Inflammatory Bowel Disease - A Holistic Perspective

The IBS Miracle

Today to Discover: My unique holistic system to immediately get symptomatic relief and completely cure your condition within 3 to 8 weeks using my powerful 100% natural system. The horrible truth about conventional Ibs treatments. A list of the original hidden research papers (together with all the details you need to locate them yourself) published by scientists and MDs reporting how they cured Ibs using natural methods so you'll see that my system is backed by scientific evidence! 78 different scientific sources to be exact! How simple over the counter products will immediately reduce cramps and abdominal pain. The dietary changes you should make to live an Ibs-free life. How to make your body combat Ibs and re-balance itself. The link between lifestyle and Ibs. The specific foods that trigger Ibs symptoms. Foods that are marketed as being ery healthy that will actually cause your Ibs to get worse. Herbs that are extremely potent in stopping diarrhea, constipation and gas. Simple alternative treatments that will cure your Ibs faster than you ever thought possible. I will show you step by step how to do this. The food items you have to include in your diet if you want to get rid of your Ibs fast. The food items you should limit if you want to get rid of Ibs. Convenient printable charts that will tell you exactly the foods to avoid and the foods to include. The secret 100% natural remedies that you should use, and are guaranteed to make a dramatic impact on your Ibs condition in just a few days! Read more here...

The IBS Miracle Summary

Rating:

4.7 stars out of 12 votes

Contents: 60 Page EBook
Author: James Walden
Official Website: theibsmiracle.com
Price: $37.00

Access Now

My The IBS Miracle Review

Highly Recommended

All of the information that the author discovered has been compiled into a downloadable ebook so that purchasers of The IBS Miracle can begin putting the methods it teaches to use as soon as possible.

Purchasing this book was one of the best decisions I have made, since it is worth every penny I invested on it. I highly recommend this to everyone out there.

Irritable Bowel Syndrome Relief Secrets

Here is just some of what you will discover inside Irritable Bowel Syndrome Relief Secrets: What causes Ibs this information may surprise you. 4 ways to improve your immune system and reduce your symptoms follow these tips and you'll put yourself on the fast track to reclaiming control of your life. The similarity in symptoms between Ibs and having a sensitive, reactive colon and what this means as far as the treatment you should pursue. Why stress is a catalyst for Ibs symptoms and what you can do to begin reducing your symptoms immediately. The common symptoms of Ibs, including the four main ones and how to manage them all effectively. How Ibs is usually diagnosed and whether the two main types of tests doctors usually run are actually effective or not. Effective strategies you can use to treat your Ibs symptoms and even eliminate them for good. Practical exercises for you to do that lead you step-by-step through the information revealed in Irritable Bowel Syndrome and Treatments and ensure that you stay on track to gaining control of your Ibs and improving the quality of your life! Read more here...

Irritable Bowel Syndrome Relief Secrets Summary

Official Website: www.natural-irritable-bowel-syndrome-relief.com
Price: $37.77

Specific Visceral And Abdominal Pain Syndromes Irritable Bowel Syndrome

The irritable bowel syndrome (IBS) is a chronic GI disorder characterized by RAP that is associated with defecation. The symptoms do not have a structural or biochemical explanation (9,10). Many population-based surveys around the globe have assessed the individual symptoms of IBS (11) and estimated the prevalence to be between 8 and 22 (12,13). The prevalence of IBS is higher in women and lower in the elderly (7,14,15). Although many studies have assessed the prevalence of IBS, data regarding incidence are much more difficult to obtain. Information on symptom onset and disappearance can be obtained by repeated surveys over time (4,16). Roughly 10 of the general population will report the onset of IBS symptoms over a one-year period (4,16). Approximately one-third of people with IBS symptoms will report symptom resolution over time (4). The incidence of a clinical diagnosis of IBS has been estimated to be 196 to 260 per 100,000 person-years (17,18). This is not the true incidence of...

