Psychology Wiki

Assessment | Biopsychology | Comparative | Cognitive | Developmental | Language | Individual differences | Personality | Philosophy | Social |
Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology |

Biological: Behavioural genetics · Evolutionary psychology · Neuroanatomy · Neurochemistry · Neuroendocrinology · Neuroscience · Psychoneuroimmunology · Physiological Psychology · Psychopharmacology (Index, Outline)

Irritable bowel syndrome synonymous with GILL/HT/IB
ICD-10 K58
ICD-9 564.1
OMIM [2]
DiseasesDB 30638
MedlinePlus 000246
eMedicine med/1190
MeSH {{{MeshNumber}}}

This is a background article. See Psychological aspects of irritable bowel syndrome

In gastro psychology and gastroenterology, irritable bowel syndrome (IBS) is a functional bowel disorder characterized by mild to severe abdominal pain, discomfort, bloating and alteration of bowel habits. In some cases, the symptoms are relieved by bowel movements.[1] Diarrhea or constipation may predominate, or they may alternate (classified as IBS-D, IBS-C or IBS-A, respectively). IBS may begin after an infection (post-infectious, IBS-PI) or a stressful life event. Other functional or pain disorders and certain psychological conditions are more common in those with IBS.

Although there is no cure for IBS, there are treatments which attempt to relieve symptoms, including dietary adjustments, medication and psychological interventions. Patient education and a good doctor-patient relationship are also important.[1]

Several conditions may present as IBS including celiac disease, mild infections, parasitic infections like giardiasis[2], several inflammatory bowel diseases, functional chronic constipation and chronic functional abdominal pain. In IBS, routine clinical tests yield no abnormalities, though the bowels may be more sensitive to certain stimuli, such as balloon insufflation testing. The exact cause of IBS is unknown. The most common theory is that IBS is a disorder of the interaction between the brain and the gastrointestinal tract, although there may also be abnormalities in the gut flora or the immune system.[3] [4]

Gastro psychology
Brain animated color nevit.gif

Functional gastrointestinal disorder
Other disorders
Related topics


The primary symptoms of IBS are abdominal pain or discomfort in association with frequent diarrhea and/or constipation, a change in bowel habits.[5] There may also be urgency for bowel movements, a feeling of incomplete evacuation (tenesmus), bloating or abdominal distention.[6] People with IBS more commonly than others have gastroesophageal reflux, symptoms relating to the genitourinary system, psychological symptoms, fibromyalgia, headache and backache.[6]

IBS can be classified as either diarrhea-predominant (IBS-D), constipation-predominant (IBS-C) or IBS with alternating stool pattern (IBS-A or pain-predominant[7]). In some individuals, IBS may have an acute onset and develop after an infectious illness characterised by two or more of the following: fever, vomiting, diarrhea, or positive stool culture. This post-infective syndrome has consequently been termed "post-infectious IBS" (IBS-PI).


There is no specific laboratory or imaging test which can be performed to diagnose irritable bowel syndrome.[8] Diagnosis of IBS involves excluding conditions which produce IBS-like symptoms, and then following a procedure to categorize the patient's symptoms.

Because there are many causes of diarrhea and IBS-like symptoms, the American Gastroenterological Association has published a set of guidelines for tests to be performed to diagnose other conditions which may have symptoms similar to IBS. These include gastrointestinal infections, lactose intolerance and Coeliac disease. Research has suggested that these guidelines are not always followed.[8] Once other causes have been excluded, the diagnosis of IBS is performed using a diagnostic algorithm. Well-known algorithms include the Manning Criteria, the Rome I Criteria, the Rome II Process, the Kruis Criteria, and studies have compared their reliability.[9] The more recent Rome III Process was published in 2006. Physicians may choose to use one of these criteria, or may use other guidelines based on their own experience and the patient's history. The algorithm may include additional tests to guard against mis-diagnosis of other diseases as IBS. Such "red flag" symptoms may include weight loss, GI bleeding, anemia, or nocturnal symptoms. However, researchers have noted that red flag conditions may not always contribute to accuracy in diagnosis — for instance, as many as 31% of IBS patients have blood in their stool.[9]

The diagnostic algorithm identifies a name which can be applied to the patient's condition based on the combination of the patient's symptoms of diarrhea, abdominal pain, and constipation. For example, the statement "50% of returning travelers had developed functional diarrhea while 25% had developed IBS" would mean that half the travelers had diarrhea while a quarter had diarrhea with abdominal pain. While some researchers believe this categorization system will help physicians understand IBS, others have questioned the value of the system and suggested that all IBS patients have the same underlying disease but with different symptoms.[10]


Published research has demonstrated that some poor patient outcomes are due to treatable causes of diarrhea being mis-diagnosed as IBS. Common examples include infectious diseases, celiac disease,[11] parasites,[4] food allergies[12] (though considered controversial), and lactose intolerance.[13] See List of causes of diarrhea for other conditions which can cause diarrhea.

Celiac disease in particular is often misdiagnosed as IBS:

Recognizing celiac disease can be difficult because some of its symptoms are similar to those of other diseases. In fact, sometimes celiac disease is confused with irritable bowel syndrome, iron-deficiency anemia caused by menstrual blood loss, Crohn's disease, diverticulitis, intestinal infections, and chronic fatigue syndrome. As a result, celiac disease is commonly underdiagnosed or misdiagnosed.[14]

Medical conditions that accompany IBS

Researchers have identified several medical conditions, or comorbidities, which appear with greater frequency in patients diagnosed with IBS.

Headache, Fibromyalgia, and Depression: A study of 97,593 individuals with IBS identified comorbidities as headache, fibromyalgia, and depression.[15] Fibromyalgia has also been identified in other studies as a comorbidity of IBS.[16][17]
Inflammatory bowel disease: Some researchers have suggested that IBS is a type of low-grade inflammatory bowel disease.[18] Researchers have suggested that IBS and IBD are interrelated diseases,[19] noting that patients with IBD experience IBS-like symptoms when their IBD is in remission.[20][21] A 3-year study found that patients diagnosed with IBS were 16.3 times more likely to develop IBD during the study period.[22] Serum markers associated with inflammation have also been found in patients with IBS (see Causes).
Abdominal surgery: A recent (2008) study found that IBS patients are at increased risk of having unnecessary cholecystectomy (gall bladder removal surgery) not due to an increased risk of gallstones, but rather to abdominal pain, awareness of having gallstones, and inappropriate surgical indications.[23] A 2005 study published in Digestive Disease Science reported that IBS patients are 87% more likely to undergo abdominal and pelvic surgery, and three times more likely to undergo gallbladder surgery.[24] A study published in Gastroenterology came to similar conclusions, and also noted IBS patients were twice as likely to undergo hysterectomy.[25]
Endometriosis: One study has reported a statistically significant link between migraine headaches, IBS, and endometriosis.[26]
Other chronic disorders: Interstitial cystitis may be associated with other chronic pain syndromes, such as irritable bowel syndrome and fibromyalgia. The connection between these syndromes is unknown.[27]


