Thursday, June 20, 2019

IBS mega file

Well I think it really started when I got •Montezuma's revenge' on holiday in the Canary Islands about 6 years ago. was only 19 and it was my first real holiday without the parents. Alter that my bowel movements have never really returned to normal, I mean they are always fairly loose and runny. il you know what I mean! But the thang I hate most is the bloating. I think I retain water really easily. Since then 't comes and goes but I think overall it's getting worse. It's embarrassing and Often gets me down. I did go to my doctor about 2 years ago and she did various blood tests but they could not find anything. Lucy (a close 'mend) told me it might be a food allergy and so cut out all wheat for a While but apart from losing a couple Of pounds it didn't seem to help that much Mth the bloating or going to the toilet."



If you Were to ask 100 from 10 countries ror definition or IBS (say for the television programme Family Fortunes) you would find significant differences between them. Ask them again 10 years later and. as well as the differences between them, many answers will have changed. This is because we UNDERSTANDING IRRITABLE BOWEL SYNDROME are still learning exactly What IBS is and how best to identify it. At present it is a condition identilied by the symptoms. These symptoms include pain. bloating or discomfort in the abdomen a mixture Of diarrhoea und constipation, In IBS rwople will experience these symptoms but we have yet to lind any disease or abnormality in the body to it. We know II'S is very common. In industrialised countries it affects around one in six Of us. That's about a dom•n lx•ople in every street! II'S will affect people in vastly different ways. Some people will only occasionally


Will affect in Vastly ditR•rent Ways. Some Will only occasionally exß•rience symC*orns. while for others the pain. diarrhoea and constipation are that it becomes distressing. and affects many areas or life. It is not but there are times it Can like it' What are the signs and symptoms Of IBS? Box 1. four symptoms 1. Abdominal pains: stomach pains. 2. Bloating: stomach swelbng or a feeling that your stomach is bloated. 3. Diarrhoea. 4. Constipation. are main symgfloms of I BS. abdominal pain. constipati»n and bloating. Other symv*oms frequently found include mucus increaq-d Wind. nauwa and ix•lching. Thesc• synWoms can vary in frequency and intensity from to and within an indivkiual J.x•rson from day-to-day. and from month to month. Not knowing What Will hamx•n tom•rrow is part Of the nature oflBS:


There arc four main symptoms or IBS. abdominal pain. diarrhoea. constipation and bloating. Other synw.orns frequently found include mucus stools, increased Wind. nausea and belching. These can vary in frequency and intensity from person to person and within an individual person from day-to-day. and from month to month. Not knowing What Will tomorrow is part of the frustrating nature oflBS: "One day it's diarrhoea and the next I can't go at all, it's the stomach pain that's the worse thing. C' I can go to the 100 up to 40 times in one day. the next day may not go at all. 't can really get me down. "When I wake up think. •Will I have a fat day or a thin day?'" s look at the symptoms in more detail.


l. Pain in the abdomen For many ry•ople abdominal pains are the unpleasant symptom. describe the pain in different ways; it is frequently described as coming in spasms (spasmodk it may be nagging. sharp. heavy or dull: get waves Of intense pain. It feels a bit like trapped wind." It can be felt anyw'here in the abdominal area Oust below the stomach) but is more frequent down the left-hand side. The wverity of this pain is the one thing most likely to drive people into Weing a d(Xtor. Some people will describe them as •stomach pains • even though these pains tend to occur in the abdomen: "Sometimes I'm in sc much pain that I can't even sit on the toilet." "It feels tike I have been cut in two, can cope with the diarrhoea. but the pain wears me down. Peoc*e may worry about what the pain may mean: "The cramps can be so bad it Can't just be IBS. it must be something more serous. But other peoNe will not exrx•rience pain but rather a 'discomfort




l. Pain in the abdomen For many ry•ople abdominal pains are the unpleasant symptom. describe the pain in different ways; it is frequently described as coming in spasms (spasmodk it may be nagging. sharp. heavy or dull: get waves Of intense pain. It feels a bit like trapped wind." It can be felt anyw'here in the abdominal area Oust below the stomach) but is more frequent down the left-hand side. The wverity of this pain is the one thing most likely to drive people into Weing a d(Xtor. Some people will describe them as •stomach pains • even though these pains tend to occur in the abdomen: "Sometimes I'm in sc much pain that I can't even sit on the toilet." "It feels tike I have been cut in two, can cope with the diarrhoea. but the pain wears me down. Peoc*e may worry about what the pain may mean: "The cramps can be so bad it Can't just be IBS. it must be something more serous. But other peoNe will not exrx•rience pain but rather a 'discomfort



describe the pain in different ways: it is frequently described as coming in spasms (spasmodic): it may be nagging. sharp, heavy or dull: I get waves cf intense pain. It feels a bit like trapped wind. It can bc felt anywhere in the abdominal area Oust below the stomach) but is more frequent down the left-hand side. The severity of this pain is the one thing most likely to drive people into seeing a doctor. Some people will describe them as 'stomach pains' even though these pains tend to occur in the abdomen: "Sometimes I'm in so much pain that I can't even sit cn the toilet." It feels like I have been cut in two. I can cope with the diarrhoea. but the pain wears me down. people may worry about what the pain may mean: "The cramps can be so bad it can't just be IBS. it must be something more senoas.


Introduction Most patients who present with gastrointestinal symptoms have no clear organic cause even after an extensive investigation and are diagnosed with a functional gastrointestinal disorder (FGID). Among the FGIDs, irritable bowel syndrome (IBS) is the most common, affecting up to 15 % of the general population. The hallmark of IBS is chronic abdominal pain associated with irregular bowel movements. The pain can be mild and intermittent or severe, constant, and debilitating. IBS patients are major healthcare utilizers and are seen and treated not only by primary care physicians and gastroenterologists but also by surgeons, gynecologists, pain specialists, and rheumatologists. Thus, it is important for physicians in diverse subspecialties to be familiar with the diagnosis and management of this disorder. The purpose of this chapter is to review the epidemiology and diagnosis of IBS and provide an in-depth look into the pathogenesis and treatment of pain in IBS patients.

Key Points • Irritable bowel syndrome (IBS) is the most common functional gastrointestinal disorder (FGID), affecting up to 15 % of the general population. • It is characterized by chronic abdominal pain that can be mild and intermittent, or severe, constant, and debilitating. Pain in IBS, as in other chronic pain disorders, is a complex symptom resulting from the interplay between peripheral (visceral) stimulation (enteric nervous system) and central modulation (central nervous system). • As the severity of pain increases central processing plays an increasingly important role compared to peripheral input. In IBS, the normal adaptive central inhibitory response to painful visceral stimuli is diminished. This change is modulated by psychosocial factors such as anxiety, depression, poor social support, and impaired coping skills. • Successful treatment begins with a therapeutic doctor– patient partnership. Medical treatment of IBS includes peripherally acting and centrally acting agents with antidepressants playing a central role. Cognitive behavioral therapy (CBT), interpersonal (psychodynamic) therapy, hypnosis, stress reduction, and mindfulness meditation have been shown to be effective in the treatment of IBS
Epidemiology IBS is a common functional disorder with a symptom-based diagnosis (Rome III diagnostic criteria, Table 6.1 ) [ 1 ]. The reported prevalence of IBS varies from study to study depending on diagnostic criteria used as well as other methodological differences among studies [ 2 ]. However, some findings on the epidemiology of IBS appear to hold true and are as follows: 1. IBS is a global problem that affects individuals all over the world [ 3 ]. The reported worldwide prevalence rates for IBS range from 5 % to 20 %. 2. In most countries IBS affects women (60–70 %) more than men [ 4 , 5 ]. The East is unique in that there are reports from China, Taiwan, and Singapore of a similar prevalence between males and females [ 6 , 7 ]. There are conflicting reports from India with community-based surveys reporting
higher prevalence of IBS among females in the general population and hospital-based surveys reporting higher proportion of males among patients in gastroenterology clinics [ 8 , 9 ]. The latter observation might reflect cultural aspects of healthcare-seeking behaviors in Indian society. 3. Although IBS can appear at any age, it is more common in young and middle-aged patients and tends to be less common in the elderly [ 10 , 11 ]. 4. Socioeconomic status may play a role in the epidemiology of IBS, which has been reported in some countries to be more prevalent in lower socioeconomic classes [ 4 , 12 , 13 ], although the data on this factor are not consistent. As a prevalent chronic disorder, IBS places a major economic burden on health care. A meta-analysis of 18 studies from the USA and the UK estimated the annual direct cost of an IBS patient (drugs, procedures, and doctor visits) at $348–8,750 and the annual indirect costs (loss of work days and deceased productivity) at $355–3,344 [ 14 , 15 ]. Another US study estimated the overall annual direct cost of IBS to be $228 million in doctor visits and $80 million in drugs [ 15 ]. Diagnosis There is no specifi c diagnostic fi nding or biomarker for IBS, so the diagnosis is based on patients’ reports of their symptoms. In the past, IBS was considered a diagnosis of exclusion, but inherent to this approach is an exhaustive diagnostic work-up that involves unpleasant and potentially risky tests for the patient and is not cost effective. Thus, a symptom- based diagnostic system, known as the Rome criteria, was developed. The main concept introduced by the Rome criteria is that the diagnostic process of a functional disorder should be based on two components. The fi rst is the presence of a typical cluster of symptoms and the second is the absence of “red fl ags” including initial presentation of symptoms at an age over 50, unexplained weight loss, fever, nocturnal symptoms, blood in the stool, a family history of gastrointestinal malignancy or disease (e.g., celiac or infl ammatory bowel disease), or an abnormal fi nding on physical examination. Basic laboratory tests, such as a complete blood count and celiac serology, are usually enough to complete the diagnostic process and establish a fi rm diagnosis. Patients who fulfi ll the criteria and do not have red fl ags need a minimal diagnostic work-up after which the diagnosis of IBS can be made with confi dence [ 16 , 17 ]. The latest update of the Rome diagnostic criteria for IBS is Rome III, in which the diagnosis of IBS requires the presence of abdominal pain or discomfort for at least 10 % of the time over the previous three months with symptom onset at least six months earlier [ 18 ]. Additionally, pain should be relieved by defecation and associated with a change in the frequency of bowel movements or a change in the form of the stool. Accompanying symptoms, although not essential for the diagnosis, are a feeling of incomplete evacuation, abnormal stool frequency (less than three times a week or more than three times a day) or consistency, straining at defecation, urgency, mucus discharge, and bloating. IBS can be further divided into three main subgroups according to bowel habit as constipation predominant (IBS-C), diarrhea predominant (IBS-D), and those exhibiting an alternating bowel pattern [ 19 ]. Patients may switch from one subclass to another during the course of their illness. It has been demonstrated repeatedly that the use of positive symptom-based diagnostic criteria in conjunction with the use of red fl ags to guide further investigation in selected cases is a reliable and cost-effective approach. After establishing the diagnosis of IBS, based on the Rome criteria, it is rarely necessary to change the diagnosis [ 20 – 22 ]. The Pathophysiology of Pain in IBS Abdominal pain is a hallmark of IBS and is essential for its diagnosis. In IBS, as in many other chronic pain syndromes, pain is a complex experience resulting from the interplay between peripheral (visceral) stimulation (enteric nervous system) and central modulation (central nervous system [CNS]). Afferent stimulation from the colon is transmitted to second- order neurons in the spinal cord and then ascends to the brain through the spinothalamic, spinoreticular, and spinomesencephalic tracts. These tracts connect to the somatosensory cortex responsible for registration and localization of painful visceral and somatic stimuli. They also connect to structures in the limbic system that are involved in the refl exive, affective, and motivational responses to pain [ 23 ]. The afferent pathways project to the perigenual anterior cingulate cortex (pACC), which is involved in affective modifi cation, and to the midcingulate cortex (MCC), which is involved in the behavioral response. The amplifi cation of afferent visceral stimulation can result from increased excitability of peripheral receptors or impaired spinal and/or central pain regulatory systems. Increased excitability can produce the two related phenomena
Table 6.1 Rome III diagnostic criteria a for IBS Recurrent abdominal pain or discomfort b at least 3 days/month in the last 3 months associated with two or more of the following: 1. Improvement with defecation 2. Onset associated with a change in frequency of stool 3. Onset associated with a change in form (appearance) of stool a Criterion fulfi lled for the last 3 months with symptom onset at least 6 mon
ths prior to diagnosis b “Discomfort” means an uncomfortable sensation not described as pain
of hyperalgesia (increased pain response to painful stimuli) and allodynia (increased pain response to nonpainful stimuli) [ 24 ]. Thus, afferent visceral stimulation can be experienced as painful not only as a result of peripheral intensity but also as a result of central processing that may be modulated by psychosocial factors such as anxiety, depression, poor social support, and impaired coping skills [ 25 ]. As the severity of pain increases central processing plays an increasingly important role compared to peripheral input. Once a pattern of central sensitization has taken hold, patients may even experience severe pain without ongoing peripheral nociceptive stimulation [ 26 , 27 ]. This is the extreme end of the IBS severity spectrum. While we do not have full knowledge of all the causes of excessive peripheral stimulation, there is good evidence that eating, infection, infl ammation, physical injury, hormones (e.g., menses), or colonic motility may play a role. Up to 15 % of IBS patients attribute the beginning of their symptoms to an acute episode of gastrointestinal infection. A meta-analysis of eight papers including almost 600,000 patients over a follow-up up to one year found that the odds ratio for developing IBS after such an episode is seven [ 28 ]. IBS that follows acute intestinal infection has been shown to be associated with a persistent or chronic state of infl ammation that cannot be identifi ed by routine clinical tests and procedures [ 29 , 30 ]. Risk factors for postinfectious IBS are related to not only to the severity of the acute infectious episode (fever, bloody stools, and need for hospitalization) but also to patient characteristics such as female gender, stress, anxiety, and depression [ 31 ]. This is a good example of how excessive afferent stimulation, induced in this case by a microinfl ammatory state, can develop into a chronic condition such as IBS-D after central sensitization occurs in a susceptible person with psychological comorbidity. Peripheral stimulation and its interplay with central amplifi cation are also refl ected in the development of chronic abdominal pain following abdominal or pelvic surgery. IBS patients reported up to twice the number of appendectomies and hysterectomies and up to three times the number of cholecystectomies compared with those without IBS [ 32 ]. Surgery may cause visceral afferent sensitization that eventually results in allodynia and chronic pain even in the presence of normal gut function. This contention is supported by a study that evaluated the development of abdominal pain after elective gynecologic surgery for nonpainful indications [ 32 ]. Patients with no prior history of chronic abdominal pain undergoing gynecological surgery for nonpainful indications were followed for the development of de novo abdominal pain following surgery. They were compared with a control group comprised of nonsurgical patients who came to a gynecologic clinic for nonpain-related reasons. At one-year follow-up significantly more patients in the surgery group complained of chronic abdominal pain (15.3 %) than in the control group (3.6 %, p = 0.003). There was no association between any surgeryrelated variables and the subsequent development of chronic abdominal pain. The only predictors of chronic abdominal pain at one-year follow-up were associated with the patients’ preoperative psychological profi le. Patients anticipating diffi culty with surgery or recovery from it and those with lower scores on the Sense of Coherence questionnaire (an index of coping skills) were more likely to develop chronic postoperative abdominal pain. In these cases, the interplay of peripheral visceral stimulus together with central sensitization related to psychosocial variables affected the de novo development of chronic abdominal pain. Studies using functional MRI and PET CT have demonstrated that the ACC, which is responsible for descending pain inhibition, is less active in IBS patients. This phenomenon is also found in other chronic pain syndromes such as fi bromyalgia [ 33 – 35 ]. In contrast, the MCC, which is associated with unpleasantness and fear, is overactive. Therefore, in IBS patients the normal adaptive inhibitory response to painful visceral stimuli is diminished and replaced by a maladaptive, presumably even aggravating, response [ 33 , 34 , 36 ]. The factors that ultimately lead to this shift into a maladaptive pattern are psychosocial in nature. This connection was elegantly demonstrated in the case report of a patient with a severe functional gastrointestinal pain syndrome and a history of abuse [ 37 ]. Her baseline brain scan demonstrated marked activation of the MCC and the somatosensory cortex. Following successful treatment with antidepressants and psychotherapy a repeated scan demonstrated diminished MCC activity and increased insular activation. Thus, maladaptive brain responses are reversible and so is the patient’s clinical situation. Treatment of Abdominal Pain in IBS As in other fields of medicine, in particular in patients with chronic painful conditions, the healing process for IBS patients begins when the patient enters the doctor’s office before any medicine has been prescribed. It is of the utmost importance to establish a good doctor–patient relationship in order to succeed in the therapeutic process [ 38 , 39 ]. Some of the essentials of a salutary doctor–patient relationship are discussed below: 1. Allow enough time especially for the first meeting. The patient should feel that the doctor is listening to and him/ her and that their symptoms are considered legitimate and are being taken seriously. 2. Take a full detailed history and perform a physical examination: These basic measures of good clinical practice help to foster the doctor–patient relationship.

