;126:952ï¿½953ciency using modern technology arethe priorities, because the cost ofhealth care and the very salaries of thehealth care personnel depend on it.The effects are profound. Physiciansare now ï¿½providers,ï¿½ guided bycase managers who decide on thelength of ï¿½clientï¿½ hospital stays, andprofessionals in business suits, notwhite coats, determine health carepolicy. Responsibility for patient careis now diffused among multiple providerswith no single person willing orable to assume final responsibility forthe patient. As a result, when decisionsare made, the patient becomesconfused and feels caught in the middle.It is no wonder that malpracticelitigations and the use of alternativemedicine have grown so dramatically.Within gastroenterology, we aremoving toward being an imaging specialty,in which patients may soonhave direct access to procedures,thereby bypassing clinical decisionmaking, as is occurring with communitycomputed tomography studies. Infact, endoscopy, the investigative andtherapeutic tool of the gastroenterologist,has become an annuity for thesurvival of academic programs andclinical practices, and the greatest respectgoes to those who endoscopethe most and the fastest.However, the cost is greatest at theacademic institutions where our physicians,teachers, and investigators ofthe future are being trained. Departmentchairs, who would like to bevalued for holding Chief of Servicerounds to show clarity in thinking tothe house staff, or for mentoring theirfaculty, are now also judged by theirability to balance the budget and todevelop a top-notch market plan forapproval by the Dean. Division chiefswho seek to promote and support thecareers of their members reluctantlyare compelled to request ï¿½bottomlineï¿½ funding sources from faculty toaccount to the department for theirtime if or when their grants run out.Recruitment strategies have shiftedfrom identifying young faculty withhopeful career paths to capturingthose either already funded, or whoare willing to work 4 days a weekdoing clinical service. For faculty,teaching is an uncompensated luxurythat fits between writing grants andsupporting oneself through clinicalservice. Furthermore, the time allottedfor teaching is compressed with theloss of formal teaching rounds, reducedtime for clinic visits, and increasednumbers of consultations. Ineffect, the value of teaching, mentoring,and caring for patients has beensupplanted by the need for each physicianand their departments in academicsor in practice to become fiscallyindependent.It is understandable, desirable, andinevitable that health care must be ef-ficient, and, in the least, financiallyneutral. However, I am concernedthat we are losing our sense of professionalismif we substitute rather thanintegrate financial management forthe time-honored values that distinguishus as physicians and educators:to develop an effective physician-patientrelationship, to mentor trainees,to establish camaraderie in peer associations,and to feel gratified in theprocess. The deeply engrained physicianethic of doing what you do forthe benefit of the patient and of teachingyoung physicians is becoming subsumedto the need to earn moremoney, often for third-party payers,and to get out on time. Technology,instead of being a resource that addsto our experience and wisdom, is believedto be sufficient for clinical decision-making. Yet, unguided technologycoupled with the speed andvolume of the workload actually increasescosts and risk to patients. Conversely,our ability to obtain criticalinformation directly from the patientwith whom we develop a relationshipreduces malpractice and improves patientsatisfaction, adherence to treatment,and even the outcome. Thesetimeless skills, if not transferred to ourstudents, will be lost.Are there solutions? There are anumber of possibilities. I believe thatwe must reward scholarly cliniciansand teachers by having the learninginstitutions, third-party payers whobenefit from these clinicians, and Congressshow their support financially.There needs to be a reallocation ofinstitutional overhead expenses, a taxto third-party payers, and, possibly, acongressional mandate to provide directeducational funds. The continuationof good educational skills must befostered. Accrediting agencies such asthe Accreditation Council for GraduateMedical Education and the LiaisonCommittee on Medical Educationcould set standards for quality assurancein teaching with more attentionpaid to basic clinical skills, evidencebasedmedicine, clinical reasoning, theuse of the biopsychosocial interview,and the cost-effective use of diagnostictests. Continuing medical educationcredits must be required in these areas.Certifying boards such as theAmerican Board of Internal Medicineand the American Board of MedicalSpecialties should call for demonstrationof these competencies for recertification.At the medical school level,deans could allocate specific fundingfor skilled teachers and reward their accomplishmentswith bonuses and promotions.Private foundations shouldsupport more fellowships and sabbaticalsfor clinician teachers. The Instituteof Medicine and other nationallyprestigious groups could influence thethinking of health care leaders by issuingappropriate directives. Ultimately,by fostering the development of educatorsand role models, we will reducecosts and improve quality of care. Isthere time to work out the solutions?Our profession and society dependon it.DOUGLAS A. DROSSMAN


----------



## skinny (Jul 27, 2002)

Eric:


> quote:I don't think calling me dense is so ice Skinny.I also know that someone else edits a lot of the writings from these doctors to the public.I do see what your talking about, but don't view it as seriously as you seem too.


I asked you two simple yes or no questions and you can't be straightforward with me? Does that mean you concede that there are errors on the Drossman paper?I'm starting to sound like a broken record here, but it's important that I do so. This may sound trivial to folks here, but it shows how you operate on this board. These are tactics that politicians do when you are trying to get them to answer a question. So I think this qualifies you as being dense. Yes I agree that is not so ice [sic].Also with Drossman being the "world authority" on GI disorders, I expect a high standard of ethics.


> quote:"Some journalists (and possibly the author) addressed the findings of this study in a very dramatic fashion: ". . . 'This is really exciting because it points to the cause of the disease. Treatments for IBS to this point have been directed at symptoms, not any cause,' said Dr. Mark Pimental." (Reuters 12/13/00) However, even when findings come from a well-designed study, the investigators are obliged to monitor and temper what is put into print. Otherwise, media coverage itself can bias decisions of physicians, patients, or regulators."He was already using the cause word before it was even figured all out? What gives with that really.


This doesn't sound like he was saying SIBO was the cause of IBS. He highly suspects it based on the study.


> quote:"SIBO symptoms are IBS symptoms"No there not really, they can mimick SOME symptoms, but not all, that is a big part of the problem here.


SIBO symptoms can mimick *all* IBS symptoms. That's what Pimentel's studies found out. Whether or not to implicate SIBO for a cause of IBS is still up for debate.


> quote:You have a lot of excuses not to just pop into the chat and ask a question, but they aren't good enough in my book.


OK and you have your excuses why you can't do what I ask. A chat session isn't the proper way to discuss this. An open forum like this allows *everyone* to see what is being discussed or debated.Eric you know better than to post long posts like that. There is a forum where you can post such articles without cluttering up the thread. Besides you made no point other than dumping several pages on this thread.IBS News, Research and Abstracts http://www.ibsgroup.org/cgi-local/ubbcgi/u...?ubb=forum;f=10 You already posted the Drossman article "What Medicine has Become" here: http://www.ibsgroup.org/ubb/ultimatebb.php...c;f=10;t=001004 Is that so difficult for you!!??Talissa, interesting book you mention there. "Angell's examples of the large consulting fees paid by industry to individual faculty members and to NIH scientists and directors are astounding." It would be interesting to find out who is behind the NIH funding. The UNC center recently got pledged $4.3 from them. How much a consultant gets paid isn't the real issue here, but it gives you an idea how much of an influence the clients are. The thing I want to know is how much these pharmaceutical companies interfere with rigging up the studies (directly and indirectly) to show them favor. That is very hard to prove.skinny


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## skinny (Jul 27, 2002)

Eric:


> quote:I don't think calling me dense is so ice Skinny.I also know that someone else edits a lot of the writings from these doctors to the public.I do see what your talking about, but don't view it as seriously as you seem too.


I asked you two simple yes or no questions and you can't be straightforward with me? Does that mean you concede that there are errors on the Drossman paper?I'm starting to sound like a broken record here, but it's important that I do so. This may sound trivial to folks here, but it shows how you operate on this board. These are tactics that politicians do when you are trying to get them to answer a question. So I think this qualifies you as being dense. Yes I agree that is not so ice [sic].Also with Drossman being the "world authority" on GI disorders, I expect a high standard of ethics.


> quote:"Some journalists (and possibly the author) addressed the findings of this study in a very dramatic fashion: ". . . 'This is really exciting because it points to the cause of the disease. Treatments for IBS to this point have been directed at symptoms, not any cause,' said Dr. Mark Pimental." (Reuters 12/13/00) However, even when findings come from a well-designed study, the investigators are obliged to monitor and temper what is put into print. Otherwise, media coverage itself can bias decisions of physicians, patients, or regulators."He was already using the cause word before it was even figured all out? What gives with that really.


This doesn't sound like he was saying SIBO was the cause of IBS. He highly suspects it based on the study.


> quote:"SIBO symptoms are IBS symptoms"No there not really, they can mimick SOME symptoms, but not all, that is a big part of the problem here.


SIBO symptoms can mimick *all* IBS symptoms. That's what Pimentel's studies found out. Whether or not to implicate SIBO for a cause of IBS is still up for debate.


> quote:You have a lot of excuses not to just pop into the chat and ask a question, but they aren't good enough in my book.


OK and you have your excuses why you can't do what I ask. A chat session isn't the proper way to discuss this. An open forum like this allows *everyone* to see what is being discussed or debated.Eric you know better than to post long posts like that. There is a forum where you can post such articles without cluttering up the thread. Besides you made no point other than dumping several pages on this thread.IBS News, Research and Abstracts http://www.ibsgroup.org/cgi-local/ubbcgi/u...?ubb=forum;f=10 You already posted the Drossman article "What Medicine has Become" here: http://www.ibsgroup.org/ubb/ultimatebb.php...c;f=10;t=001004 Is that so difficult for you!!??Talissa, interesting book you mention there. "Angell's examples of the large consulting fees paid by industry to individual faculty members and to NIH scientists and directors are astounding." It would be interesting to find out who is behind the NIH funding. The UNC center recently got pledged $4.3 from them. How much a consultant gets paid isn't the real issue here, but it gives you an idea how much of an influence the clients are. The thing I want to know is how much these pharmaceutical companies interfere with rigging up the studies (directly and indirectly) to show them favor. That is very hard to prove.skinny


----------



## eric (Jul 8, 1999)

"SIBO symptoms can mimick all IBS symptoms. That's what Pimentel's studies found out."Totally and more totally false. They explain some symptoms that can mimick IBS, your greatly confused on this. For example, please show me where they say SIBO can cause the sensation of incomplete evacuation? Please show me where SIBO can cause symptoms immediately after eating? Please show me how SIBO effects REM sleep, Please Show me how SIBO causes impairments in the prefrontal cortex and Anterior Cinculate Cortex? Please show me where SIBO can cause rectal Hypersensivity? Please show me how SIBO can cause consitpation or alternating motility symptoms. Please show me how SIBO cause molecular cell changes in the digestive tract. Please show me how SIBO cause a dysregulation of the serotonin system? Please show me how SIBO can cause altered stress ciruits. Or an increase in stress hormones. Please show me how SIBO effects the LImbic system?"Visceral pain in IBS is associated with increased prefrontal cortex activation. The normal correlation between subjective pain intensity and activation of the anterior cingulate and insula cortices is lost in IBS. The limbic system is involved in emotion, mood, and visceral autonomic control. Limbic abnormalities are seen in depression and IBS. Thus, this system is a possible site of convergence where emotional disturbance provokes intestinal dysfunction. " http://www.fdhn.org/html/education/gi/ibs_nosology.htm Please show me why more women then men get SIBO.You know not knowing who Dr Mayer is or Dr Gershon, or a lot of the other Major players are shows for sure you have not been doing your homework on IBS or have taken the time to fully research and understand IBS yourself and even the diagnoses. This is one reason why I find it personally hard for me to discuss this with you, because you are at a major disanvantage, if you don't have all the information and the bigger picture.You have never been to one of their chats, but you seem to know that is not the forum for asking a question. That is exactly what its for. And you want the anwer to your question, I feel you should ask them yourself. Why is that up to me to do your work on this? Why not email them yourself also and ask them. I posted the above in full for the sheer information on who Dr D is and what he is about. he is not in the pocket of the parm compinies, I gurantee you that, he is one of the most caring drs in all this there is, but he is a world authority and head of the Rome commitee, of course they ask him to consult and of course they ask the center to do double blind stduies to figure out if drugs work and that they are safe.You can also email them and get for free the Annual Report 2003 which is publich knowledge and shows where all the monies go, both pharm monies and NIH grants and public support, which I don't think they get enough of from all of us.I posted the second because of DR Drossman sheer concern for good doctor patient relationships and the how it shows the kind of person he really is and how important he thinks working fully with a patient is all about and how the health care is wrongly moving away from it.The majority of researchers already know this and a lot of them have poosted the same thing."Irritable Bowel Syndrome - An Evidence-Based Approach to DiagnosisPosted 06/21/2004 B.D. Cash; W.D. Chey " *The potential role of small intestinal bacterial overgrowth (SIBO) as an aetiology for IBS symptoms has been highlighted by two recent publications* .36,37 Pimentel et al.36 performed lactulose hydrogen breath testing in 202 patients fulfilling the Rome I criteria referred for evaluation of possible SIBO. Seventy-eight percent (157/202) had breath test results that were consistent with SIBO and were treated with a 10-day course of antibiotics. Forty-seven of these patients (29.9%) were restudied 7-10 days after completion of the antibiotics and SIBO eradication was achieved in 25 (53.2%). Twelve patients (48%) with SIBO eradication did not meet the Rome I criteria when their symptoms were reassessed (interpreted as improvement), while only four patients (18.2%) with persistent SIBO failed to meet the Rome I criteria after treatment. While intriguing, *a number of methodological limitations of the study by Pimental et al., including potential selection bias, the absence of a gold standard for the diagnosis of SIBO, the use of an unusual antibiotic to treat SIBO, short study duration and incomplete follow-up data for the majority of enrolled patients, limits the conclusions that can be drawn regarding the role of SIBO in patients with suspected IBS.* The same group of investigators subsequently reported the results of a double-blind randomized placebo-controlled trial evaluating the effects of therapy for SIBO upon IBS symptoms.37 The prevalence of SIBO in patients with IBS in this study was 84%, similar to the 78% rate observed in the previous trial, and *significantly greater than the 20% prevalence rate observed in healthy controls.* Seven days after completion of neomycin or placebo, patients returned for symptom assessment and lactulose breath testing. IBS patients who were successfully treated for their SIBO based upon normalization of breath test results reported significantly greater improvement in IBS symptoms than patients with a persistently abnormal breath test result. *There are no data evaluating the long-term effects and durability of antibiotic therapy in patients with IBS and SIBO. Further studies to address this highly controversial area are eagerly awaited.* Summary of the use of breath tests for the diagnosis of IBS: Current best evidence does not support the routine use of breath tests for lactose intolerance or SIBO to exclude organic gastrointestinal disease in patients who present with typical IBS symptoms without alarm features. http://www.medscape.com/viewarticle/481182_3 IRRITABLE BOWEL SYNDROMELin Chang, M.D.CNS: Center of Neurovisceral Sciences & Womenï¿½s Health, CURE: Digestive Diseases Research Center,Division of Digestive Diseases, David Geffen School of Medicine at UCLACorresponding Author:Lin Chang, M.D.Center for Neurovisceral Sciences & Womenï¿½s HealthCURE: Digestive Diseases Research CenterVA Greater Los Angeles Healthcare System11301 Wilshire Blvd., Building. 115, Room. 223" *In some centers, the presence of bacterial overgrowth is often determined because this condition may cause symptoms similar to those of IBS.* It is most commonly diagnosed by a lactulose hydrogen breath test. Two studiesfrom the same research group found that 78% to 84% of patients with IBS had bacterial overgrowth. In patients with evidence of bacterial overgrowth, those treated withan antibiotic such as neomycin had a greater reduction in their GI symptoms compared with placebo. *Although these data are intriguing, there are some methodologic limitations in these studies and, therefore, the use of widespread hydrogen breath testing for bacterial overgrowth is still not generally advocated. "* http://216.109.117.135/search/cache?p=lin+...&icp=1&.intl=us "So how far should the gastroenterologist go in the workup of patients referred to them who typically present with IBS, and have negative screening studies? One gastroenterologist, recently commented to me: "I order breath hydrogen studies and sprue serologies on all my patients referred with IBS". No doubt this comment reflects the concern that as referral gastroenterologists we have an obligation to contribute additional expertise to the diagnostic effort. Recently, the breath H2 test is being requested more actively by physicians and the public alike possibly because of media attention to a study claiming a 73% rate of bacterial overgrowth in patients with IBS referred for breath H2 testing, and a 50% improvement with antibiotic treatment (16). However, the design limitations of this study, including a high ascertainment bias, use of an uncontrolled and unblinded treatment protocol, and only a 30% follow up rate evaluated over a relatively short period of time, makes it unlikely that clinicians in practice will also obtain such dramatic results. So while this study increases awareness of bacterial overgrowth as an entity that can mimic or exacerbate IBS, clinical experience suggests that the diagnostic yield in general GI practice is probably much lower than reported, perhaps 10% or less. " http://www.romecriteria.org/reading1.html The above was written before the second stuy, that I will grant you. However, the second study had limitations also and all of this has not been worked out yet. That is a fact. They also know PI IBS can lead to IBS. They also have animal models that can give mice basically IBS, which has nothing to do with sibo. They also know there are possible molecular defects in cells in the gut that control digestion and talk to the brain. They also know parts of the brain are impaired, including the prefrontal cortex and the Anteior Cingulate cortex which are NOT SEEN IN CONTROLS. They also know the majoirty of IBSers presenting to gastronterologists, have dysregulation of the serotonin system. And a whole lot more. They also know in some IBSers there are increases in EC cells and mast cells in the digestive tract. http://www.romecriteria.org/reading1.html also if you notice above, healthy controls can have SIBO???


