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I have heard that IBS could be related to hormones, i was just wondering if anyone else knew anything about this. I am taking a birth control to regulate my periods, i have been taking it since january, and it hasn't regulated me at all. in june i was diagnosed with IBS, and i was just wondering if maybe the birth control is making my symtoms worse. The pain is getting so severe and so frequent that it's beginning to affect my life. The pains started coming every morning this week, and they used to only come at night. Also, the pain moved into my lower back today, and it was very severe. So, i'm thinking about not taking my birth control, and i think that my medicine, hyoscyamine, may be what is causing me to get such severe pain in the morning. I just started this medicine last wednesday, and on tuesday morning, i got sick, and i have been sick everymorning since then. If you have any advice or any information, please let me know. I am trying to call my doctor, but he never returns my calls, and it's hard to go see him since i am 2 hours away from him at college, but i do have an appoinment scheduled in 2 weeks. Thanks for helping me out, i really appreciate it.
 

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From what I've read in books and what I've heard on this BB, hormones and "the pill" in particular can have a direct effect on IBS. The interaction between hormones and IBS is not well understood, but there have been a lot of posts on this if you want to use the search function above to search out past posts.
 

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From what I've read in books and what I've heard on this BB, hormones and "the pill" in particular can have a direct effect on IBS. The interaction between hormones and IBS is not well understood, but there have been a lot of posts on this if you want to use the search function above to search out past posts.
 

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hey. My IBS is absolutly hormone related. For the 10 days before my period, ANYTHING will set off an IBS attack. I'm not on the pill, but I do take Sarafem (Prozac by any other name) 10 days premenstrually to keep my insane PMS in check. I find that the Sarafem helps with the IBS, maybe just because it stops the stress, panic attacks, and depression that help set off my IBS in the first place, and it supresses my cravings for those funky foods that also trigger attacks. On the other hand, I also take hyoscyamine, and have never had a problem with it, so I can't help you, there.S
 

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hey. My IBS is absolutly hormone related. For the 10 days before my period, ANYTHING will set off an IBS attack. I'm not on the pill, but I do take Sarafem (Prozac by any other name) 10 days premenstrually to keep my insane PMS in check. I find that the Sarafem helps with the IBS, maybe just because it stops the stress, panic attacks, and depression that help set off my IBS in the first place, and it supresses my cravings for those funky foods that also trigger attacks. On the other hand, I also take hyoscyamine, and have never had a problem with it, so I can't help you, there.S
 

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I agree that hormones play a big roll in IBS. My IBS-CG all started when I was 12 years old. This was the time that I was starting puberty. You know the hormones going crazy. Well years later when I was pregnant I had morning sickness for the first three months. However I did not have any IBS-CG. I could live with the morning sickness. After the first 3 months and the hormones started to stabalize then I was back to IBS-CG again.
 

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I agree that hormones play a big roll in IBS. My IBS-CG all started when I was 12 years old. This was the time that I was starting puberty. You know the hormones going crazy. Well years later when I was pregnant I had morning sickness for the first three months. However I did not have any IBS-CG. I could live with the morning sickness. After the first 3 months and the hormones started to stabalize then I was back to IBS-CG again.
 