Inflammatory Bowel Disease

Thirty-five patients (17 women and 18 men) with inflammatory bowel disease (IBD) were followed prospectively for 19 months with BMD measurements at the PA lumbar spine and proximal femur with DXA (Hologic QDR-1000) (58). Fourteen patients had Crohn's disease and 21 had ulcerative colitis. They ranged in age from 17 to 60 years with a mean age of 36 years. Crohn's disease patients lost 3.08 4.91 per year in the lumbar spine and 6.91 6.57 per year in the femoral neck. Ulcerative colitis patients without ileoanal anastomosis lost 6.42 7.5 per year in the lumbar spine and 5.59 11.12 per year in the femoral neck. No ulcerative colitis patient with ileoanal anastomosis had a significant bone loss from either site. Patients on steroids had mean bone loss of 6.23 7.04 per year in the spine and 8.97 9.57 per year in the femoral neck. Patients not on steroids had gains of 0.87 0.002 per year in the spine and 0.20 5.78 per year in the femoral neck.

Animal Models of Inflammatory Bowel Disease

Studies in experimental models of mucosal inflammation have led to major new insights into the abnormalities present in human IBD as well as to new approaches in the therapy of these diseases (Hoffmann et al. 2002 Singh et al. 2001a Strober et al. 2002). Models, based on knockout and transgenic animals, have generated the greatest interest and are commonly used. In particular, the adoptive transfer of T cells into immunodeficient mice as severe combined immune deficient (SCID) mice and recombination activation gene (RAG) deficient mice, which lack functional T and B cells, has been used to induce colitis in the recipients. The SCID transfer model will be described in more detail below, as it is one of the most widely used immunological models of inflammatory bowel disease and of major importance for the study of regulatory T cells.

Inflammatory Bowel Disease Ulcerative Colitis and Crohns Disease

There are two major forms of chronic inflammatory bowel disease (IBD). Ulcerative colitis is an ulcerative disorder of the mucosa of the colon, whereas Crohn's disease is characterized by transmural inflammation, most often in the small intestine. Both produce abdominal pain and diarrhea, which can be bloody. iBd tends to wax and wane, with periods of intense active disease followed by long periods of remission. Although the cause is not clear, IBD appears to be an autoimmune reaction, in which overzealous immune cells attack the tissues of the intestinal wall.

Abdominal Pain for Life

Talley N, Zinsmeister AR, Melton LJ III. Irritable bowel syndrome in a community symptom subgroups, risk factors and health care utilization. Am J Epidemiol 1995 142 76. 10. Talley NJ, Spiller R. Irritable bowel syndrome a little understood organic disease Lancet 2002 360(9332) 555. 12. Saito YA, Schoenfeld P, Locke GR III. The epidemiology of irritable bowel syndrome in North America a systematic review. Am J Gastroenterol 2002 97 1910. 13. Talley N et al. Epidemiology of colonic symptoms and the irritable bowel syndrome. Gastroenterol-ogy 1991 101 927. 15. Talley NJ et al. Medical costs in community subjects with irritable bowel syndrome. Gastroenterol-ogy 1995 109(6) 1736. 16. Agreus L et al. Irritable bowel syndrome and dyspepsia in the general population overlap and lack of stability over time. Gastroenterology 1995 109 671. 17. Rodriquez LG et al. Detection of colorectal tumor and inflammatory bowel disease during follow-up of patients with initial diagnosis of irritable bowel...

Transient Receptor Potential Vanilloid Receptor

The response to TRPV1 activation is generally regarded as involving two phases an initial excitation leading to transmitter release, followed by desensitization and damage after prolonged or repeated exposure (94,96,144,152,153). In the gastrointestinal tract, capsaicin evokes a powerful excitation of discharge in all classes of vagal and spinal afferents however, the relative proportion varies between location and species (71,74,109,154-156). Early reports in the cat found that the majority of vagal and spinal afferents were activated by capsai-cin (157). Similarly, in the mouse, 80 of isolated retrogradely labeled colonic lumbosacral DRG cells responded to capsaicin (158). By contrast, in the rat, in isolated retrogradely labeled cells capsaicin evoked responses in 42 of nodose ganglion cells (154), and 46 of colonic lumbosacral DRG cells (155). Capsaicin activated 29 of rat colonic LSN afferents, including 17 of mucosal afferents, 40 of serosal afferents, and no muscular afferents....