3. It is very helpful to remember four key questions that patients should be asked: a. What brings you here at this time? IBS is a chronic condition and many patients have their symptoms for years before consulting a specialist. Consultation is often driven by a specifi c anxiety or a stressful situation that should be addressed. b. What do you think is the cause of your symptoms? Many IBS patients attribute their symptoms to undiagnosed cancer, infection, infl ammatory bowel disease, or food allergy. c. What are your concerns or worries? It is important to understand the patient’s agenda and to address their primary concerns such as “What exactly do I have?” or “Do I have cancer,” or alternatively related to the symptoms like “I can’t deal with this pain anymore.” d. What are your expectations from me? Some patients have the unrealistic expectation of a “quick fix” for their situation that can lead to mutual frustration and treatment failure [ 40 ]. It should be emphasized that treating IBS is a process rather than an isolated consultation and that the goal of treatment is to reduce their suffering and to improve their quality of life rather than to “cure” them. Many IBS patients have never received a comprehensive explanation about the nature of their problem. This may be the basis for the unwarranted fears (“I might have cancer”) and feelings of frustration (“why can’t they figure out what I have”). A detailed explanation about the nature of functional disorders and their natural history is very important to deal with these issues. Treating IBS patients is an ongoing process that takes time. Throughout this process patients are likely to encounter diffi culties, setbacks, and frustration. Patients should not feel that they are left alone to deal with their setbacks. Scheduling a follow-up phone call, for example, is a simple measure that is often suffi cient to allay patients’ new concerns [ 41 ]. Physicians should inquire about comorbid gastrointestinal and nongastrointestinal functional disorders. IBS patients have a high prevalence of other functional disorders [ 42 ], leading some patients to feel that they are very ill. By providing patients with a unifying paradigm that connects different, apparently unrelated, symptoms to one disorder (i.e., central sensitization), we can alleviate much of their fears and concerns. For some patients with mild symptoms, these steps may be enough to alleviate fears and concerns regarding their symptoms. These patients often continue to cope successfully with their symptoms and need no further treatment. However, the majority of patients will require more specific treatment. The treatment options for IBS can be divided into pharmacological and nonpharmacological treatment modalities (Fig. 6.1 ). Medical Treatment Medical treatment of IBS includes peripherally acting agents and centrally acting agents. Peripherally Acting Agents These drugs act on the gut itself and are targeted against specific IBS symptoms such altered bowel movements, bloating, and cramps. Because they are not key agents in



Table 6.2 Peripheral agents used most commonly in the treatment of IBS. Peripheral agents, although not primarily directed against pain, have an important role in IBS treatment. In mild IBS cases, they might suffice but in more severe IBS cases and, where pain is a cardinal symptom, central agents are preferred Class Drug Mechanism of action Comments • Antispasmodics • Pinaverium • Direct visceral smooth muscle relaxants • Modest effect on IBS spastic pain • Mebeverin • Colpermin (peppermint oil) • Anticholinergic/antimuscarinic • Otilinium bromide, hyoscine, and colpermin; best evidence for effectiveness • Hyoscamine dicyclomine • Serotonergic and other agents • Alosetron • 5HT3 receptor antagonist • Available only through a restricted access program; increased incidence of ischemic colitis • Tegaserode • Withdrawn from the US market; an increased incidence of cardiovascular adverse events • 5HT4 receptor agonist • Linaclotide • Guanylate cyclase-C agonist • Recently approved in Europe and the US for IBS-C • Lubiprostone • Chloride channel activator • In phase 3 studies, lubiprostone was almost twice as effective for IBS symptoms as placebo


IBS pain management only some of them are discussed in detail and the rest is mentioned briefly. Table 6.2 summarizes the main facts about the different peripheral agents. Serotonin (5HT) is an important neurotransmitter that coordinates gut function and has played a key role in research and drug development. It is secreted from enterochromaffin cells in the mucosa and is involved in almost every aspect of gut function including motility, sensation, and secretion. Alosetron is a 5HT3 receptor antagonist that was shown to improve global IBS symptoms and pain in women with IBS-D. A meta- analysis comparing 12 randomized controlled trials that evaluated the efficacy of alosetron compared to placebo found an odds ratio of 1.85 for improvement in the alosetron group [ 43 ]. Unfortunately, after initial FDA approval, safety issues and in particular ischemic colitis and severe constipation led to its withdrawal from the market. It was reintroduced in 2002 under a restricted access program. Under this program, alosetron can be prescribed (under some restrictions) to women with severe IBS-D who have failed to respond to traditional medical therapies. Lubiprostone is a chloride channel activator that has been approved by the FDA for chronic constipation and IBC-C. In phase 3 studies, patients receiving lubiprostone were almost twice as likely to gain relief from overall IBS symptoms compared to patients who received placebo [ 44 ]. The main side effect of lubiprostone, nausea, is reported in 8 % of IBS-C patients who receive 8 mcg twice daily. Centrally Acting Agents Centrally acting agents should be the cornerstone of treatment in moderate-to-severe cases of IBS [ 45 ]. The main classes of drugs that are being used are the selective serotonin reuptake inhibitors (SSRIs), selective serotonin- norepinephrine reuptake inhibitors (SNRIs), and tricyclic antidepressants (TCAs). Other drugs, such as Mirtazapine, Buspiron, and the atypical antipsychotic Quetiapine, can also be used. These drugs were developed for the treatment of anxiety and depression, but can and should be used in IBS as discussed below. The different drugs and dosages are summarized in Table 6.3 . Antidepressants play a central role in medical therapy for IBS for two main reasons. First, they have a direct analgesic effect and are used in various pain syndromes, with or without concomitant depression, to elevate pain thresholds via central and peripheral effects. Second, since many IBS patient have psychological comorbidity, they can gain direct benefit from these drugs. Whether the main effect of antidepressants stems from central mechanisms (modulation of central pain processing) or from peripheral effects (effects on motility and secretion and reduction of afferent pain signals) or just from reducing depression and anxiety is still uncertain. The actual mechanism is probably a combination of all three. A recent meta-analysis found all classes of antidepressants to be effective in IBS with a number needed to treat as low as four [ 46 ]. Antidepressants in IBS (especially TCAs) are given at much lower doses then those used for the treatment of depression. The usual starting dose in 25–50 mg and can be increased as needed. SSRIs and SNRIs are usually given in the lower range of the “regular” psychiatric doses, for example, 10–20 mg of Escitalopram or 30 mg of duloxetine. Since TCAs and SNRIs have an independent indication in other pain syndromes, such as neuropathic pain and fibromyalgia, they are the drugs of choice for painful IBS. The choice between them is often based on the therapeutic profile of the drugs including potential adverse effects.


Table 6.3 Common interventions used in IBS. For optimal results these interventions can be used in combination (“augmentation” therapy). The use of more than one drug at a low dose can augment the therapeutic response and minimize the side effects Drug Drug (daily dose range [mg]) Comments TCA • Desipramine (25–150) • Begin with low dose and titrate by response • Nortriptyline (25–150) • Amitriptyline (25–150) • Allow 4–8 weeks for maximal response SSRIs • Paroxetine (20–60) • Begin with low dose and titrate by response • Escitalopram (10–20) SNRIs • Venlafaxine (25–300) • Psychological and analgesic effects • Duloxetine (20–80) Atypical antipsychotics • Quetiapine (25–100) • Preliminary reports Tetracyclic antidepressant • Mirtazepine (15–45) • Antiemetic properties Azaspirodecanediones • Buspiron (10–60) • Improves gastric receptive relaxation

For example, TCAs tend to be more constipating and have less anxiolytic properties, so an SNRI would be the preferred option in a patient with constipation or prominent anxiety. However, in many cases a combination of two drugs or more is necessary. Instead of increasing the dose of a single drug to the maximum, the use of a combination of two or more drugs from different classes and in lower doses (e.g., a TCA and an SNRI or SSRI) is recommended. This approach known as “augmentation therapy,” helps minimize adverse effects, to which patients with functional GI disorders are prone [ 45 ]. Mirtazapine is a tetracyclic antidepressant used primarily in the treatment of depression. It has serotonergic as well as noradrenergic properties. It has antagonistic alpha-2 receptor and 5HT1, 5HT2, and 5HT3 properties as well as moderated peripheral alpha-1 adrenergic and alpha-1 anticholinergic properties. Its 5HT3 antagonistic action is probably responsible for its antiemetic properties. In addition to its antidepressant effects, it is also used at times as a hypnotic, antiemetic, as an appetite stimulant, and for the treatment of anxiety. In IBS, it can be used to augment the antidepressant and anxiolytic properties of other agents (such as a TCA or an SNRI) and for nausea and vomiting or low body weight, as is often seen in patients with a comorbid eating disorder. Data regarding its use in IBS are limited and more studies are needed to explore its exact place. Quetiapine is an atypical antipsychotic approved for the treatment of schizophrenia, bipolar disorder, and as an add- on to treat depression. It has potential benefits in IBS by reducing anxiety, restoring normal sleep patterns, and potentially through a direct analgesic effect. A recent paper reported a retrospective analysis of its use in low doses (50–200 mg) in patients with severe FGIDs. Of the 21 treated patients, 10 discontinued the drug due to adverse effects or lack of effi cacy, but of the 11 patients who stayed on the drug 6 reported improvement [ 47 ]. Although this is a small and uncontrolled study, it is encouraging considering that these were patients with extremely severe IBS who did not respond to any previous treatment modality. A larger, prospective, open-label study is currently underway. Finally, Buspirone is a nonbenzodiazepine anxiolytic agent that is used in psychiatry to augment the effect of antidepressants. It also has a 5HT1 agonist effect, which may contribute to increasing gastric compliance/relaxation as has been shown to occur for functional dyspepsia. Therefore, it might be useful in patients with comorbid dyspeptic symptoms such as epigastric discomfort and early satiety. There are two main barriers that clinicians face when trying to treat IBS patients with antidepressants. The first is the general reluctance of these patients to take “chemical” and “mind altering” agents. The second is patients’ tendency to underestimate the psychological component of their symptoms. A thorough explanation regarding the mechanisms of pain (visceral hypersensitivity modulated by central mechanisms) and the drug’s independent analgesic properties is enough in many cases. Some patients view the recommendation for a psychotropic drug as evidence that the doctor does not acknowledge their pain and thinks that they are “crazy.” If we emphasize that we are recommending these drugs for their central analgesic effect, we can overcome much of this reticence to take them. This can be accomplished with a statement such as: “The same drug can be used for different reasons. For example, in the past aspirin was the leading drug for reducing fever and relieving pain, but currently it is the number one drug for the prevention of heart disease. Similarly, antidepressant drugs are effective in the treatment of depression at higher doses, but are also effective in lower dosages for pain relief”. The patient should always make the final decision regarding the drug. This can be achieved by fostering a feeling of therapeutic partnership instead of an authoritative relationship where the patient has no say about the way he is treated. An example for such an approach would be: “In IBS there are many therapeutic options, with and without drugs. Each has its advantages and disadvantages. Do you want me to tell you about options that could help you with your symptoms?” By making the drug the


patient’s choice, we can augment adherence to treatment. Finally, in our experience, the adherence rate for drug therapy increases if the physician is available to address, in real time, early adverse effects, and other concerns that otherwise may lead the patient to discontinue therapy on their own. Nonpharmacologic Therapy for IBS Nonpharmacological treatments for IBS include stress reduction, and behavioral and psychological interventions. Behavioral Interventions Behavioral interventions are commonly used to treat IBS. They are safe and their benefi t may go beyond symptomatic treatment and induce positive physiological changes. They are particularly suited to patients who do not want to take drugs. The effect of different modalities, including cognitive behavioral therapy (CBT), interpersonal (psychodynamic) therapy, hypnosis, stress reduction, and mindfulness meditation, has been evaluated for IBS. All help patients deal with issues such as maladaptive illness beliefs and behaviors, and the relationship between stress, life events, and symptomatology. CBT can help patients recognize misperceptions and maladaptive thoughts regarding their symptoms and enhance their coping abilities. It can be administered as individual or group therapy [ 48 – 50 ]. In the largest randomized placebo- controlled study conducted to date, the investigators found that 12 weekly CBT sessions were significantly more beneficial than placebo for female patients with moderate-to-severe FGIDs [ 51 ]. Interpersonal (psychodynamic) therapy presumes that symptoms are associated with difficulties in interpersonal relationships. Its focus is on the identification of interpersonal situations that lead to symptom exacerbation. The treatment itself involves psychotherapy. The symptoms improve when the conflicts are resolved. Interpersonal dynamic psychotherapy has been shown to improve symptoms and to reduce disability and healthcare costs in IBS [ 52 – 54 ]. The aim of stress reduction (relaxation training) is to counteract the physiologic effects of stress. Reduction in skeletal muscle tension can decrease autonomic arousal and subjective tension/anxiety and may improve gut motility. Stress reduction and relaxation training includes modalities such as guided imagery, relaxation response, meditation, yoga, and biofeedback. Muscle relaxation alone or in combination with CBT and other techniques was shown to reduce IBS symptoms [ 55 ]. Mindfulness meditation is a form of relaxation involving an active nonjudgmental awareness of body sensations and emotions. Group mindfulness meditation resulted in improved IBS symptoms and health-related quality of life as well as reduced stress levels in women with IBS [ 56 ], effects that persisted at a three-month follow-up assessment. Hypnosis is a form of guided imagery that uses muscle relaxation and gut-targeted suggestions to improve the gut function and reduce symptoms. Hypnosis involves nonspecifi c effects of relaxation, stress management, ego strengthening, and gut-directed suggestions of normal functioning and pleasant feeling. Data gathered from studies in different centers support the use of hypnosis as an effective, viable treatment option in IBS [ 57 ] that improves IBS symptoms and quality of life and reduces stress and anxiety. Moreover, the benefi cial effects of hypnosis have been shown to persist at long-term follow-up [ 58 – 60 ]. The predictors of a favorable outcome in behavioral interventions include confi dence in treatment success, perceived sense of control over symptoms, a good relationship with the therapist, and early response [ 61 ]. The choice of intervention depends on local expertise and availability as well as patient preference. Summary and Conclusions IBS is a common medical problem, which, although not life threatening, has a signifi cant negative impact on patients’ quality of life. Its range of severity ranges from mild intermittent symptoms to a disabling condition with a considerable loss of daily function. Pain in IBS is the result of peripheral afferent stimulation and CNS processing. A biopsychosocial perspective, taking into account the patient’s psychological status, life experiences, beliefs, and concerns can help doctors provide optimal care. The primary goal of treatment is care rather than cure, and the various treatment options can be highly effective in reducing suffering and improving quality of life. The doctor–patient relationship is the foundation of successful treatment and should be supplemented by pharmacological or nonpharmacological treatments in accordance with the clinical situation and the patient’s preference. References 1. Longstreth GF, Thompson WG, Chey WD, Houghton LA, Mearin F, Spiller RC. Functional bowel disorders. In: Drossman SA, Corazziari E, Delvaux M, Spiller RC, Talley NJ, Thompson WG, et al., editors. Rome III the functional gastrointestinal disorders. McLean, VA: Degnon Associates; 2006. p. 487–555. 2. Sperber AD. The challenge of cross-cultural, multi-national research: potential benefi ts in the functional gastrointestinal disorders. Neurogastroenterol Motil. 2009;21:351–60. 3. Drossman DA, Camilleri M, Mayer EA, Whitehead WE. AGA technical review on irritable bowel syndrome. Gastroenterology. 2002;123:2108–31. 4. Andrews EB, Eaton SC, Hollis KA, Hopkins JS, Ameen V, Hamm LR, et al. Prevalence and demographics of irritable bowel syndrome: results from a large web-based survey. Aliment Pharmacol Ther. 2005;22:935–42.
l. Pain in the abdomen For many ry•ople abdominal pains are the unpleasant symptom. describe the pain in different ways; it is frequently described as coming in spasms (spasmodic it may be nagging. sharp. heavy or dull: get waves Of intense pain. It feels a bit like trapped wind." It can be felt anywhere in the abdominal area Oust below the stomach) but is more frequent down the left-hand side. The wverity of this pain is the one thing most likely to drive people into Weing a d(Xtor. Some people will describe them as •stomach pains • even though these pains tend to occur in the abdomen: "Sometimes I'm in sc much pain that I can't even sit on the toilet." "It feels tike I have been cut in two, can cope with the diarrhoea. but the pain wears me down. Peoc*e may worry about what the pain may mean: "The cramps can be so bad it Can't just be IBS. it must be something more serous. But other peoNe will not exrx•rience pain but rather a 'discomfort


describe the pain in different ways: it is frequently described as coming in spasms (spasmodic): it may be nagging. sharp, heavy or dull: I get waves cf intense pain. It feels a bit like trapped wind. It can bc felt anywhere in the abdominal area Oust below the stomach) but is more frequent down the left-hand side. The severity of this pain is the one thing most likely to drive people into seeing a doctor. Some people will describe them as 'stomach pains' even though these pains tend to occur in the abdomen: "Sometimes I'm in so much pain that I can't even sit cn the toilet." It feels like I have been cut in two. I can cope with the diarrhoea. but the pain wears me down. people may worry about what the pain may mean: "The cramps can be so bad it can't just be IBS. it must be something more senoas.


