# Tapes and Meds



## partypooper (Mar 22, 2000)

I have typed this out 4 times now, and it will not post. I hope it works this time! I saw my GI last week and gave her a progress report. I told her that I have been doing much better since October when I started imipramine and Mikes tapes. In fact, my D has been so MUCH better that sometimes I am even a little bit C.My GI wants me to taper off my meds now. She thinks that I have a case of "post-infectious IBS" and that my body will heal itself over time. The thought of going down on my meds scares me. Should I relisten to Mike's tapes while reducing? I am worried about a relapse. Also, has anyone here gotten off IBS meds and maintained their remission through tapes or other methods? If so, I would love to hear from you and how you did it. Thanks........


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## Kathleen M. (Nov 16, 1999)

I had a big reduction in my medication needs while on CBT. Right now I'm trying to see if I can go med free using Mike's Tapes.Basically since 1998 when I did the CBT I went from 15 mgs Buspar 2X a day to 15mgs 1X a day by the time I ended the CBT.I've gotten better since then and I'm now been doing 7.5 mgs Buspar each night. And I seem to be doing OK. I'm about 1/2 way ish through the tapes, coming up on the big 50 and I'm thinking of cutting the pills in thirds when I get my next batch (they are scored for cut in 1/2 and cut in 1/3) and see if the 5 mgs will work. Then if that's OK when I finish the tapes I'll try without.It may work for you to do something similar, try cutting the dose slowly and see how it goes. That way you can go back up if you need it.It might not be a bad idea to go through the tapes again (or at least do your favorites) during the weaning off period.K.------------------I have no financial, academic, or any other stake in any commercial product mentioned by me.My story and what worked for me in greatly easing my IBS: http://www.ibsgroup.org/ubb/Forum17/HTML/000015.html


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## AZmom1 (Dec 6, 1999)

Probably a good idea to do the tapes while tapering. Interesting that your Dr. is not giving credit to hypnotherapy. Typical. I've started the tapes again after being done for about a year. Doing great and really enjoying them. AZ


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## eric (Jul 8, 1999)

Az, I did not get from the post the doctor didn't give hypno credit?Partypooper what did your doctor say about it?Anyway, I have given up all meds. for IBS. ### years of valium done deal.The effects of the hypnosis are lasting so put some trust in yourself. I had a hard time with this also at first, that I was better and not use to it. The way to find out is to cut back the meds with the doctors help and seee how you do. I have found a set back occasionally,usally I can trace the cause and they are no where near as severe, and I rebound right back to better and it has been almost two years since I did the IBS tapes.I still highly recommend practicing everyday however and I also recommend continued listening to the tapes to help at any time and reinforce the process.I am glad your doing better partypooper and trust and work with the progress you have made.







One thing how long have you had this, because post infectious IBS would be somebody who has not had this a while. It would be great and it does happen that some people just get better for no reason,but they usally still have IBS in someways.------------------I work with Mike and the IBS Audio Program. www.ibshealth.com www.ibsaudioprogram.com


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## partypooper (Mar 22, 2000)

Thanks for all of the feedback, guys!I think it is really encouraging that several BB members have gone med-free with the help pf Mike's tapes and still feel good. Hopefully, I will be one of these folks in several months.I believe that my doc thinks that the imipramine and hypno have helped. She also thinks that time will help the healing process too. I have had bad IBS-D for about 19 months which started after an acute bout of food poisoning, so bad that it resulted in my hospitalization for 3 days. She says that a significant percentage of her IBS patients really have "post-infectious IBS" and that these individuals usually experience a significant improvement in their symptoms in about 18 months to 2 years. I have acutally had two other GIs (one in California and one at the Mayo Clinic) say almost the exact same thing except that the time frame range for improvement was 2 to 3 years. Interesting that I have not read anything on the BB where someone else's doc said something similar to this, and yet I have heard it three times from three unrelated GI specialists. So is there any particular order (or frequency) in which I should relisten to Mike's tapes? Should I do the whole sequence again?Thanks!