Evidence for Altered Psychological State

Certain stressful life events have been associated with both the onset and exacerbation of a number of disorders of the GI tract including FGD (109), PI-IBS (110), and inflammatory bowel disease (111). Anxiety, somatization, neuroticism, hypochondriasis, and preceding adverse life events have all been reported to increase the risk of developing IBS after gastroenteritis (110,112). Both early-life stress in the form of abuse and an acute episode of extreme stress in adult life such as rape have been suggested as important risk factors for the development of FGD (113,114).

Clinical Presentation Based On Severity Of Pain And Implications For Treatment

Patients with chronic abdominal and visceral pain can fall under a variety of diagnostic syndromes and categories. This may include longstanding structural diagnoses such as chronic pancreatitis, a variety of functional GI diagnoses (e.g., IBS, functional chest pain or dyspepsia, functional biliary pain, levator syndrome, etc.), or combinations (e.g., inflammatory bowel disease (IBD) with IBS). In this chapter, the proposition is that, independent of diagnosis, the nature and severity of the pain as well as clinical decisions regarding treatment will depend on integrating the relative contributions of the peripheral and central determinants that affect the nature and severity of the pain and its psychosocial concomitants.

Protease Activated Receptors

From these findings, it would appear that PAR-2 antagonists have potential in the control of visceral pain and hyperalgesia. In addition, they may have anti-inflammatory activity, given that the levels of the PAR-2 agonists trypsin and mast cell tryptase are elevated in the colon of inflammatory bowel disease patients, and administration of PAR-2 agonists into the mouse colon induces inflammation via a mechanism involving sensory neurons (81,82). Furthermore, exposure of the mouse colon to a PAR-2 agonist enhances the expression of PAR-2 mRNA (81) much as the expression of PAR-2 on colonic mast cells is upregulated in ulcerative colitis (83). The available evidence indicates that the proalgesic and proinflamma-tory effects of PAR-2 activation are not necessarily interrelated, given that pain and hyperalgesia can be evoked by subinflammatory doses of PAR-2 agonists (76-78). PAR-1 antagonists may likewise display anti-inflammatory activity, given that PAR-1 stimulation induces...

Acid Sensing Ion Channels

Although an implication in visceral pain has remained unexplored, ASICs could conceivably participate in GI hypersensitivity to mechanical and chemical noxae (97). A role in GI pathology may also be envisaged from the upregulation of ASIC3, but not ASIC1 and ASIC2, in inflammatory bowel disease (168) and the stimulation of ASIC3 transcription by nerve growth factor and proinflammatory mediators such as 5-HT, interleukin-1, and bradykinin (169).

Visceral Pain Is Referred to Somatic Structures

Dorsal horn neurons in these segments have somatic receptive fields on the trunk, separate from the sacral neuron receptive fields. It would then be expected that referred pain should also be perceived as originating in the trunk. This does not occur in normal volunteers, but the area of referred pain expands into the lower abdomen following repetitive colonic distention (Fig. 3A) (34). In contrast, in patients with a functional bowel disorder or an inflammatory bowel disease, referred pain is perceived in the lower abdomen and thorax, as well as in the pelvic area (35). This dermatomal organization of referred pain suggests that acute colorectal pain is processed in the spinal cord segments receiving pelvic nerve afferent input