Introduction Most patients who present with gastrointestinal symptoms have no clear organic cause even after an extensive investigation and are diagnosed with a functional gastrointestinal disorder (FGID). Among the FGIDs, irritable bowel syndrome (IBS) is the most common, affecting up to 15 % of the general population. The hallmark of IBS is chronic abdominal pain associated with irregular bowel movements. The pain can be mild and intermittent or severe, constant, and debilitating. IBS patients are major healthcare utilizers and are seen and treated not only by primary care physicians and gastroenterologists but also by surgeons, gynecologists, pain specialists, and rheumatologists. Thus, it is important for physicians in diverse subspecialties to be familiar with the diagnosis and management of this disorder. The purpose of this chapter is to review the epidemiology and diagnosis of IBS and provide an in-depth look into the pathogenesis and treatment of pain in IBS patients.

Key Points • Irritable bowel syndrome (IBS) is the most common functional gastrointestinal disorder (FGID), affecting up to 15 % of the general population. • It is characterized by chronic abdominal pain that can be mild and intermittent, or severe, constant, and debilitating. Pain in IBS, as in other chronic pain disorders, is a complex symptom resulting from the interplay between peripheral (visceral) stimulation (enteric nervous system) and central modulation (central nervous system). • As the severity of pain increases central processing plays an increasingly important role compared to peripheral input. In IBS, the normal adaptive central inhibitory response to painful visceral stimuli is diminished. This change is modulated by psychosocial factors such as anxiety, depression, poor social support, and impaired coping skills. • Successful treatment begins with a therapeutic doctor– patient partnership. Medical treatment of IBS includes peripherally acting and centrally acting agents with antidepressants playing a central role. Cognitive behavioral therapy (CBT), interpersonal (psychodynamic) therapy, hypnosis, stress reduction, and mindfulness meditation have been shown to be effective in the treatment of IBS
Epidemiology IBS is a common functional disorder with a symptom-based diagnosis (Rome III diagnostic criteria, Table 6.1 ) [ 1 ]. The reported prevalence of IBS varies from study to study depending on diagnostic criteria used as well as other methodological differences among studies [ 2 ]. However, some fi ndings on the epidemiology of IBS appear to hold true and are as follows: 1. IBS is a global problem that affects individuals all over the world [ 3 ]. The reported worldwide prevalence rates for IBS range from 5 % to 20 %. 2. In most countries IBS affects women (60–70 %) more than men [ 4 , 5 ]. The East is unique in that there are reports from China, Taiwan, and Singapore of a similar prevalence between males and females [ 6 , 7 ]. There are confl icting reports from India with community-based surveys reporting
higher prevalence of IBS among females in the general population and hospital-based surveys reporting higher proportion of males among patients in gastroenterology clinics [ 8 , 9 ]. The latter observation might refl ect cultural aspects of healthcare-seeking behaviors in Indian society. 3. Although IBS can appear at any age, it is more common in young and middle-aged patients and tends to be less common in the elderly [ 10 , 11 ]. 4. Socioeconomic status may play a role in the epidemiology of IBS, which has been reported in some countries to be more prevalent in lower socioeconomic classes [ 4 , 12 , 13 ], although the data on this factor are not consistent. As a prevalent chronic disorder, IBS places a major economic burden on health care. A meta-analysis of 18 studies from the USA and the UK estimated the annual direct cost of an IBS patient (drugs, procedures, and doctor visits) at $348–8,750 and the annual indirect costs (loss of work days and deceased productivity) at $355–3,344 [ 14 , 15 ]. Another US study estimated the overall annual direct cost of IBS to be $228 million in doctor visits and $80 million in drugs [ 15 ]. Diagnosis There is no specifi c diagnostic fi nding or biomarker for IBS, so the diagnosis is based on patients’ reports of their symptoms. In the past, IBS was considered a diagnosis of exclusion, but inherent to this approach is an exhaustive diagnostic work-up that involves unpleasant and potentially risky tests for the patient and is not cost effective. Thus, a symptom- based diagnostic system, known as the Rome criteria, was developed. The main concept introduced by the Rome criteria is that the diagnostic process of a functional disorder should be based on two components. The fi rst is the presence of a typical cluster of symptoms and the second is the absence of “red fl ags” including initial presentation of symptoms at an age over 50, unexplained weight loss, fever, nocturnal symptoms, blood in the stool, a family history of gastrointestinal malignancy or disease (e.g., celiac or infl ammatory bowel disease), or an abnormal fi nding on physical examination. Basic laboratory tests, such as a complete blood count and celiac serology, are usually enough to complete the diagnostic process and establish a fi rm diagnosis. Patients who fulfi ll the criteria and do not have red fl ags need a minimal diagnostic work-up after which the diagnosis of IBS can be made with confi dence [ 16 , 17 ]. The latest update of the Rome diagnostic criteria for IBS is Rome III, in which the diagnosis of IBS requires the presence of abdominal pain or discomfort for at least 10 % of the time over the previous three months with symptom onset at least six months earlier [ 18 ]. Additionally, pain should be relieved by defecation and associated with a change in the frequency of bowel movements or a change in the form of the stool. Accompanying symptoms, although not essential for the diagnosis, are a feeling of incomplete evacuation, abnormal stool frequency (less than three times a week or more than three times a day) or consistency, straining at defecation, urgency, mucus discharge, and bloating. IBS can be further divided into three main subgroups according to bowel habit as constipation predominant (IBS-C), diarrhea predominant (IBS-D), and those exhibiting an alternating bowel pattern [ 19 ]. Patients may switch from one subclass to another during the course of their illness. It has been demonstrated repeatedly that the use of positive symptom-based diagnostic criteria in conjunction with the use of red fl ags to guide further investigation in selected cases is a reliable and cost-effective approach. After establishing the diagnosis of IBS, based on the Rome criteria, it is rarely necessary to change the diagnosis [ 20 – 22 ]. The Pathophysiology of Pain in IBS Abdominal pain is a hallmark of IBS and is essential for its diagnosis. In IBS, as in many other chronic pain syndromes, pain is a complex experience resulting from the interplay between peripheral (visceral) stimulation (enteric nervous system) and central modulation (central nervous system [CNS]). Afferent stimulation from the colon is transmitted to second- order neurons in the spinal cord and then ascends to the brain through the spinothalamic, spinoreticular, and spinomesencephalic tracts. These tracts connect to the somatosensory cortex responsible for registration and localization of painful visceral and somatic stimuli. They also connect to structures in the limbic system that are involved in the reflexive, affective, and motivational responses to pain [ 23 ]. The afferent pathways project to the perigenual anterior cingulate cortex (pACC), which is involved in affective modification, and to the midcingulate cortex (MCC), which is involved in the behavioral response. The amplification of afferent visceral stimulation can result from increased excitability of peripheral receptors or impaired spinal and/or central pain regulatory systems. Increased excitability can produce the two related phenomena
Table 6.1 Rome III diagnostic criteria a for IBS Recurrent abdominal pain or discomfort b at least 3 days/month in the last 3 months associated with two or more of the following: 1. Improvement with defecation 2. Onset associated with a change in frequency of stool 3. Onset associated with a change in form (appearance) of stool a Criterion fulfi lled for the last 3 months with symptom onset at least 6 mon
ths prior to diagnosis b “Discomfort” means an uncomfortable sensation not described as pain
of hyperalgesia (increased pain response to painful stimuli) and allodynia (increased pain response to nonpainful stimuli) [ 24 ]. Thus, afferent visceral stimulation can be experienced as painful not only as a result of peripheral intensity but also as a result of central processing that may be modulated by psychosocial factors such as anxiety, depression, poor social support, and impaired coping skills [ 25 ]. As the severity of pain increases central processing plays an increasingly important role compared to peripheral input. Once a pattern of central sensitization has taken hold, patients may even experience severe pain without ongoing peripheral nociceptive stimulation [ 26 , 27 ]. This is the extreme end of the IBS severity spectrum. While we do not have full knowledge of all the causes of excessive peripheral stimulation, there is good evidence that eating, infection, inflammation, physical injury, hormones (e.g., menses), or colonic motility may play a role. Up to 15 % of IBS patients attribute the beginning of their symptoms to an acute episode of gastrointestinal infection. A meta-analysis of eight papers including almost 600,000 patients over a follow-up up to one year found that the odds ratio for developing IBS after such an episode is seven [ 28 ]. IBS that follows acute intestinal infection has been shown to be associated with a persistent or chronic state of infl ammation that cannot be identifi ed by routine clinical tests and procedures [ 29 , 30 ]. Risk factors for postinfectious IBS are related to not only to the severity of the acute infectious episode (fever, bloody stools, and need for hospitalization) but also to patient characteristics such as female gender, stress, anxiety, and depression [ 31 ]. This is a good example of how excessive afferent stimulation, induced in this case by a micro inflammatory state, can develop into a chronic condition such as IBS-D after central sensitization occurs in a susceptible person with psychological comorbidity. Peripheral stimulation and its interplay with central amplification are also reflected in the development of chronic abdominal pain following abdominal or pelvic surgery. IBS patients reported up to twice the number of appendectomies and hysterectomies and up to three times the number of cholecystectomies compared with those without IBS [ 32 ]. Surgery may cause visceral afferent sensitization that eventually results in allodynia and chronic pain even in the presence of normal gut function. This contention is supported by a study that evaluated the development of abdominal pain after elective gynecologic surgery for non painful indications [ 32 ]. Patients with no prior history of chronic abdominal pain undergoing gynecological surgery for nonpainful indications were followed for the development of de novo abdominal pain following surgery. They were compared with a control group comprised of nonsurgical patients who came to a gynecologic clinic for non pain-related reasons. At one-year follow-up significantly more patients in the surgery group complained of chronic abdominal pain (15.3 %) than in the control group (3.6 %, p = 0.003). There was no association between any surgery related variables and the subsequent development of chronic abdominal pain. The only predictors of chronic abdominal pain at one-year follow-up were associated with the patients’ preoperative psychological profi le. Patients anticipating difficulty with surgery or recovery from it and those with lower scores on the Sense of Coherence questionnaire (an index of coping skills) were more likely to develop chronic postoperative abdominal pain. In these cases, the interplay of peripheral visceral stimulus together with central sensitization related to psychosocial variables affected the de novo development of chronic abdominal pain. Studies using functional MRI and PET CT have demonstrated that the ACC, which is responsible for descending pain inhibition, is less active in IBS patients. This phenomenon is also found in other chronic pain syndromes such as fibromyalgia [ 33 – 35 ]. In contrast, the MCC, which is associated with unpleasantness and fear, is overactive. Therefore, in IBS patients the normal adaptive inhibitory response to painful visceral stimuli is diminished and replaced by a maladaptive, presumably even aggravating, response [ 33 , 34 , 36 ]. The factors that ultimately lead to this shift into a maladaptive pattern are psychosocial in nature. This connection was elegantly demonstrated in the case report of a patient with a severe functional gastrointestinal pain syndrome and a history of abuse [ 37 ]. Her baseline brain scan demonstrated marked activation of the MCC and the somatosensory cortex. Following successful treatment with antidepressants and psychotherapy a repeated scan demonstrated diminished MCC activity and increased insular activation. Thus, maladaptive brain responses are reversible and so is the patient’s clinical situation. Treatment of Abdominal Pain in IBS As in other fields of medicine, in particular in patients with chronic painful conditions, the healing process for IBS patients begins when the patient enters the doctor’s office before any medicine has been prescribed. It is of the utmost importance to establish a good doctor–patient relationship in order to succeed in the therapeutic process [ 38 , 39 ]. Some of the essentials of a salutary doctor–patient relationship are discussed below: 1. Allow enough time especially for the first meeting. The patient should feel that the doctor is listening to and him/ her and that their symptoms are considered legitimate and are being taken seriously. 2. Take a full detailed history and perform a physical examination: These basic measures of good clinical practice help to foster the doctor–patient relationship.

3. It is very helpful to remember four key questions that patients should be asked: a. What brings you here at this time? IBS is a chronic condition and many patients have their symptoms for years before consulting a specialist. Consultation is often driven by a specific anxiety or a stressful situation that should be addressed. b. What do you think is the cause of your symptoms? Many IBS patients attribute their symptoms to undiagnosed cancer, infection, inflammatory bowel disease, or food allergy. c. What are your concerns or worries? It is important to understand the patient’s agenda and to address their primary concerns such as “What exactly do I have?” or “Do I have cancer,” or alternatively related to the symptoms like “I can’t deal with this pain anymore.” d. What are your expectations from me? Some patients have the unrealistic expectation of a “quick fi x” for their situation that can lead to mutual frustration and treatment failure [ 40 ]. It should be emphasized that treating IBS is a process rather than an isolated consultation and that the goal of treatment is to reduce their suffering and to improve their quality of life rather than to “cure” them. Many IBS patients have never received a comprehensive explanation about the nature of their problem. This may be the basis for the unwarranted fears (“I might have cancer”) and feelings of frustration (“why can’t they fi gure out what I have”). A detailed explanation about the nature of functional disorders and their natural history is very important to deal with these issues. Treating IBS patients is an ongoing process that takes time. Throughout this process patients are likely to encounter diffi culties, setbacks, and frustration. Patients should not feel that they are left alone to deal with their setbacks. Scheduling a follow-up phone call, for example, is a simple measure that is often suffi cient to allay patients’ new concerns [ 41 ]. Physicians should inquire about comorbid gastrointestinal and nongastrointestinal functional disorders. IBS patients have a high prevalence of other functional disorders [ 42 ], leading some patients to feel that they are very ill. By providing patients with a unifying paradigm that connects different, apparently unrelated, symptoms to one disorder (i.e., central sensitization), we can alleviate much of their fears and concerns. For some patients with mild symptoms, these steps may be enough to alleviate fears and concerns regarding their symptoms. These patients often continue to cope successfully with their symptoms and need no further treatment. However, the majority of patients will require more specifi c treatment. The treatment options for IBS can be divided into pharmacological and nonpharmacological treatment modalities (Fig. 6.1 ). Medical Treatment Medical treatment of IBS includes peripherally acting agents and centrally acting agents. Peripherally Acting Agents These drugs act on the gut itself and are targeted against specifi c IBS symptoms such altered bowel movements, bloating, and cramps. Because they are not key agents in



Table 6.2 Peripheral agents used most commonly in the treatment of IBS. Peripheral agents, although not primarily directed against pain, have an important role in IBS treatment. In mild IBS cases, they might suffi ce but in more severe IBS cases and, where pain is a cardinal symptom, central agents are preferred Class Drug Mechanism of action Comments • Antispasmodics • Pinaverium • Direct visceral smooth muscle relaxants • Modest effect on IBS spastic pain • Mebeverin • Colpermin (peppermint oil) • Anticholinergic/antimuscarinic • Otilinium bromide, hyoscine, and colpermin; best evidence for effectiveness • Hyoscamine dicyclomine • Serotonergic and other agents • Alosetron • 5HT3 receptor antagonist • Available only through a restricted access program; increased incidence of ischemic colitis • Tegaserode • Withdrawn from the US market; an increased incidence of cardiovascular adverse events • 5HT4 receptor agonist • Linaclotide • Guanylate cyclase-C agonist • Recently approved in Europe and the US for IBS-C • Lubiprostone • Chloride channel activator • In phase 3 studies, lubiprostone was almost twice as effective for IBS symptoms as placebo