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## eric (Jul 8, 1999)

"SIBO symptoms can mimick all IBS symptoms. That's what Pimentel's studies found out."Totally and more totally false. They explain some symptoms that can mimick IBS, your greatly confused on this. For example, please show me where they say SIBO can cause the sensation of incomplete evacuation? Please show me where SIBO can cause symptoms immediately after eating? Please show me how SIBO effects REM sleep, Please Show me how SIBO causes impairments in the prefrontal cortex and Anterior Cinculate Cortex? Please show me where SIBO can cause rectal Hypersensivity? Please show me how SIBO can cause consitpation or alternating motility symptoms. Please show me how SIBO cause molecular cell changes in the digestive tract. Please show me how SIBO cause a dysregulation of the serotonin system? Please show me how SIBO can cause altered stress ciruits. Or an increase in stress hormones. Please show me how SIBO effects the LImbic system?"Visceral pain in IBS is associated with increased prefrontal cortex activation. The normal correlation between subjective pain intensity and activation of the anterior cingulate and insula cortices is lost in IBS. The limbic system is involved in emotion, mood, and visceral autonomic control. Limbic abnormalities are seen in depression and IBS. Thus, this system is a possible site of convergence where emotional disturbance provokes intestinal dysfunction. " http://www.fdhn.org/html/education/gi/ibs_nosology.htm Please show me why more women then men get SIBO.You know not knowing who Dr Mayer is or Dr Gershon, or a lot of the other Major players are shows for sure you have not been doing your homework on IBS or have taken the time to fully research and understand IBS yourself and even the diagnoses. This is one reason why I find it personally hard for me to discuss this with you, because you are at a major disanvantage, if you don't have all the information and the bigger picture.You have never been to one of their chats, but you seem to know that is not the forum for asking a question. That is exactly what its for. And you want the anwer to your question, I feel you should ask them yourself. Why is that up to me to do your work on this? Why not email them yourself also and ask them. I posted the above in full for the sheer information on who Dr D is and what he is about. he is not in the pocket of the parm compinies, I gurantee you that, he is one of the most caring drs in all this there is, but he is a world authority and head of the Rome commitee, of course they ask him to consult and of course they ask the center to do double blind stduies to figure out if drugs work and that they are safe.You can also email them and get for free the Annual Report 2003 which is publich knowledge and shows where all the monies go, both pharm monies and NIH grants and public support, which I don't think they get enough of from all of us.I posted the second because of DR Drossman sheer concern for good doctor patient relationships and the how it shows the kind of person he really is and how important he thinks working fully with a patient is all about and how the health care is wrongly moving away from it.The majority of researchers already know this and a lot of them have poosted the same thing."Irritable Bowel Syndrome - An Evidence-Based Approach to DiagnosisPosted 06/21/2004 B.D. Cash; W.D. Chey " *The potential role of small intestinal bacterial overgrowth (SIBO) as an aetiology for IBS symptoms has been highlighted by two recent publications* .36,37 Pimentel et al.36 performed lactulose hydrogen breath testing in 202 patients fulfilling the Rome I criteria referred for evaluation of possible SIBO. Seventy-eight percent (157/202) had breath test results that were consistent with SIBO and were treated with a 10-day course of antibiotics. Forty-seven of these patients (29.9%) were restudied 7-10 days after completion of the antibiotics and SIBO eradication was achieved in 25 (53.2%). Twelve patients (48%) with SIBO eradication did not meet the Rome I criteria when their symptoms were reassessed (interpreted as improvement), while only four patients (18.2%) with persistent SIBO failed to meet the Rome I criteria after treatment. While intriguing, *a number of methodological limitations of the study by Pimental et al., including potential selection bias, the absence of a gold standard for the diagnosis of SIBO, the use of an unusual antibiotic to treat SIBO, short study duration and incomplete follow-up data for the majority of enrolled patients, limits the conclusions that can be drawn regarding the role of SIBO in patients with suspected IBS.* The same group of investigators subsequently reported the results of a double-blind randomized placebo-controlled trial evaluating the effects of therapy for SIBO upon IBS symptoms.37 The prevalence of SIBO in patients with IBS in this study was 84%, similar to the 78% rate observed in the previous trial, and *significantly greater than the 20% prevalence rate observed in healthy controls.* Seven days after completion of neomycin or placebo, patients returned for symptom assessment and lactulose breath testing. IBS patients who were successfully treated for their SIBO based upon normalization of breath test results reported significantly greater improvement in IBS symptoms than patients with a persistently abnormal breath test result. *There are no data evaluating the long-term effects and durability of antibiotic therapy in patients with IBS and SIBO. Further studies to address this highly controversial area are eagerly awaited.* Summary of the use of breath tests for the diagnosis of IBS: Current best evidence does not support the routine use of breath tests for lactose intolerance or SIBO to exclude organic gastrointestinal disease in patients who present with typical IBS symptoms without alarm features. http://www.medscape.com/viewarticle/481182_3 IRRITABLE BOWEL SYNDROMELin Chang, M.D.CNS: Center of Neurovisceral Sciences & Womenï¿½s Health, CURE: Digestive Diseases Research Center,Division of Digestive Diseases, David Geffen School of Medicine at UCLACorresponding Author:Lin Chang, M.D.Center for Neurovisceral Sciences & Womenï¿½s HealthCURE: Digestive Diseases Research CenterVA Greater Los Angeles Healthcare System11301 Wilshire Blvd., Building. 115, Room. 223" *In some centers, the presence of bacterial overgrowth is often determined because this condition may cause symptoms similar to those of IBS.* It is most commonly diagnosed by a lactulose hydrogen breath test. Two studiesfrom the same research group found that 78% to 84% of patients with IBS had bacterial overgrowth. In patients with evidence of bacterial overgrowth, those treated withan antibiotic such as neomycin had a greater reduction in their GI symptoms compared with placebo. *Although these data are intriguing, there are some methodologic limitations in these studies and, therefore, the use of widespread hydrogen breath testing for bacterial overgrowth is still not generally advocated. "* http://216.109.117.135/search/cache?p=lin+...&icp=1&.intl=us "So how far should the gastroenterologist go in the workup of patients referred to them who typically present with IBS, and have negative screening studies? One gastroenterologist, recently commented to me: "I order breath hydrogen studies and sprue serologies on all my patients referred with IBS". No doubt this comment reflects the concern that as referral gastroenterologists we have an obligation to contribute additional expertise to the diagnostic effort. Recently, the breath H2 test is being requested more actively by physicians and the public alike possibly because of media attention to a study claiming a 73% rate of bacterial overgrowth in patients with IBS referred for breath H2 testing, and a 50% improvement with antibiotic treatment (16). However, the design limitations of this study, including a high ascertainment bias, use of an uncontrolled and unblinded treatment protocol, and only a 30% follow up rate evaluated over a relatively short period of time, makes it unlikely that clinicians in practice will also obtain such dramatic results. So while this study increases awareness of bacterial overgrowth as an entity that can mimic or exacerbate IBS, clinical experience suggests that the diagnostic yield in general GI practice is probably much lower than reported, perhaps 10% or less. " http://www.romecriteria.org/reading1.html The above was written before the second stuy, that I will grant you. However, the second study had limitations also and all of this has not been worked out yet. That is a fact. They also know PI IBS can lead to IBS. They also have animal models that can give mice basically IBS, which has nothing to do with sibo. They also know there are possible molecular defects in cells in the gut that control digestion and talk to the brain. They also know parts of the brain are impaired, including the prefrontal cortex and the Anteior Cingulate cortex which are NOT SEEN IN CONTROLS. They also know the majoirty of IBSers presenting to gastronterologists, have dysregulation of the serotonin system. And a whole lot more. They also know in some IBSers there are increases in EC cells and mast cells in the digestive tract. http://www.romecriteria.org/reading1.html also if you notice above, healthy controls can have SIBO???


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## skinny (Jul 27, 2002)

I'm going to respond to this first...


> quote:"SIBO symptoms can mimick all IBS symptoms. That's what Pimentel's studies found out."Totally and more totally false. They explain some symptoms that can mimick IBS, your greatly confused on this.


You're telling me a half truth here. SIBO can explain *some* symptoms, but they also can explain *all* symptoms. And BTW something that "mimicks" IBS is really loaded language. IBS is defined by the symptoms.SIBO symptoms that Pimentel checked for:BloatingDiarrhea Abdominal pain Defecation relief Mucous Incomplete evacuation	Straining UrgencyAlthough the symptoms were tabulated for the whole group, almost all of the subjects had defecation relief after a bowel movement and abnormal stool form/frequency and some kind of pain/discomfort. These are IBS symptoms according to Rome II:


> quote:Rome II Diagnostic Criteria(a system for diagnosing functional gastrointestinal disorders based on symptoms) for IBS is as follows:At least 12 weeks or more, which need not be consecutive, in the preceding 12 months of abdominal discomfort or pain that is accompanied by at least two of the following features:1) It is relieved with defecation, and/or2) Onset is associated with a change in frequency of stool, and/or3) Onset is associated with a change in form (appearance) of stool.Other symptoms that are not essential but support the diagnosis of IBS: * Abnormal stool frequency (greater than 3 bowel movements/day or less than 3 bowel movements/week); * Abnormal stool form (lumpy/hard or loose/watery stool); * Abnormal stool passage (straining, urgency, or feeling of incomplete evacuation); * Passage of mucus; * Bloating or feeling of abdominal distension.


So Eric, show me what I said is _totally false_. Hmm?skinny


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## skinny (Jul 27, 2002)

I'm going to respond to this first...


> quote:"SIBO symptoms can mimick all IBS symptoms. That's what Pimentel's studies found out."Totally and more totally false. They explain some symptoms that can mimick IBS, your greatly confused on this.


You're telling me a half truth here. SIBO can explain *some* symptoms, but they also can explain *all* symptoms. And BTW something that "mimicks" IBS is really loaded language. IBS is defined by the symptoms.SIBO symptoms that Pimentel checked for:BloatingDiarrhea Abdominal pain Defecation relief Mucous Incomplete evacuation	Straining UrgencyAlthough the symptoms were tabulated for the whole group, almost all of the subjects had defecation relief after a bowel movement and abnormal stool form/frequency and some kind of pain/discomfort. These are IBS symptoms according to Rome II:


> quote:Rome II Diagnostic Criteria(a system for diagnosing functional gastrointestinal disorders based on symptoms) for IBS is as follows:At least 12 weeks or more, which need not be consecutive, in the preceding 12 months of abdominal discomfort or pain that is accompanied by at least two of the following features:1) It is relieved with defecation, and/or2) Onset is associated with a change in frequency of stool, and/or3) Onset is associated with a change in form (appearance) of stool.Other symptoms that are not essential but support the diagnosis of IBS: * Abnormal stool frequency (greater than 3 bowel movements/day or less than 3 bowel movements/week); * Abnormal stool form (lumpy/hard or loose/watery stool); * Abnormal stool passage (straining, urgency, or feeling of incomplete evacuation); * Passage of mucus; * Bloating or feeling of abdominal distension.


So Eric, show me what I said is _totally false_. Hmm?skinny


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## administrator (Aug 20, 2004)

This thread has violated posting guidelines as indicated below. Since some valid information is presented here, for the present time this thread will be monitored closely rather than closed. Please provide links rather than providing excessively long posts, and refrain from personal vindications. Keep your discussion informational, not personal.Thank you for your cooperation.The Moderator Team2) Endless debates. You can make your point on a thread in just a few posts. People will agree with you or they will not. Going on and on changes no oneï¿½s mind about the subject, and creates an atmosphere that is not appropriate for a self-help board. Threads that become a debate will be locked or deleted as appropriate. Moving the debate to a new thread will cause that thread to be locked or deleted as the individual case warrants and at the discretion of that forumï¿½s moderator.3) Long copy and paste posts. Please keep posts where you are not the author as short as possible (copy a few of the most relevant paragraphs and provide the link to the rest of the article: rule of thumb - if you have to hit scroll more than 2 X to get to the end of the post, it is too long). You may post the full article on the "Information Forums: IBS News Research and Abstract" section if it is not readily available on-line and link to that post. Excessively long posts may be truncated by the moderators without warning.


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## administrator (Aug 20, 2004)

This thread has violated posting guidelines as indicated below. Since some valid information is presented here, for the present time this thread will be monitored closely rather than closed. Please provide links rather than providing excessively long posts, and refrain from personal vindications. Keep your discussion informational, not personal.Thank you for your cooperation.The Moderator Team2) Endless debates. You can make your point on a thread in just a few posts. People will agree with you or they will not. Going on and on changes no oneï¿½s mind about the subject, and creates an atmosphere that is not appropriate for a self-help board. Threads that become a debate will be locked or deleted as appropriate. Moving the debate to a new thread will cause that thread to be locked or deleted as the individual case warrants and at the discretion of that forumï¿½s moderator.3) Long copy and paste posts. Please keep posts where you are not the author as short as possible (copy a few of the most relevant paragraphs and provide the link to the rest of the article: rule of thumb - if you have to hit scroll more than 2 X to get to the end of the post, it is too long). You may post the full article on the "Information Forums: IBS News Research and Abstract" section if it is not readily available on-line and link to that post. Excessively long posts may be truncated by the moderators without warning.


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## Jhouston (Nov 9, 2003)

Eric, question: Is Dr Drossman a psychiatrist or pychologist?


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## Jhouston (Nov 9, 2003)

Eric, question: Is Dr Drossman a psychiatrist or pychologist?


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## Guest (Nov 7, 2004)

i have a question and maybe its ignorant/misinformed, but --- Eric you said ..."I also just find it odd, I have never seen Dr Pimental talk about all the problems in IBS, I have never seen anything written by him on PI IBS or serotonin, or brain impairments and all the other research done over the years. Or how he fully explains serotonin dysregulation, how SIBO causes nerve hypersensitivity, alterations in motility the d/c c and c/d or the role of genetics the sensation of incomplete evacuation, rectal hypersensitvity and a host of other issues."could it be that Pimental is trying to show just one causal relationship i.e. between SIBO and IBS and sees IBS as a reaction to disease and not its own disease system? i think its well known that after infection the whole digestive tract can become sensitized. if that is indeed the case, if someone has SIBO then it would indeed sensitize the digest tract on a regular basis. I don't see why he should have to study the sensitization process when it seems like the more important thing would be to study the sensitizing culprit instead. how can one recover from IBS/this sensitization if SIBO is still in place and doctors are unable to detect it and don't see its relationship to IBS? also, while we know there is some back and forth play between the sensitized colon and the brain - i.e. vicious cycle established, why is it that when that cycle is stopped through drugs etc. that ibs returns in most folks? maybe in many who have been diagnosed wiht ibs - there is an ongoing bowel stressor like Celiac, bacterial overgrowth, etc. I just don't see how him not studying the brain/gut connection invalidates his research at all. There seems to be this issue with finding an organic cause outside the brain to explain some folks IBS SYMPTOMS (symptoms capitalized on purpose as its still just a collection of symptoms that could be attached to any cause - for instance Celiac and SIBO which it often is apparently).


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## Guest (Nov 7, 2004)

i have a question and maybe its ignorant/misinformed, but --- Eric you said ..."I also just find it odd, I have never seen Dr Pimental talk about all the problems in IBS, I have never seen anything written by him on PI IBS or serotonin, or brain impairments and all the other research done over the years. Or how he fully explains serotonin dysregulation, how SIBO causes nerve hypersensitivity, alterations in motility the d/c c and c/d or the role of genetics the sensation of incomplete evacuation, rectal hypersensitvity and a host of other issues."could it be that Pimental is trying to show just one causal relationship i.e. between SIBO and IBS and sees IBS as a reaction to disease and not its own disease system? i think its well known that after infection the whole digestive tract can become sensitized. if that is indeed the case, if someone has SIBO then it would indeed sensitize the digest tract on a regular basis. I don't see why he should have to study the sensitization process when it seems like the more important thing would be to study the sensitizing culprit instead. how can one recover from IBS/this sensitization if SIBO is still in place and doctors are unable to detect it and don't see its relationship to IBS? also, while we know there is some back and forth play between the sensitized colon and the brain - i.e. vicious cycle established, why is it that when that cycle is stopped through drugs etc. that ibs returns in most folks? maybe in many who have been diagnosed wiht ibs - there is an ongoing bowel stressor like Celiac, bacterial overgrowth, etc. I just don't see how him not studying the brain/gut connection invalidates his research at all. There seems to be this issue with finding an organic cause outside the brain to explain some folks IBS SYMPTOMS (symptoms capitalized on purpose as its still just a collection of symptoms that could be attached to any cause - for instance Celiac and SIBO which it often is apparently).


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## eric (Jul 8, 1999)

Jhouston "Dr. Drossman is Professor of Medicine and Psychiatry at the UNC School of Medicine, Division of Gastroenterology & Hepatology."But that is not all he is, if you read his CURRICULUM VITAE above or this He is also "Chair of the Executive Committee (since 1989) and President (since 2003) of the Rome Foundation Editor of Rome II: The Functional Gastrointestinal Disorders, 2nd edition; senior editor for Rome III to be published in 2006" http://www.med.unc.edu/wrkunits/2depts/med...dc/drossman.htm This is in regard to "Talissa If Dr Drossman is at that chat, maybe you can ask him what his "consultant" fees are for the ELEVEN pharmaceutical co's which currently use him as a "consultant"?""TREATMENTS OF IBSDouglas A. Drossman, MDCo-DirectorUNC Center for Functional GI & Motility DisordersINTRODUCTIONIn recent years, there has been increased interest by physicians and the pharmaceuticalindustry regarding newer treatments for IBS. Before discussing these new treatments, it isimportant to consider the overall management strategy in IBS. This is necessary becausepatients with IBS exhibit a wide spectrum of symptoms of varying frequencies and degreesof severity. There is no one ideal treatment for IBS, and the newer medications may workbest for only a subset of patients having this disorder. Therefore, the clinician must firstapply certain general management approaches and, following this, treatment choices willdepend on the nature (i.e., predominant diarrhea, constipation, or bloating, etc.) andseverity (mild, moderate, severe) of the symptoms." http://www.ibsgroup.org/cgi-local/ubbcgi/u...c&f=10&t=001023 Before going any further or adressing Skinny's coments on SIBO causing all IBS symptoms, Skinny have you had SIBO Testing?and for joanofarc http://www.ibsgroup.org/cgi-local/ubbcgi/u...c&f=10&t=001023


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## eric (Jul 8, 1999)

Jhouston "Dr. Drossman is Professor of Medicine and Psychiatry at the UNC School of Medicine, Division of Gastroenterology & Hepatology."But that is not all he is, if you read his CURRICULUM VITAE above or this He is also "Chair of the Executive Committee (since 1989) and President (since 2003) of the Rome Foundation Editor of Rome II: The Functional Gastrointestinal Disorders, 2nd edition; senior editor for Rome III to be published in 2006" http://www.med.unc.edu/wrkunits/2depts/med...dc/drossman.htm This is in regard to "Talissa If Dr Drossman is at that chat, maybe you can ask him what his "consultant" fees are for the ELEVEN pharmaceutical co's which currently use him as a "consultant"?""TREATMENTS OF IBSDouglas A. Drossman, MDCo-DirectorUNC Center for Functional GI & Motility DisordersINTRODUCTIONIn recent years, there has been increased interest by physicians and the pharmaceuticalindustry regarding newer treatments for IBS. Before discussing these new treatments, it isimportant to consider the overall management strategy in IBS. This is necessary becausepatients with IBS exhibit a wide spectrum of symptoms of varying frequencies and degreesof severity. There is no one ideal treatment for IBS, and the newer medications may workbest for only a subset of patients having this disorder. Therefore, the clinician must firstapply certain general management approaches and, following this, treatment choices willdepend on the nature (i.e., predominant diarrhea, constipation, or bloating, etc.) andseverity (mild, moderate, severe) of the symptoms." http://www.ibsgroup.org/cgi-local/ubbcgi/u...c&f=10&t=001023 Before going any further or adressing Skinny's coments on SIBO causing all IBS symptoms, Skinny have you had SIBO Testing?and for joanofarc http://www.ibsgroup.org/cgi-local/ubbcgi/u...c&f=10&t=001023


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## eric (Jul 8, 1999)

FYIDrossman Receives 2004 AGA Distinguished Educator Award On May 17, 2004, Douglas A. Drossman, MD, received the 2004 AGA Distinguished Educator Award. Established in 1988, this award recognizes an individual for achievements as an outstanding educator over a lifelong career. Through this award, the American Gastroenterological Association (AGA)recognizes AGA members who have made outstandingcontributions as educators in gastroenterology on both the local and national levels, including longtime efforts dedicated to training fellows, publishing educational documents, and teaching seminars and classes. The awards presentation took place during the Clinical Plenary Session of Digestive Diseases Week (DDW) at the Morial Convention Center in New Orleans,with additional recognition at the AGA Presidentï¿½s Awards"


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## eric (Jul 8, 1999)

FYIDrossman Receives 2004 AGA Distinguished Educator Award On May 17, 2004, Douglas A. Drossman, MD, received the 2004 AGA Distinguished Educator Award. Established in 1988, this award recognizes an individual for achievements as an outstanding educator over a lifelong career. Through this award, the American Gastroenterological Association (AGA)recognizes AGA members who have made outstandingcontributions as educators in gastroenterology on both the local and national levels, including longtime efforts dedicated to training fellows, publishing educational documents, and teaching seminars and classes. The awards presentation took place during the Clinical Plenary Session of Digestive Diseases Week (DDW) at the Morial Convention Center in New Orleans,with additional recognition at the AGA Presidentï¿½s Awards"


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## eric (Jul 8, 1999)

"Doug Drossman Among Americaï¿½s TopDoctorsFor the fourth year in a row, doctors at UNCHospitals have been recognized in the latestedition of ï¿½Americaï¿½s Top Doctors,ï¿½ publishedby Castle Connolly Medical Ltd. The selectionprocess begins with a mailed survey to 250,000physicians who are asked to nominate the toppeople in their specialties. Dr. DouglasDrossman, Center Co-Director, was chosen as aleading physician in Gastroenterology. He isjoined in this medical specialty recognition byhis colleague Dr. Balfour Sartour, Division ofGastroenterology and Hepatology. Dr. JohnSteege, who participated as faculty in this yearï¿½sPatient Symposium on ï¿½Understanding IBS andOther Functional GI Disorders,ï¿½ was selected inthe Obstetrics & Gynecology specialty. In all,forty-nine UNC Hospitals physicians were listedthis year."


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## eric (Jul 8, 1999)

"Doug Drossman Among Americaï¿½s TopDoctorsFor the fourth year in a row, doctors at UNCHospitals have been recognized in the latestedition of ï¿½Americaï¿½s Top Doctors,ï¿½ publishedby Castle Connolly Medical Ltd. The selectionprocess begins with a mailed survey to 250,000physicians who are asked to nominate the toppeople in their specialties. Dr. DouglasDrossman, Center Co-Director, was chosen as aleading physician in Gastroenterology. He isjoined in this medical specialty recognition byhis colleague Dr. Balfour Sartour, Division ofGastroenterology and Hepatology. Dr. JohnSteege, who participated as faculty in this yearï¿½sPatient Symposium on ï¿½Understanding IBS andOther Functional GI Disorders,ï¿½ was selected inthe Obstetrics & Gynecology specialty. In all,forty-nine UNC Hospitals physicians were listedthis year."


