Many patients experience discomfort originating in their digestive tract from time to time, but patients with IBS have ongoing symptoms. According to the Rome criteria for diagnosing IBS, patients experience abdominal pain related to defecation with altered bowel habits associated with change in the frequency or the consistency of stool. They should report pain at least 1 day a week in the last 3 months while symptoms should exist for at least 6 months.

Patient with IBS with constipation or IBS-C report hard or lumpy stools in at least 25% of their bowel movements (BM) and loose Stools in less than 25% of their BM, while patients with IBS diarrhea or IBS-D will report the opposite.

Patients might also report cramping, alternating bowels with constipation, diarrhea, or both, urgency, incomplete defecation, mucus in the stool, abdominal bloating, and gas, but these are not part of the inclusion criteria according to Rome. The Rome criteria are international standard criteria used to diagnose functional gastrointestinal disorders and the last version of Rome IV was published in May of 2016. The criteria are widely considered by experts to be 98% accurate in diagnosing IBS based on symptoms –> without the need for extensive testing for most people [1].

IBS is very common and affect about 10–20% of the population, however, most of the patients with IBS have mild symptoms that they manage with lifestyle and diet changes and OTC medications and they do not seek medical help. About 20% of the patient with IBS will have more significant symptoms that impair global function and quality of life and they are the ones primary care providers and gastroenterologists will see in clinic. This group of patient tends to have multiple doctor appointments, they undergo numerous tests and procedures, and they have greater chance of having multiple surgeries, not necessarily GI related, which results in morbidity, dysfunction, and increased health care expenses [2].

IBS is 1.5–2 times more common among females, and it cannot be explained solely by the fact that females seek more medical help and tend to report symptoms more than males. It is well established that hormones play a role in the disorder and many female patients will report different or worse symptoms during their period.

The disorder also harbors a genetic and environmental component, since patients who have first, second, or third degree relative with IBS are at increased risk of developing IBS. Comorbidity with other functional gastrointestinal disorders (FGID) , as well as non-GI conditions such as psychiatric conditions, mainly depression and anxiety, fibromyalgia, chronic fatigue syndrome, and chronic pelvic pain are observed in this group of patients [3]. A history of recurrent abdominal pain or headache during childhood and a history of physical or emotional abuse are also risk factors [4].

The pathophysiology of IBS is complex and incompletely understood, as central and peripheral pathways are involved in the development of this common disorder. There is abundant data to show that visceral hypersensitivity, alterations in the gut microbiome, intestinal permeability, gut immune function, motility, brain-gut interactions, and psychosocial status are all involved in the development of IBS. It is beyond the scope of this chapter to go through all the data that is available, moreover, the different mechanisms interplay in a sophisticated network of gut brain interactions and are not truly separable.

Studies which used a rectal balloon distention as stimulus showed that patients with IBS had visceral hypersensitivity, meaning that they experienced greater pain for the same balloon volume as compared to healthy controls [5]. Patients with IBS also have dysregulated hypothalamic-pituitary-adrenal axis (HPA) mediated by CRH secretion when visceral pain is induced during sigmoidoscopy [6].

A subgroup of patient with IBS report abdominal pain or cramping following a meal due to altered motility. While postprandial colon contractions are a physiological response to meal, some IBS patients are experiencing heightened gastro-colic reflex. Others may have blunted response to meal resulting in hard pebbly stool and constipation.

Increased permeability is another mechanism involved in the development of IBS. Studies conducted on post infectious IBS have shown disrupted tight junction between colonocytes which leads to increased permeability [7]. This process increases exposure of enteric nerve endings to stimuli such as toxins and microorganisms. This in return can lead to altered motility and visceral hypersensitivity. The severity of the enteric infection, preexisting anxiety, and female gender have been diagnosed as risk factors for the development of post infectious IBS. From long-term follow-up of this group we have learned that the majority of patients can expect complete resolution of symptoms within several years [8].

Altered gut microbiota is associated with altered gut immune function, altered gut motility, and altered neurological function that in IBS patients could lead to hypersensitivity. Several studies have demonstrated different microbiota composition in IBS compared to control, and although some of the data is conflicting, most of the studies support decreased levels of fecal Lactobacillus and Bifidobacterium in IBS patients compared to controls. We also know that manipulating the microbiota changes bowel function, as there is some evidence that probiotics improve bloating and abdominal pain [9] and that antibiotic such as Rifaximin relieves IBS-D symptoms. There is even limited data showing that fecal microbiota transplant can cure IBS [10]. Overall, data is limited and this field will need further exploration before we can offer a safe and effective microbiota manipulation.