Initially, IBS was considered a psychosomatic illness and the involvement of biological and pathogenic factors was not verified until the 1990s, a process common in the history of emerging infectious diseases. The risk of developing IBS increases six-fold after acute gastrointestinal infection. Post-infection, further risk factors are young age, prolonged fever, anxiety and depression.[28]

Psychosomatic illness


Most peptic ulcers are now treated with 1-2 weeks of antibiotic therapy, since it has been discovered that they are caused by a combination of a genetic trait in the patient and infection with the bacteria H. Pylori.[29]

One of the first references to the concept of an "irritable bowel" appeared in the Rocky Mountain Medical Journal in 1950.[30] The term was used to categorize patients who developed symptoms of diarrhea, abdominal pain, constipation, but where no well-recognized infective cause could be found. Early theories suggested that the Irritable Bowel was caused by a psychosomatic, or mental disorder. One paper from the 1980s investigated "learned illness behavior" in patients with IBS and peptic ulcers.[31] Another study suggested that both IBS and stomach ulcer patients would benefit from 15 months of psychotherapy.[32] Later, it would be found that most stomach ulcers were caused by a bacterial infection with Helicobacter pylori.[33]

Additional publications suggesting the role of brain-gut "axis" appeared in the 1990s, such as a study entitled Brain-gut response to stress and cholinergic stimulation in IBS published in the Journal of Clinical Gastroenterology in 1993.[34] A 1997 study published in Gut magazine suggested that IBS was associated with a "derailing of the brain-gut axis."[35]

Immune reaction

From the late 1990s, research publications began identifying specific biochemical changes present in tissue biopsies and serum samples from IBS patients that suggested symptoms had an organic rather than psychosomatic cause. These studies identified cytokines and secretory products in tissues taken from IBS patients. The cytokines identified in IBS patients produce inflammation and are associated with the body's immune response.

  • A study showed that intestinal biopsies from patients with constipation predominant IBS secreted higher levels of serotonin in-vitro.[36] Serotonin plays a role in regulating gastrointestinal motility and water content, and can be altered by some diseases and infections.[37][38][39]
  • A study of rectal biopsy tissue from IBS patients showed increased levels of cellular structures involved in the production of the cytokine Interleukin 1 Beta.[40]
  • A study of blood samples from IBS patients identified elevated levels of cytokines Tumor necrosis factor-alpha, Interleukin 1, and Interleukin 6 in patients with IBS.[41]
  • A study of intestinal biopsies from IBS patients showed increased levels of protease enzymes used by the body to digest proteins, and by infectious agents to combat the host's immune system.[42]
  • A study of blood samples from IBS patients found elevated levels of antibodies to the protozoan Blastocystis.[43]

Specific forms of immune response that have been implicated in IBS symptoms include Coeliac disease and other Food allergy conditions.[44] Coeliac disease (also spelled "celiac") is an immunoglobulin type A-(IgA) mediated allergic response to the Gliadin protein in gluten grains, which exhibits wide variety of symptoms and can present as IBS. "Some patients with diarrhea-predominant irritable bowel syndrome (IBS-D) may have undiagnosed celiac sprue (CS). Because the symptoms of CS respond to a gluten-free diet, testing for CS in IBS may prevent years of morbidity and attendant expense."[45] "Coeliac disease is a common finding among patients labelled as irritable bowel syndrome. In this sub-group, a gluten free diet may lead to a significant improvement in symptoms. Routine testing for coeliac disease may be indicated in all patients being evaluated for irritable bowel syndrome."[46] Food allergies, particularly those mediated by IgE and IgG-type antibodies have been implicated in IBS.[47][48][49]

Active infections


There is research to support IBS being caused by an as-yet undiscovered active infection. Most recently, a study has found that the antibiotic Rifaximin provides sustained relief for IBS patients.[50] While some researchers see this as evidence that IBS is related to an undiscovered agent, others believe IBS patients suffer from overgrowth of intestinal flora and the antibiotics are effective in reducing the overgrowth (known as small intestinal bacterial overgrowth).[51] Other researchers have focused on an unrecognized protozoal infection as a cause of IBS[4] as certain protozoal infections occur more frequently in IBS patients.[52][53] Two of the protozoa investigated have a high prevalence in industrialized countries and infect the bowel, but little is known about them as they are recently emerged pathogens.

Blastocystis is a single-celled organism which has been reported to produce symptoms of abdominal pain, constipation and diarrhea in patients, along with headaches and depression,[54] though these reports are contested by some physicians.[55] Studies from research hospitals in various countries have identified high Blastocystis infection rates in IBS patients, with 38% being reported from London School of Hygiene & Tropical Medicine,[56] 47% reported from the Department of Gastroenterology at Aga Khan University in Pakistan[52] and 18.1% reported from the Institute of Diseases and Public Health at University of Ancona in Italy.[53] Reports from all three groups indicate a Blastocystis prevalence of approximately 7% in non-IBS patients. Researchers have noted that clinical diagnostics fail to identify infection,[57] and Blastocystis may not respond to treatment with common antiprotozoals.[58][59][60][61]

Further information: Blastocystosis
File:Wiki ibs cause figures.jpg

Prevalence of protozoal infections in industrialized countries (United States and Canada) in 21st century.[62][63]

Dientamoeba fragilis is a single-celled organism which produces abdominal pain and diarrhea. Studies have reported a high incidence of infection in developed countries, and symptoms of patients resolve following antibiotic treatment.[62][64] One study reported on a large group of patients with IBS-like symptoms who were found to be infected with Dientamoeba fragilis, and experienced resolution of symptoms following treatment.[65] Researchers have noted that methods used clinically may fail to detect some Dientamoeba fragilis infections.[64]

Further information: Dientamoeba fragilis


The various conditions that can cause IBS, outlined in the Diagnosis and Etiology sections above, require specific treatments. High rates of success in resolving IBS symptoms have been reported when treatment is specifically tailored to the underlying causes revealed through proper testing for the range of known causes of IBS symptoms.[44]

A questionnaire in 2006 designed to identify patients’ perceptions about IBS, their preferences on the type of information they need, as well as educational media and expectations from health care providers, revealed misperceptions about IBS developing into other conditions, including colitis, malnutrition, and cancer.[66]

The survey found IBS patients were most interested in learning about foods to avoid (60%), causes of IBS (55%), medications (58%), coping strategies (56%), and psychological factors related to IBS (55%). The respondents indicated that they wanted their physicians to be available via phone or e-mail following a visit (80%), have the ability to listen (80%), and provide hope (73%) and support (63%).