Ionotropic Purinoceptors

Acidosis (87,97), and (iii) P2X receptors on sensory neurons are upregulated by experimental inflammation (98). Likewise, interstitial cystitis leads to an increased expression of P2X2 and P2X3 protein in the urothelium (99), and inflammatory bowel disease is associated with an increased number of P2X3 receptors in the colon (100). Pharmacologic evidence points to a role of P2X receptors in abdominal chemonociception, since trinitrophenyl-ATP (a P2X1, P2X3, and P2X2 3 receptor blocker) and A-317491 (a non-nucleotide P2X3 and P2X2 3 receptor antagonist) suppress the nociceptive behavior provoked by intraperitoneal injection of acetic acid in mice (101,102). In contrast, the visceromotor pain response to colonic distension in the rat and the colitis-induced mechanical hyperalgesia are not attenuated by A-317491 (102). The further evaluation of the therapeutic potential of P2X3 and P2X2 3 receptors in acid-related, inflammation-, and ischemia-induced disturbances of gut sensation will...

The Large Intestine Rectum and Anus

One of the postulated risk factors for irritable bowel syndrome (IBS), a key symptom of which is visceral pain, is acute transient infection, and this has been applied to animal models. Such infectious stimuli as that produced by the nematode Nippostrongylus brasiliensis or Trichinella spiralis result in hypermotility, hypersecretion, and intestinal inflammation. This is accompanied by increased visceral sensitivity and is used as a chronic model, because these effects can be seen after the inflammation has resolved, although effects may be related more directly to the jejunum rather than the colon (44). If an insult such as an infection is experienced by neonatal animals, it may induce a sensitization that can significantly affect nociceptive processing in adults, and this is the theoretical basis of animal models involving developmental stimuli. Indeed, both mechanical and chemical neonatal colonic irritation in rats have been reported to produce visceral hypersensitivity in adults...

Feeding the Inflammatory Niche Adaptive T Cell Responses Fostering the Tumor

How the adaptive immune system responds to perceived injury or infection is regulated on various levels, most intriguingly exemplified in the differential polarization of CD4+ helper cells (Reiner 2007 and Fig. 2). Cytokines such as IL-4, IL-12 and IL-23 regulate the initiation or activity of those divergent immunological pathways (McKenzie et al. 2006). IL-12 and IFN-g prime and maintain the development of Th1 cells which produce IFN-g and TNF-a and enhance antimicrobial and cytotoxic responses. IL-23 is essential in the proinflammatory function of a memory T cell subset characterized by the production of the cytokine IL-17, named therefore Th17 (Aggarwal et al. 2003 Langrish et al. 2005). Through the attraction and activation of granulocytes and other innate myeloid cells, Th17 cells are thought to safeguard against extracellular bacteria. IL-17 engages its receptor, commonly found on stromal, epithelial, endothelial cells and monocytes - resulting in the release of additional...

Anal Fissures Tears and Lacerations

A major problem in the forensic interpretation of anal fissures is that they may result from numerous other means that are unrelated to penetrative trauma, including passage of hard stools, diarrhea, inflammatory bowel disease, sexually transmitted diseases, and skin diseases (183,184).

Suppressive Effects of CD4CD25 Regulatory T Cells on the Adaptive Immune Response

In accordance with the cell-contact dependency of suppression, a large number of in vitro studies has shown that neutralization of immunosuppressive cytokines such as IL-10, TGF-3 and IL-4 did not block suppression 11,22, 50,52,53,69,70 . However, soluble factors that work at small range or in high local concentrations might still attribute to the suppressive effects. Indeed a role for IL-10 and or TGF-3 in CD4+CD25+ Treg-mediated suppression has been described in several in vivo models for transplantation tolerance 71 , colitis inflammatory bowel disease 72-74 , superantigen-induced cytokine production 75 and anterior chamber-associated immune deviation 76 . These conflicting data might be explained by differences in regulatory T cell function in vitro and in vivo, but also by recent findings that CD4+CD25+ Tregs can mediate infectious tolerance 58, 59 . The phrase 'infectious tolerance' was coined by Gershon and co-workers in 1971 3 and re-introduced by Waldmann and co-workers in...