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The common link is leokotrienes (100 times more powerful than histamine) and prostaglandins, esp. PGE2. Eleveted PGE 2 levels in stool of cyclic IBS vticms as far back as 1980, and this and other immune-response mediators have been isolated in both the small bowel and blood stream of IBS victims numerous times since. This is non-allergic reactivity to food or chemicals, not food allergy response as those patients were deselected.So if a patient is prone to dysmenorrhea, adding more arachadonic acid metabolites atop the existing problem just makes it worse, and the severity will fluctuate as the levels of these chemicals fluctaute with the cycle. The way they fluctuate varies somewhat pre and post menopause, which can also have an effect.Here is one article which shows the metabolites linked to the menstrual cycle normall, and a bit about HETE and non-IBS comorbid dysmenorrhea, and another which is the very first time they found PGE2 in the cyclic IBS effluvia.So in patients with comorbid dysmenorrhea and cyclic or d-type IBS which will reduce or block the effects of prostaglandins will certainly reduce the intensity of symptoms produced by prostaglandins and leukotrienes. Since these have been shown actively released my the small bowel in response to food challenges in IBS patients WITHOUT food allergy, (in vitro and in vivo methods), the link between the gut immune system source of arachadonic acid metabolites and their known effects on the bowel and endometrium makes alot of sense. Esp. if you provoke a response at a time when Pg or leukotriene levels are normally high, or in a person predisposed to dysmenorrhea already.AGHHHH its a good but comples subject and I have to run.....since some other work starts linking the NK receptor effect and PAF and other mediators....anyway here is an abstract about the hormones in question then the abstract of the very first time PGE2 was found in the cyclic IBS effluvia. _____________________________: Gynecol Endocrinol 1995 Dec;9(4):307-12 Concentrations of various arachidonic acid metabolites in menstrual fluid are associated with menstrual pain and are influenced by hormonal contraceptives.Bieglmayer C, Hofer G, Kainz C, Reinthaller A, Kopp B, Janisch H.Institute for Medical and Chemical Laboratory Diagnostics, University Hospital, Vienna, Austria.In a pilot study we investigated the association between concentrations of various eicosanoids in menstrual blood with pain and oral contraceptive use. Menstrual fluid was collected on tampons by 12 women who did not use an oral contraceptive but suffered from slight primary dysmenorrhea and by three pain-free women who used an oral contraceptive. Eicosanoids (cyclooxygenase products: 6-ketoprostaglandin F1 alpha, thromboxane B2, prostaglandin E2, prostaglandin F2 alpha, 13,14-dihydro-15-ketoprostaglandin F2 alpha, 12-hydroxy-heptadecatrienoic acid; lipoxygenase products: 5-, 12-, 15-hydroxy-eicosatetraenoic acid (HETE), leukotriene B4, leukotriene C4, leukotriene D4, leukotriene E4) and female sex steroids (17 beta-estradiol and progesterone) were analyzed by the combined use of high-performance liquid chromatography and radioimmunoassay. 12-HETE was the main arachidonic acid metabolite. An increased metabolism of arachidonic acid was associated with pain, especially when synthesis of 12-HETE was elevated. Oral contraceptive use decreased the synthesis of prostaglandins as well as leukotrienes. The concordant changes of cyclooxygenase and lipoxygenase products in dysmenorrhea or in oral contraceptive use may be explained by an increased or decreased phospholipid metabolism, respectively. _____________________________Adv Prostaglandin Thromboxane Res 1980;8:1627-31 Related Articles, Books, LinkOut An approach to evaluation of local intestinal PG production and clinical assessment of its inhibition by indomethacin in chronic diarrhea. Bukhave K, Rask-Madsen J No abstract ON LINE..Summary of Findings:The connection between gut motility and prostaglandin release was studied. PGE2 levels in the jejunal secretions IBS patients were elevated in 10 of 17 with cyclic IBS (D & C) and in �gluten enteropathy�. Six IBS patients treated with indomethacin (INDOCIN: non-steroidal analgesic anti-inflammatory which works by inhibiting prostaglandins, which are inflammatory and pain mediators of various types) had a 50% reduction in stool volume and frequency. And withdrawal of the indocin caused the symptoms to return.Due to the absence of indicators of Type I inflammatory-allergic response, the authors said the findings suggested localized or gut-wall reactions . _____________________This also sort of makes sense out of how the BC Pills, by blocking formation of arachadonic acid metabolites, can affect both symptom sets.Eat well. Think well. Be well.MNL_________________ www.leapallergy.com
 