There are a number of dietary changes a person with IBS can make to prevent the overreaction of the gastrocolic reflex and lessen pain, discomfort, and bowel dysfunction. Having soluble fiber foods and supplements, substituting milk products with soy or rice products, being careful with fresh fruits and vegetables that are high in insoluble fiber, and eating frequent meals of small amounts of food, can all help to lessen the symptoms of IBS. Foods and beverages to be avoided or minimized include red meat, oily or fatty and fried products, milk products (even when there is no lactose intolerance), solid chocolate, coffee (regular and decaffeinated), alcohol, carbonated beverages, especially those containing sorbitol or other artificial sweeteners. Care, however, should be taken to avoid adding foods to the diet to which the patient is allergic or intolerant.[67]

Definitive determination of dietary issues can be accomplished by testing for the physiological effects of specific foods. The ELISA food allergy panel can identify specific foods to which a patient has a reaction. Other testing can determine if there are nutritional deficiencies secondary to diet that may also play a role. Removal of foods causing IgG immune response as measured using the ELISA food panel has been shown to substantially decrease symptoms of IBS in several studies.[68]

There is no evidence that digestion of food or absorption of nutrients is problematic for those with IBS at rates different from those without IBS. However, the very act of eating or drinking can provoke an overreaction of the gastrocolic response in some patients with IBS due to their heightened visceral sensitivity, and this can lead to abdominal pain, diarrhea, and/or constipation.[69]

Several of the most common dietary triggers are well-established by clinical studies at this point; research has shown that IBS patients are hypersensitive to fats and fructose.[70][71]

It also appears that some foods are more difficult for the gut as evidenced by elevated food-specific IgG4 antibodies being present,[72][73] while others increase colonic contractions, which may be painful, due to increased visceral sensitivity in IBS sufferers.[74]


In patients who do not have diarrhea predominant irritable bowel, soluble fiber at doses of 20 grams per day can reduce overall symptoms but will not reduce pain. The research supporting dietary fiber contains conflicting, small studies that are complicated by the heterogeneity of types of fiber and doses used.[75] The one meta-analysis that controlled for solubility found that only soluble fiber improved global symptoms of irritable bowel and neither type of fiber reduced pain[75] Positive studies have used 20-30 grams per day of psyllium seed.[76][77] One study specifically examined the effect of dose and found that 20 grams of ispaghula husk was better than 10 grams and equivalent to 30 grams per day[78]An uncontrolled study noted increased symptoms with insoluble fibers.[79] It is unclear if these symptoms are truly increased compared to a control group. If the symptoms are increased, it is unclear if these patients were diarrhea predominant (which can be exacerbated by insoluble fiber[80][81]), or if the increase is temporary before benefit occurs. There is a mistaken presumption that fiber therapy only works for those with constipation. In actuality soluble fiber can act as a counterbalance to both constipation, by retaining water in the bowel, and for diarrhea, by absorbing excess water.


Initial treatments

Medications may consist of stool softeners and laxatives in constipation-predominant IBS, and antidiarrheals (e.g., opioid or opioid analogs such as loperamide, diphenoxylate or codeine) in diarrhea-predominant IBS for mild symptoms.[82][83][84]

Main article: Laxative

For patients who do not adequately respond to dietary fiber, osmotic agents such as polyethylene glycol, sorbitol, and lactulose can help avoid 'cathartic colon' which has been associated with stimulant laxatives.[85] Among the osmotic laxatives, 17 to 26 grams/day of polyethylene glycol (PEG) has been well studied.

Main article: Antispasmodic

The use of antispasmodic drugs (e.g. anticholinergics such as hyoscyamine or dicyclomine) may help patients, especially those with cramps or diarrhea. A meta-analysis by the Cochrane Collaboration concludes that if 6 patients are treated with antispasmodics, 1 patient will benefit (number needed to treat = 6).[82] Antispasmodics can be divided in two groups: neurotropics and musculotropics. Neurotropics, such as atropine, act at the nerve fibre of the parasympathicus but also affect other nerves and have side effects. Musculotropics such as mebeverine act directly at the smooth muscle of the gastrointestinal tract, relieving spasm without affecting normal gut motility. Since this action is not mediated by the autonomic nervous system, the usual anticholinergic side effects are absent. Antispasmodic drugs are also available in combination with tranquilizers or barbiturates, such as chlordiazepoxide and Donnatal. The value of the combination therapies has not been established.

Drugs affecting serotonin

Drugs affecting serotonin (5-HT) in the intestines can help reduce symptoms.[86] Serotonin stimulates the gut motility and so agonists can help constipation predominate irritable bowel while antagonists can help diarrhea predominant irritable bowel:

  • Tegaserod, a selective 5-HT4 agonist for IBS-C, is available for relieving IBS constipation in women and chronic idiopathic constipation in men and women. On March 30, 2007, the Food and Drug Administration (FDA) requested that Novartis Pharmaceuticals voluntarily discontinue marketing of Zelnorm (tegaserod) based on the recently identified finding of an increased risk of serious cardiovascular adverse events (heart problems) associated with use of the drug. Novartis agreed to voluntarily suspend marketing of the drug in the United States and in many other countries. On July 27, 2007 the Food and Drug Administration (FDA) approved a limited treatment IND program for Zelnorm in the USA to allow restricted access to the medication for patients in need if no comparable alternative drug or therapy is available to treat the disease. The USA FDA had issued two previous warnings about the serious consequences of Tegaserod. In 2005, Tegaserod was rejected as an IBS medication by the European Union. Tegaserod, marketed as Zelnorm in the United States, was the only agent approved to treat the multiple symptoms of IBS (in women only), including constipation, abdominal pain and bloating. A meta-analysis by the Cochrane Collaboration concludes that if 17 patients are treated with typical doses of tegaserod, 1 patient will benefit (number needed to treat = 17).[87]
  • Selective serotonin reuptake inhibitor anti-depressants (SSRIs), because of their serotonergic effect, would seem to help IBS, especially patients who are constipation predominant. Initial crossover studies[88] and randomized controlled trials[89][90][91] support this role.
  • Alosetron, a selective 5-HT3 antagonist for IBS-D, which is only available for women in the United States under a restricted access program, due to severe risks of side-effects if taken mistakenly by IBS-A or IBS-C sufferers.
  • Cilansetron, also a selective 5-HT3 antagonist, is undergoing further clinical studies in Europe for IBS-D sufferers. In 2005, Solvay Pharmaceuticals withdrew Cilansetron from the United States regulatory approval process after receiving a "not approvable" action letter from the FDA requesting additional clinical trials.

Other agents

Anti-depressants include both tricyclic antidepressants (TCAs) and the newer selective serotonin reuptake inhibitors (SSRIs). In addition to improving symptoms via treating any co-existing depression, TCAs have anti-cholinergic actions while SSRIs are serotonergic. Thus in theory, TCAs would best treat diarrhea-predominant IBS while SSRIs would best treat constipation-predominant IBS. A meta-analysis of randomized controlled trials of mainly TCAs found 3 patients have to be treated with TCAs for one patient to improve (number needed to treat = 3).[92] A separate randomized controlled trial found that TCAs are best for patients with diarrhea-predominant IBS.[93]

Recent studies have suggested that rifaximin can be used as an effective treatment for abdominal bloating and flatulence,[94][50] giving more credibility to the potential role of bacterial overgrowth in some patients with IBS.[95]

Ibodutant is a tachykinin receptor antagonist currently under investigation for the use against IBS.