Leptin and Cancer Anorexia Cachexia

The persistence of anorexia and the onset of cachexia in cancer patients, therefore, implies a failure of this adaptive feeding response 86 . Leptin, a member of the gp 130 family of cytokines, induces a strong T helper-1 lymphocyte response and is regarded as a proin-flammatory inducer 87 . Several data suggested a role of leptin in inflammatory diseases. Proinflammatory cytokines up-regulate leptin expression in white adipose tissue and increase plasma leptin levels in hamsters and mice 88 . However, in many common diseases associated with cachexia, such as chronic obstructive pulmonary disease and chronic inflammatory bowel disease, there is an inflammatory status caused by high proinflammatory cytokine levels, whereby leptin concentrations are decreased related to body fat mass. In patients with advanced non-small-cell lung cancer, serum leptin levels were lower than in controls and lower still in those who were cachectic who also showed an increase of...

Autoimmune Gastritis Model of CD4CD25 T Cell Mediated Suppression

Over the years, many autoimmune models have been employed to investigate the in vivo biology of suppressor T cells (Shevach 2000). One of the original autoimmune models used in the study of CD4+CD25+ biology is AIG induced by thymectomy on day 3 of life (d3Tx) or CD25- T cell transfer to immunocompromised animals. Another widely utilized autoimmune disease model is inflammatory bowel disease (IBD) or colitis. Transfer of CD4+CD45Rbhi (Powrie et al. 1994) or CD4+CD25- T cells (Liu et al. 2003

Calcium and Vitamin D

Osteoporosis is increasingly being recognised as a leading extra-intestinal complication of inflammatory bowel disease. Calcium is absorbed in the proximal small intestine by a vitamin D-depend-ent Ca2+-binding protein, and vitamin D is absorbed in the duodenum and jejunum. Therefore, in Crohn's disease patients with extended inflammation or resection of the small intestine, osteoporosis results from impaired absorption of calcium and vitamin D.

Regulatory T Cells in Experimental Colitis

2 Inflammatory Bowel 3 Bacterial Flora in Inflammatory Bowel Disease 181 4 Animal Models of Inflammatory Bowel Disease 182 for Inflammatory Bowel Disease 199 Abstract Induction and maintenance of peripheral tolerance are important mechanisms to maintain the balance of the immune system. Growing evidence indicates that dysregulation of mucosal T cell responses may lead to loss of tolerance to commensal flora and to the development of inflammatory bowel diseases (IBD). Many studies suggest that active suppression of enteroantigen reactive cells mediated by regulatory

Current serum biomarkers of cancer

CEA, for example, is a human tumour marker typically associated with malignant epithelial neoplasms. The CEA gene belongs to a family of more than 20 members, clustered on the long arm of chromosome 19 31 and belonging to the immunoglobulin supergene family. Its main use is to monitor patients with colorectal carcinoma, but the antigen is not specific and elevated levels may be observed with some nonmalignant diseases including inflammatory bowel disease, liver disease 32 , pancreatitis and renal failure 33 . In healthy individuals, plasma levels are in a range of 0-5 ng ml and 3-10 ng ml in smokers, whereas patients with colorectal cancer exhibit levels 20 ng ml.

Phenotypic Alterations in Cancer Cells

Since hyperproliferative conditions in patients, such as inflammatory bowel disease or psoriasis, may mimic some of the characteristics of malignant cells, it is important to use a number of criteria that define the malignant state. The evidence that these phenotypic properties found in transformed cells in culture are related to malignant neoplasia in vivo is discussed below.