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## skinny (Jul 27, 2002)

TheModeratorTeam: Thanks for intervening and reminding us of the posting etiquette.Eric:To recap, here is the contention I have with you:1) You misrepresented SIBO and its association to IBS. Lin is someone who has clinical experience with it and his paper put out a theory that's is well supported by recent studies. Whether or not SIBO is a cause of IBS, I'd say it still up for debate. Yes there needs to be more studies. There are limitations with the breath test and it's accuracy in diagnosing bacterial growth. The long term effects and durability of the treatment needs to be studied. In every study you can find limitations and problems.2) You didn't provide any evidence that Pimentel's studies were replicated.3) You ignore other research that is challenging the views of what IBS is. It's no longer safe to assume that IBS presumes the absence or biochemical or structural explanation. You seem to be looking for a unifying theory that explains it all and there may not be one.For example the article that you quoted challenges this view of IBS:


> quote:Much remains unknown about the potential causes of IBS. *There may not be a unifying hypothesis to link all the aspects of this diverse syndrome. Nevertheless, markers of low-grade inflammation, which were initially found in diarrhea-predominant and postinfectious cases of IBS, are increasingly being found in constipation-predominant patients as well. Thus, inflammation may figure as an underlying factor in visceral hypersensitivity in more cases of IBS than previously was suspected.* http://www.pulsus.com/Gastro/18_10/andr_ed.htm


4) You aren't forthcoming with the questions that I ask. I don't have a general contempt for Drossman although I am wary of his position of SIBO. I'm sure he's done a lot in the field of GI disorders, but experts can be wrong sometimes. It shouldn't be taken as a personal attack if I critique his position. Now my comments about "covering his tracks" was speculation. I could be wrong here too. Maybe one of his peers just botched it up.5) You say that SIBO symptoms don't reflect all IBS symptoms, but studies have shown that they do. I know that some people have SIBO and not IBS.


> quote:For example, please show me where they say SIBO can cause the sensation of incomplete evacuation? Please show me where SIBO can cause symptoms immediately after eating? Please show me how SIBO effects REM sleep, Please Show me how SIBO causes impairments in the prefrontal cortex and Anterior Cinculate Cortex? Please show me where SIBO can cause rectal Hypersensivity? Please show me how SIBO can cause consitpation or alternating motility symptoms. Please show me how SIBO cause molecular cell changes in the digestive tract. Please show me how SIBO cause a dysregulation of the serotonin system? Please show me how SIBO can cause altered stress ciruits. Or an increase in stress hormones. Please show me how SIBO effects the LImbic system?


I don't have all the answers of the universe. If we can get other GI researchers in on this, it would be great. I know progress in science is slow and painstaking. The Drossman article "What medicine has become" shows how difficult it is for doctors to do their work.


> quote:You know not knowing who Dr Mayer is or Dr Gershon, or a lot of the other Major players are shows for sure you have not been doing your homework on IBS or have taken the time to fully research and understand IBS yourself and even the diagnoses. This is one reason why I find it personally hard for me to discuss this with you, because you are at a major disanvantage, if you don't have all the information and the bigger picture.


First of all, I don't take the time to fully research IBS. I read enough to get a basic understanding somewhere between an expert level and layman's level.like this article: http://www.hopkins-gi.org/pages/latin/temp...an=6&disease=43 I don't see what is so hard to understand about the diagnoses of IBS?? Now what gets me is that you present misinformation on a focus such as SIBO, yet you say you understand the bigger picture. What I'm talking about are simpler ideas and you don't answer me in a straightforward manner. That makes me wary. I don't get the big picture and most experts don't get big picture either simply because there is a lot that remains to be known.skinny


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## skinny (Jul 27, 2002)

TheModeratorTeam: Thanks for intervening and reminding us of the posting etiquette.Eric:To recap, here is the contention I have with you:1) You misrepresented SIBO and its association to IBS. Lin is someone who has clinical experience with it and his paper put out a theory that's is well supported by recent studies. Whether or not SIBO is a cause of IBS, I'd say it still up for debate. Yes there needs to be more studies. There are limitations with the breath test and it's accuracy in diagnosing bacterial growth. The long term effects and durability of the treatment needs to be studied. In every study you can find limitations and problems.2) You didn't provide any evidence that Pimentel's studies were replicated.3) You ignore other research that is challenging the views of what IBS is. It's no longer safe to assume that IBS presumes the absence or biochemical or structural explanation. You seem to be looking for a unifying theory that explains it all and there may not be one.For example the article that you quoted challenges this view of IBS:


> quote:Much remains unknown about the potential causes of IBS. *There may not be a unifying hypothesis to link all the aspects of this diverse syndrome. Nevertheless, markers of low-grade inflammation, which were initially found in diarrhea-predominant and postinfectious cases of IBS, are increasingly being found in constipation-predominant patients as well. Thus, inflammation may figure as an underlying factor in visceral hypersensitivity in more cases of IBS than previously was suspected.* http://www.pulsus.com/Gastro/18_10/andr_ed.htm


4) You aren't forthcoming with the questions that I ask. I don't have a general contempt for Drossman although I am wary of his position of SIBO. I'm sure he's done a lot in the field of GI disorders, but experts can be wrong sometimes. It shouldn't be taken as a personal attack if I critique his position. Now my comments about "covering his tracks" was speculation. I could be wrong here too. Maybe one of his peers just botched it up.5) You say that SIBO symptoms don't reflect all IBS symptoms, but studies have shown that they do. I know that some people have SIBO and not IBS.


> quote:For example, please show me where they say SIBO can cause the sensation of incomplete evacuation? Please show me where SIBO can cause symptoms immediately after eating? Please show me how SIBO effects REM sleep, Please Show me how SIBO causes impairments in the prefrontal cortex and Anterior Cinculate Cortex? Please show me where SIBO can cause rectal Hypersensivity? Please show me how SIBO can cause consitpation or alternating motility symptoms. Please show me how SIBO cause molecular cell changes in the digestive tract. Please show me how SIBO cause a dysregulation of the serotonin system? Please show me how SIBO can cause altered stress ciruits. Or an increase in stress hormones. Please show me how SIBO effects the LImbic system?


I don't have all the answers of the universe. If we can get other GI researchers in on this, it would be great. I know progress in science is slow and painstaking. The Drossman article "What medicine has become" shows how difficult it is for doctors to do their work.


> quote:You know not knowing who Dr Mayer is or Dr Gershon, or a lot of the other Major players are shows for sure you have not been doing your homework on IBS or have taken the time to fully research and understand IBS yourself and even the diagnoses. This is one reason why I find it personally hard for me to discuss this with you, because you are at a major disanvantage, if you don't have all the information and the bigger picture.


First of all, I don't take the time to fully research IBS. I read enough to get a basic understanding somewhere between an expert level and layman's level.like this article: http://www.hopkins-gi.org/pages/latin/temp...an=6&disease=43 I don't see what is so hard to understand about the diagnoses of IBS?? Now what gets me is that you present misinformation on a focus such as SIBO, yet you say you understand the bigger picture. What I'm talking about are simpler ideas and you don't answer me in a straightforward manner. That makes me wary. I don't get the big picture and most experts don't get big picture either simply because there is a lot that remains to be known.skinny


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## flux (Dec 13, 1998)

[qquote]Now my comments about "covering his tracks" was speculation. I could be wrong here too.[/quote]Could be wrong?


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## flux (Dec 13, 1998)

[qquote]Now my comments about "covering his tracks" was speculation. I could be wrong here too.[/quote]Could be wrong?


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## Talissa (Apr 10, 2004)

I'm sure Drossman has the best intentions, yet this is why I'm leery of someone tied to so many Rx companies...ï¿½The United States needs to watch over the ties between the scientists who study drugs and the drug companies that pay for the research, because industry funding makes it 3.6 times more likely that a study result will be favorable to the sponsor, say researchers led by Yale's Cary Gross.Reporting in today's Journal of the American Medical Association, Gross' group finds that about one-fourth of biomedical researchers have financial ties to companies whose products they are studying, while about two-thirds of schools have financial ties to start-ups investigating new drugs. The group pooled the results of 37 past studies of conflicts of interest, building on a decade's worth of similar reportsï¿½ï¿½ http://www.usatoday.com/news/education/200...rch-funds_x.htm ï¿½ï¿½And weï¿½re talking serious money here. In addition to the salaries built into company-sponsored research grants, academic clinicians at medical schools can pad their already decent incomes with $1,000-a-day consulting contracts with pharmaceutical companies, patent royalties, licensing fees, and big-payoff stock optionsï¿½.At many of the top research universities and medical schools around the country, a substantial percentage of the faculty enjoys the perks of industry relationships. ï¿½By penetrating the wall that once existed around academic researchers, drug companies have gained access to the ï¿½thought leadersï¿½ in medicine, the big names whose good opinion of an idea or a product carries enormous weight with other physicians.ï¿½ï¿½ http://www.drugawareness.org/Archives/2ndQ...record0048.html ï¿½ï¿½The scientific community has responded by saying that industry cash fuels discovery and, moreover, that no amount of money can corrupt a researcher who is trained to seek the truth. But a review by Courant, a small newspaper in the US, of more than 40 recently developed drugs, as well as interviews with dozens of researchers across the nation, has found that scientists are getting answers in their research that neatly fit the agenda of their corporate sponsorsï¿½ï¿½ http://www.delhiscienceforum.org/pharm6.html T-


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## Talissa (Apr 10, 2004)

I'm sure Drossman has the best intentions, yet this is why I'm leery of someone tied to so many Rx companies...ï¿½The United States needs to watch over the ties between the scientists who study drugs and the drug companies that pay for the research, because industry funding makes it 3.6 times more likely that a study result will be favorable to the sponsor, say researchers led by Yale's Cary Gross.Reporting in today's Journal of the American Medical Association, Gross' group finds that about one-fourth of biomedical researchers have financial ties to companies whose products they are studying, while about two-thirds of schools have financial ties to start-ups investigating new drugs. The group pooled the results of 37 past studies of conflicts of interest, building on a decade's worth of similar reportsï¿½ï¿½ http://www.usatoday.com/news/education/200...rch-funds_x.htm ï¿½ï¿½And weï¿½re talking serious money here. In addition to the salaries built into company-sponsored research grants, academic clinicians at medical schools can pad their already decent incomes with $1,000-a-day consulting contracts with pharmaceutical companies, patent royalties, licensing fees, and big-payoff stock optionsï¿½.At many of the top research universities and medical schools around the country, a substantial percentage of the faculty enjoys the perks of industry relationships. ï¿½By penetrating the wall that once existed around academic researchers, drug companies have gained access to the ï¿½thought leadersï¿½ in medicine, the big names whose good opinion of an idea or a product carries enormous weight with other physicians.ï¿½ï¿½ http://www.drugawareness.org/Archives/2ndQ...record0048.html ï¿½ï¿½The scientific community has responded by saying that industry cash fuels discovery and, moreover, that no amount of money can corrupt a researcher who is trained to seek the truth. But a review by Courant, a small newspaper in the US, of more than 40 recently developed drugs, as well as interviews with dozens of researchers across the nation, has found that scientists are getting answers in their research that neatly fit the agenda of their corporate sponsorsï¿½ï¿½ http://www.delhiscienceforum.org/pharm6.html T-


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## flux (Dec 13, 1998)

> quote:yet this is why I'm leery of someone tied to so many Rx companies


Most experts are "tied" to drug companies. So does that mean there are no real experts? Who do we trust for real information? skinny and talissa?


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## flux (Dec 13, 1998)

> quote:yet this is why I'm leery of someone tied to so many Rx companies


Most experts are "tied" to drug companies. So does that mean there are no real experts? Who do we trust for real information? skinny and talissa?


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## eric (Jul 8, 1999)

"I'm sure Drossman has the best intentions"He does and I know this for sure as do many many others and why I posted this for you, but perhaps need to calirify it again. Lets not go on a witch hunts before we understand who people are and what they are about? I believe its one thing to argue research, but another altogether to accuse people of their character and intensions, unless something is totally blatant or found out.""TREATMENTS OF IBSDouglas A. Drossman, MDCo-DirectorUNC Center for Functional GI & Motility DisordersINTRODUCTIONIn recent years, there has been increased interest by physicians and the pharmaceuticalindustry regarding newer treatments for IBS. Before discussing these new treatments, it isimportant to consider the overall management strategy in IBS. This is necessary becausepatients with IBS exhibit a wide spectrum of symptoms of varying frequencies and degreesof severity. There is no one ideal treatment for IBS, and the newer medications may workbest for only a subset of patients having this disorder. Therefore, the clinician must firstapply certain general management approaches and, following this, treatment choices willdepend on the nature (i.e., predominant diarrhea, constipation, or bloating, etc.) andseverity (mild, moderate, severe) of the symptoms." http://www.ibsgroup.org/cgi-local/ubbcgi/u...c&f=10&t=001023


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## eric (Jul 8, 1999)

"I'm sure Drossman has the best intentions"He does and I know this for sure as do many many others and why I posted this for you, but perhaps need to calirify it again. Lets not go on a witch hunts before we understand who people are and what they are about? I believe its one thing to argue research, but another altogether to accuse people of their character and intensions, unless something is totally blatant or found out.""TREATMENTS OF IBSDouglas A. Drossman, MDCo-DirectorUNC Center for Functional GI & Motility DisordersINTRODUCTIONIn recent years, there has been increased interest by physicians and the pharmaceuticalindustry regarding newer treatments for IBS. Before discussing these new treatments, it isimportant to consider the overall management strategy in IBS. This is necessary becausepatients with IBS exhibit a wide spectrum of symptoms of varying frequencies and degreesof severity. There is no one ideal treatment for IBS, and the newer medications may workbest for only a subset of patients having this disorder. Therefore, the clinician must firstapply certain general management approaches and, following this, treatment choices willdepend on the nature (i.e., predominant diarrhea, constipation, or bloating, etc.) andseverity (mild, moderate, severe) of the symptoms." http://www.ibsgroup.org/cgi-local/ubbcgi/u...c&f=10&t=001023


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## eric (Jul 8, 1999)

From Dr Drossman"Dear Shawn Eric,I do feel that the issue of bacterial overgrowth is an important considerations in IBS, and these authors have gone a long way to advance this area of investigation and raise awareness of bacterial overgrowth as a possible player in IBS. It kind of relates to other work being done in the area of post-infectious IBS and altered mucosal immunity in subsets of IBS. However, there is some disagreement within the community with regard to the prevalence in patients with IBS, these authors claiming up to 80% and others finding far less by standard methods. Another issue of concern is that explaining bacterial overgrowth as the cause of so many other aspects of the condition is going beyond the available scientific data. Their work should be considered more in the way of opinion/speculation, rather than accepted dogma within the medical community, and further confirmation is needed. You should keep in mind that all scientists will from time to time try to extend their data into understanding other aspects of a condition, but the checks and balances within medicine lead to common acceptance when there is confirmation from other groups and more conclusive evidence. That has not happenned as of yet but remains an area of interest in the field.Doug"


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## eric (Jul 8, 1999)

From Dr Drossman"Dear Shawn Eric,I do feel that the issue of bacterial overgrowth is an important considerations in IBS, and these authors have gone a long way to advance this area of investigation and raise awareness of bacterial overgrowth as a possible player in IBS. It kind of relates to other work being done in the area of post-infectious IBS and altered mucosal immunity in subsets of IBS. However, there is some disagreement within the community with regard to the prevalence in patients with IBS, these authors claiming up to 80% and others finding far less by standard methods. Another issue of concern is that explaining bacterial overgrowth as the cause of so many other aspects of the condition is going beyond the available scientific data. Their work should be considered more in the way of opinion/speculation, rather than accepted dogma within the medical community, and further confirmation is needed. You should keep in mind that all scientists will from time to time try to extend their data into understanding other aspects of a condition, but the checks and balances within medicine lead to common acceptance when there is confirmation from other groups and more conclusive evidence. That has not happenned as of yet but remains an area of interest in the field.Doug"


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## eric (Jul 8, 1999)

One more thing, Hopefully Talissa and Skinny will read this."The pathophysiology of irritable bowel syndrome.Schwetz I, Bradesi S, Mayer EA.Center of Neurovisceral Sciences and Women's Health (CNS),, Division of Digestive Diseases and Brain Research Institute, Department of Medicine, Los Angeles, CA, USA.Recent studies have provided evidence to suggest a possible role for mucosal immune activation in the pathophysiology of irritable bowel syndrome (IBS). On the other hand, novel findings using functional brain-imaging techniques support the concept that altered perception of visceral stimuli plays a key role in IBS symptom generation. These seemingly contradictory findings have revived the discussion about the relative contribution of peripheral versus central mechanisms in the symptom generation of IBS. In this review, we will provide evidence for the hypothesis that, in the absence of changes in visceral perception and alterations in endogenous pain modulation systems, chronic inflammatory mucosal changes in the gut are not a plausible mechanism to explain the presence of chronic abdominal pain, a clinical hallmark of IBS."Full text"Not sure if this would work for everyone...it is a link to the journal and the abstract there is in italian, but the .pdf link on the bottom gives me the whole article in English.K." http://www.minervamedica.it/index2.t?show=R10Y2004N05A0419 Full text at the bottom of the page in PDF"Full-Text (PDF) "


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## eric (Jul 8, 1999)

One more thing, Hopefully Talissa and Skinny will read this."The pathophysiology of irritable bowel syndrome.Schwetz I, Bradesi S, Mayer EA.Center of Neurovisceral Sciences and Women's Health (CNS),, Division of Digestive Diseases and Brain Research Institute, Department of Medicine, Los Angeles, CA, USA.Recent studies have provided evidence to suggest a possible role for mucosal immune activation in the pathophysiology of irritable bowel syndrome (IBS). On the other hand, novel findings using functional brain-imaging techniques support the concept that altered perception of visceral stimuli plays a key role in IBS symptom generation. These seemingly contradictory findings have revived the discussion about the relative contribution of peripheral versus central mechanisms in the symptom generation of IBS. In this review, we will provide evidence for the hypothesis that, in the absence of changes in visceral perception and alterations in endogenous pain modulation systems, chronic inflammatory mucosal changes in the gut are not a plausible mechanism to explain the presence of chronic abdominal pain, a clinical hallmark of IBS."Full text"Not sure if this would work for everyone...it is a link to the journal and the abstract there is in italian, but the .pdf link on the bottom gives me the whole article in English.K." http://www.minervamedica.it/index2.t?show=R10Y2004N05A0419 Full text at the bottom of the page in PDF"Full-Text (PDF) "


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## skinny (Jul 27, 2002)

Talissa, thanks for the links. These are some good articles to show you what we are up against. The regulatory function of the FDA is so corrupt that it needs a major overhaul. Good thing that a few organizations like the LEF have cracked the gestapo like control on their powers. I believe that we wouldn't be able to buy health supplements off the shelf if it wasn't for the fight of these people, but there are still a lot of battles to be won.Victory over the FDABy Saul Kent, President of the Life Extension Foundation (very interesting story!) http://tinyurl.com/5lk2a


> quote:After an 11-year reign of terror by the U.S. Food & Drug Administration (FDA) against The Life Extension Foundation, the FDA has "thrown in the towel".In November 1995, Federal Judge Daniel Hurley dismissed all but one of the 56 criminal charges filed against Foundation officers Saul Kent and William Faloon. In February 1996, Judge Hurley dismissed the final charge (see above).This is the first time in its 88-year history that the FDA has been forced to give up on a criminal prosecution. After spending millions of taxpayer dollars, the FDA has abandoned its crusade to destroy The Foundation and throw its leaders into prison


What's wrong with the FDA (May 2001) http://www.lef.org/LEFCMS/aspx/PrintVersio...spx?CmsID=34703 
Delaying the introduction of life-saving therapies
Suppressing safe methods of preventing disease
Causing the price of drugs to be so high that some Americans do without
Denying Americans access to effective drugs approved in other countries
Intimidating those who develop innovative methods to treat disease
Approving lethal prescription drugs that kill
Censoring medical information that would let consumers protect their health
Censoring medical information that would better educate doctors
Failing to protect the safety of our food
Misleading the public about scientific methods to increase longevity
Drugs the FDA says you can't have (July 2001) http://www.lef.org/LEFCMS/aspx/PrintVersio...spx?CmsID=34817 New Website Speaks Out on FDA's Unhealthy Policies (August 2002) http://www.lef.org/LEFCMS/aspx/PrintVersio...spx?CmsID=77823 Interview with Durk Pearson & Sandy Shaw (July 1999) http://www.lef.org/LEFCMS/aspx/PrintVersio...spx?CmsID=35607


> quoteurk Pearson and Sandy Shaw are two leading independent experts in anti-aging research and brain biochemistry. Since 1968, they have been pioneers in the life extension field. Among other best sellers, Durk & Sandy are the authors of "Freedom of Informed Choice: FDA Versus Nutrient Supplements" that discusses constitutional and scientific issues relating to the FDA's regulation of the dissemination of scientific information.Durk & Sandy's battle began in 1992, when they started filing Public Comments in response to the FDA's proposed rules regulating what health claims they would permit for dietary supplements. On January 15th, 1999, Durk Pearson and Sandy Shaw, along with The American Preventative Medical Association and (from a separate appeal) Citizens for Health, won a long and hard-fought battle with the U.S. Food and Drug Administration. In a landmark decision upholding the First Amendment right of free speech, as opposed to government (FDA) regulation of truthful non-misleading "health claims," the U.S. Court of Appeals for the District of Columbia ruled against the FDA on all issues by a 3-0 vote. The FDA appealed to the U.S. Court of Appeals for the D.C. Circuit. On April 2, 1999, the Court turned down the FDA's request for a re-hearing 11-0.


