christy sounds like IBS and what IBS can do to a person.There are a few ways to address the problems.Here is some info
http://hopkins-gi.nts.jhu.edu/pages/latin/...se=43&lang_id=1IBS is a physical condition and they have found
abnormalities.Question:What progress has been made in finding a theory in the development of IBS? Answer: IBS occurs when there is a dysfunction in the regulation of how the brain and gut talk to each other. Diet, stress, hormones, and infection can all affect a person's sensitivity to this condition. There's a brain-gut connection, and if the bowel is distressed, it's not unusual to get anxious. Mental stress may also cause the bowel to become distressed. -- Douglas Drossman, professor of medicine and psychiatry at the University of North Carolina, Chapel Hill and co-director of the UNC Center for Functional GI and Utility Disorders. What's happening now is that there is an increasing recognition that IBS is a problem that is occurring in both the central nervous system and the gut and the interplay between the two. That is giving us a much better handle on mechanisms involved. Therefore, we now have a lot of new ideas and more scientific evidence that are leading to more effective treatments. -- Ray E. Clouse, MD, professor of medicine and psychiatry in the division of gastroenterology at the Washington University School of Medicine in St. Louis.
http://www.webmd.com/content/article/65/79519.htmboth the gut and the brain are operational to cause the symptoms.Many people don't know there is a kind of "brain" in the gut directly connected to the brain. Both the gut and the brain are "operational" to cause the symptoms.Complex and Hidden Brain in Gut Makes Bellyaches and Butterflies
http://www.aikidoaus.com.au/dojo/docs/2nd_braina.htmHavard, John Hopkins, UNC, IFFGD, UCLA, Vanderbuilt, Ohio State and many others.The Gut-Brain Connection Recent studies show that functional GI symptoms are not necessarily the result of dysfunction in the bowel, but may be due to disturbances in brain-gut pathways. By Harvard Health Reports
http://www.lhj.com/lhj/story.jhtml?storyid...atref=cat910018Gastro ProDiagnosis and management of irritable bowel syndrome
http://www.gastro-pro.org/index.html?http&...ibs/ibs-03.htmlandMedGenMed GastroenterologyIBS -- Review and What's NewPosted 07/26/2006"Serotonin SignalingOf the putative mechanisms underlying the pathophysiology of IBS, the strongest evidence points to the role of serotonin in the GI tract. The effect of serotonergic mechanisms in the manifestation of IBS symptoms has led to development of a new drug class for the treatment of IBS patients: the GI serotonergic agents.Normal GI function relies on a properly functioning brain-gut axis, which involves the coordinated interplay of the GI musculature, the CNS, the autonomic nervous system, and the enteric nervous system (ENS). The ENS contains millions of neurons embedded in the wall of the digestive tract and functions, at least in part, independently of the CNS. The size, complexity, and independent function of the ENS has resulted in application of the terms "the second brain" and "the mini-brain."[81] Impaired function or coordination of any of these systems, or the communication between these systems and the GI musculature, can lead to symptoms of dysmotility and altered sensory perception, which are characteristic of IBS and select other GI motility disorders.[82]The neurotransmitter serotonin (5-hydroxytryptamine [5-HT]) is a predominant signaling molecule in the ENS. Most (90% to 95%) of the body's serotonin is found in the gut, and smaller amounts are found in the brain (about 3%) and in platelets (about 2%).[83] In the GI tract, serotonin facilitates communication between the ENS and its effector systems (muscles, secretory endothelium, endocrine cells, and vasculature of the GI tract), thus playing a key role in normal GI tract functioning.[84] In addition, serotonin plays a role in the communication between the ENS and the CNS.In the gut, serotonin is synthesized by and stored in the enterochromaffin cells, which are located within the mucosa of the intestinal wall. When material passes through the lumen and the mucosa is stimulated, enterochromaffin cells release serotonin, which then binds to its receptors (primarily 5-HT1P receptors) on intrinsic primary afferent neurons, initiating peristalsis and secretion. Serotonin also binds to 5-HT4 receptors on interneurons, which augments the transmission of signals to motor neurons, resulting in enhanced peristaltic activity. In transgenic mice lacking 5-HT4 receptors, colonic motility is abnormally slow, confirming the role of these receptors in facilitating normal colonic motility.[85] By binding to 5-HT3 receptors on efferent sensory innervations coming from the vagus and the spinal nerves, serotonin mediates signaling between the ENS and the CNS and, thus, modulates pain perception.To regulate the signaling process, excess serotonin must be removed; this is accomplished by the SERT molecule expressed by intestinal epithelial cells.[86] Human studies have shown that defects in serotonin signaling contribute to the pathophysiology of IBS and, potentially, other GI motility disorders. In a recent study by Coates and colleagues,[87] biopsy specimens from patients with IBS showed significantly lower mucosal serotonin concentrations than those from healthy controls, potentially the result of lower mRNA levels for tryptophan hydroxylase (the rate-limiting enzyme in serotonin synthesis), which were also significantly lower in patients with inflammatory bowel disease.[87] There was no significant difference in the number of enterochromaffin cells or in the capacity of these cells to release serotonin under stimulated conditions. In another study, higher serotonin levels were observed in mucosal biopsy samples from patients with IBS with constipation (IBS-C) than in patients with IBS-D or in healthy volunteers.[88]Serotonin levels may also be affected by altering the amount or function of SERT. The study by Coates and colleagues[87] showed a significant decrease in the level of SERT mRNA and SERT protein expressed in the intestinal epithelial cells of IBS patients compared with that of healthy volunteers. In another study,[89] SERT expression and binding capacity in platelets were decreased in women with IBS-D compared with expression and binding capacity in healthy controls. Furthermore, Chen and colleagues[90] showed that mice with a SERT gene deletion had altered colonic motility. It is interesting to note that the mice thrived in laboratory housing conditions, indicating that other transporters could compensate for the lack of SERT. Additional studies have focused on SERT polymorphisms. Yeo and colleagues[91] showed an association between patients with IBS-D and the homozygous short polymorphism of the SERT gene promoter. This mutation results in lower levels of SERT gene transcription and reduced amounts of SERT protein available for reuptake of serotonin. In addition, Camilleri and colleagues[92] showed a possible link between the long promoter polymorphism and patient response to therapy.Thus, a substantially large body of work shows that normal gut physiology is predicated on the interplay between the GI musculature and the ENS, autonomic nervous system, and CNS. One of the central mediators of this complex interplay is the neurotransmitter serotonin. Impairment or imbalance in serotonergic signaling, which can affect GI motility, secretion, and visceral sensitivity, may be affected by defects or deficiencies in serotonin production, specific serotonin receptors, or proteins such as SERT. These changes can manifest in symptoms associated with IBS, including abdominal pain, altered bowel habits (constipation, diarrhea, or alternation between these 2 states), and bloating."
http://www.medscape.com/viewarticle/532089_printand some good food infoNutritional Intervention for IBS
http://ibsgroup.org/groupee/forums/a/tpc/f...261/m/474108222