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## eric (Jul 8, 1999)

Partypooper, very honestly doing the whole sequence again is probably optimal. However, listening to side two on occasion and picking your favorite tape would also help.Here is something on Post infectious IBS you might take to them and ask about. The link and this article. http://www.gastro.org/reuters/2000/July/17...713scie001.html Digestive Disease Week 2000Day 3 - May 23, 2000 Irritable Bowel Syndrome: A Postinfectious andInflammatory Disorder?Nicholas J. Talley, MD, PhD The pathophysiology of the functional gastrointestinal disorders remains obscure, but there is increasing evidence that, in at least a subset of patients, infection and inflammation may play key roles.[1] After an episode of severe gastroenteritis requiring hospitalization, it has been observed that approximately 1 in 4 patients has long-standing irritable bowel syndrome (IBS)-like symptoms on follow-up 6 months later.[2,3] A topic forum was therefore devoted to infection and inflammation in functional bowel disease. A number of other key abstracts were also presented on this topic, and a review of the new data and the clinical implications will be highlighted. Can Infection Change Gut Sensory Perception? It is established that patients with IBS usually have visceral hypersensitivity, particularly in the colon, although pan-gut involvement has been documented. A key question is whether infection can directly alter colonic sensory pathways. A useful model developed in mice involves infection with the parasite Trichomonas spiralis, which results in neuromuscular abnormalities in both the colon and small bowel that persist despite healing of the initial injury and loss of the organism.[1] Dr. Yukang Mao and colleagues from McMaster University in Hamilton, Ontario, Canada, examined the acute and chronic effects of T spiralis on colonic sensory function by measuring the dorsal root ganglion single-unit discharges in adult male NIH Swiss mice.[4] The investigators placed a latex balloon in the colon distally following the introduction of T spiralis. There was jejunal enteritis at 6 days postinfection, which returned to normal in 28 days. There were no T spiralis remaining in the bowel after 3 weeks. The investigators found postinfection hyperalgesic sensory response following distension of the colon that persisted despite healing of the acute inflammation. Furthermore, the authors were able to show that the induced response was blocked by a neurokinin (NK)-1 receptor antagonist (SR140333). The results confirm that postinfection inflammation can alter visceral sensitivity and imply that NK-1 antagonists may be therapeutically useful in this situation. There is increasing interest in NK receptor antagonists as visceral analgesics,[5] and these drugs are currently being tested in IBS. Is There Evidence of Increased Inflammation in IBS? Direct evidence of an active inflammatory component in IBS remains to be confirmed. Earlier reports suggested that there is a small, albeit significant, quantitative increase of colonic inflammatory cells in patients with IBS as well as an increase in terminal ileal mast cells.[1,6] More direct evidence has become available during this year's DDW. Dr. Maria A O'Sullivan and colleagues from Dublin, Ireland, aimed to determine whether there is evidence of increased inducible nitric oxide (NO) synthase (iNOS) and nitrotyrosine (NT) in IBS.[7] Nitric oxide is known to have a number of effects on gastrointestinal function, and increased infiltration of mast cells could potentially be effectors of nitric oxide generation. They studied 11 patients with IBS, 4 normal controls, and 3 with inactive inflammatory bowel disease of the colon. Biopsies from the colon were stained for iNOS and NT by applying validated immunohistochemistry and quantified image analysis techniques. Of interest, compared with the controls, both iNOS and NT were significantly increased in IBS at all colonic sites except the rectum. Not surprising, those with inactive colitis had more iNOS than IBS, although this was not significant. The other observation of interest was that iNOS was colocalized with B and T cells in IBS. The results imply that B cells and T cells are activated, and via nitric oxide release may be mediators of functional changes in IBS. An important poster from Dr. Hans Tornblom and colleagues[8] from the University of Lund in Malmo, Sweden, reported direct evidence of inflammation in IBS. They examined 6 patients with documented, severe IBS. These patients fulfilled the Rome criteria and had normal antro-duodenal manometry, implying they were not misdiagnosed cases of chronic idiopathic intestinal pseudo-obstruction. At laparoscopy, full-thickness biopsies from the proximal jejunum were obtained. In all 6 patients, inflammatory infiltration of lymphocytes in the myenteric plexus was observed. These lymphocytes were situated in peri- and intraganglionic locations. The authors also noted hypertrophy of the longitudinal muscle layer in 4 patients and abnormalities in the interstitial cells of the Cajal (the pacemakers of the gut) in 5 patients. These results are provocative. The major concern remains misdiagnosis of pseudo-obstruction. Furthermore, it is unclear whether these results can be generalized to all IBS patients. At the distinguished abstract plenary session on Monday, Dr. Joyce Chan and colleagues, from Manchester, United Kingdom, reported further provocative evidence supporting a direct role for inflammation in IBS.