IBS pain management only some of them are discussed in detail and the rest is mentioned briefly. Table 6.2 summarizes the main facts about the different peripheral agents. Serotonin (5HT) is an important neurotransmitter that coordinates gut function and has played a key role in research and drug development. It is secreted from enterochromaffin cells in the mucosa and is involved in almost every aspect of gut function including motility, sensation, and secretion. Alosetron is a 5HT3 receptor antagonist that was shown to improve global IBS symptoms and pain in women with IBS-D. A meta- analysis comparing 12 randomized controlled trials that evaluated the efficacy of alosetron compared to placebo found an odds ratio of 1.85 for improvement in the alosetron group [ 43 ]. Unfortunately, after initial FDA approval, safety issues and in particular ischemic colitis and severe constipation led to its withdrawal from the market. It was reintroduced in 2002 under a restricted access program. Under this program, alosetron can be prescribed (under some restrictions) to women with severe IBS-D who have failed to respond to traditional medical therapies. Lubiprostone is a chloride channel activator that has been approved by the FDA for chronic constipation and IBC-C. In phase 3 studies, patients receiving lubiprostone were almost twice as likely to gain relief from overall IBS symptoms compared to patients who received placebo [ 44 ]. The main side effect of lubiprostone, nausea, is reported in 8 % of IBS-C patients who receive 8 mcg twice daily. Centrally Acting Agents Centrally acting agents should be the cornerstone of treatment in moderate-to-severe cases of IBS [ 45 ]. The main classes of drugs that are being used are the selective serotonin reuptake inhibitors (SSRIs), selective serotonin- norepinephrine reuptake inhibitors (SNRIs), and tricyclic antidepressants (TCAs). Other drugs, such as Mirtazapine, Buspiron, and the atypical antipsychotic Quetiapine, can also be used. These drugs were developed for the treatment of anxiety and depression, but can and should be used in IBS as discussed below. The different drugs and dosages are summarized in Table 6.3 . Antidepressants play a central role in medical therapy for IBS for two main reasons. First, they have a direct analgesic effect and are used in various pain syndromes, with or without concomitant depression, to elevate pain thresholds via central and peripheral effects. Second, since many IBS patient have psychological comorbidity, they can gain direct benefit from these drugs. Whether the main effect of antidepressants stems from central mechanisms (modulation of central pain processing) or from peripheral effects (effects on motility and secretion and reduction of afferent pain signals) or just from reducing depression and anxiety is still uncertain. The actual mechanism is probably a combination of all three. A recent meta-analysis found all classes of antidepressants to be effective in IBS with a number needed to treat as low as four [ 46 ]. Antidepressants in IBS (especially TCAs) are given at much lower doses then those used for the treatment of depression. The usual starting dose in 25–50 mg and can be increased as needed. SSRIs and SNRIs are usually given in the lower range of the “regular” psychiatric doses, for example, 10–20 mg of Escitalopram or 30 mg of duloxetine. Since TCAs and SNRIs have an independent indication in other pain syndromes, such as neuropathic pain and fibromyalgia, they are the drugs of choice for painful IBS. The choice between them is often based on the therapeutic profile of the drugs including potential adverse effects.


Table 6.3 Common interventions used in IBS. For optimal results these interventions can be used in combination (“augmentation” therapy). The use of more than one drug at a low dose can augment the therapeutic response and minimize the side effects Drug Drug (daily dose range [mg]) Comments TCA • Desipramine (25–150) • Begin with low dose and titrate by response • Nortriptyline (25–150) • Amitriptyline (25–150) • Allow 4–8 weeks for maximal response SSRIs • Paroxetine (20–60) • Begin with low dose and titrate by response • Escitalopram (10–20) SNRIs • Venlafaxine (25–300) • Psychological and analgesic effects • Duloxetine (20–80) Atypical antipsychotics • Quetiapine (25–100) • Preliminary reports Tetracyclic antidepressant • Mirtazepine (15–45) • Antiemetic properties Azaspirodecanediones • Buspiron (10–60) • Improves gastric receptive relaxation

For example, TCAs tend to be more constipating and have less anxiolytic properties, so an SNRI would be the preferred option in a patient with constipation or prominent anxiety. However, in many cases a combination of two drugs or more is necessary. Instead of increasing the dose of a single drug to the maximum, the use of a combination of two or more drugs from different classes and in lower doses (e.g., a TCA and an SNRI or SSRI) is recommended. This approach known as “augmentation therapy,” helps minimize adverse effects, to which patients with functional GI disorders are prone [ 45 ]. Mirtazapine is a tetracyclic antidepressant used primarily in the treatment of depression. It has serotonergic as well as noradrenergic properties. It has antagonistic alpha-2 receptor and 5HT1, 5HT2, and 5HT3 properties as well as moderated peripheral alpha-1 adrenergic and alpha-1 anticholinergic properties. Its 5HT3 antagonistic action is probably responsible for its antiemetic properties. In addition to its antidepressant effects, it is also used at times as a hypnotic, antiemetic, as an appetite stimulant, and for the treatment of anxiety. In IBS, it can be used to augment the antidepressant and anxiolytic properties of other agents (such as a TCA or an SNRI) and for nausea and vomiting or low body weight, as is often seen in patients with a comorbid eating disorder. Data regarding its use in IBS are limited and more studies are needed to explore its exact place. Quetiapine is an atypical antipsychotic approved for the treatment of schizophrenia, bipolar disorder, and as an add- on to treat depression. It has potential benefi ts in IBS by reducing anxiety, restoring normal sleep patterns, and potentially through a direct analgesic effect. A recent paper reported a retrospective analysis of its use in low doses (50–200 mg) in patients with severe FGIDs. Of the 21 treated patients, 10 discontinued the drug due to adverse effects or lack of effi cacy, but of the 11 patients who stayed on the drug 6 reported improvement [ 47 ]. Although this is a small and uncontrolled study, it is encouraging considering that these were patients with extremely severe IBS who did not respond to any previous treatment modality. A larger, prospective, open-label study is currently underway. Finally, Buspirone is a nonbenzodiazepine anxiolytic agent that is used in psychiatry to augment the effect of antidepressants. It also has a 5HT1 agonist effect, which may contribute to increasing gastric compliance/relaxation as has been shown to occur for functional dyspepsia. Therefore, it might be useful in patients with comorbid dyspeptic symptoms such as epigastric discomfort and early satiety. There are two main barriers that clinicians face when trying to treat IBS patients with antidepressants. The fi rst is the general reluctance of these patients to take “chemical” and “mind altering” agents. The second is patients’ tendency to underestimate the psychological component of their symptoms. A thorough explanation regarding the mechanisms of pain (visceral hypersensitivity modulated by central mechanisms) and the drug’s independent analgesic properties is enough in many cases. Some patients view the recommendation for a psychotropic drug as evidence that the doctor does not acknowledge their pain and thinks that they are “crazy.” If we emphasize that we are recommending these drugs for their central analgesic effect, we can overcome much of this reticence to take them. This can be accomplished with a statement such as: “The same drug can be used for different reasons. For example, in the past aspirin was the leading drug for reducing fever and relieving pain, but currently it is the number one drug for the prevention of heart disease. Similarly, antidepressant drugs are effective in the treatment of depression at higher doses, but are also effective in lower dosages for pain relief”. The patient should always make the fi nal decision regarding the drug. This can be achieved by fostering a feeling of therapeutic partnership instead of an authoritative relationship where the patient has no say about the way he is treated. An example for such an approach would be: “In IBS there are many therapeutic options, with and without drugs. Each has its advantages and disadvantages. Do you want me to tell you about options that could help you with your symptoms?” By making the drug the


patient’s choice, we can augment adherence to treatment. Finally, in our experience, the adherence rate for drug therapy increases if the physician is available to address, in real time, early adverse effects, and other concerns that otherwise may lead the patient to discontinue therapy on their own. Nonpharmacologic Therapy for IBS Nonpharmacological treatments for IBS include stress reduction, and behavioral and psychological interventions. Behavioral Interventions Behavioral interventions are commonly used to treat IBS. They are safe and their benefi t may go beyond symptomatic treatment and induce positive physiological changes. They are particularly suited to patients who do not want to take drugs. The effect of different modalities, including cognitive behavioral therapy (CBT), interpersonal (psychodynamic) therapy, hypnosis, stress reduction, and mindfulness meditation, has been evaluated for IBS. All help patients deal with issues such as maladaptive illness beliefs and behaviors, and the relationship between stress, life events, and symptomatology. CBT can help patients recognize misperceptions and maladaptive thoughts regarding their symptoms and enhance their coping abilities. It can be administered as individual or group therapy [ 48 – 50 ]. In the largest randomized placebo- controlled study conducted to date, the investigators found that 12 weekly CBT sessions were signifi cantly more benefi cial than placebo for female patients with moderate-to-severe FGIDs [ 51 ]. Interpersonal (psychodynamic) therapy presumes that symptoms are associated with diffi culties in interpersonal relationships. Its focus is on the identifi cation of interpersonal situations that lead to symptom exacerbation. The treatment itself involves psychotherapy. The symptoms improve when the confl icts are resolved. Interpersonal dynamic psychotherapy has been shown to improve symptoms and to reduce disability and healthcare costs in IBS [ 52 – 54 ]. The aim of stress reduction (relaxation training) is to counteract the physiologic effects of stress. Reduction in skeletal muscle tension can decrease autonomic arousal and subjective tension/anxiety and may improve gut motility. Stress reduction and relaxation training includes modalities such as guided imagery, relaxation response, meditation, yoga, and biofeedback. Muscle relaxation alone or in combination with CBT and other techniques was shown to reduce IBS symptoms [ 55 ]. Mindfulness meditation is a form of relaxation involving an active nonjudgmental awareness of body sensations and emotions. Group mindfulness meditation resulted in improved IBS symptoms and health-related quality of life as well as reduced stress levels in women with IBS [ 56 ], effects that persisted at a three-month follow-up assessment. Hypnosis is a form of guided imagery that uses muscle relaxation and gut-targeted suggestions to improve the gut function and reduce symptoms. Hypnosis involves nonspecifi c effects of relaxation, stress management, ego strengthening, and gut-directed suggestions of normal functioning and pleasant feeling. Data gathered from studies in different centers support the use of hypnosis as an effective, viable treatment option in IBS [ 57 ] that improves IBS symptoms and quality of life and reduces stress and anxiety. Moreover, the benefi cial effects of hypnosis have been shown to persist at long-term follow-up [ 58 – 60 ]. The predictors of a favorable outcome in behavioral interventions include confi dence in treatment success, perceived sense of control over symptoms, a good relationship with the therapist, and early response [ 61 ]. The choice of intervention depends on local expertise and availability as well as patient preference. Summary and Conclusions IBS is a common medical problem, which, although not life threatening, has a signifi cant negative impact on patients’ quality of life. Its range of severity ranges from mild intermittent symptoms to a disabling condition with a considerable loss of daily function. Pain in IBS is the result of peripheral afferent stimulation and CNS processing. A biopsychosocial perspective, taking into account the patient’s psychological status, life experiences, beliefs, and concerns can help doctors provide optimal care. The primary goal of treatment is care rather than cure, and the various treatment options can be highly effective in reducing suffering and improving quality of life. The doctor–patient relationship is the foundation of successful treatment and should be supplemented by pharmacological or nonpharmacological treatments in accordance with the clinical situation and the patient’s preference. References 1. Longstreth GF, Thompson WG, Chey WD, Houghton LA, Mearin F, Spiller RC. Functional bowel disorders. In: Drossman SA, Corazziari E, Delvaux M, Spiller RC, Talley NJ, Thompson WG, et al., editors. Rome III the functional gastrointestinal disorders. McLean, VA: Degnon Associates; 2006. p. 487–555. 2. Sperber AD. The challenge of cross-cultural, multi-national research: potential benefi ts in the functional gastrointestinal disorders. Neurogastroenterol Motil. 2009;21:351–60. 3. Drossman DA, Camilleri M, Mayer EA, Whitehead WE. AGA technical review on irritable bowel syndrome. Gastroenterology. 2002;123:2108–31. 4. Andrews EB, Eaton SC, Hollis KA, Hopkins JS, Ameen V, Hamm LR, et al. Prevalence and demographics of irritable bowel syndrome: results from a large web-based survey. Aliment Pharmacol Ther. 2005;22:935–42.

l. Pain in the abdomen For many ry•ople abdominal pains are the unpleasant symptom. describe the pain in different ways; it is frequently described as coming in spasms (spasmodk it may be nagging. sharp. heavy or dull: get waves Of intense pain. It feels a bit like trapped wind." It can be felt anyw'here in the abdominal area Oust below the stomach) but is more frequent down the left-hand side. The wverity of this pain is the one thing most likely to drive people into Weing a d(Xtor. Some people will describe them as •stomach pains • even though these pains tend to occur in the abdomen: "Sometimes I'm in sc much pain that I can't even sit on the toilet." "It feels tike I have been cut in two, can cope with the diarrhoea. but the pain wears me down. Peoc*e may worry about what the pain may mean: "The cramps can be so bad it Can't just be IBS. it must be something more serous. But other peoNe will not exrx•rience pain but rather a 'discomfort


describe the pain in different ways: it is frequently described as coming in spasms (spasmodic): it may be nagging. sharp, heavy or dull: I get waves cf intense pain. It feels a bit like trapped wind. It can bc felt anywhere in the abdominal area Oust below the stomach) but is more frequent down the left-hand side. The severity of this pain is the one thing most likely to drive people into seeing a doctor. Some people will describe them as 'stomach pains' even though these pains tend to occur in the abdomen: "Sometimes I'm in so much pain that I can't even sit cn the toilet." It feels like I have been cut in two. I can cope with the diarrhoea. but the pain wears me down. people may worry about what the pain may mean: "The cramps can be so bad it can't just be IBS. it must be something more senoas.


Introduction Most patients who present with gastrointestinal symptoms have no clear organic cause even after an extensive investigation and are diagnosed with a functional gastrointestinal disorder (FGID). Among the FGIDs, irritable bowel syndrome (IBS) is the most common, affecting up to 15 % of the general population. The hallmark of IBS is chronic abdominal pain associated with irregular bowel movements. The pain can be mild and intermittent or severe, constant, and debilitating. IBS patients are major healthcare utilizers and are seen and treated not only by primary care physicians and gastroenterologists but also by surgeons, gynecologists, pain specialists, and rheumatologists. Thus, it is important for physicians in diverse subspecialties to be familiar with the diagnosis and management of this disorder. The purpose of this chapter is to review the epidemiology and diagnosis of IBS and provide an in-depth look into the pathogenesis and treatment of pain in IBS patients.