The multi-herbal extract Iberogast was found to be significantly superior to placebo via both an abdominal pain scale and an IBS symptom score after four weeks of treatment.[96]

Enteric coated peppermint oil capsules has been advocated for IBS symptoms in adults and children;[97] however, results from trials have been inconsistent.[98][99]

For severe diarrhea-predominant IBS, more potent opioids may be used, such as codeine or propoxyphene; refractory cases may even be treated with paregoric, or, more rarely, deodorized tincture of opium or morphine sulfate. The use of opioids remains controversial due to the lack of evidence supporting their benefit and the potential risk of tolerance, physical dependence and addiction.[100]

Cannabis has theoretical support for its role,[101][102] but has not been subject of clinical studies. Although illegal in many countries, it has been prescribed to patients in nations such as Canada and The Netherlands. Some of the argued benefits of cannabis are the reduction of pain and nausea, appetite stimulation, and assisting in falling asleep.

Psychotherapy and hypnotherapy

There is a strong brain-gut component to IBS, and cognitive therapy may improve symptoms in a portion of patients in conjunction with antidepressants.[103] In a randomized controlled trial of referred patients, cognitive behavioral therapy helped even though patients in this study did not have any psychiatric diagnoses.[104]

Gut-directed or gut-specific hypnotherapy or self-hypnosis is one of the most promising areas of IBS treatment. An uncontrolled study shows that symptom reduction/elimination from IBS hypnotherapy can last at least five years.[105]

Relaxation therapy in four 90-minute group sessions was found to help in a randomized controlled trial.[106]

Alternative treatments


Probiotics are generally accepted to be potentially beneficial strains of bacteria and yeast, often found in the human gut. One research study has shown a clear link between the ingestion of Lactobacillus plantarum 299v (Lp299v) and sufferers of IBS who reported resolution of their abdominal pain.[107] Another study showed the utility of B. infantis 35625, a strain of Bifidobacteria, in normalizing bowel movement frequency in sufferers of IBS.[108] Some practitioners of Integrative Medicine now recommend a strain of Lactobacillus rhamnosus known commonly as "LGG" after its discoverers Gorbach and Goldin. This strain in particular has shown an ability to endure the acidic environment of the stomach and survive until presentation to the intestinal tract.

A prospective placebo-controlled study found patients with diarrhea predominant IBS taking Saccharomyces boulardii, a probiotic yeast, had a significant reduction on the number and improvement in consistency of bowel movements.[109]


Many sufferers of IBS seek relief using Acupuncture, a component of Traditional Chinese Medicine. The meta-analysis by the Cochrane Collaboration concluded 'Most of the trials included in this review were of poor quality and were heterogeneous in terms of interventions, controls, and outcomes measured. With the exception of one outcome in common between two trials, data were not combined. Therefore, it is still inconclusive whether acupuncture is more effective than sham acupuncture or other interventions for treating IBS'.[110] One practitioner of Traditional Chinese Medicine asserts that IBS has become a bit of a "garbage diagnosis" for some medical practitioners. Traditional Chinese Medicine does not recognize the Western diagnosis of IBS per se, as the named condition has no definitive single test for diagnosis, clear cause, or cure. Traditional Chinese Medicine approaches IBS on an individual symptom-by-symptom basis, rather than recognizing a standard "IBS" diagnosis, which then warrants a blanket "IBS" treatment.[111] According to the National Institutes of Health, "Preclinical studies have documented acupuncture's effects, but they have not been able to fully explain how acupuncture works within the framework of the Western system of medicine that is commonly practiced in the United States."[112]


File:Wiki ibs prevalence.jpg

Percentage of population with IBS reported in various studies in different countries

By Country: Studies have reported that the prevalence of IBS varies by country and by age range examined. The bar graph at right shows the percentage of the population reporting symptoms of IBS in studies from various geographic regions (see table below for references).

The following table contains a list of studies performed in different countries that measured the prevalence of IBS and IBS-like symptoms:

Percentage of Population Reporting Symptoms of IBS in Various Studies from Various Geographic Areas ** Check the Rome criteria studies (eg, at PubMed) and see how the reported prevalence rates drop! Also, one should be wary of trusting many of these study results - ref. 'Havidol'.
Country Prevalence Author/Year Notes
Canada 6%[113] Boivin,2001
Japan 10%[114] Quigley,2006 Study measured prevalence of GI abdominal pain/cramping
United Kingdom 8.2%[115]




Prevalence increased substantially 1970-2004
United States 14.1%[117] Hungin, 2005 Most undiagnosed
United States 15%[113] Boivin,2001 Estimate
Pakistan 14%[118] Jafri, 2007 Much more common in 16-30 age range. Of IBS patients, 56% male, 44% female
Pakistan 34%[119] Jafri,2005 College students
Mexico City 35%[120] Schmulson, 2006 n=324. Also measured functional diarrhea and functional vomiting. High rates attributed to "stress of living in a populated city."
Brazil 43%[114] Quigley,2006 Study measured prevalence of GI abdominal pain/cramping
Mexico 46%[114] Quigley,2006 Study measured prevalence of GI abdominal pain/cramping

Returning Travelers: A study of United States residents returning from international travel found a high rate of IBS and persistent diarrhea which developed during travel and persisted upon return. The study examined 83 subjects in Utah, most of whom were returning missionaries. Of the 68 who completed the gastrointestinal questionnaire, 27 reported persistent diarrhea that developed while traveling, and 10 reported persistent IBS that developed while traveling.[121]

Economic cost of IBS

The aggregate cost of irritable bowel syndrome in the United States has been estimated at $1.7-$10 billion in direct medical costs, with an additional $20 billion in indirect costs, for a total of $21.7-$30 billion.[122] A study by a managed care company comparing medical costs of IBS patients to non-IBS controls identified a 49% annual increase in medical costs associated with a diagnosis of IBS.[123] A 2007 study from a managed care oganization found that IBS patients incurred average annual direct costs of $5,049 and $406 in out-of-pocket expenses.[124]A study of workers with IBS found that they reported a 34.6% loss in productivity, corresponding to 13.8 hours lost per 40 hour week.[125] A study of employer-related health costs from a Fortune 100 company conducted with data from the 1990s found IBS patients incurred US $4527 in claims costs vs. $3276 for controls.[126] A study on Medicaid costs conducted in 2003 by the University of Georgia's College of Pharmacy and Novartis found IBS was associated in an increase of $962 in Medicaid costs in California, and $2191 in North Carolina. IBS patients had higher costs for physician visits, outpatients visits, and prescription drugs. The study suggested the costs associated with IBS were comparable to those found in asthma patients.[127]

Research spending on IBS

Further information: NIH funding of IBS Research

The National Institutes of Health provides a searchable database for grant awards since 1974 on its CRISP database, and provides dollar amounts for recent awards on its Intramural Grant Award Page. In 2006, the NIH awarded approximately 56 grants related to IBS, totalling approximately $18,787,710.


IBS does not lead to more serious conditions in most patients.[18][19][20][21][22] But it is a source of chronic pain, fatigue and other symptoms, and it increases a patient's medical costs,[124][123] and contributes to work absenteeism.[125][128] Researchers have reported that the high prevalence of IBS,[113][116][120] in conjunction with increased costs produces a disease with a high societal cost.[122] It is also regared as a chronic illness and can dramatically affect the quality of a sufferer's life.