[9] In ulcerative colitis, it has been reported that lower amounts of the anti-inflammatory cytokine interleukin (IL)-10 is produced and this is associated with a reduced frequency of the -1082*G allele. The authors therefore postulated that in IBS there would be a reduced frequency of the IL-10 allele as is observed in ulcerative colitis. This hypothesis was tested by extracting DNA from the peripheral blood leukocytes of 140 IBS patients. The genotypes for IL-10 as well as other inflammatory cytokines were determined using standardized techniques. Of great interest, the IL-10 -1082*G allele was significantly reduced in IBS patients compared with healthy controls. Similarly, the TGF-beta high producer (+915*G allele) was reduced in IBS vs controls. The authors speculate that high production of anti-inflammatory cytokines may protect against IBS, but those who are genetically predisposed to lower amounts may be more likely to develop the condition. As there is other evidence supporting a genetic predisposition in IBS,[10] these results are exciting. Moreover, the findings may lead to the development of testable disease markers in IBS. Post-Campylobacter Enteritis and IBS Gwee and colleagues have previously established a relationship between Campylobacter enteritis and the subsequent risk of IBS.[2] The risk of IBS appears to be increased in those with psychological distress.[3] The exact role of bacterial virulence and the risk of IBS remains unknown. Dr. Thornley and coworkers from Nottingham, England, studied the effect of specific bacterial toxins and their relationship to outcome following Campylobacter enteritis.[11] They evaluated 188 patients who had clinically isolated Campylobacter species. Seventeen (9%) patients at 6 months met the Rome I criteria for IBS. The toxigenic effects of HEP-2, VERO, and CHO-K1 toxins were obtained by testing epithelial cell monolayers; the toxigenic effects were measured at 12 and 24 hours in duplicate. They observed that persistently altered bowel habit was more common in subjects with HEP-2 toxin positive infections, compared with those who were negative for this toxin, but this was not significant. There was no association with the CHO or VERO toxins. These results imply that bacterial factors are less important than presumably other largely unidentified host factors in the pathogenesis of postinfectious IBS. As there is increasing interest in potentially targeting those who develop acute bacterial gastroenteritis with prophylactic therapy to try and prevent the development of IBS (eg, with local steroids), these observations are potentially of major clinical relevance if confirmed. It is well established that patients with IBS have more psychiatric and psychological disturbances than non-IBS controls, although this may be explained at least in part by a healthcare-seeking bias (those presenting in tertiary care centers are more likely to have psychological disturbances that drive them to seek this level of care). Dr. Simeran and colleagues from Gothenburg, Sweden, investigated the relationship between psychological factors and IBS by studying patients with ulcerative colitis in remission.[12] It is known that IBS-like symptoms are more common in patients with IBS in remission (about one third) than in controls. The reasons for this relationship remain unclear. However, in view of the postinflammatory IBS hypothesis, this is a fruitful group of patients to study. The investigators evaluated 43 patients with ulcerative colitis and 40 with Crohn's disease in remission. IBS-like symptoms were reported in 33% of ulcerative colitis patients and 59% of Crohn's disease patients; results were similar in men and women. Those with IBS-like symptoms (compared with those who did not have IBS-like symptoms) had more anxiety and depression as well as lower psychological well-being, based on standardized psychological self-rating scales. The authors speculated that previous inflammation can result in persisting gut dysfunction, and psychological factors are important in mediating symptom persistence. However, it is also possible that distressing, persistent gut symptoms may alter psychological function and result in the association observed. Further studies of patients with inflammatory bowel disease in remission are indicated; these studies will need to include appropriate controls and preferably assess psychological status before and after disease onset (which will represent a challenge). Conclusions The results of these new studies are exciting. There appears to be increasing evidence that IBS and probably other functional gastrointestinal disorders are, at least in a subset, due to structural disease. Host and bacterial factors may both be important. The development of new disease markers appears likely from the novel work in progress. This in turn should lead to characterization of more homogenous groups of patients and the development of better-targeted therapeutic approaches (perhaps NK-1 antagonists). Clinicians should watch this space!------------------I work with Mike and the IBS Audio Program. www.ibshealth.com www.ibsaudioprogram.com


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## partypooper (Mar 22, 2000)

Thanks for the info, Eric. That article was particularly interesting.


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## Guest (Mar 24, 2001)

Hi All,Partp, I work with patients in med reduction as outlined by Kmottus. A gentle weaning off is the way to go. That way its managed and structured. Best RegardsMike


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