Key Points • Irritable bowel syndrome (IBS) is the most common functional gastrointestinal disorder (FGID), affecting up to 15 % of the general population. • It is characterized by chronic abdominal pain that can be mild and intermittent, or severe, constant, and debilitating. Pain in IBS, as in other chronic pain disorders, is a complex symptom resulting from the interplay between peripheral (visceral) stimulation (enteric nervous system) and central modulation (central nervous system). • As the severity of pain increases central processing plays an increasingly important role compared to peripheral input. In IBS, the normal adaptive central inhibitory response to painful visceral stimuli is diminished. This change is modulated by psychosocial factors such as anxiety, depression, poor social support, and impaired coping skills. • Successful treatment begins with a therapeutic doctor– patient partnership. Medical treatment of IBS includes peripherally acting and centrally acting agents with antidepressants playing a central role. Cognitive behavioral therapy (CBT), interpersonal (psychodynamic) therapy, hypnosis, stress reduction, and mindfulness meditation have been shown to be effective in the treatment of IBS
Epidemiology IBS is a common functional disorder with a symptom-based diagnosis (Rome III diagnostic criteria, Table 6.1 ) [ 1 ]. The reported prevalence of IBS varies from study to study depending on diagnostic criteria used as well as other methodological differences among studies [ 2 ]. However, some fi ndings on the epidemiology of IBS appear to hold true and are as follows: 1. IBS is a global problem that affects individuals all over the world [ 3 ]. The reported worldwide prevalence rates for IBS range from 5 % to 20 %. 2. In most countries IBS affects women (60–70 %) more than men [ 4 , 5 ]. The East is unique in that there are reports from China, Taiwan, and Singapore of a similar prevalence between males and females [ 6 , 7 ]. There are confl icting reports from India with community-based surveys reporting
higher prevalence of IBS among females in the general population and hospital-based surveys reporting higher proportion of males among patients in gastroenterology clinics [ 8 , 9 ]. The latter observation might refl ect cultural aspects of healthcare-seeking behaviors in Indian society. 3. Although IBS can appear at any age, it is more common in young and middle-aged patients and tends to be less common in the elderly [ 10 , 11 ]. 4. Socioeconomic status may play a role in the epidemiology of IBS, which has been reported in some countries to be more prevalent in lower socioeconomic classes [ 4 , 12 , 13 ], although the data on this factor are not consistent. As a prevalent chronic disorder, IBS places a major economic burden on health care. A meta-analysis of 18 studies from the USA and the UK estimated the annual direct cost of an IBS patient (drugs, procedures, and doctor visits) at $348–8,750 and the annual indirect costs (loss of work days and deceased productivity) at $355–3,344 [ 14 , 15 ]. Another US study estimated the overall annual direct cost of IBS to be $228 million in doctor visits and $80 million in drugs [ 15 ]. Diagnosis There is no specifi c diagnostic fi nding or biomarker for IBS, so the diagnosis is based on patients’ reports of their symptoms. In the past, IBS was considered a diagnosis of exclusion, but inherent to this approach is an exhaustive diagnostic work-up that involves unpleasant and potentially risky tests for the patient and is not cost effective. Thus, a symptom- based diagnostic system, known as the Rome criteria, was developed. The main concept introduced by the Rome criteria is that the diagnostic process of a functional disorder should be based on two components. The fi rst is the presence of a typical cluster of symptoms and the second is the absence of “red fl ags” including initial presentation of symptoms at an age over 50, unexplained weight loss, fever, nocturnal symptoms, blood in the stool, a family history of gastrointestinal malignancy or disease (e.g., celiac or infl ammatory bowel disease), or an abnormal fi nding on physical examination. Basic laboratory tests, such as a complete blood count and celiac serology, are usually enough to complete the diagnostic process and establish a fi rm diagnosis. Patients who fulfi ll the criteria and do not have red fl ags need a minimal diagnostic work-up after which the diagnosis of IBS can be made with confi dence [ 16 , 17 ]. The latest update of the Rome diagnostic criteria for IBS is Rome III, in which the diagnosis of IBS requires the presence of abdominal pain or discomfort for at least 10 % of the time over the previous three months with symptom onset at least six months earlier [ 18 ]. Additionally, pain should be relieved by defecation and associated with a change in the frequency of bowel movements or a change in the form of the stool. Accompanying symptoms, although not essential for the diagnosis, are a feeling of incomplete evacuation, abnormal stool frequency (less than three times a week or more than three times a day) or consistency, straining at defecation, urgency, mucus discharge, and bloating. IBS can be further divided into three main subgroups according to bowel habit as constipation predominant (IBS-C), diarrhea predominant (IBS-D), and those exhibiting an alternating bowel pattern [ 19 ]. Patients may switch from one subclass to another during the course of their illness. It has been demonstrated repeatedly that the use of positive symptom-based diagnostic criteria in conjunction with the use of red fl ags to guide further investigation in selected cases is a reliable and cost-effective approach. After establishing the diagnosis of IBS, based on the Rome criteria, it is rarely necessary to change the diagnosis [ 20 – 22 ]. The Pathophysiology of Pain in IBS Abdominal pain is a hallmark of IBS and is essential for its diagnosis. In IBS, as in many other chronic pain syndromes, pain is a complex experience resulting from the interplay between peripheral (visceral) stimulation (enteric nervous system) and central modulation (central nervous system [CNS]). Afferent stimulation from the colon is transmitted to second- order neurons in the spinal cord and then ascends to the brain through the spinothalamic, spinoreticular, and spinomesencephalic tracts. These tracts connect to the somatosensory cortex responsible for registration and localization of painful visceral and somatic stimuli. They also connect to structures in the limbic system that are involved in the refl exive, affective, and motivational responses to pain [ 23 ]. The afferent pathways project to the perigenual anterior cingulate cortex (pACC), which is involved in affective modifi cation, and to the midcingulate cortex (MCC), which is involved in the behavioral response. The amplifi cation of afferent visceral stimulation can result from increased excitability of peripheral receptors or impaired spinal and/or central pain regulatory systems. Increased excitability can produce the two related phenomena
Table 6.1 Rome III diagnostic criteria a for IBS Recurrent abdominal pain or discomfort b at least 3 days/month in the last 3 months associated with two or more of the following: 1. Improvement with defecation 2. Onset associated with a change in frequency of stool 3. Onset associated with a change in form (appearance) of stool a Criterion fulfi lled for the last 3 months with symptom onset at least 6 mon
ths prior to diagnosis b “Discomfort” means an uncomfortable sensation not described as pain
of hyperalgesia (increased pain response to painful stimuli) and allodynia (increased pain response to nonpainful stimuli) [ 24 ]. Thus, afferent visceral stimulation can be experienced as painful not only as a result of peripheral intensity but also as a result of central processing that may be modulated by psychosocial factors such as anxiety, depression, poor social support, and impaired coping skills [ 25 ]. As the severity of pain increases central processing plays an increasingly important role compared to peripheral input. Once a pattern of central sensitization has taken hold, patients may even experience severe pain without ongoing peripheral nociceptive stimulation [ 26 , 27 ]. This is the extreme end of the IBS severity spectrum. While we do not have full knowledge of all the causes of excessive peripheral stimulation, there is good evidence that eating, infection, infl ammation, physical injury, hormones (e.g., menses), or colonic motility may play a role. Up to 15 % of IBS patients attribute the beginning of their symptoms to an acute episode of gastrointestinal infection. A meta-analysis of eight papers including almost 600,000 patients over a follow-up up to one year found that the odds ratio for developing IBS after such an episode is seven [ 28 ]. IBS that follows acute intestinal infection has been shown to be associated with a persistent or chronic state of infl ammation that cannot be identifi ed by routine clinical tests and procedures [ 29 , 30 ]. Risk factors for postinfectious IBS are related to not only to the severity of the acute infectious episode (fever, bloody stools, and need for hospitalization) but also to patient characteristics such as female gender, stress, anxiety, and depression [ 31 ]. This is a good example of how excessive afferent stimulation, induced in this case by a microinfl ammatory state, can develop into a chronic condition such as IBS-D after central sensitization occurs in a susceptible person with psychological comorbidity. Peripheral stimulation and its interplay with central amplifi cation are also refl ected in the development of chronic abdominal pain following abdominal or pelvic surgery. IBS patients reported up to twice the number of appendectomies and hysterectomies and up to three times the number of cholecystectomies compared with those without IBS [ 32 ]. Surgery may cause visceral afferent sensitization that eventually results in allodynia and chronic pain even in the presence of normal gut function. This contention is supported by a study that evaluated the development of abdominal pain after elective gynecologic surgery for nonpainful indications [ 32 ]. Patients with no prior history of chronic abdominal pain undergoing gynecological surgery for nonpainful indications were followed for the development of de novo abdominal pain following surgery. They were compared with a control group comprised of nonsurgical patients who came to a gynecologic clinic for nonpain-related reasons. At one-year follow-up signifi cantly more patients in the surgery group complained of chronic abdominal pain (15.3 %) than in the control group (3.6 %, p = 0.003). There was no association between any surgeryrelated variables and the subsequent development of chronic abdominal pain. The only predictors of chronic abdominal pain at one-year follow-up were associated with the patients’ preoperative psychological profi le. Patients anticipating diffi culty with surgery or recovery from it and those with lower scores on the Sense of Coherence questionnaire (an index of coping skills) were more likely to develop chronic postoperative abdominal pain. In these cases, the interplay of peripheral visceral stimulus together with central sensitization related to psychosocial variables affected the de novo development of chronic abdominal pain. Studies using functional MRI and PET CT have demonstrated that the ACC, which is responsible for descending pain inhibition, is less active in IBS patients. This phenomenon is also found in other chronic pain syndromes such as fi bromyalgia [ 33 – 35 ]. In contrast, the MCC, which is associated with unpleasantness and fear, is overactive. Therefore, in IBS patients the normal adaptive inhibitory response to painful visceral stimuli is diminished and replaced by a maladaptive, presumably even aggravating, response [ 33 , 34 , 36 ]. The factors that ultimately lead to this shift into a maladaptive pattern are psychosocial in nature. This connection was elegantly demonstrated in the case report of a patient with a severe functional gastrointestinal pain syndrome and a history of abuse [ 37 ]. Her baseline brain scan demonstrated marked activation of the MCC and the somatosensory cortex. Following successful treatment with antidepressants and psychotherapy a repeated scan demonstrated diminished MCC activity and increased insular activation. Thus, maladaptive brain responses are reversible and so is the patient’s clinical situation. Treatment of Abdominal Pain in IBS As in other fi elds of medicine, in particular in patients with chronic painful conditions, the healing process for IBS patients begins when the patient enters the doctor’s offi ce before any medicine has been prescribed. It is of the outmost importance to establish a good doctor–patient relationship in order to succeed in the therapeutic process [ 38 , 39 ]. Some of the essentials of a salutary doctor–patient relationship are discussed below: 1. Allow enough time especially for the fi rst meeting. The patient should feel that the doctor is listening to and him/ her and that their symptoms are considered legitimate and are being taken seriously. 2. Take a full detailed history and perform a physical examination: These basic measures of good clinical practice help to foster the doctor–patient relationship.

3. It is very helpful to remember four key questions that patients should be asked: a. What brings you here at this time? IBS is a chronic condition and many patients have their symptoms for years before consulting a specialist. Consultation is often driven by a specifi c anxiety or a stressful situation that should be addressed. b. What do you think is the cause of your symptoms? Many IBS patients attribute their symptoms to undiagnosed cancer, infection, infl ammatory bowel disease, or food allergy. c. What are your concerns or worries? It is important to understand the patient’s agenda and to address their primary concerns such as “What exactly do I have?” or “Do I have cancer,” or alternatively related to the symptoms like “I can’t deal with this pain anymore.” d. What are your expectations from me? Some patients have the unrealistic expectation of a “quick fi x” for their situation that can lead to mutual frustration and treatment failure [ 40 ]. It should be emphasized that treating IBS is a process rather than an isolated consultation and that the goal of treatment is to reduce their suffering and to improve their quality of life rather than to “cure” them. Many IBS patients have never received a comprehensive explanation about the nature of their problem. This may be the basis for the unwarranted fears (“I might have cancer”) and feelings of frustration (“why can’t they fi gure out what I have”). A detailed explanation about the nature of functional disorders and their natural history is very important to deal with these issues. Treating IBS patients is an ongoing process that takes time. Throughout this process patients are likely to encounter diffi culties, setbacks, and frustration. Patients should not feel that they are left alone to deal with their setbacks. Scheduling a follow-up phone call, for example, is a simple measure that is often suffi cient to allay patients’ new concerns [ 41 ]. Physicians should inquire about comorbid gastrointestinal and nongastrointestinal functional disorders. IBS patients have a high prevalence of other functional disorders [ 42 ], leading some patients to feel that they are very ill. By providing patients with a unifying paradigm that connects different, apparently unrelated, symptoms to one disorder (i.e., central sensitization), we can alleviate much of their fears and concerns. For some patients with mild symptoms, these steps may be enough to alleviate fears and concerns regarding their symptoms. These patients often continue to cope successfully with their symptoms and need no further treatment. However, the majority of patients will require more specifi c treatment. The treatment options for IBS can be divided into pharmacological and nonpharmacological treatment modalities (Fig. 6.1 ). Medical Treatment Medical treatment of IBS includes peripherally acting agents and centrally acting agents. Peripherally Acting Agents These drugs act on the gut itself and are targeted against specifi c IBS symptoms such altered bowel movements, bloating, and cramps. Because they are not key agents in



Table 6.2 Peripheral agents used most commonly in the treatment of IBS. Peripheral agents, although not primarily directed against pain, have an important role in IBS treatment. In mild IBS cases, they might suffi ce but in more severe IBS cases and, where pain is a cardinal symptom, central agents are preferred Class Drug Mechanism of action Comments • Antispasmodics • Pinaverium • Direct visceral smooth muscle relaxants • Modest effect on IBS spastic pain • Mebeverin • Colpermin (peppermint oil) • Anticholinergic/antimuscarinic • Otilinium bromide, hyoscine, and colpermin; best evidence for effectiveness • Hyoscamine dicyclomine • Serotonergic and other agents • Alosetron • 5HT3 receptor antagonist • Available only through a restricted access program; increased incidence of ischemic colitis • Tegaserode • Withdrawn from the US market; an increased incidence of cardiovascular adverse events • 5HT4 receptor agonist • Linaclotide • Guanylate cyclase-C agonist • Recently approved in Europe and the US for IBS-C • Lubiprostone • Chloride channel activator • In phase 3 studies, lubiprostone was almost twice as effective for IBS symptoms as placebo


IBS pain management only some of them are discussed in detail and the rest is mentioned briefly. Table 6.2 summarizes the main facts about the different peripheral agents. Serotonin (5HT) is an important neurotransmitter that coordinates gut function and has played a key role in research and drug development. It is secreted from enterochromaffin cells in the mucosa and is involved in almost every aspect of gut function including motility, sensation, and secretion. Alosetron is a 5HT3 receptor antagonist that was shown to improve global IBS symptoms and pain in women with IBS-D. A meta- analysis comparing 12 randomized controlled trials that evaluated the efficacy of alosetron compared to placebo found an odds ratio of 1.85 for improvement in the alosetron group [ 43 ]. Unfortunately, after initial FDA approval, safety issues and in particular ischemic colitis and severe constipation led to its withdrawal from the market. It was reintroduced in 2002 under a restricted access program. Under this program, alosetron can be prescribed (under some restrictions) to women with severe IBS-D who have failed to respond to traditional medical therapies. Lubiprostone is a chloride channel activator that has been approved by the FDA for chronic constipation and IBC-C. In phase 3 studies, patients receiving lubiprostone were almost twice as likely to gain relief from overall IBS symptoms compared to patients who received placebo [ 44 ]. The main side effect of lubiprostone, nausea, is reported in 8 % of IBS-C patients who receive 8 mcg twice daily. Centrally Acting Agents Centrally acting agents should be the cornerstone of treatment in moderate-to-severe cases of IBS [ 45 ]. The main classes of drugs that are being used are the selective serotonin reuptake inhibitors (SSRIs), selective serotonin- norepinephrine reuptake inhibitors (SNRIs), and tricyclic antidepressants (TCAs). Other drugs, such as Mirtazapine, Buspiron, and the atypical antipsychotic Quetiapine, can also be used. These drugs were developed for the treatment of anxiety and depression, but can and should be used in IBS as discussed below. The different drugs and dosages are summarized in Table 6.3 . Antidepressants play a central role in medical therapy for IBS for two main reasons. First, they have a direct analgesic effect and are used in various pain syndromes, with or without concomitant depression, to elevate pain thresholds via central and peripheral effects. Second, since many IBS patient have psychological comorbidity, they can gain direct benefit from these drugs. Whether the main effect of antidepressants stems from central mechanisms (modulation of central pain processing) or from peripheral effects (effects on motility and secretion and reduction of afferent pain signals) or just from reducing depression and anxiety is still uncertain. The actual mechanism is probably a combination of all three. A recent meta-analysis found all classes of antidepressants to be effective in IBS with a number needed to treat as low as four [ 46 ]. Antidepressants in IBS (especially TCAs) are given at much lower doses then those used for the treatment of depression. The usual starting dose in 25–50 mg and can be increased as needed. SSRIs and SNRIs are usually given in the lower range of the “regular” psychiatric doses, for example, 10–20 mg of Escitalopram or 30 mg of duloxetine. Since TCAs and SNRIs have an independent indication in other pain syndromes, such as neuropathic pain and fibromyalgia, they are the drugs of choice for painful IBS. The choice between them is often based on the therapeutic profile of the drugs including potential adverse effects.