See also


  1. 1.0 1.1 Mayer EA (2008). Clinical practice. Irritable bowel syndrome. N. Engl. J. Med. 358 (16): 1692–9.
  2. Intestinal Infection
  3. Yang CM, Li YQ (2007). [The therapeutic effects of eliminating allergic foods according to food-specific IgG antibodies in irritable bowel syndrome]. Zhonghua Nei Ke Za Zhi 46 (8): 641–3.
  4. 4.0 4.1 4.2 Stark D, van Hal S, Marriott D, Ellis J, Harkness J (2007). Irritable bowel syndrome: a review on the role of intestinal protozoa and the importance of their detection and diagnosis. Int. J. Parasitol. 37 (1): 11–20.
  5. Schmulson MW, Chang L (1999). Diagnostic approach to the patient with irritable bowel syndrome. Am. J. Med. 107 (5A): 20S–26S.
  6. 6.0 6.1 Talley NJ (2006). Irritable bowel syndrome. Intern Med J 36 (11): 724–8.
  7. Holten KB, Wetherington A, Bankston L (2003). Diagnosing the patient with abdominal pain and altered bowel habits: is it irritable bowel syndrome?. Am Fam Physician 67 (10): 2157–62.
  8. 8.0 8.1 Yawn BP, Lydick E, Locke GR, Wollan PC, Bertram SL, Kurland MJ (2001). Do published guidelines for evaluation of irritable bowel syndrome reflect practice?. BMC gastroenterology 1: 11.
  9. 9.0 9.1 Fass R, Longstreth GF, Pimentel M, et al (2001). Evidence- and consensus-based practice guidelines for the diagnosis of irritable bowel syndrome. Arch. Intern. Med. 161 (17): 2081–8.
  10. Talley NJ (2006). A unifying hypothesis for the functional gastrointestinal disorders: really multiple diseases or one irritable gut?. Reviews in gastroenterological disorders 6 (2): 72–8.
  11. Spiegel BM, DeRosa VP, Gralnek IM, Wang V, Dulai GS (2004). Testing for celiac sprue in irritable bowel syndrome with predominant diarrhea: a cost-effectiveness analysis. Gastroenterology 126 (7): 1721–32.
  12. Drisko et al (2006). Treating Irritable Bowel Syndrome with a Food Elimination Diet Followed by Food Challenge and Probiotics. Journal of the American College of Nutrition 25 (6): 514–22.
  13. Vernia P, Ricciardi MR, Frandina C, Bilotta T, Frieri G (1995). Lactose malabsorption and irritable bowel syndrome. Effect of a long-term lactose-free diet. The Italian journal of gastroenterology 27 (3): 117–21.
  14. - The United States National Institutes of Health Celiac Disease Page
  15. Cole JA, Rothman KJ, Cabral HJ, Zhang Y, Farraye FA (2006). Migraine, fibromyalgia, and depression among people with IBS: a prevalence study. BMC gastroenterology 6: 26.
  16. Kurland JE, Coyle WJ, Winkler A, Zable E (2006). Prevalence of irritable bowel syndrome and depression in fibromyalgia. Dig. Dis. Sci. 51 (3): 454–60.
  17. Frissora CL, Koch KL (2005). Symptom overlap and comorbidity of irritable bowel syndrome with other conditions. Current gastroenterology reports 7 (4): 264–71.
  18. 18.0 18.1 Bercik P, Verdu EF, Collins SM (2005). Is irritable bowel syndrome a low-grade inflammatory bowel disease?. Gastroenterol. Clin. North Am. 34 (2): 235–45, vi-vii.
  19. 19.0 19.1 Quigley EM (2005). Irritable bowel syndrome and inflammatory bowel disease: interrelated diseases?. Chinese journal of digestive diseases 6 (3): 122–32.
  20. 20.0 20.1 Simrén M, Axelsson J, Gillberg R, Abrahamsson H, Svedlund J, Björnsson ES (2002). Quality of life in inflammatory bowel disease in remission: the impact of IBS-like symptoms and associated psychological factors. Am. J. Gastroenterol. 97 (2): 389–96.
  21. 21.0 21.1 Minderhoud IM, Oldenburg B, Wismeijer JA, van Berge Henegouwen GP, Smout AJ (2004). IBS-like symptoms in patients with inflammatory bowel disease in remission; relationships with quality of life and coping behavior. Dig. Dis. Sci. 49 (3): 469–74.
  22. 22.0 22.1 García Rodríguez LA, Ruigómez A, Wallander MA, Johansson S, Olbe L (2000). Detection of colorectal tumor and inflammatory bowel disease during follow-up of patients with initial diagnosis of irritable bowel syndrome. Scand. J. Gastroenterol. 35 (3): 306–11.
  23. Corazziari et al. (2008). Gallstones, cholecystectomy and irritable bowel syndrome (IBS) MICOL population-based study.. Dig Liver Dis..
  24. Cole JA, Yeaw JM, Cutone JA, et al (2005). The incidence of abdominal and pelvic surgery among patients with irritable bowel syndrome. Dig. Dis. Sci. 50 (12): 2268–75.
  25. Longstreth GF, Yao JF (2004). Irritable bowel syndrome and surgery: a multivariable analysis. Gastroenterology 126 (7): 1665–73.
  26. Tietjen GE, Bushnell CD, Herial NA, Utley C, White L, Hafeez F (2007). Endometriosis is associated with prevalence of comorbid conditions in migraine. Headache 47 (7): 1069–78.
  27. Interstitial cystitis (Mayo Clinic)
  28. Thabane M, Kottachchi DT, Marshall JK (2007). The incidence and prognosis of post-infectious irritable bowel syndrome.. Aliment Pharmacol Ther 26 (4): 535–44.
  29. El-Omar EM, Carrington M, Chow WH, et al (2000). Interleukin-1 polymorphisms associated with increased risk of gastric cancer. Nature 404 (6776): 398–402.
  30. Brown PW (1950). The irritable bowel syndrome. Rocky Mountain medical journal 47 (5): 343–6.
  31. Whitehead WE, Winget C, Fedoravicius AS, Wooley S, Blackwell B (1982). Learned illness behavior in patients with irritable bowel syndrome and peptic ulcer. Dig. Dis. Sci. 27 (3): 202–8.
  32. Svedlund J, Sjödin I (1985). A psychosomatic approach to treatment in the irritable bowel syndrome and peptic ulcer disease with aspects of the design of clinical trials. Scand. J. Gastroenterol. Suppl. 109: 147–51.
  33. Damianos AJ, McGarrity TJ (1997). Treatment strategies for Helicobacter pylori infection. American family physician 55 (8): 2765–74, 2784–6.
  34. Fukudo S, Nomura T, Muranaka M, Taguchi F (1993). Brain-gut response to stress and cholinergic stimulation in irritable bowel syndrome. A preliminary study. J. Clin. Gastroenterol. 17 (2): 133–41.
  35. Orr WC, Crowell MD, Lin B, Harnish MJ, Chen JD (1997). Sleep and gastric function in irritable bowel syndrome: derailing the brain-gut axis. Gut 41 (3): 390–3.