Some other good websites... http://www.stopfda.org/ http://www.fdareview.org skinny


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## skinny (Jul 27, 2002)

Talissa, thanks for the links. These are some good articles to show you what we are up against. The regulatory function of the FDA is so corrupt that it needs a major overhaul. Good thing that a few organizations like the LEF have cracked the gestapo like control on their powers. I believe that we wouldn't be able to buy health supplements off the shelf if it wasn't for the fight of these people, but there are still a lot of battles to be won.Victory over the FDABy Saul Kent, President of the Life Extension Foundation (very interesting story!) http://tinyurl.com/5lk2a


> quote:After an 11-year reign of terror by the U.S. Food & Drug Administration (FDA) against The Life Extension Foundation, the FDA has "thrown in the towel".In November 1995, Federal Judge Daniel Hurley dismissed all but one of the 56 criminal charges filed against Foundation officers Saul Kent and William Faloon. In February 1996, Judge Hurley dismissed the final charge (see above).This is the first time in its 88-year history that the FDA has been forced to give up on a criminal prosecution. After spending millions of taxpayer dollars, the FDA has abandoned its crusade to destroy The Foundation and throw its leaders into prison


What's wrong with the FDA (May 2001) http://www.lef.org/LEFCMS/aspx/PrintVersio...spx?CmsID=34703 
Delaying the introduction of life-saving therapies
Suppressing safe methods of preventing disease
Causing the price of drugs to be so high that some Americans do without
Denying Americans access to effective drugs approved in other countries
Intimidating those who develop innovative methods to treat disease
Approving lethal prescription drugs that kill
Censoring medical information that would let consumers protect their health
Censoring medical information that would better educate doctors
Failing to protect the safety of our food
Misleading the public about scientific methods to increase longevity
Drugs the FDA says you can't have (July 2001) http://www.lef.org/LEFCMS/aspx/PrintVersio...spx?CmsID=34817 New Website Speaks Out on FDA's Unhealthy Policies (August 2002) http://www.lef.org/LEFCMS/aspx/PrintVersio...spx?CmsID=77823 Interview with Durk Pearson & Sandy Shaw (July 1999) http://www.lef.org/LEFCMS/aspx/PrintVersio...spx?CmsID=35607


> quoteurk Pearson and Sandy Shaw are two leading independent experts in anti-aging research and brain biochemistry. Since 1968, they have been pioneers in the life extension field. Among other best sellers, Durk & Sandy are the authors of "Freedom of Informed Choice: FDA Versus Nutrient Supplements" that discusses constitutional and scientific issues relating to the FDA's regulation of the dissemination of scientific information.Durk & Sandy's battle began in 1992, when they started filing Public Comments in response to the FDA's proposed rules regulating what health claims they would permit for dietary supplements. On January 15th, 1999, Durk Pearson and Sandy Shaw, along with The American Preventative Medical Association and (from a separate appeal) Citizens for Health, won a long and hard-fought battle with the U.S. Food and Drug Administration. In a landmark decision upholding the First Amendment right of free speech, as opposed to government (FDA) regulation of truthful non-misleading "health claims," the U.S. Court of Appeals for the District of Columbia ruled against the FDA on all issues by a 3-0 vote. The FDA appealed to the U.S. Court of Appeals for the D.C. Circuit. On April 2, 1999, the Court turned down the FDA's request for a re-hearing 11-0.


Some other good websites... http://www.stopfda.org/ http://www.fdareview.org skinny


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## SpAsMaN* (May 11, 2002)

Drossman is hot!!!Wow Eric,i would be impress to meet him!!Kmottus said that she had an appointment with him


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## SpAsMaN* (May 11, 2002)

Drossman is hot!!!Wow Eric,i would be impress to meet him!!Kmottus said that she had an appointment with him


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## flux (Dec 13, 1998)

> quote: These are some good articles to show you what we are up against.


I don't think they are so good.


> quote:The scientific community has responded by saying that industry cash fuels discovery and, moreover, that no amount of money can corrupt a researcher who is trained to seek the truth


Actually, the scientific community disagrees with this statement. The article is so biased, it argues against the very side who agrees with it (to a point).


> quote: The regulatory function of the FDA is so corrupt that it needs a major overhaul


I don't see any corruption, let alone anything needs a major overhaul.Seems to me that only one or two administrators are just not good at their jobs.


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## flux (Dec 13, 1998)

> quote: These are some good articles to show you what we are up against.


I don't think they are so good.


> quote:The scientific community has responded by saying that industry cash fuels discovery and, moreover, that no amount of money can corrupt a researcher who is trained to seek the truth


Actually, the scientific community disagrees with this statement. The article is so biased, it argues against the very side who agrees with it (to a point).


> quote: The regulatory function of the FDA is so corrupt that it needs a major overhaul


I don't see any corruption, let alone anything needs a major overhaul.Seems to me that only one or two administrators are just not good at their jobs.


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## Jhouston (Nov 9, 2003)

Eric, Interesting Dr D is a psychiatrist......... wonder why he joined the airforce after becomming a doctor? any info on that. He is my peer and we grew up in the same neighborhood. feel like I "know" him a bit better from the bio post. Joann


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## Jhouston (Nov 9, 2003)

Eric, Interesting Dr D is a psychiatrist......... wonder why he joined the airforce after becomming a doctor? any info on that. He is my peer and we grew up in the same neighborhood. feel like I "know" him a bit better from the bio post. Joann


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## SpAsMaN* (May 11, 2002)

Apparently,the SIBO is gaining credibility because no other "treatment" are available for bloater.I'm on a french forum where a guy have been diagnose with a small bowel bacterial infection.I guess his doctor follow the Pimentel protocol.BTW,WHEN the PImentel "kit" will be available???I think i will die of poisonous gas.


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## SpAsMaN* (May 11, 2002)

Apparently,the SIBO is gaining credibility because no other "treatment" are available for bloater.I'm on a french forum where a guy have been diagnose with a small bowel bacterial infection.I guess his doctor follow the Pimentel protocol.BTW,WHEN the PImentel "kit" will be available???I think i will die of poisonous gas.


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## Talissa (Apr 10, 2004)

Thank YOU for those links skinny. Wow. I've read many articles from lef, but didn't realize what a difference they've made on our behalf...And this newest FDA action in response to vioxx--appointing a new drug safety director...I've heard it was largely a PR move, the Rx co.s aren't concerned...


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## Talissa (Apr 10, 2004)

Thank YOU for those links skinny. Wow. I've read many articles from lef, but didn't realize what a difference they've made on our behalf...And this newest FDA action in response to vioxx--appointing a new drug safety director...I've heard it was largely a PR move, the Rx co.s aren't concerned...


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## eric (Jul 8, 1999)

Talissa Did you get a chance to read the article here?From the same author of this article.Inflammatory Bowel Disease and Irritable Bowel Syndrome: Separate or Unified? "Not sure if this would work for everyone...it is a link to the journal and the abstract there is in italian, but the .pdf link on the bottom gives me the whole article in English.K."The pathophysiology of irritable bowel syndrome. http://www.minervamedica.it/index2.t?show=R10Y2004N05A0419 Full text at the bottom of the page in PDF"Full-Text (PDF) "From the same author of this article.Inflammatory Bowel Disease and Irritable Bowel Syndrome: Separate or Unified? Jhouston Have never talked to Dr Drossman about why he joined the air force. Were you in the air force, or are you a psychiatrist?Spasman, SIBO is not the only cause for bloating, nor is the treatment for sibo, the only treatment for bloating, and there is very good information other mechansims can cause bloating in IBS as well as other reasons for bloating being a symptom. There is also some differences in bloating and abdominal distension and possibles causes of each of them.


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## eric (Jul 8, 1999)

Talissa Did you get a chance to read the article here?From the same author of this article.Inflammatory Bowel Disease and Irritable Bowel Syndrome: Separate or Unified? "Not sure if this would work for everyone...it is a link to the journal and the abstract there is in italian, but the .pdf link on the bottom gives me the whole article in English.K."The pathophysiology of irritable bowel syndrome. http://www.minervamedica.it/index2.t?show=R10Y2004N05A0419 Full text at the bottom of the page in PDF"Full-Text (PDF) "From the same author of this article.Inflammatory Bowel Disease and Irritable Bowel Syndrome: Separate or Unified? Jhouston Have never talked to Dr Drossman about why he joined the air force. Were you in the air force, or are you a psychiatrist?Spasman, SIBO is not the only cause for bloating, nor is the treatment for sibo, the only treatment for bloating, and there is very good information other mechansims can cause bloating in IBS as well as other reasons for bloating being a symptom. There is also some differences in bloating and abdominal distension and possibles causes of each of them.


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## Talissa (Apr 10, 2004)

Hi Eric, yes, I read it...as I've said before, I don't have pain anymore, just chronic D, controlled by supplements, and inflammation as shown in my CDSA 2.0 test...I can't agree with the "hypothesis" they've given evidence toward because its based on IBS HAVING to include pain...the first Rome didn't include this in defining IBS...will the 3rd? We'll see.And I've been quoting the "IBD & IBS:Sep or Unified?" article since I've come on this board, so yes, I've read it...I doubt we'll ever agree on some things Eric. That's just the way it is. We both like cats, that's something...







How's life in the restaurant biz treating you? Your newlywed life? Hope it's all fantastic for you.T-


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## Talissa (Apr 10, 2004)

Hi Eric, yes, I read it...as I've said before, I don't have pain anymore, just chronic D, controlled by supplements, and inflammation as shown in my CDSA 2.0 test...I can't agree with the "hypothesis" they've given evidence toward because its based on IBS HAVING to include pain...the first Rome didn't include this in defining IBS...will the 3rd? We'll see.And I've been quoting the "IBD & IBS:Sep or Unified?" article since I've come on this board, so yes, I've read it...I doubt we'll ever agree on some things Eric. That's just the way it is. We both like cats, that's something...








How's life in the restaurant biz treating you? Your newlywed life? Hope it's all fantastic for you.T-


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## eric (Jul 8, 1999)

Skinny, I asked the question for you."Whitehead: Eric, the Cedar Sinai group believe small bowel bacterial overgrowth causes all types of IBS, but the association with diarrhea is certainly the strongest. I don't share their view that SIBO is the cause of IBS but think SIBO is a different problem which can produce similar symptoms. ""Whitehead: FG74, I think others have already responded. It is unlikely but possible for SIBO to persist for years. SIBO is usually the consequence of poor motility in the small intestine that allows bacteria to remain in the area rather than sweeping them out. "Talissa, in order for a diagnoses to be made for IBS, it must include pain or discomfort. You may also disagree, but he is one of the major leading experts in Neurogastroenterology and IBS and viceral pain and the leading center just funded with 4 million from the NIH to do pet scan research and fmri research on IBS patients and pain and the brain and the cause of IBS pain.alsoTABLE 1 *Rome I Criteria* -------------------------------------------------------------------------------- *At least three months of continuous or recurrent symptoms of abdominal pain * that is: Relieved by defecation and/or Associated with a change in stool consistency and/or Associated with a change in frequency of stool Plus two or more of the following greater than 25 percent of the time: Altered stool frequency (more than three per day or less than three per week) Altered stool form (lumpy, hard or watery, loose) Altered stool passage (straining, urgency, or incomplete evacuation) Passage of mucus Bloating or feeling of abdominal distention -------------------------------------------------------------------------------- TABLE 2 *Rome II Criteria * -------------------------------------------------------------------------------- 12 or more weeks of continuous or * recurrent abdominal pain or discomfort * Plus at least two of the following: Relieved by defecation and/or Associated with change in frequency of stool and/or Associated with a change in form (appearance) of stool "Symptom-Based Diagnostic CriteriaBecause, by definition, IBS symptoms cannot be explained by structural or known biochemical abnormalities, diagnosis has been difficult. Until recently, IBS was considered a diagnosis of exclusion. Thus, extensive, invasive, and costly testing has frequently been utilized to rule out other conditions before arriving at a diagnosis of IBS. This may no longer be necessary in many IBS patients because symptomatic criteria are now available. Consensus diagnostic guidelines for IBS were developed by committee in the late 1980s and were later referred to as the "Rome criteria" (Table).(8,9) These subsequently became the standard for patient selection in clinical trials of IBS but were not widely adopted in clinical practice. To facilitate their use in clinical practice, the criteria were recently simplified. The revised criteria are called the Rome II criteria and also are presented in Table.(11) *"The main difference between the Rome criteria and the Rome II criteria is that pain moved from being one of the main criteria to being the absolute diagnostic sign, with other symptoms being merely supportive of the diagnosis"* and"But microscopic inflammation cannot be a diagnostic marker for IBS because it does not typically produce pain in those who have it. All patients with active celiac disease have microscopic inflammation, but a large proportion do not have abdominal pain, and patients with ulcerative colitis who also have microscopic inflammation when compared to patients with IBS appear to have higher pain thresholds" http://www.romecriteria.org/reading1.html This does not mean they have not seen MACROSCOPIC specific inflammation in some subgroups of IBS patients either, especially PI IBS.Many things can cause gi inflammation, aspirin or nasids for example, but inflammation does not always cause pain in the gi tract.These observations are not part of rome criteria, which is symptom based, not specific abnormalities, the total picture and cause of IBS is not known, they are diagnostic and research generated insights into gastroenterology, functional disorders and diseases. At the moment also there is very good research on "Whitehead: Eric, Dr. Gershon's research on serotonin is an important part of the story in IBS. There is evidence that differences between people in how their body clears serotonin from the synapses can affect both mood and gut motility."Which in part explains altered motility but also is connected as a very important neurotransmitter which helps report up nerve fibers, sensations of the digestive tract reported to the brain as pain or discomfort.


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## eric (Jul 8, 1999)

Skinny, I asked the question for you."Whitehead: Eric, the Cedar Sinai group believe small bowel bacterial overgrowth causes all types of IBS, but the association with diarrhea is certainly the strongest. I don't share their view that SIBO is the cause of IBS but think SIBO is a different problem which can produce similar symptoms. ""Whitehead: FG74, I think others have already responded. It is unlikely but possible for SIBO to persist for years. SIBO is usually the consequence of poor motility in the small intestine that allows bacteria to remain in the area rather than sweeping them out. "Talissa, in order for a diagnoses to be made for IBS, it must include pain or discomfort. You may also disagree, but he is one of the major leading experts in Neurogastroenterology and IBS and viceral pain and the leading center just funded with 4 million from the NIH to do pet scan research and fmri research on IBS patients and pain and the brain and the cause of IBS pain.alsoTABLE 1 *Rome I Criteria* -------------------------------------------------------------------------------- *At least three months of continuous or recurrent symptoms of abdominal pain * that is: Relieved by defecation and/or Associated with a change in stool consistency and/or Associated with a change in frequency of stool Plus two or more of the following greater than 25 percent of the time: Altered stool frequency (more than three per day or less than three per week) Altered stool form (lumpy, hard or watery, loose) Altered stool passage (straining, urgency, or incomplete evacuation) Passage of mucus Bloating or feeling of abdominal distention -------------------------------------------------------------------------------- TABLE 2 *Rome II Criteria * -------------------------------------------------------------------------------- 12 or more weeks of continuous or * recurrent abdominal pain or discomfort * Plus at least two of the following: Relieved by defecation and/or Associated with change in frequency of stool and/or Associated with a change in form (appearance) of stool "Symptom-Based Diagnostic CriteriaBecause, by definition, IBS symptoms cannot be explained by structural or known biochemical abnormalities, diagnosis has been difficult. Until recently, IBS was considered a diagnosis of exclusion. Thus, extensive, invasive, and costly testing has frequently been utilized to rule out other conditions before arriving at a diagnosis of IBS. This may no longer be necessary in many IBS patients because symptomatic criteria are now available. Consensus diagnostic guidelines for IBS were developed by committee in the late 1980s and were later referred to as the "Rome criteria" (Table).(8,9) These subsequently became the standard for patient selection in clinical trials of IBS but were not widely adopted in clinical practice. To facilitate their use in clinical practice, the criteria were recently simplified. The revised criteria are called the Rome II criteria and also are presented in Table.(11) *"The main difference between the Rome criteria and the Rome II criteria is that pain moved from being one of the main criteria to being the absolute diagnostic sign, with other symptoms being merely supportive of the diagnosis"* and"But microscopic inflammation cannot be a diagnostic marker for IBS because it does not typically produce pain in those who have it. All patients with active celiac disease have microscopic inflammation, but a large proportion do not have abdominal pain, and patients with ulcerative colitis who also have microscopic inflammation when compared to patients with IBS appear to have higher pain thresholds" http://www.romecriteria.org/reading1.html This does not mean they have not seen MACROSCOPIC specific inflammation in some subgroups of IBS patients either, especially PI IBS.Many things can cause gi inflammation, aspirin or nasids for example, but inflammation does not always cause pain in the gi tract.These observations are not part of rome criteria, which is symptom based, not specific abnormalities, the total picture and cause of IBS is not known, they are diagnostic and research generated insights into gastroenterology, functional disorders and diseases. At the moment also there is very good research on "Whitehead: Eric, Dr. Gershon's research on serotonin is an important part of the story in IBS. There is evidence that differences between people in how their body clears serotonin from the synapses can affect both mood and gut motility."Which in part explains altered motility but also is connected as a very important neurotransmitter which helps report up nerve fibers, sensations of the digestive tract reported to the brain as pain or discomfort.