Table 6.3 Common interventions used in IBS. For optimal results these interventions can be used in combination (“augmentation” therapy). The use of more than one drug at a low dose can augment the therapeutic response and minimize the side effects Drug Drug (daily dose range [mg]) Comments TCA • Desipramine (25–150) • Begin with low dose and titrate by response • Nortriptyline (25–150) • Amitriptyline (25–150) • Allow 4–8 weeks for maximal response SSRIs • Paroxetine (20–60) • Begin with low dose and titrate by response • Escitalopram (10–20) SNRIs • Venlafaxine (25–300) • Psychological and analgesic effects • Duloxetine (20–80) Atypical antipsychotics • Quetiapine (25–100) • Preliminary reports Tetracyclic antidepressant • Mirtazepine (15–45) • Antiemetic properties Azaspirodecanediones • Buspiron (10–60) • Improves gastric receptive relaxation

For example, TCAs tend to be more constipating and have less anxiolytic properties, so an SNRI would be the preferred option in a patient with constipation or prominent anxiety. However, in many cases a combination of two drugs or more is necessary. Instead of increasing the dose of a single drug to the maximum, the use of a combination of two or more drugs from different classes and in lower doses (e.g., a TCA and an SNRI or SSRI) is recommended. This approach known as “augmentation therapy,” helps minimize adverse effects, to which patients with functional GI disorders are prone [ 45 ]. Mirtazapine is a tetracyclic antidepressant used primarily in the treatment of depression. It has serotonergic as well as noradrenergic properties. It has antagonistic alpha-2 receptor and 5HT1, 5HT2, and 5HT3 properties as well as moderated peripheral alpha-1 adrenergic and alpha-1 anticholinergic properties. Its 5HT3 antagonistic action is probably responsible for its antiemetic properties. In addition to its antidepressant effects, it is also used at times as a hypnotic, antiemetic, as an appetite stimulant, and for the treatment of anxiety. In IBS, it can be used to augment the antidepressant and anxiolytic properties of other agents (such as a TCA or an SNRI) and for nausea and vomiting or low body weight, as is often seen in patients with a comorbid eating disorder. Data regarding its use in IBS are limited and more studies are needed to explore its exact place. Quetiapine is an atypical antipsychotic approved for the treatment of schizophrenia, bipolar disorder, and as an add- on to treat depression. It has potential benefi ts in IBS by reducing anxiety, restoring normal sleep patterns, and potentially through a direct analgesic effect. A recent paper reported a retrospective analysis of its use in low doses (50–200 mg) in patients with severe FGIDs. Of the 21 treated patients, 10 discontinued the drug due to adverse effects or lack of effi cacy, but of the 11 patients who stayed on the drug 6 reported improvement [ 47 ]. Although this is a small and uncontrolled study, it is encouraging considering that these were patients with extremely severe IBS who did not respond to any previous treatment modality. A larger, prospective, open-label study is currently underway. Finally, Buspirone is a nonbenzodiazepine anxiolytic agent that is used in psychiatry to augment the effect of antidepressants. It also has a 5HT1 agonist effect, which may contribute to increasing gastric compliance/relaxation as has been shown to occur for functional dyspepsia. Therefore, it might be useful in patients with comorbid dyspeptic symptoms such as epigastric discomfort and early satiety. There are two main barriers that clinicians face when trying to treat IBS patients with antidepressants. The fi rst is the general reluctance of these patients to take “chemical” and “mind altering” agents. The second is patients’ tendency to underestimate the psychological component of their symptoms. A thorough explanation regarding the mechanisms of pain (visceral hypersensitivity modulated by central mechanisms) and the drug’s independent analgesic properties is enough in many cases. Some patients view the recommendation for a psychotropic drug as evidence that the doctor does not acknowledge their pain and thinks that they are “crazy.” If we emphasize that we are recommending these drugs for their central analgesic effect, we can overcome much of this reticence to take them. This can be accomplished with a statement such as: “The same drug can be used for different reasons. For example, in the past aspirin was the leading drug for reducing fever and relieving pain, but currently it is the number one drug for the prevention of heart disease. Similarly, antidepressant drugs are effective in the treatment of depression at higher doses, but are also effective in lower dosages for pain relief”. The patient should always make the fi nal decision regarding the drug. This can be achieved by fostering a feeling of therapeutic partnership instead of an authoritative relationship where the patient has no say about the way he is treated. An example for such an approach would be: “In IBS there are many therapeutic options, with and without drugs. Each has its advantages and disadvantages. Do you want me to tell you about options that could help you with your symptoms?” By making the drug the


patient’s choice, we can augment adherence to treatment. Finally, in our experience, the adherence rate for drug therapy increases if the physician is available to address, in real time, early adverse effects, and other concerns that otherwise may lead the patient to discontinue therapy on their own. Nonpharmacologic Therapy for IBS Nonpharmacological treatments for IBS include stress reduction, and behavioral and psychological interventions. Behavioral Interventions Behavioral interventions are commonly used to treat IBS. They are safe and their benefi t may go beyond symptomatic treatment and induce positive physiological changes. They are particularly suited to patients who do not want to take drugs. The effect of different modalities, including cognitive behavioral therapy (CBT), interpersonal (psychodynamic) therapy, hypnosis, stress reduction, and mindfulness meditation, has been evaluated for IBS. All help patients deal with issues such as maladaptive illness beliefs and behaviors, and the relationship between stress, life events, and symptomatology. CBT can help patients recognize misperceptions and maladaptive thoughts regarding their symptoms and enhance their coping abilities. It can be administered as individual or group therapy [ 48 – 50 ]. In the largest randomized placebo- controlled study conducted to date, the investigators found that 12 weekly CBT sessions were signifi cantly more benefi cial than placebo for female patients with moderate-to-severe FGIDs [ 51 ]. Interpersonal (psychodynamic) therapy presumes that symptoms are associated with diffi culties in interpersonal relationships. Its focus is on the identifi cation of interpersonal situations that lead to symptom exacerbation. The treatment itself involves psychotherapy. The symptoms improve when the confl icts are resolved. Interpersonal dynamic psychotherapy has been shown to improve symptoms and to reduce disability and healthcare costs in IBS [ 52 – 54 ]. The aim of stress reduction (relaxation training) is to counteract the physiologic effects of stress. Reduction in skeletal muscle tension can decrease autonomic arousal and subjective tension/anxiety and may improve gut motility. Stress reduction and relaxation training includes modalities such as guided imagery, relaxation response, meditation, yoga, and biofeedback. Muscle relaxation alone or in combination with CBT and other techniques was shown to reduce IBS symptoms [ 55 ]. Mindfulness meditation is a form of relaxation involving an active nonjudgmental awareness of body sensations and emotions. Group mindfulness meditation resulted in improved IBS symptoms and health-related quality of life as well as reduced stress levels in women with IBS [ 56 ], effects that persisted at a three-month follow-up assessment. Hypnosis is a form of guided imagery that uses muscle relaxation and gut-targeted suggestions to improve the gut function and reduce symptoms. Hypnosis involves nonspecifi c effects of relaxation, stress management, ego strengthening, and gut-directed suggestions of normal functioning and pleasant feeling. Data gathered from studies in different centers support the use of hypnosis as an effective, viable treatment option in IBS [ 57 ] that improves IBS symptoms and quality of life and reduces stress and anxiety. Moreover, the benefi cial effects of hypnosis have been shown to persist at long-term follow-up [ 58 – 60 ]. The predictors of a favorable outcome in behavioral interventions include confi dence in treatment success, perceived sense of control over symptoms, a good relationship with the therapist, and early response [ 61 ]. The choice of intervention depends on local expertise and availability as well as patient preference. Summary and Conclusions IBS is a common medical problem, which, although not life threatening, has a signifi cant negative impact on patients’ quality of life. Its range of severity ranges from mild intermittent symptoms to a disabling condition with a considerable loss of daily function. Pain in IBS is the result of peripheral afferent stimulation and CNS processing. A biopsychosocial perspective, taking into account the patient’s psychological status, life experiences, beliefs, and concerns can help doctors provide optimal care. The primary goal of treatment is care rather than cure, and the various treatment options can be highly effective in reducing suffering and improving quality of life. The doctor–patient relationship is the foundation of successful treatment and should be supplemented by pharmacological or nonpharmacological treatments in accordance with the clinical situation and the patient’s preference. References 1. Longstreth GF, Thompson WG, Chey WD, Houghton LA, Mearin F, Spiller RC. Functional bowel disorders. In: Drossman SA, Corazziari E, Delvaux M, Spiller RC, Talley NJ, Thompson WG, et al., editors. Rome III the functional gastrointestinal disorders. McLean, VA: Degnon Associates; 2006. p. 487–555. 2. Sperber AD. The challenge of cross-cultural, multi-national research: potential benefi ts in the functional gastrointestinal disorders. Neurogastroenterol Motil. 2009;21:351–60. 3. Drossman DA, Camilleri M, Mayer EA, Whitehead WE. AGA technical review on irritable bowel syndrome. Gastroenterology. 2002;123:2108–31. 4. Andrews EB, Eaton SC, Hollis KA, Hopkins JS, Ameen V, Hamm LR, et al. Prevalence and demographics of irritable bowel syndrome: results from a large web-based survey. Aliment Pharmacol Ther. 2005;22:935–42.



People may worry about what the pain may mean: "The cramps can be go bad it can't just be IBS, il must be something more serious. But other people will not experience pain but rather a 'discomfort': ' 'It's not that painful, but it ig a nagging feeling. Some women have found that the pains are worse prior to and during menstruation: just know it's going to be worse with my periods." Abdominal pain is often but not always relieved by passing a stool or passing wind. 2. Bloating

2. Bloating Bloating or abdominal distension is common and, although for most people it is not the most severe aspect of IBS, it can be embarrassing and a nuisance: "My stomach sticks out so far that it looks Like I'm pregnant. It is so embarrassing. G 'l spend most of my time in tracksuits to cover it up.


1 STARTED MY CAREER AS a dietitian in a gastroenterology practice, fresh out of graduate school. I was light on real-life experience with people who had digestive problems, but I arrived full of textbook knowl- edge about all of the conditions I thought I'd encounter in my new job. I'd done my homework and read up about how to use diet to manage diarrhea and constipation, the pain of irritable bowel syndrome (IBS), and the heartburn associated with acid reflux. I felt ready to address whatever complaints my patients would bring. But in the three years of my dietetics education and all those months spent training in the hospital, I had never once heard of the problem that patient after patient showed up complaining about: bloating. Bloating? What did that even mean? It wtlsn't a clinical condition I had ever learned about, and as far as I could tell, there was no official

definition of what it was and how it should be treated. So each time patients told me they were bloated, I probed deeply to understand exactly what they meant. I asked them to describe the feeling of being bloated, what times Of day it happened, what circumstances brought it on, how long it lasted, what made it better, what made it worse, whether it was painful, what it looked like, what other symptoms accompanied it. I needed to understand what this "bloating" thing was so that I could help fix it. The more bloated patients I questioned, the more I came to under- stand that bloating was not a single, uniform experience that could be fixed with a one-size-fits-all solution. To some, bloating described a feeling of excessive fullness after eating—sometimes even after eating very little. TO others, it described a distended belly that looked "pregnant" after eating. Some people belched when bloated; others farted. When bloating was accompanied by gas from either end, it might be painful ...


or not. And when bloating was painful, it was sometimes a pressure-type pain at the top of the stomach underneath the rib cage, a series of sharp gas pains on the sides, or a crampy pain below the belly button. Some bloating was relieved after going to the bathroom, and some wasn't. Some people woke up feeling bloated, while others found that their bloating built as the day progressed. Bloating meant so many different things. Bloating is a symptom Of something else, not a medical condition unto itself, and after spending years in my medical nutrition practice interviewing thousands of patients with digestive problems, I earne to recognize distinct patterns among the different types of bloating that patients presented. As these patterns became clear to me, I became bet- ter and better at matching a description Of their bloating expe- rience with its most likely underlying medical cause. was then able to recommend tailored dietary advice that would address my patient's

rience with its most likely underlying medical cause. I was then able to recommend tailored dietary advice that would address my patient's unique brand of bloating and collaborate with their doctor to help them get the proper diagnosis and, when appropriate, the right treatment. My bloated patients were getting better, often within days of initiating the right diet regimen. So I started writing about bloating online in an attempt to share what I'd learned with people who might not have access to a local dieti-

tian who was highly specialized in digestive disorders. And that's when the emails and calls started pouring in. I've heard from athletes in the Middle East battling bloating as they trained for endurance competi- tions and computer programmers from India who suffered tough diges- tive consequences when following their family's traditional vegetarian diet. Mostly, though, I heard from countless people all across America who just couldn't figure out why they were so darn bloated all the time, who felt that they'd tried everything and were desperate for a solution. A grateful patient once remarked to me that I was like her "bloating whisperer," and my husband got a good laugh about that nickname. But it stuck. While it's certainly not a title I ever aspired to as a little girl fantasizing about what be when I grew up, I embrace it nonetheless. As fate would have it, learning the secret language of bloating has become something of my calling in life, and this book is my way of sharing this knowledge with all the bloated bellies I won't have occasion to meet

Every Unhappy Belly Is Unhappy in Its Own Way A hundred and fifty years ago, the Russian author Leo Tolstoy wrote in his famous book Anna Karenina: "Happy families are all alike; every unhappy family is unhappy in its own way." I think the same can be said about bellies. All happy bellies are alike; every unhappy belly is unhappy in its own way. What I mean by this is that people with happy bellies have digestive systems that function exactly as they*re supposed to. Their stomachs secrete the right amount of acid to get the digestion process under way efficiently. The muscle separating their stomach from their esophagus (food pipe) prevents acid or other stomach contents from re- fluxing baclovard. The nerves that control their stomachs and abdomi- nal wall muscles direct these muscles to stretch just the right amount after eating a meal. The pacemaker cells that control stomach emptying kee food movin alon into the intestines at a normal rate. Their stom-

keep food moving along into the intestines at a normal rate. Their stom- achs and small intestines have sufficient levels of enzymes to break down food into absorbable nutrients effectively. Their small intestines harbor the right number of bacteria and fully absorb the nutrients in Every Unhappy Belly Is Unhappy in Its Own Way: The Many Ways to Be Bloated their food. Their large intestines (colons) keep undigested fiber and waste moving along at a regular pace, resulting in bathroom patterns that are

Then there's everyone else. People with unhappy bellies have digestive systems that misbehave along any number of these dimensions. Bloating can result from dys- function at one or more of these steps in the digestive process. The trick is to figure out the underlying cause of your bloating so that effective dietary—and, when appropriate, medical—remedies can be applied. After all, every bloated belly can be bloated in its own way. When You Hear Hoofbeats, Look for Horses, Not Zebras Most of my bloated patients have sought answers elsewhere before they ended up in my offlce. They've seen at least one doctor—and often several of them. They've consulted the internet and sometimes even seen

trasounds. (All normal.) Sometimes they've also tried a variety of medi- cations, supplements, gone gluten—free, and spent hundreds Of dollars on "food sensitivity" tests, still to no avail. This lack of diagnosis and resolution despite what feels like an extensive search invariably leaves my patients with the impression that whatever is causing their problems must be pretty rare, exotic, and serious. In reality, though, almost all of the bloated patients I see are af- flicted by one Of just ten reasonably common and easily diagnosable med— ical conditions. If your doctor or other health-care provider knows what she or he is looking for, a very detailed food and symptom history is often all it takes to narrow down the possibilities to one or two leading contenders. From there, you may be just a blood test, breath test, motil- ity test, or diet trial away from the answers youve been looking for. To be sure, there are plenty of rarer medical conditions that cause Copyfish

To be sure, there are plenty of rarer medical conditions that cause bloating—what we call zebras in the clinical world—that are not covered in this book. That's why books like mine aren't meant to be a substitute for personalized medical advice from a well-credentialed doctor. Some very serious medical conditions—including ovarian cancer—can first The Bloated Belly Whisperer appear with a bloated, pregnant-looking belly—in that case, one that's fillin with fluid. If thin don't feel lite ri ht I encoura vou to make

But the odds are still overwhelming that the medical explanation for your bloating—and the range of treatment options—is indeed con- tained somewhere in this book. You'll understand what I mean when you encounter that one paragraph that describes your bloating experi- ence to a T, and you feel as though I'm talking exactly about you. This book describes those ten most common medical causes of bloat- ing I encounter in my clinical practice—the "horses" rather than the "zebras." Chapter 2 will help you navigate this book by introducing you to your digestive anatomy, equipping you with some vocabulary, and giving you a short quiz that will help you prioritize which chapters in parts 2 and 3 to start reading first. These chapters are grouped based on the origin of your bloating—stomach or intestines—and describe each type of bloating in great detail and its medical cause, including:

a detailed description of what that type of bloating feels like and other symptoms with which it's typically associated; an explanation Of the underlying cause Of that type Of bloating; a discussion of the typos of tests a doctor might use to diagnose the cause; a review Of medical treatments commonly used to treat that type Of bloating; a review of dietary remedies that are effective for the condition; and stories about patients Of mine who experienced that type Of bloating, with details about how they were diagnosed and then treated with diet, supplements, medication, and/or lifestyle changes.