Control of CD25CD4 TR Cell Development by Foxp3

Higher than that in CD25-CD4+ T cells. Activation of CD25-CD4+ T cells, Th1, or Th2 cells failed to induce Foxp3 expression, in contrast with their expression of CD25, CTLA-4, and GITR, which are generally expressed on any activated T cells (Hori et al. 2003). Importantly, retroviral transduction of Foxp3 FOXP3 into CD25-CD4+ T cells converted them to CD25+CD4+ TR-like cells (Hori et al. 2003, Yagi et al. 2004). Such Foxp3-transduced T cells showed hypoproliferation and low production of cytokines in response to in vitro antigenic stimulation, and suppressed the activation of co-cultured CD25-CD4+ naive T cells in a similar manner to natural TR cells. Foxp3-transduced T cells were also able to negatively control self-reactive T cells in vivo for example, co-transfer of Foxp3-transduced T cells inhibited the development of inflammatory bowel disease and autoimmune gastritis that can be induced in SCID mice by the transfer of CD25-CD45RBhighCD4+ T cells from normal mice. Foxp3 is also...

Future Directions

Jeremy D Gale is a drug developer with 17 years experience in major R&D-based pharmaceutical companies working across the continuum of drug discovery and development. He graduated in pharmacology and then completed a PhD in pharmacology and neuroscience at the University of London. He joined Glaxo in 1988 and for almost 8 years worked in gastrointestinal pharmacology, leading the biology teams that formed part of the irritable bowel syndrome (IBS) and emesis research programes. Jeremy joined Pfizer in 1995 to lead the biology research team focused on gastroenterological diseases, developing expertise in IBS, inflammatory bowel disease (IBD), and gastroesophageal reflux disease (GERD). In 2002, he moved into Exploratory Clinical Development, becoming clinical leader for programs targeting GERD and IBD. In addition, Jeremy leads translational medicine activities and biomarker development for the gastroenterology and hepatology therapeutic area.

Pathogenesis of Crohns Disease

Crohn Disease

Although significant advances in understanding the pathogenesis of CD have been made, there are many unknowns. CD is believed to be caused by a combination of genetic and environmental factors, affecting the mucosal immune system and culminating in an aberrant inflammatory response (Korzenik and Podolsky 2006) (Fig. 12.3). It is a polygenic disease with probable genetic heterogeneity. Some genes are associated with the disease itself, whereas others increase the risk of the disease or are associated with the location or behavior of the disease (Lakatos et al. 2006). Caspase recruitment domain family member 15 (CARD15, also known as IBD1 or NOD2) was the first specific gene associated with inflammatory bowel disease (IBD) and is believed to confer the critical mutation on chromosome 16 Fig. 12.4. Novel therapeutic targets in inflammatory bowel disease (IBD). Potential therapies in IBD encompass interventions targeting a variety of pathways in the inflammatory cascade. These include...

Dendritic Cells Mucosa Intestine Treg Cell

Epithelial cells in other mucosal tissues, such as the lung and genitourinary tract. Blocking monoclonal antibodies specific for the a4 chain of a4p7 have been used to treat patients with inflammatory bowel disease on the basis of the knowledge that effector T cells use this integrin to enter gut tissues in this disease. (We will discuss inflammatory bowel disease later in the chapter.)

Innate Immunity in the Gastrointestinal Tract

Adiposse Tissue Expansion

Defensins produced by intestinal epithelial cells provide innate immune protection against luminal bacteria, and defects in their production are associated with bacterial invasion and inflammatory bowel disease. Defensins are peptides produced by various cell types in the body that exert lethal toxic effects on microbes by inserting into and causing loss of integrity of their outer phospholipid membranes (see Chapter 4). In the small bowel, the major defensins are the a-defensins, including human defensin 5 (HD5) and HD6, produced constitutively as inactive precursor proteins by Paneth cells located at the base of crypts between microvilli. Active HD5 and HD6 peptides are generated by proteolytic cleavage mediated by trypsin, also produced by Paneth cells. In the colon, P-defensins are produced by absorptive epithelial cells in the intestinal crypts, some constitutively and others in response to IL-1 or invasive bacteria. In addition, neutrophil granules are rich in a-defensins, which...