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## eric (Jul 8, 1999)

By the way if a person does not have pain or discomfort, then they may have another functional disorder, of which there are some 25 of them."These are the established criteria for making the diagnosis of irritable bowel syndrome. They are known as the Rome criteria since they were designated by an international group of experts on IBS at a Rome conference. If you meet the criteria, then you have IBS. If you don't, e.g. you have functional constipation or diarrhea but no abdominal pain, or you have bloating and gas with normal bowel movements, then you have a different functional syndrome. The Rome Committee has completed a revision of the IBS criteria which is known as Rome II. Having specific criteria for the diagnosis of IBS allows researchers, medical and psychological clinicians, patients and pharmaceutical companies to compare their observations and treatments on the same category of patients. This has been a significant advance in the management of IBS. " http://www.mindbodydigestive.com/doyouhaveibs.html


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## eric (Jul 8, 1999)

By the way if a person does not have pain or discomfort, then they may have another functional disorder, of which there are some 25 of them."These are the established criteria for making the diagnosis of irritable bowel syndrome. They are known as the Rome criteria since they were designated by an international group of experts on IBS at a Rome conference. If you meet the criteria, then you have IBS. If you don't, e.g. you have functional constipation or diarrhea but no abdominal pain, or you have bloating and gas with normal bowel movements, then you have a different functional syndrome. The Rome Committee has completed a revision of the IBS criteria which is known as Rome II. Having specific criteria for the diagnosis of IBS allows researchers, medical and psychological clinicians, patients and pharmaceutical companies to compare their observations and treatments on the same category of patients. This has been a significant advance in the management of IBS. " http://www.mindbodydigestive.com/doyouhaveibs.html


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## eric (Jul 8, 1999)

American College of Gastroenterology 69th Annual Scientific Meeting and Postgraduate CourseAdvances in Chronic Constipation and Irritable Bowel Syndrome With ConstipationBrooks D. Cash, MD, FACP Orlando, Florida; Wednesday, November 3, 2004 FYI"Antibiotic Therapy for Bloating and FlatulencePatients with functional gastrointestinal disorders will often report symptoms that extend beyond the primary symptoms elicited by the Rome diagnostic criteria. These include -- but are not limited to -- bloating, distension, incomplete evacuation, mucus in the stool, or urgency. In many cases, it is these symptoms, especially bloating and distension, that are the most bothersome to patients. Effective therapeutic interventions for these complaints are limited, with no agents proven superior to placebo in rigorous clinical trials. Previous investigators have reported that small intestinal bacterial overgrowth may be more common in IBS patients and that antibiotic therapy in such patients may therefore result in symptomatic improvement.4 Validation of these observations in routine clinical practice, however, has largely been lacking. Sharara and colleagues 5 from Beirut, Lebanon, presented the results of a trial involving the newly approved nonabsorbable antibiotic rifaximin as a therapy for bloating and flatulence. Rifaximin is a rifamycin derivative that inhibits bacterial RNA synthesis and is approved for the treatment of traveler's diarrhea. In this randomized, double-blind, placebo-controlled trial, 103 patients received rifaximin 400 mg twice daily or placebo for 10 days. The primary endpoint was a subjective feeling of general symptom improvement. A symptom score incorporating abdominal pain, bloating, change in bowel habits, feeling of incomplete evacuation, and urgency was also calculated. Symptoms were assessed at the end of therapy and again at the end of a 10-day posttreatment phase. At the end of 10 days of rifaximin therapy, 37.5% of patients in the rifaximin group reported general symptom improvement compared with 20.4% of patients in the placebo group (P = .04). These differences persisted at the end of the 10-day posttreatment phase, with 28.6% of the rifaximin group reporting improvement vs 11.1% of the placebo group (P = .02). Although changes in lactulose hydrogen breath test values were not significantly different between the rifaximin and placebo groups, changes in the lactulose hydrogen breath test scores for patients in the rifaximin group did correlate with symptom response (P = .04). It remains unclear as to whether this therapeutic approach can be generalized to a Western population or whether these observed benefits will persist for a clinically meaningful period of time. Assessment of symptom response to fulfillment of the Rome criteria for IBS is currently under way. Additional investigations, such as combining this therapy with a promotility agent or further evaluating the utility and safety of cyclic or prolonged rifaximin for functional gastrointestinal symptoms, are eagerly awaited." http://www.medscape.com/viewarticle/493065


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## eric (Jul 8, 1999)

American College of Gastroenterology 69th Annual Scientific Meeting and Postgraduate CourseAdvances in Chronic Constipation and Irritable Bowel Syndrome With ConstipationBrooks D. Cash, MD, FACP Orlando, Florida; Wednesday, November 3, 2004 FYI"Antibiotic Therapy for Bloating and FlatulencePatients with functional gastrointestinal disorders will often report symptoms that extend beyond the primary symptoms elicited by the Rome diagnostic criteria. These include -- but are not limited to -- bloating, distension, incomplete evacuation, mucus in the stool, or urgency. In many cases, it is these symptoms, especially bloating and distension, that are the most bothersome to patients. Effective therapeutic interventions for these complaints are limited, with no agents proven superior to placebo in rigorous clinical trials. Previous investigators have reported that small intestinal bacterial overgrowth may be more common in IBS patients and that antibiotic therapy in such patients may therefore result in symptomatic improvement.4 Validation of these observations in routine clinical practice, however, has largely been lacking. Sharara and colleagues 5 from Beirut, Lebanon, presented the results of a trial involving the newly approved nonabsorbable antibiotic rifaximin as a therapy for bloating and flatulence. Rifaximin is a rifamycin derivative that inhibits bacterial RNA synthesis and is approved for the treatment of traveler's diarrhea. In this randomized, double-blind, placebo-controlled trial, 103 patients received rifaximin 400 mg twice daily or placebo for 10 days. The primary endpoint was a subjective feeling of general symptom improvement. A symptom score incorporating abdominal pain, bloating, change in bowel habits, feeling of incomplete evacuation, and urgency was also calculated. Symptoms were assessed at the end of therapy and again at the end of a 10-day posttreatment phase. At the end of 10 days of rifaximin therapy, 37.5% of patients in the rifaximin group reported general symptom improvement compared with 20.4% of patients in the placebo group (P = .04). These differences persisted at the end of the 10-day posttreatment phase, with 28.6% of the rifaximin group reporting improvement vs 11.1% of the placebo group (P = .02). Although changes in lactulose hydrogen breath test values were not significantly different between the rifaximin and placebo groups, changes in the lactulose hydrogen breath test scores for patients in the rifaximin group did correlate with symptom response (P = .04). It remains unclear as to whether this therapeutic approach can be generalized to a Western population or whether these observed benefits will persist for a clinically meaningful period of time. Assessment of symptom response to fulfillment of the Rome criteria for IBS is currently under way. Additional investigations, such as combining this therapy with a promotility agent or further evaluating the utility and safety of cyclic or prolonged rifaximin for functional gastrointestinal symptoms, are eagerly awaited." http://www.medscape.com/viewarticle/493065


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## Talissa (Apr 10, 2004)

FYIï¿½ï¿½These criteria should not be used in treatment trials. This is because the presence of pain, now a requirement for the diagnosis of IBS, was not listed as such in these documents, and this did not occur until 1992 (7). ï¿½From the same page as aboveï¿½and why I now, like skinny, have low expectations for Rome III~ï¿½Because of the success of the Rome II process, support from the pharmaceutical industry was secured almost immediately to begin the Rome III process. ï¿½ http://www.romecriteria.org/rome12biblio.html Itï¿½s all about medicating and covering up symptoms with this groupï¿½itï¿½s not about finding & fixing the root cause.FYIï¿½Much remains unknown about the potential causes of IBS. There may not be a unifying hypothesis to link all the aspects of this diverse syndrome. Nevertheless, markers of low-grade inflammation, which were initially found in diarrhea-predominant and postinfectious cases of IBS, are increasingly being found in constipation-predominant patients as well. Thus, inflammation may figure as an underlying factor in visceral hypersensitivity in more cases of IBS than previously was suspected. These intriguing inroads may be the key to our understanding of the basis for the IBS and may yield exciting therapeutic possibilities.ï¿½ http://www.pulsus.com/Gastro/18_10/andr_ed.htm Yes, I posted this already in news & abstracts, but if Eric has to be redundant, for the sake of any newcomers, I feel the need to stoop to his levelï¿½Thereï¿½s also this to revisit from the Journal of the American Medical Association, the FULL conclusion by Lin, who obviously wonï¿½t be on the Rome III committee~ï¿½In this effort, it is biologically plausible that the gastrointestinal and extraintestinal symptoms and findings of IBS have a single, unifying explanation. Specifically, SIBO provides a framework for understanding IBS by accounting for the following observations in IBS patients. Nearly all of the symptoms and findings of IBS are wholly consistent with SIBO, including postprandial bloating (which is nearly universal), physical evidence of small bowel gas irrespective of predominant symptoms, high prevalence of abnormal lactulose breath test results, dramatic reduction in symptoms when antibiotic therapy is given and breath tests subsequently normalize, altered gut motility, visceral hypersensitivity, abnormal brain-gut interactions, evidence of autonomic dysfunction, nearly uniform immune activation regardless of prior acute gastroenteritis, and extraintestinal symptoms that are often flu-like in quality. As a unifying framework for understanding IBS and other functional disorders, SIBO provides a target for exciting research that may lead to better diagnostic and treatment approaches. SIBO is a condition characterized by a chronic relapsing clinical course.76 Since indefinite use of antibiotics is not an attractive option, future research should be directed at understanding and controlling the interaction between host and gut bacteria. ï¿½ http://jama.ama-assn.org/cgi/content/full/...ournalcode=jama


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## Talissa (Apr 10, 2004)

FYIï¿½ï¿½These criteria should not be used in treatment trials. This is because the presence of pain, now a requirement for the diagnosis of IBS, was not listed as such in these documents, and this did not occur until 1992 (7). ï¿½From the same page as aboveï¿½and why I now, like skinny, have low expectations for Rome III~ï¿½Because of the success of the Rome II process, support from the pharmaceutical industry was secured almost immediately to begin the Rome III process. ï¿½ http://www.romecriteria.org/rome12biblio.html Itï¿½s all about medicating and covering up symptoms with this groupï¿½itï¿½s not about finding & fixing the root cause.FYIï¿½Much remains unknown about the potential causes of IBS. There may not be a unifying hypothesis to link all the aspects of this diverse syndrome. Nevertheless, markers of low-grade inflammation, which were initially found in diarrhea-predominant and postinfectious cases of IBS, are increasingly being found in constipation-predominant patients as well. Thus, inflammation may figure as an underlying factor in visceral hypersensitivity in more cases of IBS than previously was suspected. These intriguing inroads may be the key to our understanding of the basis for the IBS and may yield exciting therapeutic possibilities.ï¿½ http://www.pulsus.com/Gastro/18_10/andr_ed.htm Yes, I posted this already in news & abstracts, but if Eric has to be redundant, for the sake of any newcomers, I feel the need to stoop to his levelï¿½Thereï¿½s also this to revisit from the Journal of the American Medical Association, the FULL conclusion by Lin, who obviously wonï¿½t be on the Rome III committee~ï¿½In this effort, it is biologically plausible that the gastrointestinal and extraintestinal symptoms and findings of IBS have a single, unifying explanation. Specifically, SIBO provides a framework for understanding IBS by accounting for the following observations in IBS patients. Nearly all of the symptoms and findings of IBS are wholly consistent with SIBO, including postprandial bloating (which is nearly universal), physical evidence of small bowel gas irrespective of predominant symptoms, high prevalence of abnormal lactulose breath test results, dramatic reduction in symptoms when antibiotic therapy is given and breath tests subsequently normalize, altered gut motility, visceral hypersensitivity, abnormal brain-gut interactions, evidence of autonomic dysfunction, nearly uniform immune activation regardless of prior acute gastroenteritis, and extraintestinal symptoms that are often flu-like in quality. As a unifying framework for understanding IBS and other functional disorders, SIBO provides a target for exciting research that may lead to better diagnostic and treatment approaches. SIBO is a condition characterized by a chronic relapsing clinical course.76 Since indefinite use of antibiotics is not an attractive option, future research should be directed at understanding and controlling the interaction between host and gut bacteria. ï¿½ http://jama.ama-assn.org/cgi/content/full/...ournalcode=jama


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## flux (Dec 13, 1998)

> quote:Itï¿½s all about medicating and covering up symptoms with this groupï¿½itï¿½s not about finding & fixing the root cause


*False*. There is research on the symptom of IBS but that's intended to identify it better and more precisely. Most IBS research is certainly about finding & fixing the root causes, and not symptoms.


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## flux (Dec 13, 1998)

> quote:Itï¿½s all about medicating and covering up symptoms with this groupï¿½itï¿½s not about finding & fixing the root cause


*False*. There is research on the symptom of IBS but that's intended to identify it better and more precisely. Most IBS research is certainly about finding & fixing the root causes, and not symptoms.


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## Talissa (Apr 10, 2004)

Also, if I quit taking all the vit's, probiotics and fiber, of course I'll get D the next day....but how long until the pain returns? I think the pain would eventually return, but I'm not willing to find out. The longest I've tried going w/o fiber is threee days, then I go back to it because who wants D? I'm not giving up my other supp's to see if the pain returns. Pain is not my friend...Thus, the inflammation, in my mind, is causing the diarrhea...as I've read in medscape this can be caused simply because the epithelial cells that are increased are right next to the nerve endings, causing the D, in my case.


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## Talissa (Apr 10, 2004)

Also, if I quit taking all the vit's, probiotics and fiber, of course I'll get D the next day....but how long until the pain returns? I think the pain would eventually return, but I'm not willing to find out. The longest I've tried going w/o fiber is threee days, then I go back to it because who wants D? I'm not giving up my other supp's to see if the pain returns. Pain is not my friend...Thus, the inflammation, in my mind, is causing the diarrhea...as I've read in medscape this can be caused simply because the epithelial cells that are increased are right next to the nerve endings, causing the D, in my case.


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## Talissa (Apr 10, 2004)

" Thus changes in enteroendocrine cell populations and 5-HT availability could contribute to the altered motility and secretion associated with intestinal inflammation by disrupting mucosal signaling to enteric nerves involved in peristaltic and secretory reflexes."http://ajpgi.physiology.org/cgi/content/ab...owel%22&andorex actfulltext=phrase&searchid=1097302106981_43641&stored_search=&FIRSTINDEX=&fdate=10/7/2004&usestrictdates=yes&journalcode=ajpgi&ct[/URL]


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## Talissa (Apr 10, 2004)

" Thus changes in enteroendocrine cell populations and 5-HT availability could contribute to the altered motility and secretion associated with intestinal inflammation by disrupting mucosal signaling to enteric nerves involved in peristaltic and secretory reflexes."http://ajpgi.physiology.org/cgi/content/ab...owel%22&andorex actfulltext=phrase&searchid=1097302106981_43641&stored_search=&FIRSTINDEX=&fdate=10/7/2004&usestrictdates=yes&journalcode=ajpgi&ct[/URL]


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## eric (Jul 8, 1999)

You had PI IBS, in some people PI IBS resolves. Although you may still be left with cell changes in your gut causing the d still. Or functional d even. This may not have anything to do with inflammation. Nor is all IBS based on you and your symptoms. probiotics may help PI IBS in the intial stages of infection inflammation as well, before the full clinical presentation of IBS develops. The rome ll diagnoses is a stable diagnoses with less then 5 percent after two to five years re diagnosed with an organic condition. There has not yet been evidence to show inflammation in all IBSers.Nor does SIBO explain SPECIFIC cell changes in the gut in PI IBS? Which is how you say you personally developed it. SIBO is not enteric infection. It does not cause and increase in mast cells and enteroendocrine in the digestive lining. Which they see in PI IBS after the *resolution* of the intial infection. and as Flux said"Itï¿½s all about medicating and covering up symptoms with this groupï¿½itï¿½s not about finding & fixing the root cause"What group is that? The 50 Gastroenterologist experts on the rome committees? Or the group of researchers in every country around the world? Or the fact you left out the rest of the quote, which is bias."Having specific criteria for the diagnosis of IBS allows researchers, medical and psychological clinicians, patients and pharmaceutical companies to compare their observations and treatments on the same category of patients. This has been a significant advance in the management of IBS. "This is not what its about at all. Its exactly about finding out what causes IBS and if there are subgroups or if its an even bigger problem.Review article: the overlap between functional dyspepsia and irritable bowel syndrome - a tale of one or two disorders?"The evidence available suggests that at least subsets of functional dyspepsia and irritable bowel syndrome represent different manifestations of a single entity. " http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15521854 Lin here only searched medline and books for bloating to come to that conclusion, it was not from clinical research."EVIDENCE ACQUISITION: Ovid MEDLINE was searched through May 2004 for *relevant* *English-language articles* beginning with those *related to bloating, gas, and IBS.* Bibliographies of *pertinent articles * and books were also scanned for additional suitable citations."What about the hundreds and hundreads of other researched IBS abstracts. There is A LOT KNOWN ALREADY ABOUT IBS.Lin's framework is not researched science in the labratory. Its just a search looking for what you want to look for. Why don't you also take a look at the "The 6th International Symposium on Functional Gastrointestinal Disorders is being developed to enhance the knowledge and skills of physicians, psychologists, nurses and allied health professionals in their care of patients with functional gastrointestinal and motility disorders. " and see all they are researching and talking about. http://www.iffgd.org/images/FGID_brochure2005.pdf and for your last one.Your quote"Thus changes in enteroendocrine cell populations and 5-HT availability could contribute to "The enteroendocrine cells store the majoirty of the guts serotonin. Serotonin is released from these cells and its function is to start contractions. They know there is a problem with this and they are starting to understand it and narrow down the problem. To much causes d and to little cause c and back and forth causes the alternating. They have known this for a while now, which is why they can in part explain motility problems in IBS. They also have very good animal studies showing they can create a type of IBS.Review article: serotonin receptors and transporters - roles in normal and abnormal gastrointestinal motility.Gershon MD.Department of Anatomy & Cell Biology, Columbia University, New York, NY, USA." *The observation that molecular defects occur in the human gut in irritable bowel syndrome strengthens the hand of those seeking to legitimize the disease. At least it is not 'all in your head'. The bowel contributes."*


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## eric (Jul 8, 1999)

You had PI IBS, in some people PI IBS resolves. Although you may still be left with cell changes in your gut causing the d still. Or functional d even. This may not have anything to do with inflammation. Nor is all IBS based on you and your symptoms. probiotics may help PI IBS in the intial stages of infection inflammation as well, before the full clinical presentation of IBS develops. The rome ll diagnoses is a stable diagnoses with less then 5 percent after two to five years re diagnosed with an organic condition. There has not yet been evidence to show inflammation in all IBSers.Nor does SIBO explain SPECIFIC cell changes in the gut in PI IBS? Which is how you say you personally developed it. SIBO is not enteric infection. It does not cause and increase in mast cells and enteroendocrine in the digestive lining. Which they see in PI IBS after the *resolution* of the intial infection. and as Flux said"Itï¿½s all about medicating and covering up symptoms with this groupï¿½itï¿½s not about finding & fixing the root cause"What group is that? The 50 Gastroenterologist experts on the rome committees? Or the group of researchers in every country around the world? Or the fact you left out the rest of the quote, which is bias."Having specific criteria for the diagnosis of IBS allows researchers, medical and psychological clinicians, patients and pharmaceutical companies to compare their observations and treatments on the same category of patients. This has been a significant advance in the management of IBS. "This is not what its about at all. Its exactly about finding out what causes IBS and if there are subgroups or if its an even bigger problem.Review article: the overlap between functional dyspepsia and irritable bowel syndrome - a tale of one or two disorders?"The evidence available suggests that at least subsets of functional dyspepsia and irritable bowel syndrome represent different manifestations of a single entity. " http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=15521854 Lin here only searched medline and books for bloating to come to that conclusion, it was not from clinical research."EVIDENCE ACQUISITION: Ovid MEDLINE was searched through May 2004 for *relevant* *English-language articles* beginning with those *related to bloating, gas, and IBS.* Bibliographies of *pertinent articles * and books were also scanned for additional suitable citations."What about the hundreds and hundreads of other researched IBS abstracts. There is A LOT KNOWN ALREADY ABOUT IBS.Lin's framework is not researched science in the labratory. Its just a search looking for what you want to look for. Why don't you also take a look at the "The 6th International Symposium on Functional Gastrointestinal Disorders is being developed to enhance the knowledge and skills of physicians, psychologists, nurses and allied health professionals in their care of patients with functional gastrointestinal and motility disorders. " and see all they are researching and talking about. http://www.iffgd.org/images/FGID_brochure2005.pdf and for your last one.Your quote"Thus changes in enteroendocrine cell populations and 5-HT availability could contribute to "The enteroendocrine cells store the majoirty of the guts serotonin. Serotonin is released from these cells and its function is to start contractions. They know there is a problem with this and they are starting to understand it and narrow down the problem. To much causes d and to little cause c and back and forth causes the alternating. They have known this for a while now, which is why they can in part explain motility problems in IBS. They also have very good animal studies showing they can create a type of IBS.Review article: serotonin receptors and transporters - roles in normal and abnormal gastrointestinal motility.Gershon MD.Department of Anatomy & Cell Biology, Columbia University, New York, NY, USA." *The observation that molecular defects occur in the human gut in irritable bowel syndrome strengthens the hand of those seeking to legitimize the disease. At least it is not 'all in your head'. The bowel contributes."*


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## eric (Jul 8, 1999)

I just want to point out also so far you have disagreed with personally the Lead chairman of the rome commitee to diagnose IBS. An a leading expert of functional disorders and gastrointestinal diseases.The senior gastroenterologists for 15 years at John hopkins.Dr WhiteheadThe head of the UCLA Center for Neurovisceral Sciences & Women's Health.Dr Mayerand the leading world expert on the enteric nervous system. The head of Department of Anatomy & Cell Biology, Columbia University, New York, NY, USA.Dr Gershon.