The fourth part of the book goes deeper into the specifics of the various therapeutic diets I recommend for each type of bloating, with specific food lists and meal ideas. Rather than focus on laundry lists of everything you can't eat, I focus more on teaching you what you can eat. That's why I teamed up with world-class recipe developer Kristine Kidd, Every unhappy Belly Is Unhappy in Its Own Way: The Many Ways to Be Bloated who created fifty fantastic recipes for this book that are tailored to the specifications required for each therapeutic diet. Kristine spent twenty

specifications required for each therapeutic diet. Kristine spent twenty years as food editor at Bon Appétit magazine and is no stranger to re- stricted diets herself; she's got celiac disease and a garlic allergy. But when life hands a true foodie a couple of diet restrictions, she hits the kitchen and finds delicious work-arounds. In other words, don't think for a minute that you'll need to subsist on bland chicken and white rice for the rest of your life just to keep your bloating at bay! Finally, I've included an encyclopedia Of dietary supplements com- monly used for digestive health, with a sciencebased evaluation of their effectiveness and safety. Because there is so much contradictory infor- mation on these products in circulation, I believe important to offer an unbiased opinion about which products may be helpful and which products may be hype. For the record, I do not sell any dietary supple- ments•, I don't get commissions or kickbacks for referring people to sup-


plement marketers. To avoid conflicts of interest, my clinical practice has a policy of refusing visits from pharmaceutical company representa- fives. If I green-light a product, because I've seen published evidence— or have firsthand clinical experience—that it works and that it's safe. My intention is for you to use this book to facilitate a productive con- versation with your doctor. I want to equip you with the descriptive language and relevant issues to mention during your appointment so that you can help your doctor home in on the problem most likely afflict- ing you. I also want to familiarize you with the diagnostic process asso- ciated with these common digestive disorders so that you won't be surprised when your doctor suggests various tests, procedures, or medi- Copyfish

cations. Most important to me as a dietitian, I want to empower you with effective nutritional remedies so that you can control your own symptoms. In some cases, dietary change alone can completely control bloating. In other cases, medical therapy may be called for in addition to diet. Your doctor will help you decide on the most appropriate plan for your individual case, and your belly will offer feedback as to what's working best. This book should not replace the advice ofa doctor. I am not a doe
tor, and I cannot dispense medical diagnoses. Even if you recognize your brand of bloating to a T in this book, you cannot assume that the associ- ated medical diagnosis applies to you without proper testing. Your doctor may look at other pieces Of information, including family history, your personal medical history, blood test results, and any other symptoms you may be experiencing to determine whether there might be another cause of your bloating that should be investigated other than the one(s) I've suggested in this book. A good gastroenterologist is worth his or her weight in gold. Find one—and never let him or her go. Finally, if your bloating is accompanied by any of the following symptoms, you should see a doctor promptly:

blood in your stool difficulty swallowing recurrent vomiting unintentional weight loss of more than a few pounds nutritional deficiencies, including anemia sudden onset of constipation not related to a change in diet fever jaundice (yellowing of your skin and the whites of your eyes) a "pregnant-looking" belly that is always equally distended, even when you wake up and/or haven't eaten anything in hours (in other words,

jaundice (yellowing of your skin and the whites of your eyes) a "pregnant-looking" belly that is always equally distended, even when you wake up and/or haven't eaten anything in hours (in other words, there are no circumstances under which it gets flatter) persistent, excessive hiccuping Now. If you're ready to figure out how to get rid of that bloated belly of yours once and for all, then let's move on to chapter 2 so you can learn the language and take my diagnostic quiz!

IF YOU'RE READING THIS BOOK, then you Ve got a bloated belly in need of some answers. Your quickest path to finding them is to start reading the chapters most likely to pertain to you. To help steer you to the right ones, I've designed a quiz to help you identify the causes of bloating that are most consistent with your symptoms, and I'd recommend you start reading the chapters indicated by your quiz results. Once you rec- Copyfish jaundice (yellowing Of your skin and whites Of your eyes) a "pregnant-looking" belly that is always equally distended. even you wake up and/or haven't eaten anything in hours (in other w there are no circumstances under which it gets natter)

feels like and to read each one consecutively until you find the descrip— tion that feels like you're reading about yourself. Then, start reading that chapter from the beginning, in its entirety, before moving on to part 4. If you're a fellow dietitian or other clinician using this book for con- tinuing education, then get out your highlighter and read it start to finish. Pay special attention to the types of questions asked in the quiz below as key clues to your assessment detective v,ork, and study the descriptions of bloating in each chapter; this will help you discern the unique character- istics of each type so you'll recognize it readily when you see it.
Know the Lingo a lot Of terms throughout this book to describe different parts Of your digestive system and its, ahem, outputs. Let's take a moment to make sure we're all on the same page with terminology. I use the terms stool. bowel rnovement. and int«changeaNy to feces. it's ttw stuff of I use the term interchangeÖly With poopmg bowels. I use the terms gut and bowel interchangeably to refer to the entirety ot yoa.r the small intestine and ttw cdon combined. (Rrists out Wt the but. we're to

I use the terms gut and bowel interchangeably to refer to me entirety of intestines—both the and ttw combined. (Purists would ctyrectty point out that. biobgically speaking, gut the but. we're term nwre narrowty. ttw way nwst of my pat•nts of n.) the terms abdomen and belly to to nudsection Of where the digestive housed. Outside. stut and an the way where starts. and farts to gas that 0' Your have it

I use the terms abdominal distension distended, and bulge/bulging to an in girth or circumference in such as when your belly is protruding out from its natter. emptier state. It's what forces you to unbutton when you're bbated. FOS is a common abbreviation that some doctors use when talking unong th«nselvos: it stands for "fu" of stool." It describes a situation in which there is so much stool in your colon that it extends all the way practically right up to the junction with your small intestine. I use the terms FOS and backed up interchangeably. DO not confuse it With tructo.oliøosaccharides. a tw» o' carbohydrate that causes gas in susceptible as described in chapters 6 and 9 that is also sorne- times referred by this acronym. Next. on to y•our anatomy. The location Of your bloating and/or pain Copyfish

can often provide a clue as to its origin, so I've provided the diagrams on the following pages to help orient you to the organs that play a role in your digestive drama and show you where they reside. For starters, note that the abdomen is divided into four quadrants: the right upper and lower, and left upper and lower. •l •he labels right and Iep refer to your right and left, so the labels will actually appear flipped on the diagrams (since the model is facing you). These quadrants are markers that doctors Often use to describe the location of abdominal pain and discomfort. The diagram on page 13 shows the outlines of the stomach, small intestine, and colon; they are shaded so you can see roughly where they dwell beneath external landmarks. The stomach, you may note, is quite high up—right underneath the rib cage and a bit over to your left (in the picture, it Will be on the model's left side, which is on your right side, since you are facing her). The small intestine is squarely in the middle of the belly, and the colon is pretty spread out: A portion of it

lives in the center of the abdomen beneath the belly button, but seg- ments of it actually snake up and down the perimeters of your abdomi- nal cavity, crossing over above your small intestine. Ifyou're feeling a bit rusty as to what each of these organs actually does, the list below offers a mini refresher. be talking a lot more about all of these in later chapters, where I'll explain how they may play a role in various types of bloating.

The Bloated Belly Whisperer Quiz I developed this quiz in collaboration with my gastroenterologist cd- league Dr. Eric Goldstein as a simplified version of the detective pro- cess that goes on in our office when a new patient arrives complaining of being bloated. If you were sitting in my office, I'd pepper you with a variety of questions such as the ones following, first to help me isolate

which section of pur digestive tract the bloating seems to originate in. and then to narrow down the most likely one or two possibilities. While this nine-question quiz certainly doeslfi cover every medical possibility under the sun, it should certainly help focus your attention on a few of the most likely possibilities. Two tylX'S of bloating that result from malabsorption that is disease- related—celiac discasc and pancreatic insufficiency—arc not included in the quiz. That is because a bloated belly from either of these condi- tions Often takes a backseat to several more troubling syrmRoms: amounts of (foul-smelling) diarrhea; stomach pain; a significant amount of unintentional weight loss; unexplained vitamin and iron deficiencies. If this sounds familiar, then call a gastroenterologist to make an ap- pointment and flip straight to chapter 10 while his or her office has you on hold. If chapter 10 with then check out chayxer 8, SIBO, next before trying out the quiz.

Directions for Taking the Quiz: 2. 3. 4. Copyfish Read each question and identity the most fitting option(s) that best your bloating For questions that allow it, you thm answer. Alongside each mswer, Will find one or empty circles. in a" Of the ernpty circles the row alongside the answerß Of choice. For any given there are no answers provided that you feel are accurate for yow situation, Or if you are simply unsure of an answer, leave that Nank- DO not choose an answer that is me closest thing to something you experience if it is not an accurate representation of yow experience. When you finished taking the quiz. Cm_Jnt the total nun-Iber Of Shaded
5. 6. 7. Make note Of which column numbers have the highest number Of shaded boxes. Look tor the corresponding diagnosis and chapter/ page number in the key provided after the quiz. You should start read- ing the chapter/section that corresponds to the diagnosis with which you scored tho most symptom matches. After reading your top-ranked chapter/section. if you feel that it did not accurately describe your type Of bloating, proceed to the chapter/ section where you had the second-highest number of symptom mat. ches. (And so on.) If your symptom matches score pretty evenly across multiple different types Of bloating. and these include types Of bloating that originate in the stomach as well as ones that originate in the intestines. you should start by reading chapter 8 on SIBCX If that description doesn't fit well, you may need to read several chapters that scored high to find the

7. If your symptom matches score pretty evenly across multiple different types of bloating, and these include types of bloating that originate in the stomach as well as ones that originate in the intestines, you should start by reading chapter 8 on SIBO. If that description doesn't fit well, you may need to read several chapters that scored high to find the combination of diagnoses that feels most familiar. (And read the next section on common bloating combos, which may help shed some light.) Hopefully, the very detailed and differentiated descriptions of bloating I included in each chapter/section will help you narrow things down, even if your quiz results seem a little bit vague.

The following quiz was designed to help you identify the most likely cause of your bloating among ten of the most common possibilities. ever, it's important to mention that the causes of bloating I've outlined are not mutually exclusive. In other words, it's possible—and even common—for people to have more than one reason for their bloating. This is because a single underlying medical issue can affect different parts of the digestive system. If a particular bloating description you read feels very accurate but also somewhat incomplete, you should also consider that your bloating may be the result Of more than one problem. Simi- larly, if you follow the recommendations to address one particular type of bloating and wind up feeling a substantial improvement but still not as well controlled as you'd like, I suggest you retake the quiz with your residual symptoms in mind to see whether a second type of bloating


emerges as a front-runner. Consider some Of the following examples Of common medical com- bos that result in a double whammy of bloating and see if any of these sound familiar after reading their associated chapters: • GASTROPARESIS (GP, CHAPTER 3) AND CONSTIPATION (CHAPTER 7): Sometimes problems with your digestive system's nerves will cause your entire digestive tract to operate in slow motion. The slow-to- empty stomach will produce bloating and associated symptoms in the upper GI tract, like nausea, acid reflux, or vomiting, and the slow-to- empty colon will produce bloating and associated symptoms in the lower GI tract, like farting, constipation, and crampy pain.

emerges as a front-runner. Consider some Of the following examples Of common medical com- bos that result in a double whammy of bloating and see if any of these sound familiar after reading their associated chapters: • GASTROPARESIS (GP, CHAPTER 3) AND CONSTIPATION (CHAPTER 7): Sometimes problems with your digestive system's nerves will cause your entire digestive tract to operate in slow motion. The slow-to- empty stomach will produce bloating and associated symptoms in the upper GI tract, like nausea, acid reflux, or vomiting, and the slow-to- empty colon will produce bloating and associated symptoms in the lower GI tract, like farting, constipation, and crampy pain.


frequent bowel movements and lower-abdominal discomfort resulting from the inability to empty your bowels completely. CELIAC DISEASE (CHAPTER 10) AND CARBOHYDRATE INTOLERANCES (CHAP- TER 9): The inflammation caused by celiac disease typically damages the fingerlike projections lining your small intestine called villi. Since the tips of these villi produce digestive enzymes that help you absorb cer- tain sugars, people with newly diagnosed celiac disease may find them- selves bloated not just from gluten but also from dairy foods, as the result of a temporary lactose intolerance, and/or some more sugary foods. Lactose and sugar tolerance should be restored within several months On a gluten-free diet Once the gut has time to heal. CONSTIPATION (CHAPTER 7) AND SIBO (CHAPTER a): If you've got a sluggish colon that causes chronic consti tion it's ossible could also


CONSTIPATION (CHAPTER 7) AND SIBO (CHAPTER 8): If you've got a sluggish colon that causes chronic constipation, it's possible you could also have some slowness farther upstream in the small intestine, as well. (There are motility tests your doctor can order to determine whether this is the case.) Slow motility in the small intestine can predispose you to developing an overgrowth Of bacteria there, and this may be particularly so if you've been dabbling with probiotic supplements to try to fix your constipation. If those probiotic bacteria get the chance to linger too long in the small intestine while en route to the colon, they may just take the opportunity to establish more permanent residency there.


(DO not count): My bloating feels worse after chewing sugarless gum False 1. Choose one: My bloated belly is... inflated like a balloon solid/hard as a rock 2. Choose one: The location of my bloating is concentrated ... broadly across the upper abdomen (above the belly button) centered. right underneath the breastbone in the lower-abdominal area (underneath the belly button) all over/ varying locations


3 Bloating onset (check up to three Of the most relevant) is worse/more likely with large-volume meals builds as day progresses; always at night immediately after eating if I was extremely hungry at mealtime after eating anything at all does not Seem particularly related to 4. The foods that would trigger significant bloating for me would be (chock all that apply) water large salad with olive oil and vinegar small plate of pasta with generous portion of red sauce McDonald's-size burger and small fries small soft-serve frozen yogurt

8. In to bloating, I also have the following lower-digestive system issues (check all that apply); bowel movements (fewer than 3 per week) feeling to completely evacuate my bowels when I are hard to wipe hard like little bans or •rabbit pellets- and Stools my bowel habits are not a problem 9. Choose or

w: My bloating is associated with the following type of pain:


9. Choose one: My bloating is associated with the following type of pain: no overt pain (though being bloated is generally uncomfortable) burning pain toward the top of my abdomen sharp pain annvhere throughout my abdomen crampy pain in my lower abdomen (beneath the belly button) dull pain an»vhere throughout my abdomen o o o o o o O o o o o o •ei•iiii o Scoring the Bloated Belly VVhisperer Quiz: If you Scored the m t matches With column your symptoms resemble this diagnosis most Closely Gastroparesis (GP) so start on this Chapter / page chapter 3 p. 23


Scoring the Bloated Belly Whisperer Quiz: Scored the most m atc hes Copyfish symptoms this most Gastroparesis (G P) Abdomino-phrenic dyssynergia (APO) Classic indigestion Functional dyspepsia (ED) Aeroph agia Constipation Small Intestinal Bacterial Overgrowth (SIBO) Carbohydrate into rances so Stut on this Chapter chapter 3 p. 23 chapter 3 p. 37 chapter 4 p. 45 chapter 5 p. 55 chapter 6 p. 69 chapter 7 p. 79 chapter 8 p. 101 chapter 9 p. 118


If I did my job well, this chapter should have generated some promising leads in your quest to identify the cause Of your bloating, and you've got your rank-ordered list of chapters to read. Without further ado, it's time to dive into the depths of your digestive tract and solve some mysteries!