Diseases Related to Immune Responses in the

Inflammatory bowel disease is a heterogeneous group of disorders characterized by chronic remitting inflammation in the small or large bowel, likely due to poorly regulated responses to commensal bacteria. The two main types of inflammatory bowel disease are Crohn's disease, which can affect the entire thickness of the bowel wall tissue in any part of the gastrointestinal tract but most frequently involves the terminal ileum, and ulcerative colitis, which is restricted to the colonic mucosa. Symptoms include abdominal pain, vomiting, diarrhea, and weight loss. Treatments include various anti-inflammatory drugs, such as sulfasalazine, corticoste-roids, TNF antagonists, and antimetabolites. Although the etiology of Crohn's disease and ulcerative colitis is poorly understood, several types of evidence suggest that these disorders are a result of defects in the regulation of immune responses to commensal organisms in the gut in a genetically susceptible host. A number of immunologic...

What is Mycobacterium avium subsp paratuberculosis and how is it controlled

Mycobacterium avium subsp. paratuberculosis (MAP) causes paratuberculosis, or Johne's disease, an inflammatory bowel disease affecting ruminants. This disease is chronic and contagious and eventually results in death of affected animals. In the US, approximately 22 of the dairy herds are affected with Johne's disease. Infected dairy cattle are able to shed MAP in milk. This pathogen has been epidemiologically implicated in association with Crohn's disease in humans. While pasteurisation is thought to provide public health protection from this organism, several studies have revealed the presence of MAP in retail fluid pasteurised milk.

Regulation of Immunity in the Gastrointestinal Tract by Regulatory T Cells and Cytokines

Several cytokines, including TGF-fi, IL-10, and IL-2, appear to play crucial roles in maintaining homeostasis in the gut immune system, and deficiencies in these cyto-kines or their receptors result in pathologic bowel inflammation. Much of our knowledge of cytokine-mediated regulation in the gut comes from studies with cytokine or cytokine receptor gene knockout mice. A major feature of the phenotype of mice with engineered deficiencies in TGF-P, IL-10, IL-10 receptor, IL-2, and IL-2 receptor is uncontrolled inflammation in the bowel. Mutations in the IL-10 and IL-10 receptor genes are also associated with severe inflammatory bowel disease in children, confirming the importance of IL-10 in preventing pathologic gut inflammation in humans. The uncontrolled inflammation observed in the gut in the absence of these cyto-kines or their receptors is most likely caused by innate and adaptive immune responses to commensal gut flora because the inflammation does not occur in mice raised in...

Telephone Systems

On how to cope with specific pain conditions. Hicks et al. (16) demonstrated that a Web-based intervention can effectively treat headache and recurrent abdominal pain. A coach who e-mailed or spoke to the participants on the telephone augmented the material presented on the Web. We have developed and are currently testing a second Web-based intervention for inflammatory bowel disease in adolescents. The program is part of our Family Help program and consists of Web pages that explain the disease and its treatment, as well as Web pages that teach coping skills. Videos model specific skills and attitudes, and a coach contacts the adolescent weekly to help him or her stay on track and problem solve any difficulties the adolescent may have.

Quality of Life

IBD patients have significantly lower health-related QoL across a number of domains when compared with healthy controls. Two IBD-specific questionnaires have been developed to allow the assessment of health-related QoL in this patient group the inflammatory bowel disease questionnaire (IBDQ) and the rating form of inflammatory bowel disease patient concerns (RFIPCs). The IBDQ has been used in many clinical trials and is considered to be robust in measuring therapeutic efficacy. A short form of this questionnaire has been developed, but not yet tested in a clinical trial setting.

How To Manage Irritable Bowel Syndrome

How To Manage Irritable Bowel Syndrome

Having issues with irritable bowel syndrome and want to know the correct way to manage the problem? Finally, This Books Explains Everything You'll Never Wonder If The Misery Will End... This Book Will Ease Your Pain And Enable Your Old Day-To-Day Life Stop Fighting Irritable Bowel Syndromes With Products And Home Remedies That Always Seem To Make Things Worse Than They Ever Were. Stop the suffering once and for all, YOU don't have to live with IBS anymorebr There's finallya new, breakthroughbookcreated just for people like you

Get My Free Ebook