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## eric (Jul 8, 1999)

I just want to point out also so far you have disagreed with personally the Lead chairman of the rome commitee to diagnose IBS. An a leading expert of functional disorders and gastrointestinal diseases.The senior gastroenterologists for 15 years at John hopkins.Dr WhiteheadThe head of the UCLA Center for Neurovisceral Sciences & Women's Health.Dr Mayerand the leading world expert on the enteric nervous system. The head of Department of Anatomy & Cell Biology, Columbia University, New York, NY, USA.Dr Gershon.


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## Talissa (Apr 10, 2004)

> quote:Because of the success of the Rome II process, support from the pharmaceutical industry was secured almost immediately to begin the Rome III process.


Do you think they mean emotional support???It's all about the $$$...But that doesn't mean I think these amazing minds are idiots. I simply feel they are being led by the nose by Big Pharma.And remember Eric, UNC as well as Spiller are doing studies right now to determine if inflammation in IBS can cause symptoms. It's not been ruled out. And as sure as night follows day, if it found to be so, they'll have some drug to "fix" it, rather than go about it homeostatically via microbial manipulation or natural anit-inflammatories...


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## Talissa (Apr 10, 2004)

> quote:Because of the success of the Rome II process, support from the pharmaceutical industry was secured almost immediately to begin the Rome III process.


Do you think they mean emotional support???It's all about the $$$...But that doesn't mean I think these amazing minds are idiots. I simply feel they are being led by the nose by Big Pharma.And remember Eric, UNC as well as Spiller are doing studies right now to determine if inflammation in IBS can cause symptoms. It's not been ruled out. And as sure as night follows day, if it found to be so, they'll have some drug to "fix" it, rather than go about it homeostatically via microbial manipulation or natural anit-inflammatories...


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## flux (Dec 13, 1998)

> quote:It's all about the $$$..


That's *fantastic*. There are many diseases not so lucky.


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## flux (Dec 13, 1998)

> quote:It's all about the $$$..


That's *fantastic*. There are many diseases not so lucky.


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## skinny (Jul 27, 2002)

> quote:"The main difference between the Rome criteria and the Rome II criteria is that pain moved from being one of the main criteria to being the absolute diagnostic sign, with other symptoms being merely supportive of the diagnosis"and"But microscopic inflammation cannot be a diagnostic marker for IBS because it does not typically produce pain in those who have it. All patients with active celiac disease have microscopic inflammation, but a large proportion do not have abdominal pain, and patients with ulcerative colitis who also have microscopic inflammation when compared to patients with IBS appear to have higher pain thresholds" http://www.romecriteria.org/reading1.html


So what? Right now Rome II includes pain *or discomfort.* Those with microscopic inflammation may have a lower pain threshold, but they still have some sort of discomfort if they have D or C everyday.So is there an objective way to qualify pain and tell the difference between pain and discomfort?


> quote:"EVIDENCE ACQUISITION: Ovid MEDLINE was searched through May 2004 for relevant English-language articles beginning with those related to bloating, gas, and IBS. Bibliographies of pertinent articles and books were also scanned for additional suitable citations."What about the hundreds and hundreads of other researched IBS abstracts. There is A LOT KNOWN ALREADY ABOUT IBS.Lin's framework is not researched science in the labratory. Its just a search looking for what you want to look for.


Hello? Lin's paper is also based off of positive results of clinical trials he was not involved in not "just a search" as you claim it to be.Eradication of Small Intestinal Bacterial Overgrowth Reduces Symptoms of Irritable Bowel Syndrome http://www-east.elsevier.com/ajg/issues/9512/ajg3368fla.htm Normalization of lactulose breath testing correlates with symptom improvement in irritable bowel syndrome: a double-blind, randomized, placebo-controlled study. http://www.ncbi.nlm.nih.gov/entrez/query.f...2&dopt=Abstract A 14-day elemental diet is highly effective in normalizing the lactulose breath test. (Lin not listed here, but FYI)Pimentel M, Constantino T, Kong Y, Bajwa M, Rezaei A, Park S. http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=14992438 skinny


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## skinny (Jul 27, 2002)

> quote:"The main difference between the Rome criteria and the Rome II criteria is that pain moved from being one of the main criteria to being the absolute diagnostic sign, with other symptoms being merely supportive of the diagnosis"and"But microscopic inflammation cannot be a diagnostic marker for IBS because it does not typically produce pain in those who have it. All patients with active celiac disease have microscopic inflammation, but a large proportion do not have abdominal pain, and patients with ulcerative colitis who also have microscopic inflammation when compared to patients with IBS appear to have higher pain thresholds" http://www.romecriteria.org/reading1.html


So what? Right now Rome II includes pain *or discomfort.* Those with microscopic inflammation may have a lower pain threshold, but they still have some sort of discomfort if they have D or C everyday.So is there an objective way to qualify pain and tell the difference between pain and discomfort?


> quote:"EVIDENCE ACQUISITION: Ovid MEDLINE was searched through May 2004 for relevant English-language articles beginning with those related to bloating, gas, and IBS. Bibliographies of pertinent articles and books were also scanned for additional suitable citations."What about the hundreds and hundreads of other researched IBS abstracts. There is A LOT KNOWN ALREADY ABOUT IBS.Lin's framework is not researched science in the labratory. Its just a search looking for what you want to look for.


Hello? Lin's paper is also based off of positive results of clinical trials he was not involved in not "just a search" as you claim it to be.Eradication of Small Intestinal Bacterial Overgrowth Reduces Symptoms of Irritable Bowel Syndrome http://www-east.elsevier.com/ajg/issues/9512/ajg3368fla.htm Normalization of lactulose breath testing correlates with symptom improvement in irritable bowel syndrome: a double-blind, randomized, placebo-controlled study. http://www.ncbi.nlm.nih.gov/entrez/query.f...2&dopt=Abstract A 14-day elemental diet is highly effective in normalizing the lactulose breath test. (Lin not listed here, but FYI)Pimentel M, Constantino T, Kong Y, Bajwa M, Rezaei A, Park S. http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=14992438 skinny


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## Jhouston (Nov 9, 2003)

Eric, Recall in the past I have brought up the fact that some IBS dxed patients do NOT have IBS per rome criteria? Really, all this is moot once the above is accepted. Don't ya' think? If only the "pain" symptom is REALLY checked out. if a person had pain once, does that qualify? once a month? 3 times in last year? every day? avoiding "triggers" gives relief...does that qualify? What about the word "discomfort"? someone explain to me how that could be a "standard" for IBS? one person's ceiling is another person's floor. Perception of either pain or discomfort is a psycosomatic problem, no? PI IBS? how can we be sure that the very first "attack" of IBS was or wasn't an infection of greater or lesser degree? Joann


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## Jhouston (Nov 9, 2003)

Eric, Recall in the past I have brought up the fact that some IBS dxed patients do NOT have IBS per rome criteria? Really, all this is moot once the above is accepted. Don't ya' think? If only the "pain" symptom is REALLY checked out. if a person had pain once, does that qualify? once a month? 3 times in last year? every day? avoiding "triggers" gives relief...does that qualify? What about the word "discomfort"? someone explain to me how that could be a "standard" for IBS? one person's ceiling is another person's floor. Perception of either pain or discomfort is a psycosomatic problem, no? PI IBS? how can we be sure that the very first "attack" of IBS was or wasn't an infection of greater or lesser degree? Joann


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## eric (Jul 8, 1999)

Lin and Pimentel have three studies. They are partners. Skinny, you have noit answered my question yet either. Have you been tested for sibo?If SIBO is suspected it should be tested for, but it mainly causes d, bloating and pain. Usally brought on by eating and hour to an hour and a half after eating. It can mimick some IBS symptoms. Those authors have NOT SHOWN ITS IBS.In IBS some people get pain before they even eat from smelling food even, or 15 minutes after they eat, because in IBS they have also found an altered gastro colonic responce. Some from drinking cold water even. In IBS there are a lot of triggers, not just eating. Show a study also how sibo causes mast cell inflammtion in the deeper tissues of the bowel wall or an increase of EC cells or mast cells? Who says? "microscopic inflammation may have a lower pain threshold" One more time, inflammation does not always cause pain!!!! "patients with ulcerative colitis who also have microscopic inflammation when compared to patients with IBS appear to have higher pain thresholds"They can have higher pain thresholds to pain singaling from the gut!IBSers have a lower pain threshold to distension of the gut and gut nerve sensitvity. Inflammation is already known in PI IBS and even some of the reasons for it. Yes it is being studied further, just like serotonin, the brain, the gut, neurotransmitters, hormones, cells changes, genetics and a lot of other combined research. Much progress has been made recently in not only IBS but functional disorders in general. Inflammation in those mast cells can even be brought on by stress. or previous inflammation of mast cells after resolution, can be reinflammed by stress. Only that microscopic inflammation may contribute to the pain in IBS. They know quite a bit about this already and it involves mast cells for one and there are numerous studies on this, and a lot of evidence on brain center impairment in pain processing the anterior cinulate cortex and the prefrontal cortex from signals that arrive to the brain via the gut of which serotonin is a player also and has been majorally implicated in IBS, and there are numerous studies on that as well. Hence why some of the new IBS drugs that effect serotonin, help with motility and pain and hence why antidepressants that work on serotonin, help with pain and sometimes motility via the spinal cord and brain and action on recptors in the gut. As well as Hypnotherapy helping with pain in IBS via the anterior cinculate cortex, which is impaired in IBS patients verses controls and they have quite a bit of research on all of this combined. There are also numerous studies where they can cause pain in IBS by inserting a ballon up the rectum. They also see specific brain changes when they do so, in IBSers as opposed to normals. They alreay know things that help IBS, ranging from natural treatments to medications. In reality, the most effective treatments for IBS to date as a whole are education, life style changes, diet changes and stress reduction. These treatments have been the most effective to date for the majority of IBSers long term. IBSers have a lower pain threshold of nerves in the digestive system, in classic IBS specifically the sigmoid colon and rectum. also JUST motility does not fully explain IBS.Historyhttp://216.109.117.135/search/cache?p=the+...istory+function al+bowel+disorders&d=056341B916&icp=1&.intl=us[/URL]Motilityviceral hypersensitvityand brain gut axis dysfuntionanyone who has seriously studied IBS has heard the words.Viceral hypersensitvity."Visceral hypersensitivity (intestinal): Enhanced perception, or enhanced responsiveness within the gut -- even to normal events." http://www.iffgd.org/GIDisorders/glossary.html "Eric,Recall in the past I have brought up the fact that some IBS dxed patients do NOT have IBS per rome criteria? "True they may have another of the twenty five functional disorders or a disease, even sibo is a functional disorder. There is functional d with no pain and functional constipation with no pain. There is also chronic abdominal pain, with no d or c. There are other functional disorders, one being functional dyspepsia, which is known to overlap IBS. There are functional disorders in the entire digestive system. There are also diseases.Talissa, who is suppose to create new drugs and safe drugs? Or are you saying the whole world does not need any drugs what so ever? So AIDS patients for example should not be given any drugs or drugs that have ever been research? What about cancer drugs, what about antibiotics also which have saved millions of lives, even though they can be problematic? What about conditions that require drugs? There are such conditions? You are complaining about drug compainies and doctors being in their pockets. So what is your suggestion to create safe drugs that are needed in the world we live in to treat diseases? Also the experts in IBS, only recommend drugs as a last resort for moderate to severe IBS, after all other treatment methods fail. There is also a big percentage of people, who only want a drug. Some IBSers feel IBS can only be treated by drugs.You might also really be interested in this.Jhouston There are mild, moderate and severe IBS patients. Some have more pain then others, a mild IBS patient usally has less pain then a moderate one and a moderate one less then a severe one. However, your right in pain itself is subjective and as well as a matter of a persons persception. Genetics even plays a role in how much pain a person can tolerate.Doctors go to school however and are taught differences in pain and pain symptoms and discomfort and chronic pain and short term pain and even the causes of pain and areas where a problem may cause pain. Pain and discomfort in IBS actually has some characteritics to it. One its chronic. Chronic pain is usally harder to diagnose. However, the diagnoses of IBS is pain or discomfort a must, with a SPECIFIC cluster of symptoms along with it to make a more accurate diagnoses. Yes a good doctor needs to truly understand the diagnoses and use the criteria and evaluate the persons mendical history. But IBS is no longer a diagnoses of exclusion. Using the criteria and the specific cluster of symptoms, minus alarm symptoms, it is a stable diagnoses and most people if they do not have a change in symptoms, are rrarely diagnosed with an organic disorder years later. One reason why they may diagnose someone and ask them to come back six months later to find out if they have a change in symptoms for one.PainAbdominal Pain, Long-Term http://familydoctor.org/528.xml Abdominal Pain, Short-Term http://familydoctor.org/x2593.xml Medical EncyclopediaAbdominal pain http://www.nlm.nih.gov/medlineplus/ency/article/003120.htm http://search.nlm.nih.gov/medlineplusEncy/...=Abdominal+Pain Abdominal Pain http://www.medicinenet.com/abdominal_pain/article.htm Also in IBS, pain can sometimes be relieved by defecation, which helps support the diagnoses.Again, pain or discomfort is a must, but its a specific cluster of symptoms, seen together to help establish and IBS diagnoses and to help rule out organic diseases. "In the past two decades, medical opinion has changed regarding how to diagnose IBS. The older view emphasized that IBS should be regarded primarily as a "diagnosis of exclusion;" that is, diagnosed only after diagnostic testing excludes many disorders that could possibly cause the symptoms. Because many medical disorders can produce the cardinal IBS features of abdominal discomfort or pain and disturbed bowel habit as well as other symptoms caused by IBS, this approach often led to extensive diagnostic testing in many patients. Since the era when such thinking about IBS was common, laboratory, motility, radiologic, and endoscopic tests have proliferated. Although each of these tests is useful in evaluating certain problems, their routine or indiscriminate use can cause unnecessary inconvenience and cost for patients, and complications even occur infrequently from some of the tests. Fortunately, physicians can now diagnose IBS in most patients by recognizing certain symptom details, performing a physical examination, and undertaking limited diagnostic testing. This simpler approach is grounded on recent knowledge of the typical symptoms of IBS, and it leads to a reliable diagnosis in most cases. Extensive testing is usually reserved for special situations." http://www.aboutibs.org/Publications/diagnosis.html Jhouston the defintion of psyï¿½choï¿½soï¿½matï¿½icin the case of IBS and pain yes. Pain involves the mind and body and yes emotional factors can influnces both pain and motility. That does not in any way mean however, IBS is not a physical disorder orginating from the gut, it is and the experts know this, but both pain and motility and other influences are effected or controled by the brain. The gut can cause symptoms and the brain can cause symptoms. In fact both are operational to cause the symptoms.Pronunciation: (sI"kO-su-mat'ik, -sO-), ï¿½adj. 1. of or pertaining to a physical disorder that is caused by or notably influenced by emotional factors. 2. pertaining to or involving both the mind and the body.


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## eric (Jul 8, 1999)

Lin and Pimentel have three studies. They are partners. Skinny, you have noit answered my question yet either. Have you been tested for sibo?If SIBO is suspected it should be tested for, but it mainly causes d, bloating and pain. Usally brought on by eating and hour to an hour and a half after eating. It can mimick some IBS symptoms. Those authors have NOT SHOWN ITS IBS.In IBS some people get pain before they even eat from smelling food even, or 15 minutes after they eat, because in IBS they have also found an altered gastro colonic responce. Some from drinking cold water even. In IBS there are a lot of triggers, not just eating. Show a study also how sibo causes mast cell inflammtion in the deeper tissues of the bowel wall or an increase of EC cells or mast cells? Who says? "microscopic inflammation may have a lower pain threshold" One more time, inflammation does not always cause pain!!!! "patients with ulcerative colitis who also have microscopic inflammation when compared to patients with IBS appear to have higher pain thresholds"They can have higher pain thresholds to pain singaling from the gut!IBSers have a lower pain threshold to distension of the gut and gut nerve sensitvity. Inflammation is already known in PI IBS and even some of the reasons for it. Yes it is being studied further, just like serotonin, the brain, the gut, neurotransmitters, hormones, cells changes, genetics and a lot of other combined research. Much progress has been made recently in not only IBS but functional disorders in general. Inflammation in those mast cells can even be brought on by stress. or previous inflammation of mast cells after resolution, can be reinflammed by stress. Only that microscopic inflammation may contribute to the pain in IBS. They know quite a bit about this already and it involves mast cells for one and there are numerous studies on this, and a lot of evidence on brain center impairment in pain processing the anterior cinulate cortex and the prefrontal cortex from signals that arrive to the brain via the gut of which serotonin is a player also and has been majorally implicated in IBS, and there are numerous studies on that as well. Hence why some of the new IBS drugs that effect serotonin, help with motility and pain and hence why antidepressants that work on serotonin, help with pain and sometimes motility via the spinal cord and brain and action on recptors in the gut. As well as Hypnotherapy helping with pain in IBS via the anterior cinculate cortex, which is impaired in IBS patients verses controls and they have quite a bit of research on all of this combined. There are also numerous studies where they can cause pain in IBS by inserting a ballon up the rectum. They also see specific brain changes when they do so, in IBSers as opposed to normals. They alreay know things that help IBS, ranging from natural treatments to medications. In reality, the most effective treatments for IBS to date as a whole are education, life style changes, diet changes and stress reduction. These treatments have been the most effective to date for the majority of IBSers long term. IBSers have a lower pain threshold of nerves in the digestive system, in classic IBS specifically the sigmoid colon and rectum. also JUST motility does not fully explain IBS.Historyhttp://216.109.117.135/search/cache?p=the+...istory+function al+bowel+disorders&d=056341B916&icp=1&.intl=us[/URL]Motilityviceral hypersensitvityand brain gut axis dysfuntionanyone who has seriously studied IBS has heard the words.Viceral hypersensitvity."Visceral hypersensitivity (intestinal): Enhanced perception, or enhanced responsiveness within the gut -- even to normal events." http://www.iffgd.org/GIDisorders/glossary.html "Eric,Recall in the past I have brought up the fact that some IBS dxed patients do NOT have IBS per rome criteria? "True they may have another of the twenty five functional disorders or a disease, even sibo is a functional disorder. There is functional d with no pain and functional constipation with no pain. There is also chronic abdominal pain, with no d or c. There are other functional disorders, one being functional dyspepsia, which is known to overlap IBS. There are functional disorders in the entire digestive system. There are also diseases.Talissa, who is suppose to create new drugs and safe drugs? Or are you saying the whole world does not need any drugs what so ever? So AIDS patients for example should not be given any drugs or drugs that have ever been research? What about cancer drugs, what about antibiotics also which have saved millions of lives, even though they can be problematic? What about conditions that require drugs? There are such conditions? You are complaining about drug compainies and doctors being in their pockets. So what is your suggestion to create safe drugs that are needed in the world we live in to treat diseases? Also the experts in IBS, only recommend drugs as a last resort for moderate to severe IBS, after all other treatment methods fail. There is also a big percentage of people, who only want a drug. Some IBSers feel IBS can only be treated by drugs.You might also really be interested in this.Jhouston There are mild, moderate and severe IBS patients. Some have more pain then others, a mild IBS patient usally has less pain then a moderate one and a moderate one less then a severe one. However, your right in pain itself is subjective and as well as a matter of a persons persception. Genetics even plays a role in how much pain a person can tolerate.Doctors go to school however and are taught differences in pain and pain symptoms and discomfort and chronic pain and short term pain and even the causes of pain and areas where a problem may cause pain. Pain and discomfort in IBS actually has some characteritics to it. One its chronic. Chronic pain is usally harder to diagnose. However, the diagnoses of IBS is pain or discomfort a must, with a SPECIFIC cluster of symptoms along with it to make a more accurate diagnoses. Yes a good doctor needs to truly understand the diagnoses and use the criteria and evaluate the persons mendical history. But IBS is no longer a diagnoses of exclusion. Using the criteria and the specific cluster of symptoms, minus alarm symptoms, it is a stable diagnoses and most people if they do not have a change in symptoms, are rrarely diagnosed with an organic disorder years later. One reason why they may diagnose someone and ask them to come back six months later to find out if they have a change in symptoms for one.PainAbdominal Pain, Long-Term http://familydoctor.org/528.xml Abdominal Pain, Short-Term http://familydoctor.org/x2593.xml Medical EncyclopediaAbdominal pain http://www.nlm.nih.gov/medlineplus/ency/article/003120.htm http://search.nlm.nih.gov/medlineplusEncy/...=Abdominal+Pain Abdominal Pain http://www.medicinenet.com/abdominal_pain/article.htm Also in IBS, pain can sometimes be relieved by defecation, which helps support the diagnoses.Again, pain or discomfort is a must, but its a specific cluster of symptoms, seen together to help establish and IBS diagnoses and to help rule out organic diseases. "In the past two decades, medical opinion has changed regarding how to diagnose IBS. The older view emphasized that IBS should be regarded primarily as a "diagnosis of exclusion;" that is, diagnosed only after diagnostic testing excludes many disorders that could possibly cause the symptoms. Because many medical disorders can produce the cardinal IBS features of abdominal discomfort or pain and disturbed bowel habit as well as other symptoms caused by IBS, this approach often led to extensive diagnostic testing in many patients. Since the era when such thinking about IBS was common, laboratory, motility, radiologic, and endoscopic tests have proliferated. Although each of these tests is useful in evaluating certain problems, their routine or indiscriminate use can cause unnecessary inconvenience and cost for patients, and complications even occur infrequently from some of the tests. Fortunately, physicians can now diagnose IBS in most patients by recognizing certain symptom details, performing a physical examination, and undertaking limited diagnostic testing. This simpler approach is grounded on recent knowledge of the typical symptoms of IBS, and it leads to a reliable diagnosis in most cases. Extensive testing is usually reserved for special situations." http://www.aboutibs.org/Publications/diagnosis.html Jhouston the defintion of psyï¿½choï¿½soï¿½matï¿½icin the case of IBS and pain yes. Pain involves the mind and body and yes emotional factors can influnces both pain and motility. That does not in any way mean however, IBS is not a physical disorder orginating from the gut, it is and the experts know this, but both pain and motility and other influences are effected or controled by the brain. The gut can cause symptoms and the brain can cause symptoms. In fact both are operational to cause the symptoms.Pronunciation: (sI"kO-su-mat'ik, -sO-), ï¿½adj. 1. of or pertaining to a physical disorder that is caused by or notably influenced by emotional factors. 2. pertaining to or involving both the mind and the body.