  36. Miwa J, Echizen H, Matsueda K, Umeda N (2001). Patients with constipation-predominant irritable bowel syndrome (IBS) may have elevated serotonin concentrations in colonic mucosa as compared with diarrhea-predominant patients and subjects with normal bowel habits. Digestion 63 (3): 188–94.
  37. McGowan K, Kane A, Asarkof N, et al (1983). Entamoeba histolytica causes intestinal secretion: role of serotonin. Science 221 (4612): 762–4.
  38. McGowan K, Guerina V, Wicks J, Donowitz M (1985). Secretory hormones of Entamoeba histolytica. Ciba Found. Symp. 112: 139–54.
  39. Banu, Naheed, et al. (2005). Neurohumoral alterations and their role in amoebiasis.. Indian J. Clin Biochem 20 (2): 142–5.
  40. Gwee KA, Collins SM, Read NW, et al (2003). Increased rectal mucosal expression of interleukin 1beta in recently acquired post-infectious irritable bowel syndrome. Gut 52 (4): 523–6.
  41. Liebregts T, Adam B, Bredack C, et al (2007). Immune activation in patients with irritable bowel syndrome. Gastroenterology 132 (3): 913–20.
  42. Cenac N, Andrews CN, Holzhausen M, et al (2007). Role for protease activity in visceral pain in irritable bowel syndrome. J. Clin. Invest. 117 (3): 636–47.
  43. Hussain R, Jaferi W, Zuberi S, et al (1997). Significantly increased IgG2 subclass antibody levels to Blastocystis hominis in patients with irritable bowel syndrome. Am. J. Trop. Med. Hyg. 56 (3): 301–6.
  44. 44.0 44.1 Stephen Wangen (2006). Irritable bowel syndrome solution, Seattle, WA: Innate Health Group. Excerpted with author's permission at [1]
  45. Spiegel BM, et al (2004). Testing for celiac sprue in irritable bowel syndrome with predominant diarrhea: a cost-effectiveness analysis.. Gastroenterology 126 (7): 1721–32.
  46. Shahbazkhani B, et al (2003). Coeliac disease presenting with symptoms of irritable bowel syndrome.. Aliment Pharmacol Therapy 18 (2): 231–5.
  47. Li H, et al (2007). Allergen-IgE complexes trigger CD23-dependent CCL20 release from human intestinal epithelial cells.. Gastroenterology 133 (6): 1905–15.
  48. (2007). The therapeutic effects of eliminating allergic foods according to food-specific IgG antibodies in irritable bowel syndrome - Article in Chinese. Zhonghua Nei Ke Za Zhi. 46 (8): 641–3.
  49. Drisko et al (2006). Treating Irritable Bowel Syndrome with a Food Elimination Diet Followed by Food Challenge and Probiotics. Journal of the American College of Nutrition 25 (6): 514–22.
  50. 50.0 50.1 Pimentel M, Park S, Mirocha J, Kane SV, Kong Y (2006). The effect of a nonabsorbed oral antibiotic (rifaximin) on the symptoms of the irritable bowel syndrome: a randomized trial. Ann. Intern. Med. 145 (8): 557–63. Cite error: Invalid <ref> tag; name "pmid17043337" defined multiple times with different content
  51. Posserud I, Stotzer PO, Björnsson ES, Abrahamsson H, Simrén M (2007). Small intestinal bacterial overgrowth in patients with irritable bowel syndrome. Gut 56 (6): 802–8.
  52. 52.0 52.1 Yakoob J, Jafri W, Jafri N, et al (2004). Irritable bowel syndrome: in search of an etiology: role of Blastocystis hominis. Am. J. Trop. Med. Hyg. 70 (4): 383–5.
  53. 53.0 53.1 Giacometti A, Cirioni O, Fiorentini A, Fortuna M, Scalise G (1999). Irritable bowel syndrome in patients with Blastocystis hominis infection. Eur. J. Clin. Microbiol. Infect. Dis. 18 (6): 436–9.
  54. Qadri SM, al-Okaili GA, al-Dayel F (1989). Clinical significance of Blastocystis hominis. J. Clin. Microbiol. 27 (11): 2407–9.
  55. Markell EK, Udkow MP (1986). Blastocystis hominis: pathogen or fellow traveler?. Am. J. Trop. Med. Hyg. 35 (5): 1023–6.
  56. Windsor J (2007). B. hominis and D. fragilis: Neglected human protozoa. British Biomedical Scientist: 524–7.
  57. Stensvold R, Brillowska-Dabrowska A, Nielsen HV, Arendrup MC (2006). Detection of Blastocystis hominis in unpreserved stool specimens by using polymerase chain reaction. J. Parasitol. 92 (5): 1081–7.
  58. Yakoob J, Jafri W, Jafri N, Islam M, Asim Beg M (2004). In vitro susceptibility of Blastocystis hominis isolated from patients with irritable bowel syndrome. Br. J. Biomed. Sci. 61 (2): 75–7.
  59. Haresh K, Suresh K, Khairul Anus A, Saminathan S (1999). Isolate resistance of Blastocystis hominis to metronidazole. Trop. Med. Int. Health 4 (4): 274–7.
  60. Markell EK, Udkow MP (1986). Blastocystis hominis: pathogen or fellow traveler?. Am. J. Trop. Med. Hyg. 35 (5): 1023–6.
  61. Ok UZ, Girginkardeşler N, Balcioğlu C, Ertan P, Pirildar T, Kilimcioğlu AA (1999). Effect of trimethoprim-sulfamethaxazole in Blastocystis hominis infection. Am. J. Gastroenterol. 94 (11): 3245–7.
  62. 62.0 62.1 Lagacé-Wiens PR, VanCaeseele PG, Koschik C (2006). Dientamoeba fragilis: an emerging role in intestinal disease. CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne 175 (5): 468–9.
  63. Amin OM (2002). Seasonal prevalence of intestinal parasites in the United States during 2000. Am. J. Trop. Med. Hyg. 66 (6): 799–803.
  64. 64.0 64.1 Stensvold CR, Arendrup MC, Mølbak K, Nielsen HV (2007). The prevalence of Dientamoeba fragilis in patients with suspected enteroparasitic disease in a metropolitan area in Denmark. Clin. Microbiol. Infect. 13 (8): 839–42.
  65. Borody T, Warren E, Wettstein A, et al. (2002). Eradication of Dientamoeba fragilis can resolve IBS-like symptoms.. J Gastroenterol Hepatol 17 (Suppl; pages=A103).
  66. Halpert AD, Thomas AC, Hu Y, Morris CB, Bangdiwala SI, Drossman DA (2006). A survey on patient educational needs in irritable bowel syndrome and attitudes toward participation in clinical research. J Clin Gastroenterol 40 (1): 37–43.
  67. Heather Van Vorous (2000). Eating for IBS: 175 Delicious, Nutritious, Low-Fat, Low-Residue Recipes to Stabilize the Touchiest Tummy, Marlowe & Company. Excerpted with author's permission at Help for Irritable Bowel Syndrome (see IBS Diet Section)
  68. Atkinson W, Sheldon TA, Shaath N, Whorwell PJ (2004). Food elimination based on IgG antibodies in irritable bowel syndrome: a randomised controlled trial. Gut 53 (10): 1459–64.