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The common link is leokotrienes (100 times more powerful than histamine) and prostaglandins, esp. PGE2. Eleveted PGE 2 levels in stool of cyclic IBS vticms as far back as 1980, and this and other immune-response mediators have been isolated in both the small bowel and blood stream of IBS victims numerous times since. This is non-allergic reactivity to food or chemicals, not food allergy response as those patients were deselected.So if a patient is prone to dysmenorrhea, adding more arachadonic acid metabolites atop the existing problem just makes it worse, and the severity will fluctuate as the levels of these chemicals fluctaute with the cycle. The way they fluctuate varies somewhat pre and post menopause, which can also have an effect.Here is one article which shows the metabolites linked to the menstrual cycle normall, and a bit about HETE and non-IBS comorbid dysmenorrhea, and another which is the very first time they found PGE2 in the cyclic IBS effluvia.So in patients with comorbid dysmenorrhea and cyclic or d-type IBS which will reduce or block the effects of prostaglandins will certainly reduce the intensity of symptoms produced by prostaglandins and leukotrienes. Since these have been shown actively released my the small bowel in response to food challenges in IBS patients WITHOUT food allergy, (in vitro and in vivo methods), the link between the gut immune system source of arachadonic acid metabolites and their known effects on the bowel and endometrium makes alot of sense. Esp. if you provoke a response at a time when Pg or leukotriene levels are normally high, or in a person predisposed to dysmenorrhea already.AGHHHH its a good but comples subject and I have to run.....since some other work starts linking the NK receptor effect and PAF and other mediators....anyway here is an abstract about the hormones in question then the abstract of the very first time PGE2 was found in the cyclic IBS effluvia. _____________________________: Gynecol Endocrinol 1995 Dec;9(4):307-12 Concentrations of various arachidonic acid metabolites in menstrual fluid are associated with menstrual pain and are influenced by hormonal contraceptives.Bieglmayer C, Hofer G, Kainz C, Reinthaller A, Kopp B, Janisch H.Institute for Medical and Chemical Laboratory Diagnostics, University Hospital, Vienna, Austria.In a pilot study we investigated the association between concentrations of various eicosanoids in menstrual blood with pain and oral contraceptive use. Menstrual fluid was collected on tampons by 12 women who did not use an oral contraceptive but suffered from slight primary dysmenorrhea and by three pain-free women who used an oral contraceptive. Eicosanoids (cyclooxygenase products: 6-ketoprostaglandin F1 alpha, thromboxane B2, prostaglandin E2, prostaglandin F2 alpha, 13,14-dihydro-15-ketoprostaglandin F2 alpha, 12-hydroxy-heptadecatrienoic acid; lipoxygenase products: 5-, 12-, 15-hydroxy-eicosatetraenoic acid (HETE), leukotriene B4, leukotriene C4, leukotriene D4, leukotriene E4) and female sex steroids (17 beta-estradiol and progesterone) were analyzed by the combined use of high-performance liquid chromatography and radioimmunoassay. 12-HETE was the main arachidonic acid metabolite. An increased metabolism of arachidonic acid was associated with pain, especially when synthesis of 12-HETE was elevated. Oral contraceptive use decreased the synthesis of prostaglandins as well as leukotrienes. The concordant changes of cyclooxygenase and lipoxygenase products in dysmenorrhea or in oral contraceptive use may be explained by an increased or decreased phospholipid metabolism, respectively. _____________________________Adv Prostaglandin Thromboxane Res 1980;8:1627-31 Related Articles, Books, LinkOut An approach to evaluation of local intestinal PG production and clinical assessment of its inhibition by indomethacin in chronic diarrhea. Bukhave K, Rask-Madsen J No abstract ON LINE..Summary of Findings:The connection between gut motility and prostaglandin release was studied. PGE2 levels in the jejunal secretions IBS patients were elevated in 10 of 17 with cyclic IBS (D & C) and in �gluten enteropathy�. Six IBS patients treated with indomethacin (INDOCIN: non-steroidal analgesic anti-inflammatory which works by inhibiting prostaglandins, which are inflammatory and pain mediators of various types) had a 50% reduction in stool volume and frequency. And withdrawal of the indocin caused the symptoms to return.Due to the absence of indicators of Type I inflammatory-allergic response, the authors said the findings suggested localized or gut-wall reactions . _____________________This also sort of makes sense out of how the BC Pills, by blocking formation of arachadonic acid metabolites, can affect both symptom sets.Eat well. Think well. Be well.MNL_________________ www.leapallergy.com
 

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I do most certainly believe hormones can affect IBS. I am 53, and menopausal and my IBS has never been worse since starting menopause. A breast cancer history in my family prevents me from taking hormone replacement therapy, but I do wonder if I would see some improvement if I were on HRT...unfortunately, I'll never know.
------------------"Remember To Stop and Smell the Roses"Rose (C-type)
 

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I do most certainly believe hormones can affect IBS. I am 53, and menopausal and my IBS has never been worse since starting menopause. A breast cancer history in my family prevents me from taking hormone replacement therapy, but I do wonder if I would see some improvement if I were on HRT...unfortunately, I'll never know.
------------------"Remember To Stop and Smell the Roses"Rose (C-type)
 
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