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## Talissa (Apr 10, 2004)

"One more time, inflammation does not always cause pain!!!! "I'm proof of that.I'm not against all drugs. I'm against researchers working on the behalf of pharmaceutical companies as opp to working on patients behalf. I'm ag researchers hiding or downplaying side effects in order to meet the demands of their benefactors who only want to make huge profits. I'm ag pharm's using highly respected academic dept heads as marketing tools and paying them off with hugh fees, stock options and hawaiin vacations.


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## Talissa (Apr 10, 2004)

"One more time, inflammation does not always cause pain!!!! "I'm proof of that.I'm not against all drugs. I'm against researchers working on the behalf of pharmaceutical companies as opp to working on patients behalf. I'm ag researchers hiding or downplaying side effects in order to meet the demands of their benefactors who only want to make huge profits. I'm ag pharm's using highly respected academic dept heads as marketing tools and paying them off with hugh fees, stock options and hawaiin vacations.


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## Talissa (Apr 10, 2004)

Actually Eric, I disagree with you, but not necessarily with your ï¿½expertsï¿½ï¿½From Spiller~~ï¿½ *Associated with these changes there is also evidence of low grade inflammation and elevated enteroendocrine cells which resolves in most patients, but persists in those with persistent symptoms * ï¿½ http://www.google.hn/search?q=cache:sCV_-u...mptoms%22&hl=en From Drossman~~ï¿½I recently attended an international meeting that focused on potential new mechanisms to help understand the functional gastrointestinal (GI) disorders. It was exciting to hear experts address new concepts on how:ï¿½ mucosal inflammation could alter neurotransmitter, ion channel, or nerve growth factor activity and early gene expression, all of which might influence motility and visceral sensation;ï¿½ï¿½ http://www.med.unc.edu/medicine/fgidc/organification.htm From the UNC`ï¿½Inflammatory Mediators in Irritable Bowel Syndromeï¿½ï¿½ConclusionWe believe that low-grade inflammation may play a role in the pathogenesis of a sub-set of IBS. There is now evidence from several different studies to suggest that a range of inflammatory mediators may be increased in IBS. It is important to point out, however, that most of this evidence, including our data is preliminary and will need to be confirmed by larger research studies. Important challenges for future work will be to demonstrate the role of specific inflammatory mediators in the generation and resolution of IBS symptoms. Continued research into this area is likely to improve our understanding of the underlying mechanisms in IBS and may lead to the development to better therapeutic approaches for this condition. ï¿½ http://www.med.unc.edu/medicine/fgidc/infl...rymediators.htm ï¿½The development and use of biologic markers identifying low-grade inflammation would improve the characterization of subsets of IBS patients in whom peripheral mechanisms may participate in specific symptom genesis and could be considered in the choice of the therapy.ï¿½ http://www.medscape.com/viewarticle/457728_5


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## Talissa (Apr 10, 2004)

Actually Eric, I disagree with you, but not necessarily with your ï¿½expertsï¿½ï¿½From Spiller~~ï¿½ *Associated with these changes there is also evidence of low grade inflammation and elevated enteroendocrine cells which resolves in most patients, but persists in those with persistent symptoms * ï¿½ http://www.google.hn/search?q=cache:sCV_-u...mptoms%22&hl=en  From Drossman~~ï¿½I recently attended an international meeting that focused on potential new mechanisms to help understand the functional gastrointestinal (GI) disorders. It was exciting to hear experts address new concepts on how:ï¿½ mucosal inflammation could alter neurotransmitter, ion channel, or nerve growth factor activity and early gene expression, all of which might influence motility and visceral sensation;ï¿½ï¿½ http://www.med.unc.edu/medicine/fgidc/organification.htm From the UNC`ï¿½Inflammatory Mediators in Irritable Bowel Syndromeï¿½ï¿½ConclusionWe believe that low-grade inflammation may play a role in the pathogenesis of a sub-set of IBS. There is now evidence from several different studies to suggest that a range of inflammatory mediators may be increased in IBS. It is important to point out, however, that most of this evidence, including our data is preliminary and will need to be confirmed by larger research studies. Important challenges for future work will be to demonstrate the role of specific inflammatory mediators in the generation and resolution of IBS symptoms. Continued research into this area is likely to improve our understanding of the underlying mechanisms in IBS and may lead to the development to better therapeutic approaches for this condition. ï¿½ http://www.med.unc.edu/medicine/fgidc/infl...rymediators.htm ï¿½The development and use of biologic markers identifying low-grade inflammation would improve the characterization of subsets of IBS patients in whom peripheral mechanisms may participate in specific symptom genesis and could be considered in the choice of the therapy.ï¿½ http://www.medscape.com/viewarticle/457728_5


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## eric (Jul 8, 1999)

You said you disagree with Dr Drossman and Inflammation.You said you disagree with Dr Mayer, tht just inflammation in the gut is not a plausible mechansims to cause pain in all IBS patients.You said you disagree with Dr WHite head.Dr Spiller is a leading PI IBS researcher, who will be at the 6th International Symposium on Functional Gastrointestinal Disorders. Where DR Spiller, Dr Drossman, Dr Whitehead, Dr Mayer, Dr Gershon and many other very important experts will be gathering to review state of the art IBS research.as stated before evalvated enteroendocrine cells store serotonin and that is even what the post from Dr Spiller you posted is talking about. Elavated mast cells and the specific cells seen inflammmed you have misinterpreted the research on for quite a while now as well.Robin Spiller"Irritable bowel syndrome - still causing problems Robin Spiller, Professor of Gastroenterology at Nottingham has a particular interest in irritable bowel syndrome (IBS), particularly the form of IBS that develops after a gastrointestinal infection. His presentation in Barcelona raised a number of important question which still cause trouble. What is IBS? Why do our patients consult? How do and should general practitioners respond to them? And what is the evidence of current and planned therapies? Spiller emphasised the importance of the Rome Criteria in making a diagnosis; although few of us use these in a formal way, it is increasingly evident that not only do we consider them in a rather more intuitive way but that our diagnoses based on this approach have pretty good concordance with formal diagnoses made on the basis of elaborate criteria. Spiller questioned the relevance of bloating as a diagnostic criterion and also emphasised the additional diagnostic value of the associated, non-gastrointestinal symptoms that are frequent found in IBS patients. He made two other important suggestions for evaluating patients with IBS. The first of these was the use of symptom diaries, which are self-completed forms containing information about the frequency, duration and severity of pain and other symptoms, episodes of urgency and description of stool form. These, Spiller believes, have the important added value of assuring patients that they are being listened to, as well as providing valuable clinical and possibly diagnostic information. The other innovation that he discussed was the use of telephone symptom recording and the use of palm pilots to make contemporaneous records of the occurrence of symptoms. Using these methods a number of studies had shown that most IBS patients experience their symptoms around once every week, and that they last for 1-2 days on each occasion, with a wide range of duration. A second telephone symptom recording study, whilst revealing similar clusters and peaks of symptoms, was unable to demonstrate a relationship between anxiety and stress and the onset or exacerbation of symptoms. The General Practitioner Research Database (GPRD) has been used to study primary care management of IBS. Amongst 2956 patients identified in the GPRD with a first diagnosis of IBS made in 1994, one-third had received a diagnostic test, 85% had received drugs and consulting and referral rates in primary and secondary care seemed to be unaltered after diagnosis, compared with pre-diagnosis rates. Spiller interpreted this, possibly incorrectly, as a failure of reassurance, but whether or not this is the case, he made the important point that no formal studies of the outcome of reassurance in IBS patients have been conducted. I thought that his review of the effect of drug therapy in IBS was over-selective, referring only to early studies and very limited meta-analyses, which have been superseded by more recent work. However, the bottom line that there is only slim evidence of efficacy for most interventions, including mebeverine, bran and bulking agents is an important message. Interestingly, Spiller concentrated on hypnosis as the most valuable 'psychological' modality of treatment in IBS. He emphasised the importance of chronic life stresses and continuing difficulties in the maintenance of IBS symptoms and the reasonable evidence of efficacy of anti-depressants in IBS, although once again good quality primary care trials are lacking. Gut-directed hypnotherapy, particularly as undertaken in Peter Whorwell's unit in Manchester, is particular efficacious and there is now good evidence of enduring efficacy. Cognitive behaviour therapy is also emerging as a useful treatment modality in IBS. Finally, Robin Spiller reviewed the importance of 5HT in gut function and the likely contribution that 5HT3 antagonists and 5HT4 agonists may make to the management of IBS in the future. Both promising 5HT3-active agents are currently unavailable but interest in the management of IBS is high, which means that there are real opportunities for primary care research into diagnosis and management." http://www.pcsg.org.uk/html/GIP/gip02/7thWyethEndoSymp.html


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## eric (Jul 8, 1999)

You said you disagree with Dr Drossman and Inflammation.You said you disagree with Dr Mayer, tht just inflammation in the gut is not a plausible mechansims to cause pain in all IBS patients.You said you disagree with Dr WHite head.Dr Spiller is a leading PI IBS researcher, who will be at the 6th International Symposium on Functional Gastrointestinal Disorders. Where DR Spiller, Dr Drossman, Dr Whitehead, Dr Mayer, Dr Gershon and many other very important experts will be gathering to review state of the art IBS research.as stated before evalvated enteroendocrine cells store serotonin and that is even what the post from Dr Spiller you posted is talking about. Elavated mast cells and the specific cells seen inflammmed you have misinterpreted the research on for quite a while now as well.Robin Spiller"Irritable bowel syndrome - still causing problems Robin Spiller, Professor of Gastroenterology at Nottingham has a particular interest in irritable bowel syndrome (IBS), particularly the form of IBS that develops after a gastrointestinal infection. His presentation in Barcelona raised a number of important question which still cause trouble. What is IBS? Why do our patients consult? How do and should general practitioners respond to them? And what is the evidence of current and planned therapies? Spiller emphasised the importance of the Rome Criteria in making a diagnosis; although few of us use these in a formal way, it is increasingly evident that not only do we consider them in a rather more intuitive way but that our diagnoses based on this approach have pretty good concordance with formal diagnoses made on the basis of elaborate criteria. Spiller questioned the relevance of bloating as a diagnostic criterion and also emphasised the additional diagnostic value of the associated, non-gastrointestinal symptoms that are frequent found in IBS patients. He made two other important suggestions for evaluating patients with IBS. The first of these was the use of symptom diaries, which are self-completed forms containing information about the frequency, duration and severity of pain and other symptoms, episodes of urgency and description of stool form. These, Spiller believes, have the important added value of assuring patients that they are being listened to, as well as providing valuable clinical and possibly diagnostic information. The other innovation that he discussed was the use of telephone symptom recording and the use of palm pilots to make contemporaneous records of the occurrence of symptoms. Using these methods a number of studies had shown that most IBS patients experience their symptoms around once every week, and that they last for 1-2 days on each occasion, with a wide range of duration. A second telephone symptom recording study, whilst revealing similar clusters and peaks of symptoms, was unable to demonstrate a relationship between anxiety and stress and the onset or exacerbation of symptoms. The General Practitioner Research Database (GPRD) has been used to study primary care management of IBS. Amongst 2956 patients identified in the GPRD with a first diagnosis of IBS made in 1994, one-third had received a diagnostic test, 85% had received drugs and consulting and referral rates in primary and secondary care seemed to be unaltered after diagnosis, compared with pre-diagnosis rates. Spiller interpreted this, possibly incorrectly, as a failure of reassurance, but whether or not this is the case, he made the important point that no formal studies of the outcome of reassurance in IBS patients have been conducted. I thought that his review of the effect of drug therapy in IBS was over-selective, referring only to early studies and very limited meta-analyses, which have been superseded by more recent work. However, the bottom line that there is only slim evidence of efficacy for most interventions, including mebeverine, bran and bulking agents is an important message. Interestingly, Spiller concentrated on hypnosis as the most valuable 'psychological' modality of treatment in IBS. He emphasised the importance of chronic life stresses and continuing difficulties in the maintenance of IBS symptoms and the reasonable evidence of efficacy of anti-depressants in IBS, although once again good quality primary care trials are lacking. Gut-directed hypnotherapy, particularly as undertaken in Peter Whorwell's unit in Manchester, is particular efficacious and there is now good evidence of enduring efficacy. Cognitive behaviour therapy is also emerging as a useful treatment modality in IBS. Finally, Robin Spiller reviewed the importance of 5HT in gut function and the likely contribution that 5HT3 antagonists and 5HT4 agonists may make to the management of IBS in the future. Both promising 5HT3-active agents are currently unavailable but interest in the management of IBS is high, which means that there are real opportunities for primary care research into diagnosis and management." http://www.pcsg.org.uk/html/GIP/gip02/7thWyethEndoSymp.html


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## eric (Jul 8, 1999)

second you are extremely biased in what yu post and interpret from the links you provide.Dr DrossmanThe "Organification" of Functional GI Disorders:Implications for Research"mucosal inflammation could alter neurotransmitter, ion channel, or nerve growth factor activity and early gene expression, all of which might *influence* motility and visceral sensation; distention of in series tension-sensitive mechanoreceptors in the proximal gastric fundus may lead to dyspeptic symptoms; animal models now exist to show that chemical stimulation of gut mucosa alters visceral sensitivity, and can even be modified via descending input from higher brain centers; and early genetic studies suggest that 5HT or G-protein receptor polymorphisms may help explain the variability in the clinical expression of irritable bowel syndrome (IBS) or in the response to pharmacological agents. "5ht serotonin once again!as well as"Thus, as perhaps most clinicians know, it is not likely that an altered gene or set of specific biological etiologies will explain these complex human disorders, let alone their treatments. Furthermore, if there were major breakthroughs in basic or translational research, their clinical application may take years, if not decades, to bear relevancy. There are major health care needs that need to be addressed now. For the moment, the clinician must appraise, within a clinical context, the degree to which any of several physiological determinants (e.g., visceral hypersensitivity, dysmotility, postinfectious inflammation, psychosocial factors, or any combination) explain the clinical presentation, and this will determine the proper set of treatments.So if knowledge of the basic mechanisms of GI motor and neuroenteric function is not sufficient to explain the complexity of these human illnesses and does not currently meet the needs of clinicians or their patients, what else can be done? What is also needed is good clinical research that seeks to understand the biopsychosocial interactions affecting the illness experience and health behaviors of our patients, and applies this information in treatment. This would include: research on the biological and physiological (gut and brain) influences on symptom experience and behavior and the factors that modulate these outcomes; the study of coping and adaptation to chronic illness, outcome, and health services research to help physicians identify more efficient and economic treatment methods for patients; clinical trials of pharmaceutical and behavioral treatments to reduce symptoms and improve quality of life; research on educational methods to help health care providers become more efficient, compassionate, and knowledgeable about their patients; and helping patients find the ways to help themselves. " http://www.med.unc.edu/medicine/fgidc/organification.htm


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## eric (Jul 8, 1999)

second you are extremely biased in what yu post and interpret from the links you provide.Dr DrossmanThe "Organification" of Functional GI Disorders:Implications for Research"mucosal inflammation could alter neurotransmitter, ion channel, or nerve growth factor activity and early gene expression, all of which might *influence* motility and visceral sensation; distention of in series tension-sensitive mechanoreceptors in the proximal gastric fundus may lead to dyspeptic symptoms; animal models now exist to show that chemical stimulation of gut mucosa alters visceral sensitivity, and can even be modified via descending input from higher brain centers; and early genetic studies suggest that 5HT or G-protein receptor polymorphisms may help explain the variability in the clinical expression of irritable bowel syndrome (IBS) or in the response to pharmacological agents. "5ht serotonin once again!as well as"Thus, as perhaps most clinicians know, it is not likely that an altered gene or set of specific biological etiologies will explain these complex human disorders, let alone their treatments. Furthermore, if there were major breakthroughs in basic or translational research, their clinical application may take years, if not decades, to bear relevancy. There are major health care needs that need to be addressed now. For the moment, the clinician must appraise, within a clinical context, the degree to which any of several physiological determinants (e.g., visceral hypersensitivity, dysmotility, postinfectious inflammation, psychosocial factors, or any combination) explain the clinical presentation, and this will determine the proper set of treatments.So if knowledge of the basic mechanisms of GI motor and neuroenteric function is not sufficient to explain the complexity of these human illnesses and does not currently meet the needs of clinicians or their patients, what else can be done? What is also needed is good clinical research that seeks to understand the biopsychosocial interactions affecting the illness experience and health behaviors of our patients, and applies this information in treatment. This would include: research on the biological and physiological (gut and brain) influences on symptom experience and behavior and the factors that modulate these outcomes; the study of coping and adaptation to chronic illness, outcome, and health services research to help physicians identify more efficient and economic treatment methods for patients; clinical trials of pharmaceutical and behavioral treatments to reduce symptoms and improve quality of life; research on educational methods to help health care providers become more efficient, compassionate, and knowledgeable about their patients; and helping patients find the ways to help themselves. " http://www.med.unc.edu/medicine/fgidc/organification.htm


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## Talissa (Apr 10, 2004)

> quote:You said you disagree with Dr Drossman and Inflammation.You said you disagree with Dr Mayer, tht just inflammation in the gut is not a plausible mechansims to cause pain in all IBS patients.You said you disagree with Dr WHite head.


Why, why, why?...Do you say I say things which I've never said?I only question Dr Drossman's impartiality. I think as a psychiatrist, his studies lean toward that end and his conclusions are conveniently in line with the pharm's goal of selling us drugs and raking in $$$...I think that those, what 6 pharmaceutical companies?(ie, Lilly) for whom he "consults" which also market SSRI's make him biased...But like with Solvay & this new drug he's helped develop for IBS-D, his Rx influence extends beyond SSRI's. He's one busy guy!I only disagree with the wild absolutes you throw around here, the faulty conclusions you draw, when all the answers re:IBS are far from being answered...I say I disagree with YOU and you read it as me disagreeing with Dr Drossman...as a shrink, I wonder what he would think of that???


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## Talissa (Apr 10, 2004)

> quote:You said you disagree with Dr Drossman and Inflammation.You said you disagree with Dr Mayer, tht just inflammation in the gut is not a plausible mechansims to cause pain in all IBS patients.You said you disagree with Dr WHite head.