  69. Sjölund K, Ekman R, Lindgren S, Rehfeld J (1996). Disturbed motilin and cholecystokinin release in the irritable bowel syndrome.. Scand J Gastroenterol 31 (11): 1110–4.
  70. Caldarella MP, Milano A, Laterza F, Sacco F, Balatsinou C, Lapenna D, Pierdomenico SD, Cuccurullo F, Neri M (2005). Visceral sensitivity and symptoms in patients with constipation- or diarrhea-predominant irritable bowel syndrome (IBS): effect of a low-fat intraduodenal infusion. Am J Gastroenterol 100 (2): 383–9.
  71. Choi, Y. Fats, Fructose May Contribute to IBS Symptoms. ACG 68th Annual Scientific Meeting: Abstract 21, presented October 13, 2003; Abstract 547, presented October 14, 2003.
  72. Zar S, Benson MJ, Kumar D (2005). Food-specific serum IgG4 and IgE titers to common food antigens in irritable bowel syndrome. Am J Gastroenterol 100 (7): 1550–7.
  73. Zar S, Mincher L, Benson MJ, Kumar D (2005). Food-specific IgG4 antibody-guided exclusion diet improves symptoms and rectal compliance in irritable bowel syndrome. Scand J Gastroenterol 40 (7): 800–7.
  74. Mayer EA, Berman S, Suyenobu B, Labus J, Mandelkern MA, Naliboff BD, Chang L (2005). Differences in brain responses to visceral pain between patients with irritable bowel syndrome and ulcerative colitis. Pain 115 (3): 398–409.
  75. 75.0 75.1 Bijkerk C, Muris J, Knottnerus J, Hoes A, de Wit N (2004). Systematic review: the role of different types of fiber in the treatment of irritable bowel syndrome.. Aliment Pharmacol Ther 19 (3): 245–51. Cite error: Invalid <ref> tag; name "pmid14984370" defined multiple times with different content
  76. Prior A, Whorwell P (1987). Double blind study of ispaghula in irritable bowel syndrome.. Gut 28 (11): 1510–3.
  77. Jalihal A, Kurian G (1990). Ispaghula therapy in irritable bowel syndrome: improvement in overall well-being is related to reduction in bowel dissatisfaction.. J Gastroenterol Hepatol 5 (5): 507–13.
  78. Kumar A, Kumar N, Vij J, Sarin S, Anand B (1987). Optimum dosage of ispaghula husk in patients with irritable bowel syndrome: correlation of symptom relief with whole gut transit time and stool weight.. Gut 28 (2): 150–5.
  79. Francis CY, Whorwell PJ (1994). Bran and irritable bowel syndrome: time for reappraisal. Lancet 344 (8914): 39–40.
  80. Cann P, Read N, Holdsworth C, Barends D (1984). Role of loperamide and placebo in management of irritable bowel syndrome (IBS).. Dig Dis Sci 29 (3): 239–47.
  81. Cann P, Read N, Holdsworth C (1984). What is the benefit of coarse wheat bran in patients with irritable bowel syndrome?. Gut 25 (2): 168–73.
  82. 82.0 82.1 Quartero A, Meineche-Schmidt V, Muris J, Rubin G, de Wit N (2005). Bulking agents, antispasmodic and antidepressant medication for the treatment of irritable bowel syndrome.. Cochrane Database Syst Rev: CD003460.
  83. Lesbros-Pantoflickova D, Michetti P, Fried M, Beglinger C, Blum A (2004). Meta-analysis: The treatment of irritable bowel syndrome.. Aliment Pharmacol Ther 20 (11-12): 1253–69.
  84. Jailwala J, Imperiale T, Kroenke K (2000). Pharmacologic treatment of the irritable bowel syndrome: a systematic review of randomized, controlled trials.. Ann Intern Med 133 (2): 136–47.
  85. Joo J, Ehrenpreis E, Gonzalez L, Kaye M, Breno S, Wexner S, Zaitman D, Secrest K (1998). Alterations in colonic anatomy induced by chronic stimulant laxatives: the cathartic colon revisited.. J Clin Gastroenterol 26 (4): 283–6.
  86. Talley N (2001). Serotoninergic neuroenteric modulators.. Lancet 358 (9298): 2061–8.
  87. Evans B, Clark W, Moore D, Whorwell P (2004). Tegaserod for the treatment of irritable bowel syndrome.. Cochrane Database Syst Rev: CD003960.
  88. Tack J, Broekaert D, Fischler B, Oudenhove L, Gevers A, Janssens J (2006). A controlled crossover study of the selective serotonin reuptake inhibitor citalopram in irritable bowel syndrome.. Gut 55 (8): 1095–103.
  89. Vahedi H, Merat S, Rashidioon A, Ghoddoosi A, Malekzadeh R (2005). The effect of fluoxetine in patients with pain and constipation-predominant irritable bowel syndrome: a double-blind randomized-controlled study.. Aliment Pharmacol Ther 22 (5): 381–5.
  90. Creed F, Fernandes L, Guthrie E, Palmer S, Ratcliffe J, Read N, Rigby C, Thompson D, Tomenson B (2003). The cost-effectiveness of psychotherapy and paroxetine for severe irritable bowel syndrome.. Gastroenterology 124 (2): 303–17.
  91. Tabas G, Beaves M, Wang J, Friday P, Mardini H, Arnold G (2004). Paroxetine to treat irritable bowel syndrome not responding to high-fiber diet: a double-blind, placebo-controlled trial.. Am J Gastroenterol 99 (5): 914–20.
  92. Jackson J, O'Malley P, Tomkins G, Balden E, Santoro J, Kroenke K (2000). Treatment of functional gastrointestinal disorders with antidepressant medications: a meta-analysis.. Am J Med 108 (1): 65–72.
  93. Drossman D, Toner B, Whitehead W, Diamant N, Dalton C, Duncan S, Emmott S, Proffitt V, Akman D, Frusciante K, Le T, Meyer K, Bradshaw B, Mikula K, Morris C, Blackman C, Hu Y, Jia H, Li J, Koch G, Bangdiwala S (2003). Cognitive-behavioral therapy versus education and desipramine versus placebo for moderate to severe functional bowel disorders.. Gastroenterology 125 (1): 19–31.
  94. Sharara AI, Aoun E, Abdul-Baki H, Mounzer R, Sidani S, Elhajj I (2006). A randomized double-blind placebo-controlled trial of rifaximin in patients with abdominal bloating and flatulence. Am J Gastroenterol 101 (2): 326–33.
  95. Quigley EM (2006). Germs, gas and the gut; the evolving role of the enteric flora in IBS. Am J Gastroenterol 101 (2): 334–5.
  96. Madisch A, Holtmann G, Plein K, Holz J (2004). Treatment of irritable bowel syndrome with herbal preparations: results of a double-blind, randomized, placebo-controlled, multi-centre trial. Aliment Pharmacol Ther 19: 271–9.
  97. Hadley SK, Gaarder SM (2005). Treatment of irritable bowel syndrome. Am Fam Physician 72 (12): 2501–6.
  98. Nash P, Gould SR, Bernardo DE (1986). Peppermint oil does not relieve the pain of irritable bowel syndrome. Br J Clin Pract 40 (7): 292–3.