Early life stress is involved in the development of exaggerated pain perception. Many patients with IBS report history of abuse either emotional or physical, anxiety or depression. Not only stress underlies the mechanism of hypersensitivity, but it can also aggravate symptoms and induces anxiety [11].

Although the diagnosis of IBS is based on symptoms and fulfilling Rome criteria with an accuracy of 95–98%, most primary care providers and gastroenterologists believe this is a diagnosis of exclusion [12, 13].

IBS guidelines do no support extensive workup for patient with FGID; however, in reality providers and patients who seek GI consultation expect testing and will not be satisfied without completing additional tests. Workup is also driven by exposure to media and the remote possibility of missing a significant diagnosis. In fact, colonoscopy in individuals with suspected IBS has low yield and there is not an increased risk for colon cancer [14]. In regard to bowel disease inflammatory (IBD), in the presence of normal inflammatory markers such as CRP and fecal calprotectin, and in the absence of alarming symptoms, fewer than 1% of patients undergoing a colonoscopy will be diagnosed with IBD.

Additional tests are indicated in the presence of alarming symptoms such as rectal bleeding, iron deficiency anemia, unintentional weight loss, fever, vomiting, family history of colon cancer, or in patient older than 50 years.

Symptoms of IBS and celiac disease overlap and differentiating them by taking the history is not accurate. Blood tests can help rule out this disease with high sensitivity, and it is cost effective to screen for celiac disease when the prevalence of celiac is greater than 1% [15].

Most if not all patients with IBS believe that their symptoms are affected by their diet. Up to 80% of patients are able to identify food trigger of which the most common are fatty food, fiber, dairy products, legumes, caffeine, and alcohol. Moreover, the majority of the patients have tried to eliminate trigger foods from the diet along the course of their disease. Food triggers were more commonly reported by women, and patients who identified high number of triggers had reduced quality of life [16].

In general, if the patient can point to specific food that triggers symptoms, the best would be to avoid the food, unless the diet becomes very limited and there is concern for malnutrition or nutrients deficiency. Eating large volume meals can trigger abdominal distention, fatty of fried food delays gastric emptying and might increase gas production and diarrhea. Consuming non-absorbable sugars, legumes, and cruciferous vegetables (broccoli, cauliflower, etc.) can cause gas, bloating, and diarrhea.

In the past several years we were introduced to the low FODMAP diet , which is a diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols . Several randomized controlled trials showed improvement of abdominal pain, bloating, flatulence, and altered bowel movements in IBS patients who followed a low FODMAP diet. When guided by a dedicated dietician and with good adherence, success can be up to 80%. Since the diet is relatively new, there is no data on the long-term consequences mainly in regard to nutrient deficiencies and altered gut microbiota [17].

Many of our patients find the diet hard to follow and there is some encouraging data regarding a more simple traditional diet. In one randomized study that was recently published, “traditional IBS diet ” was as effective a low FODMAP diet [18]. The standard diet consisted of three average size meals and three snacks spread through the day with reduced fat, spicy foods, coffee, alcohol, onions, cabbage, beans and discontinuing carbonated beverages and artificial sweeteners that are made of poorly absorbable sugars.

Recommending gluten-free diet is still debatable, since the symptoms of IBS and non-celiac gluten sensitivity overlap. In the only double-blind randomized controlled trial of gluten-free diet (GFD) in IBS patients with no celiac disease, Biesiekierski JR and colleagues reported significant improvement of GI symptoms on GFD [19]. If a patient is already on a low FODMAP diet it is unlikely that adhering to gluten-free diet will have additional benefit [20].

There is not a definitive cure for IBS, since it is a chronic disorder that is the consequence of multiple processes. Our goal when treating IBS is to establish good rapport with the patient and it is a major factor in treatment success and in patient satisfaction. During the interview we should listen to the patient and believe his symptoms. One should not let the patient feel that his symptoms are imaginary nor that we believe that everything he says is driven by anxiety and somatization. Patient also needs to understand that the responsibility for treatment is mutual and it is not the sole responsibility of the provider, and the patient should be fully engaged in the treatment plan. Next would be to set realistic expectations. We do not “fix the bowel function,” we can’t “take the IBS away,” rather we can work together and set a treatment plan that we both agree upon.

This is a process that will not happen overnight, but with good patient and physician relationship we have a good chance of helping and improving symptoms and function [21].

There are several treatment options including medications and nondrug interventions which can help improve symptoms of IBS. The choice depends on the severity of symptoms, the impact of quality of life and global function, and on the provider and patients preferences. Treatment is individually tailored to meet the patient needs after good rapport was established.