Why, why, why?...Do you say I say things which I've never said?I only question Dr Drossman's impartiality. I think as a psychiatrist, his studies lean toward that end and his conclusions are conveniently in line with the pharm's goal of selling us drugs and raking in $$$...I think that those, what 6 pharmaceutical companies?(ie, Lilly) for whom he "consults" which also market SSRI's make him biased...But like with Solvay & this new drug he's helped develop for IBS-D, his Rx influence extends beyond SSRI's. He's one busy guy!I only disagree with the wild absolutes you throw around here, the faulty conclusions you draw, when all the answers re:IBS are far from being answered...I say I disagree with YOU and you read it as me disagreeing with Dr Drossman...as a shrink, I wonder what he would think of that???


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## eric (Jul 8, 1999)

Next once again you quote dr Mayer, yet disagree with his theories? What is that all about, even that article posted important information, between inflammatory bowel disease and IBS. Inflammation may help to indentify certain subgroups of IBS patients for specific treatments, NOT ALL, but certain subtypes, for example PI IBS patinets.One of the newer drugs being developed for inflammation in IBS and mast cells, is for stress hormones, via CRH a stress hormone released from the HPA axis that down regulates and can cause mast cell degrandulation and inflammation from chronic stress.Second. You disagree with a newer article that the same author wrote that inflammation in IBS cannot be a plausible mechanism for pain in IBS, without the brain impairment seen in IBS. I can also tell you that more info on this has not been released, but will be soon. "The pathophysiology of irritable bowel syndrome.Schwetz I, Bradesi S, Mayer EA.Center of Neurovisceral Sciences and Women's Health (CNS),, Division of Digestive Diseases and Brain Research Institute, Department of Medicine, Los Angeles, CA, USA.Recent studies have provided evidence to suggest a possible role for mucosal immune activation in the pathophysiology of irritable bowel syndrome (IBS). On the other hand, novel findings using functional brain-imaging techniques support the concept that altered perception of visceral stimuli plays a key role in IBS symptom generation. These seemingly contradictory findings have revived the discussion about the relative contribution of peripheral versus central mechanisms in the symptom generation of IBS. In this review, we will provide evidence for the hypothesis that, in the absence of changes in visceral perception and alterations in endogenous pain modulation systems, chronic inflammatory mucosal changes in the gut are not a plausible mechanism to explain the presence of chronic abdominal pain, a clinical hallmark of IBS.""http://www.minervamedica.it/index2.t?show=R10Y2004N05A0419Not sure if this would work for everyone...it is a link to the journal and the abstract there is in italian, but the .pdf link on the bottom gives me the whole article in English.K."I am done with this thread now, unless you even know who all these IBS experts are and many more of them, a lot of them world experts in their fields and what there research is totally about and the bigger picture of all research in IBS. And your disagreement and a lot of times, flat out wrong interpretations on the research, with almost all of these experts. I cannot seriously continue this discussion, before you learn even the basic science on IBS, before trying to interpret very complex theories and brain gut mechanisms. Which I have to add personally belive I think is a shame since I really see and active part on your behalf in trying to fully research and understand IBS. I believe before you joined this group, it is quite likely you did not know who Dr Drossman was, or Dr Spiller, or Dr Mayer, Or Dr Whitehead, or Dr Gershon the doctor who discovered serotonin in the digestive tract and how it operates gut function, or Dr Ester Sternberg, or Dr Talley, Dr Lin Chang, Dr Wood the doctor who coined "the brain in the gut", Dr Michael Camilleri, Dr Palsson, Dr Peter J. Whorwell and many others attending from around the world. http://www.ibsgroup.org/cgi-local/ubbcgi/u...b=newtopic;f=10


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## eric (Jul 8, 1999)

Next once again you quote dr Mayer, yet disagree with his theories? What is that all about, even that article posted important information, between inflammatory bowel disease and IBS. Inflammation may help to indentify certain subgroups of IBS patients for specific treatments, NOT ALL, but certain subtypes, for example PI IBS patinets.One of the newer drugs being developed for inflammation in IBS and mast cells, is for stress hormones, via CRH a stress hormone released from the HPA axis that down regulates and can cause mast cell degrandulation and inflammation from chronic stress.Second. You disagree with a newer article that the same author wrote that inflammation in IBS cannot be a plausible mechanism for pain in IBS, without the brain impairment seen in IBS. I can also tell you that more info on this has not been released, but will be soon. "The pathophysiology of irritable bowel syndrome.Schwetz I, Bradesi S, Mayer EA.Center of Neurovisceral Sciences and Women's Health (CNS),, Division of Digestive Diseases and Brain Research Institute, Department of Medicine, Los Angeles, CA, USA.Recent studies have provided evidence to suggest a possible role for mucosal immune activation in the pathophysiology of irritable bowel syndrome (IBS). On the other hand, novel findings using functional brain-imaging techniques support the concept that altered perception of visceral stimuli plays a key role in IBS symptom generation. These seemingly contradictory findings have revived the discussion about the relative contribution of peripheral versus central mechanisms in the symptom generation of IBS. In this review, we will provide evidence for the hypothesis that, in the absence of changes in visceral perception and alterations in endogenous pain modulation systems, chronic inflammatory mucosal changes in the gut are not a plausible mechanism to explain the presence of chronic abdominal pain, a clinical hallmark of IBS.""http://www.minervamedica.it/index2.t?show=R10Y2004N05A0419Not sure if this would work for everyone...it is a link to the journal and the abstract there is in italian, but the .pdf link on the bottom gives me the whole article in English.K."I am done with this thread now, unless you even know who all these IBS experts are and many more of them, a lot of them world experts in their fields and what there research is totally about and the bigger picture of all research in IBS. And your disagreement and a lot of times, flat out wrong interpretations on the research, with almost all of these experts. I cannot seriously continue this discussion, before you learn even the basic science on IBS, before trying to interpret very complex theories and brain gut mechanisms. Which I have to add personally belive I think is a shame since I really see and active part on your behalf in trying to fully research and understand IBS. I believe before you joined this group, it is quite likely you did not know who Dr Drossman was, or Dr Spiller, or Dr Mayer, Or Dr Whitehead, or Dr Gershon the doctor who discovered serotonin in the digestive tract and how it operates gut function, or Dr Ester Sternberg, or Dr Talley, Dr Lin Chang, Dr Wood the doctor who coined "the brain in the gut", Dr Michael Camilleri, Dr Palsson, Dr Peter J. Whorwell and many others attending from around the world. http://www.ibsgroup.org/cgi-local/ubbcgi/u...b=newtopic;f=10


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## flux (Dec 13, 1998)

> quote: I'm against researchers working on the behalf of pharmaceutical companies as opp to working on patients behalf. I'm ag researchers hiding or downplaying side effects in order to meet the demands of their benefactors who only want to make huge profits.


Can you name one such researcher?


> quote:I think that those, what 6 pharmaceutical companies?(ie, Lilly) for whom he "consults" which also market SSRI's make him biased..


How does that make him biased?


> quote:I say I disagree with YOU and you read it as me disagreeing with Dr Drossman


Doesn't the fact that you think he is biased make *you* biased about judging your position relative to his?


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## flux (Dec 13, 1998)

> quote: I'm against researchers working on the behalf of pharmaceutical companies as opp to working on patients behalf. I'm ag researchers hiding or downplaying side effects in order to meet the demands of their benefactors who only want to make huge profits.


Can you name one such researcher?


> quote:I think that those, what 6 pharmaceutical companies?(ie, Lilly) for whom he "consults" which also market SSRI's make him biased..


How does that make him biased?


> quote:I say I disagree with YOU and you read it as me disagreeing with Dr Drossman


Doesn't the fact that you think he is biased make *you* biased about judging your position relative to his?


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## Talissa (Apr 10, 2004)

PS...I've never said I think low grade inflammation exists in ALL IBS patients...that has yet to be determined.But it does exist in MANY, from what I've read. For example, it's being found in IBS-D as well as in IBS-C now as cited in the above article: http://www.pulsus.com/Gastro/18_10/andr_ed.htm You've also quoted from the above article on a diff thread.And you said to me: "second you are extremely biased in what yu post "No, I just stay on topic. I'm not writing a full dissertation on IBS every time I post.Why is it a dare utter the obvious truism that there are some things we'll never agree on and you can't just agree with even that? We've already had these arguments. Don't you feel like the crazy fly beat up against the burning lightbulb. Are you thinking that by doing the same thing over & over you'll get a diff result? You know what THAT's supposed to mean...if not I'm betting Drossman does.


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## Talissa (Apr 10, 2004)

PS...I've never said I think low grade inflammation exists in ALL IBS patients...that has yet to be determined.But it does exist in MANY, from what I've read. For example, it's being found in IBS-D as well as in IBS-C now as cited in the above article: http://www.pulsus.com/Gastro/18_10/andr_ed.htm You've also quoted from the above article on a diff thread.And you said to me: "second you are extremely biased in what yu post "No, I just stay on topic. I'm not writing a full dissertation on IBS every time I post.Why is it a dare utter the obvious truism that there are some things we'll never agree on and you can't just agree with even that? We've already had these arguments. Don't you feel like the crazy fly beat up against the burning lightbulb. Are you thinking that by doing the same thing over & over you'll get a diff result? You know what THAT's supposed to mean...if not I'm betting Drossman does.


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## Talissa (Apr 10, 2004)

Flux, I'd respond to your comments but you're just too freaky for me.{{{shudder}}}


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## Talissa (Apr 10, 2004)

Flux, I'd respond to your comments but you're just too freaky for me.{{{shudder}}}


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## Talissa (Apr 10, 2004)

Eric, I said I disagree with many of your absolutes, based on faulty conclusion, that aren't proven--I NEVER said I disagree with these doctors. Most of the doctors are circumspect enough to also say more studies are needed and there's still much to learn.Something you never do.


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## Talissa (Apr 10, 2004)

Eric, I said I disagree with many of your absolutes, based on faulty conclusion, that aren't proven--I NEVER said I disagree with these doctors. Most of the doctors are circumspect enough to also say more studies are needed and there's still much to learn.Something you never do.


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## eric (Jul 8, 1999)

You read this nwer Dr Mayer article and disagreed, its on this thread.You disagreed with Dr Drossman and inflammation not be a biological marker in all IBS patinets on numerous threads. You also misinterpreted what the rome diagnostics meant in reagrds to specific abnormalities seen in IBS, when IBS and Rome is based on symptoms, because there is no unifying marker in ALL IBSers yet. So they cannot diagnose IBS based on just abnormalities yet. The exact cause is not known, just that they see many abnormalities and have divided IBS into different subgroups, with different pathologies, all leading to altered motility, viceral hypersensitivity and brain gut axis dysfunction, all of which are a part of or contribute to IBS symptoms. Many of the functional disorders also overlap, as well as causing many non gi symptoms, as well as being seen a lot in fibro, CFIS, and irritable bladder to name a few.And more disagreement, I am not going to waste my time looking up through all the threads, on the bb.Talissa, my website is listed on the iffgd website and the UNC website, and Dr Drossman and Dr Whithead, evaluated it before adding it.The IFFGD also evaulated my website and added it to there website. They know who I am for sure.Your error in thinking Dr Drssoman is only a psychiatrist is very much wrong again.Please read his bio carefully this time."Dr. Drossman is Professor of Medicine and Psychiatry at the UNC School of Medicine, Division of Gastroenterology & Hepatology. He has had a long-standing interest in the research and evaluation of difficult to diagnose and treat GI disorders. He established a program of research in functional GI disorders at UNC more than 25 years ago and has published more than 350 books, articles and abstracts relating to epidemiology, psychosocial and quality of life assessment, design of treatment trials, and outcomes of research in GI disorders. He has also published two books, a GI procedures manual, and a textbook on FGIDs (Rome I and Rome II editions)." http://www.med.unc.edu/wrkunits/2depts/med...dc/drossman.htm Or what he believes, you don't even know him, yet accuse him of things that are again flat out wrong. He constantly promotes natural ways to treat IBS before drugs are used. A major focus on their center is on natural and safe ways to treat IBS first and for most, with drugs prescribe for specific reasons or as a last resort. full text 6th International Symposium on FUNCTIONAL GASTROINTESTINAL DISORDERS http://www.ibsgroup.org/cgi-local/ubbcgi/u...c;f=10;t=001028


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## eric (Jul 8, 1999)

You read this nwer Dr Mayer article and disagreed, its on this thread.You disagreed with Dr Drossman and inflammation not be a biological marker in all IBS patinets on numerous threads. You also misinterpreted what the rome diagnostics meant in reagrds to specific abnormalities seen in IBS, when IBS and Rome is based on symptoms, because there is no unifying marker in ALL IBSers yet. So they cannot diagnose IBS based on just abnormalities yet. The exact cause is not known, just that they see many abnormalities and have divided IBS into different subgroups, with different pathologies, all leading to altered motility, viceral hypersensitivity and brain gut axis dysfunction, all of which are a part of or contribute to IBS symptoms. Many of the functional disorders also overlap, as well as causing many non gi symptoms, as well as being seen a lot in fibro, CFIS, and irritable bladder to name a few.And more disagreement, I am not going to waste my time looking up through all the threads, on the bb.Talissa, my website is listed on the iffgd website and the UNC website, and Dr Drossman and Dr Whithead, evaluated it before adding it.The IFFGD also evaulated my website and added it to there website. They know who I am for sure.Your error in thinking Dr Drssoman is only a psychiatrist is very much wrong again.Please read his bio carefully this time."Dr. Drossman is Professor of Medicine and Psychiatry at the UNC School of Medicine, Division of Gastroenterology & Hepatology. He has had a long-standing interest in the research and evaluation of difficult to diagnose and treat GI disorders. He established a program of research in functional GI disorders at UNC more than 25 years ago and has published more than 350 books, articles and abstracts relating to epidemiology, psychosocial and quality of life assessment, design of treatment trials, and outcomes of research in GI disorders. He has also published two books, a GI procedures manual, and a textbook on FGIDs (Rome I and Rome II editions)." http://www.med.unc.edu/wrkunits/2depts/med...dc/drossman.htm Or what he believes, you don't even know him, yet accuse him of things that are again flat out wrong. He constantly promotes natural ways to treat IBS before drugs are used. A major focus on their center is on natural and safe ways to treat IBS first and for most, with drugs prescribe for specific reasons or as a last resort. full text 6th International Symposium on FUNCTIONAL GASTROINTESTINAL DISORDERS http://www.ibsgroup.org/cgi-local/ubbcgi/u...c;f=10;t=001028


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## Talissa (Apr 10, 2004)

> quote:Your error in thinking Dr Drssoman is only a psychiatrist is very much wrong again.


I didn't say that.I said "as a psychiatrist". He is also, well, you already said, but I was addressing that particular aspect of who he is, not giving his bio...Faulty conclusions. This is the problem.And using old info when newer info has come out making it questionable.


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## Talissa (Apr 10, 2004)

> quote:Your error in thinking Dr Drssoman is only a psychiatrist is very much wrong again.


I didn't say that.I said "as a psychiatrist". He is also, well, you already said, but I was addressing that particular aspect of who he is, not giving his bio...Faulty conclusions. This is the problem.And using old info when newer info has come out making it questionable.


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## flux (Dec 13, 1998)

> quote:And using old info when newer info has come out making it questionable.


When has that happened? Or this something that you are predicting will happen? How long do we wait?


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## flux (Dec 13, 1998)

> quote:And using old info when newer info has come out making it questionable.


When has that happened? Or this something that you are predicting will happen? How long do we wait?


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## eric (Jul 8, 1999)

FYIDiagnosis, Pathophysiology, and Treatment of Irritable Bowel Syndrome "Pathophysiology of IBSThe pathophysiology of IBS is a work in progress. Roughly 200 years after its initial description by the English physician William Powell, our understanding of what causes IBS symptoms remains incompletely understood. For most of the second half of the 20th century, tremendous attention was paid to the concept of altered gut motility as a cause of IBS symptoms.20 However, several difficulties are apparent in this approach. *First, although altered motility of the colon and small bowel can be demonstrated in patients with IBS, there is a very poor correlation between IBS symptomatology and the presence of alterations in gastrointestinal motility.* 21 *Likewise, drugs that alter gastrointestinal motility alone, such as antispasmodic22,23 and prokinetic drugs like metoclopramide and cisapride,24,25 have not been shown to be of any significant benefit in relieving IBS symptoms.* The third dilemma facing investigators in this area is that no pathognomonic pattern of gut dysmotility can be identified specifically with IBS, as opposed to other functional or organic disorders of the gut.20 *Altered motility, as occurs in IBS, is currently seen as one of many epiphenomena associated with the disorder, as opposed to being a cause of the disorder itself.* *In the early 1980s, it was discovered that upon balloon distention in the rectum, individuals suffering from IBS were more sensitive to distention than were individuals who did not suffer from IBS.26 This means that IBS patients feel discomfort at lower levels of balloon inflation in the rectum and lower bowel than do normal controls.* *This finding has been replicated in numerous studies, and the concept of "visceral" hypersensitivity has been established.27 A second level of investigation in this area is the fascinating finding that individuals with IBS not only have a unique local response (in the rectum) to visceral stimulation, but they also tend to process signals in the brain differently from non-IBS controls. Mertz and others[27] have shown that IBS patients have differential responses in the anterior cingulate cortex and other areas of the brain when stimulated with rectal or sigmoid colon distention, compared with controls.* *These findings have been replicated by other investigators.28 These data certainly suggest the possibility of a "brain-gut axis" where peripheral symptoms are processed in the end organ (ie, the colon), and then neural signals are carried via visceral afferents to the spinal cord, and then to the brain, where they are subject to additional processing.* 29 *It is this brain-gut axis that has received considerable attention recently in IBS research. The findings of enhanced visceral sensitivity in the colon and rectum, as well as altered processing of signals in the brain, have provided new insight. Regarding the pathophysiology of IBS, the altered processing of neural sensation in IBS patients logically raises the question as to which neurotransmitters play a role in this abnormal signal transmission."* http://www.cfids-cab.org/cfs-inform/Ibs/ibs.medscape03.htm


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## eric (Jul 8, 1999)

FYIDiagnosis, Pathophysiology, and Treatment of Irritable Bowel Syndrome "Pathophysiology of IBSThe pathophysiology of IBS is a work in progress. Roughly 200 years after its initial description by the English physician William Powell, our understanding of what causes IBS symptoms remains incompletely understood. For most of the second half of the 20th century, tremendous attention was paid to the concept of altered gut motility as a cause of IBS symptoms.20 However, several difficulties are apparent in this approach. *First, although altered motility of the colon and small bowel can be demonstrated in patients with IBS, there is a very poor correlation between IBS symptomatology and the presence of alterations in gastrointestinal motility.* 21 *Likewise, drugs that alter gastrointestinal motility alone, such as antispasmodic22,23 and prokinetic drugs like metoclopramide and cisapride,24,25 have not been shown to be of any significant benefit in relieving IBS symptoms.* The third dilemma facing investigators in this area is that no pathognomonic pattern of gut dysmotility can be identified specifically with IBS, as opposed to other functional or organic disorders of the gut.20 *Altered motility, as occurs in IBS, is currently seen as one of many epiphenomena associated with the disorder, as opposed to being a cause of the disorder itself.* *In the early 1980s, it was discovered that upon balloon distention in the rectum, individuals suffering from IBS were more sensitive to distention than were individuals who did not suffer from IBS.26 This means that IBS patients feel discomfort at lower levels of balloon inflation in the rectum and lower bowel than do normal controls.* *This finding has been replicated in numerous studies, and the concept of "visceral" hypersensitivity has been established.27 A second level of investigation in this area is the fascinating finding that individuals with IBS not only have a unique local response (in the rectum) to visceral stimulation, but they also tend to process signals in the brain differently from non-IBS controls. Mertz and others[27] have shown that IBS patients have differential responses in the anterior cingulate cortex and other areas of the brain when stimulated with rectal or sigmoid colon distention, compared with controls.* *These findings have been replicated by other investigators.28 These data certainly suggest the possibility of a "brain-gut axis" where peripheral symptoms are processed in the end organ (ie, the colon), and then neural signals are carried via visceral afferents to the spinal cord, and then to the brain, where they are subject to additional processing.* 29 *It is this brain-gut axis that has received considerable attention recently in IBS research. The findings of enhanced visceral sensitivity in the colon and rectum, as well as altered processing of signals in the brain, have provided new insight. Regarding the pathophysiology of IBS, the altered processing of neural sensation in IBS patients logically raises the question as to which neurotransmitters play a role in this abnormal signal transmission."* http://www.cfids-cab.org/cfs-inform/Ibs/ibs.medscape03.htm


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