  99. Liu JH, Chen GH, Yeh HZ, Huang CK, Poon SK (1997). Enteric-coated peppermint-oil capsules in the treatment of irritable bowel syndrome: a prospective, randomized trial. J. Gastroenterol. 32 (6): 765–8.
  100. Warfield, Carol A.; Zahid H. Bajwa (2003). Principles and Practice of Pain Medicine, McGraw-Hill Professional.
  101. Massa F, Storr M, Lutz B (2005). The endocannabinoid system in the physiology and pathophysiology of the gastrointestinal tract.. J Mol Med 83 (12): 944–54.
  102. Russo EB (2004). Clinical endocannabinoid deficiency (CECD): can this concept explain therapeutic benefits of cannabis in migraine, fibromyalgia, irritable bowel syndrome and other treatment-resistant conditions?. Neuro Endocrinol. Lett. 25 (1-2): 31–9.
  103. Kennedy T, Jones R, Darnley S, Seed P, Wessely S, Chalder T (2005). Cognitive behaviour therapy in addition to antispasmodic treatment for irritable bowel syndrome in primary care: randomised controlled trial. BMJ 331 (7514): 435.
  104. Heymann-Mönnikes I, Arnold R, Florin I, Herda C, Melfsen S, Mönnikes H (2000). The combination of medical treatment plus multicomponent behavioral therapy is superior to medical treatment alone in the therapy of irritable bowel syndrome.. Am J Gastroenterol 95 (4): 981–94.
  105. Gonsalkorale WM, Miller V, Afzal A, Whorwell PJ (2003). Long term benefits of hypnotherapy for irritable bowel syndrome. Gut 52 (11): 1623–9.
  106. van der Veek PP, van Rood YR, Masclee AA (2007). Clinical trial: short- and long-term benefit of relaxation training for irritable bowel syndrome. Aliment. Pharmacol. Ther. 26 (6): 943–52.
  107. Niedzielin K, Kordecki H, Birkenfeld B (2001). A controlled, double-blind, randomized study on the efficacy of Lactobacillus plantarum 299V in patients with irritable bowel syndrome. Eur J Gastroenterol Hepatol 13 (10): 1143–7.
  108. New Studies Examine the Evidence of Probiotics on IBS (Oct 2005). American College of Gastrointerologists. Retrieved on March 2, 2006
  109. Maupas J, Champemont P, Delforge M (1983). Treatment of irritable bowel syndrome with Saccharomyces boulardii: a double blind, placebo controlled study. Medicine Chirurgie Digestives 12(1): 77–9.
  110. Lim B, Manheimer E, Lao L, Ziea E, Wisniewski J, Liu J, Berman B (2006). Acupuncture for treatment of irritable bowel syndrome.. Cochrane Database Syst Rev: CD005111.
  111. Irritable Bowel Syndrome - A Traditional Chinese Medicine Perspective, (2006). Al Stone L.Ac. Retrieved on February 14, 2006.
  112. Get the Facts, Acupuncture, (2006). National Institute of Health. Retrieved on March 2, 2006.
  113. 113.0 113.1 113.2 Boivin M. (2001 Oct;15). Socioeconomic impact of irritable bowel syndrome in. Canada. Can J Gastroenterol. Suppl B: :8B–11B..
  114. 114.0 114.1 114.2 Quigley EM, Locke GR, Mueller-Lissner S, Paulo LG, Tytgat GN, Helfrich I, Schaefer E. Prevalence and management of abdominal cramping and pain: a multinational survey. (2006 Jul). Aliment Pharmacol Ther.. Alimentary Pharmacology &amp Therapeutics 24 (2): 411–9.
  115. Ehlin AG, Montgomery SM, Ekbom A, Pounder RE, Wakefield AJ. (2003 Aug). Prevalence of gastrointestinal diseases in two British national birth cohorts.. Gut. 52 (8): 1117–21..
  116. 116.0 116.1 Wilson S, Roberts L, Roalfe A, Bridge P, Singh S. (2004). Prevalence of irritable bowel syndrome: a community survey.. Br J Gen Pract. 54 (504): 495–502..
  117. Hungin AP, Chang L, Locke GR, Dennis EH, Barghout V (2005). Irritable bowel syndrome in the United States: prevalence, symptom patterns and impact. Aliment. Pharmacol. Ther. 21 (11): 1365–75.
  118. Jafri W, Yakoob J, Jafri N Islam M, Ali QM. (2007). Irritable bowel syndrome and health seeking behaviour in different communities of Pakistan.. J Pak Med Assoc. 57 (6): 285–7.
  119. Jafri W, Yakoob J, Jafri N, Islam M, Ali QM. (2005). Frequency of irritable bowel syndrome in college students.. J Ayub Med Coll Abbottabad. 4 (17): 9–11.
  120. 120.0 120.1 Schmulson M, Ortiz O, Santiago-Lomeli M, Gutierrez-Reyes G, Gutierrez-Ruiz MC, Robles-Diaz G, Morgan D. (2006). Frequency of functional bowel disorders among healthy volunteers in Mexico City.. Dig Dis. 24: 342.
  121. Tuteja AK, Talley NJ, Gelman SS, Adler SC, Thompson C, Tolman K, Hale DC. E. (2007). Development of Functional Diarrhea, Constipation, Irritable Bowel Syndrome, and Dyspepsia During and After Traveling Outside the USA.. Dig. Dis. Sci 53: 271.
  122. 122.0 122.1 Hulisz D. (2004). The burden of illness of irritable bowel syndrome: current challenges and hope for the future.. J Manag Care Pharm. 10 (4): 299–309.
  123. 123.0 123.1 Levy RL, Von Korff M, Whitehead WE, Stang P, Saunders K, Jhingran P, Barghout V, Feld AD. (2001). Costs of care for irritable bowel syndrome patients in a health maintenance organization. Am J Gastroenterol 96 (11): 3122–9.
  124. 124.0 124.1 Nyrop KA, Palsson OS, Levy RL, Korff MV, Feld AD, Turner MJ, Whitehead WE. (2007). Costs of health care for irritable bowel syndrome, chronic constipation, functional diarrhoea and functional abdominal pain.. Aliment Pharmacol Ther 26 (2): 237–48.
  125. 125.0 125.1 Paré P, Gray J, Lam S, et al (2006). Health-related quality of life, work productivity, and health care resource utilization of subjects with irritable bowel syndrome: baseline results from LOGIC (Longitudinal Outcomes Study of Gastrointestinal Symptoms in Canada), a naturalistic study. Clinical therapeutics 28 (10): 1726–35; discussion 1710–1.
  126. Leong SA, Barghout V, Birnbaum HG, et al (2003). The economic consequences of irritable bowel syndrome: a US employer perspective. Arch. Intern. Med. 163 (8): 929–35.
  127. Martin B, Ganguly R, Pannicker S, Feride F, Barghout V (2003). Utilization Patterns and Net Direct Medical Costs Medicaid of Irritable Bowel Syndrome. Curr Med Res Opin 19 (8): 771–80.
  128. Maxion-Bergemann S, Thielecke F, Abel F, Bergemann R (2006). Costs of irritable bowel syndrome in the UK and US. PharmacoEconomics 24 (1): 21–37.

External links