UPPER-ABDOMINAL BLOATING THAT ORIGINATES IN THE STOMACH

The "Food Baby" Twins: Gastroparesis and Dyssynergia

THE FIRST TYPES OF BLOATING we'll address have their roots in the stomach, an organ whose job it is to serve as a food storage chamber and blender. Your stomach holds the food you eat, liquefies it, and then squirts it out a little bit at a time through a tiny opening toward its bottom the Pylorus. The pylorus leads from the stomach into the small intestine, where the absorption of all nutrients actually happens. Your stomach's muscular walls blend food through waves Of contraction and relaxation, which mix its contents with acid and enzymes to liquefy them. Then these muscular walls push the liquefied food through the pylorus to continue its path to digestion. But when the nerves and other cells that govern your stomacl* ac- tivities are not coordinating their actions properly, two distinct types of


bloating can result. Both types of bloating set in quickly after eating, and they're more severe the larger the volume Of the meal. Because the bloated belly in both cases results from a stomach literally filled with food, I've nicknamed this category Of bloating the food baby." Copyfish

Gastroparesis (GP; Delayed Stomach Emptying) When you eat a solid meal—or food that must be chewed, rather than a soup or a smoothie—your stomach should empty at least 65 percent of that meal's volume after two hours and at least 90 percent of the meal's volume after four hours. Your stomac}fi rate of emptying is controlled by "pacemaker" cells, which are stimulated by a number of triggers: the stretch Of the stomach after being full from a meal, and signals from the network of nerves and hormones throughout the digestive tract. But in some cases, the stomach's pacemaker cells don't operate normallv, Copyfish bloating can result. Both types of bloating set in quickly after eating


and this can result in a delayed rate of stomach emptying called gas- troparesis (GP). affects about 2 percent Of the population, and it's more common in women than in men. In many cases, the cause Of GP is unknown, but it often starts in the aftermath of a viral infection; this is called postin- fectious For example, you may begin to experience symptoms Of after recovering from a bout of food poisoning or the "stomach flu." GP is also a common side effect of both type 1 and type 2 diabetes, and in these cases, it results from damage to the digestive system's nerves as a result of chronically high blood sugar. Some medications can also in- duce GP, including injectable diabetes medications called GLP-I recep- mc • so Cowfish I sof h s in I

tor agonists; some examples Of these include Byetta (exenatide), Victoza (liraglutide), and Trulicity (dulaglutide). GP can also result from certain types Of surgery in which a major digestive system nerve is Cut in a procedure called vagotomy. What Bloating from GP Feels Like Whatever the cause of your GP, its effect is the same. Bloating from GP is not typically painful, but it produces a belly that feels full and is often visibly distended. The distension is least noticeable in the morning and, in many cases, it isn't too bad after eating breakfast either. But your
belly bulge grows with each subsequent meal as the day progresses, and there's usually a noticeable worsening soon after lunch. The bloating is at its absolute worst at night—particularly for those who follow the typi- cal American Custom of a relatively big dinner. While mornings are generally the best time of day for people with GP, sometimes you might still wake up with a visibly distended belly, particularly if you’ve eaten a large, high-fat, and/or late dinner the night before. My patients with GP often describe feeling as if their food "just sits there" after eating, and as if they have a "brick" in their stomachs. They often experience heartburn or other symptoms of acid reflux, which can include belching or regurgitating small amounts Of your acidic Stomach Bloating from GP is almost always accompanied by both a loss of appetite and early satiety, which means feeling very full even after eat- ing only a small amount of food. My patients with GP rarely ever feel hungry, they often eat meals just because "l know I should" based on the time of day. With GP, you can easily go five to seven hours between meals and not feel hungry at all. Often, you'll have no appetite at all for dinner after having eaten a few small meals earlier in the day. Sometimes you may experience a strange sensation Of feeling both weak from hunger but also physically too full to eat. This results from the lag time between eating food and actually absorbing its nutrients in your small intestine. In other words, blood sugar levels remain low while your slow stomach takes its time releasing its contents into your small intestine for absorption

Nausea is very common with GP, and vomiting may occur too. This vomiting often happens at night after dinner, overnight (it vmkes you from sleep), or first thing in the morning. Often, you may vomit a few hours after eating a high-fat meal (steak house dinners are a pretty com- mon trigger) or a very bulky, high-fiber meal—like a big salad or a bucket of movie popcorn. In fact, GP is one of the few causes of bloat- ing that is accompanied by vomiting. Bloating from GP is not usually accompanied by excess flatulence (farting) or gas pain. It is typically described as uncomfortably full but not overtly painful per se. People with GP may also experience an unintentional weight change.


In severe cases, you may have such a reduced appetite that you wind up eating very little and lose a substantial amount of weight in a short period Of time. In less severe cases, you may actually gain a little bit Of weight. This results from gravitating toward foods that are easier to digest and cause less bloating. For example, you may come to realize that you feel awful after eating salads—which take a long time to leave the stomach—so you start eating more foods like bread, rice, mashed potatoes, and pasta, which leave the stomach faster. This increases your daily calorie intake, and weight gain follows. Sometimes the underlying cause of (GP will also affect Other parts of the digestive tract, causing slow motility not just in the stomach but also in the small intestine or the colon. In these eases, the bloating from

Gastric Emptying Scan If your doctor suspects GP based on your description of its symp- toms above, then he or she will typically order a test called a gastric emp— tying scan (GFS), also known as gastric emptying scintigrapby. This is considered the best method for diagnosis. A gastric emptying scan is usually a two- to four-hour test conducted at a radiologist's offce, and it measures how long it takes for a standard- ized portion of food or liquid to leave your stomach. Your stomach's emp- tying rate is compared against the normal emptying rate by analyzing what percentage of the food you ate remains in your stomach at regular intervals. If a amount Of food remains in your Stom- ach at the end of the test, you'll be diagnosed with GP. GP is also graded
ach at the end of the test, you'll be diagnosed with GP. (GP is also graded into levels Of severity based on what percentage Of the food remains in your stomach at the end Of the test; it Can be mild, moderate, or severe. When you arrive for the test, you'll be given a small meal to eat— usually oatmeal or eggs and toast. The food is mixed with a bit of radio- active material so that the radiologist can track its movement through your digestive tract by photographing your abdomen using a specialized camera. It does not use x-ray technology. Gastric emptying scans can be

conducted with either liquids or solids to measure your stomach's emp- tying time for either of these textures. It's possible to have delayed emptying Of solids but not Of liquids, and even when both are delayed, generally speaking, liquids empty the stomach faster than solids. In some cases, if your doctor suspects you may have motility prob- lems that affect other parts of the digestive tract in addition to your stomach, he or she may order a more extensive version of this test, one which tracks the transit time of food throughout the stomach, small intestine, and colon. This test is called a transenteric study. A transen- teric study will usually require you to be at the radiologist's office for six hours on the first day and then to come back for a quick photograph •il f r h n x hr Ish

Medical Treatment for Gastroparesis The primary medical treatments for GP are medications called pro- kinetic agents. Prokinetics work by stimulating motility in the stomach, causing it to contract more frequently so that it will empty more rapidly and alleviate the feelings of bloating, fullness, poor appetite, nausea, reflux, and/or vomiting. Examples of prokinetic medications include Reglan (metoclopramide) and Motilium (domperidone), though the lat- ter is not licensed for use in the United States, so most patients who use this dru im ort it from Canada or elsewhere overseas. The antibiotics

erythromycin and Zithromax (azithromycin) also have prokinetic prop- erties. These medications are rarely a silver bullet for GP, and diet change is almost always necessary as well. Other medications may help control the symptoms of GP, particu- larly nausea and vomiting, but they don't actually address the under- lying cause of the condition. Antinausea drugs (also called antiemetics) are one such option, though their benefit should be weighed against pos- Sible side effects. Some antiemetics may be constipating and can make bloating worse for people affected by overall slow motility in both the stomach and the colon, who are already experiencing "backed-up bloat- ing" (see chapter 7 for more on this type of bloating).

Dietary Treatment for Gastroparesis Dietary therapy for GP is designed to help you manage your symp- toms, not to cure the disease. This is because diet cannot actually speed up the rate of your stomach's contractions. But the texture, volume, fat content, and fiber content of meals can certainly influence how quickly a meal is able to clear your slow stomach and make its way to the next phase of the digestive journey. Choose Soft, Low-Fat, Moderate-Fiber Foods Eaten in Small, Well-Spaced Meals Think back to the image of your stomach as a blender that I de- scribed earlier in this chapter. If your stomach blender needs to liquefy a meal for it to empty, and if the blender isn't working very well—say, it n onl ulse instead of urée—whatt e of foods are most likel to

 Symptoms & Causes
 Last Updated: 04 September 2015
Most foods that contain carbohydrates can cause gas. By contrast, fats and proteins cause little gas (although certain proteins may intensify the odor of gas).
Sugars
The sugars that cause gas are raffinose, lactose, fructose, and sorbitol.
  • Raffinose — Beans contain large amounts of this complex sugar. Smaller amounts are found in cabbage, Brussels sprouts, broccoli, asparagus, other vegetables, and whole grains.
  • Lactose — Lactose is the natural sugar in milk. It is also found in milk products, such as cheese and ice cream, and processed foods, such as bread, cereal, and salad dressing. Many people, particularly those of African, Native American, or Asian background, have low levels of the enzyme lactase needed to digest lactose. Also, as people age, their enzyme levels decrease. As a result, over time people may experience increasing amounts of gas after eating food containing lactose.
  • Fructose — Fructose is naturally present in onions, artichokes, pears, and wheat. It is also used as a sweetener in some soft drinks and fruit drinks.
  • Sorbitol — Sorbitol is a sugar found naturally in fruits, including apples, pears, peaches, and prunes. It is also used as an artificial sweetener in many dietetic foods and sugarfree candies and gums.
Starches
Most starches, including potatoes, corn, noodles, and wheat, produce gas as they are broken down in the large intestine. Rice is the only starch that does not cause gas.
Fiber
Dietary fiber is carbohydrate that is indigestible in the small intestine and reaches the colon relatively intact. In the colon, certain bacteria digest fiber (fermentation), which produces gas. Dietary fiber can be classified as either soluble or insoluble.
Soluble fiber dissolves in water and becomes a soft gel. It is found in oat bran, beans, barley, nuts, seeds, lentils, peas, and most fruits. Insoluble fiber does not dissolve or gel in water. It absorbs liquid and adds bulk to stool. Cellulose (found in legumes, seeds, root vegetables, and vegetables in the cabbage family), wheat bran, and corn bran are examples of insoluble fiber.
High fiber substances containing both soluble and insoluble fibers have the properties of both. They include oat bran, psyllium, and soy fiber. Methylcellulose is a semi-synthetic fiber. It is soluble and gel forming, but not fermentable.
Types of fiber differ in the speed and extent to which they are digested in the GI tract, and in the process of fermentation. The solubility and fermentation of a particular fiber affects how it is handled in the GI tract. However, the effect of identical fibers varies from person to person.
A gradual increase in dietary fiber can modify and improve symptoms. But individual responses vary and too much of a type of fiber can worsen symptoms. It may be necessary to try different types of fiber. With any dietary fiber it is best to start low and go slow.
Read More

Controlling Intestinal Gas

Everybody produces gas, and everybody needs to pass gas. The amount depends on the individual, and there is a wide range of "normal." Passing gas is normal; nevertheless, it can be embarrassing or cause discomfort. A better understanding of what causes intestinal gas can help most people reduce symptoms and find some relief.

Sources of Intestinal Gas

Gas in the digestive tract (the esophagus, stomach, small intestine, and large intestine) comes from two sources:
  • swallowed air and
  • the normal breakdown of certain undigested foods by harmless bacteria that are naturally present in the large intestine.
Swallowed Air – Air swallowing (aerophagia) is a common cause of gas in the stomach. Everyone swallows small amounts of air when eating and drinking. However, eating or drinking rapidly, talking while eating, chewing gum, smoking, or wearing loose dentures can cause some people to take in more air.
Burping, or belching, is the way most swallowed air leaves the stomach. The remaining gas moves into the small intestine where it is partially absorbed. A small amount travels into the large intestine for release through the rectum. (The stomach also releases carbon dioxide when stomach acid and bicarbonate mix, but most of this gas is absorbed into the bloodstream and does not enter the large intestine.)
Bacteria – Gases are produced as a by-product when certain food materials are digested by naturally occurring bacteria in the large intestine, or colon. These bacteria are responsible for digesting materials like complex carbohydrates (sugar, starches, and fiber found in many foods) and cellulose, which are not normally digested in the upper gastrointestinal tract.
The quantity and mixture of gases depend on the types of bacteria in the colon; everyone has a unique assortment of bacteria from the time of birth. These gases include hydrogen, carbon dioxide, and, in some people methane. Trace gases, such as hydrogen sulfide, are responsible for the odor. Foods that produce gas in one person may not cause gas in another.
 Symptoms & Causes
 Last Updated: 04 September 2015
The most common ways to reduce the discomfort of gas are changing diet, taking medicines, and reducing the amount of air swallowed.
Diet Changes That May Help Gas
Avoiding fermentable vegetables/carbohydrates like beans, broccoli, cabbage, and some artificial sweeteners like sorbitol (which is found in gum, candies, and some soft drinks) can lessen the amount of gas produced. Those who are truly lactose intolerant may improve if they avoid milk products.
Alcohol may impair intestinal digestion so that more food is available for gas production. Certain proteins may enhance the odor of gas. If gas is a problem for you, try monitoring your diet (time of day and description of foods eaten and drinks ingested, and times of each episode of gas) for a week or so to identify what may cause increased gas production or what may effect odor.
Doctors may tell people to eat fewer foods that cause gas. However, for some people this may mean cutting out healthy foods, such as fruits and vegetables, whole grains, and milk products. Doctors may also suggest limiting high-fat foods to reduce bloating and discomfort. This helps the stomach empty faster, allowing gases to move into the small intestine.
The amount of gas caused by certain foods varies from person to person. Effective dietary changes depend on learning through trial and error how much of the offending foods one can handle.
Medications to Help Gas
Many nonprescription, over-the-counter medicines are available to help reduce symptoms. Products containing chlorophyllin copper (e.g., Nullo, Derifil) can help minimize offending odor. 
Digestive enzymes, such as lactase supplements, actually help digest carbohydrates and may allow people to eat foods that normally cause gas.
Simethicone (e.g., Gas-X, Mylanta Gas, Phazyme) is a foaming agent that joins gas bubbles in the stomach so that gas is more easily belched away. However, these medicines have no effect on intestinal gas.
The enzyme lactase, which aids with lactose digestion, is available in liquid and tablet form without a prescription (e.g., Dairy Ease, Lactaid). Adding a few drops of liquid lactase to milk before drinking it or chewing lactase tablets just before eating helps digest foods that contain lactose. Also, lactose-reduced milk and other products are available at many grocery stores.
Beano, an over-the-counter digestive aid, contains the sugar-digesting enzyme that the body lacks to digest the sugar in beans and many vegetables. The enzyme comes in liquid or tablet form. Beano has no effect on gas caused by lactose or fiber. Heat degrades the enzyme in Beano so it cannot be added to food while it is being cooked.
Beano is made from an enzyme (alpha-galactosidase) extracted from a food-grade mold; if you are allergic to molds you may react to Beano. Those with galactosemia (an inherited disorder characterized by the inability to metabolize galactose) should not use Beano without first consulting their physician.
Reduce Air Swallowing
For those who have chronic belching, doctors may suggest ways to reduce the amount of air swallowed. Recommendations are to avoid chewing gum and to avoid eating hard candy. Eating at a slow pace and checking with a dentist to make sure dentures fit properly should also help.


Tips on Controlling Gas

  1. Everyone has gas in the digestive tract.
  2. People often believe normal passage of gas to be excessive.
  3. Gas comes from two main sources: swallowed air and normal breakdown of certain foods by harmless bacteria naturally present in the large intestine.
  4. Swallowed air can be affected by a number of contributing factors. Dentures that do not fit well can cause people to swallow more saliva which carries air bubbles; postnasal drip tends to make people swallow more often, carrying more air to the stomach; smoking a cigar or pipe may increase the amount of saliva produced and swallowed; eating too fast increases the amount of air swallowed; gum chewing and sucking on hard candies also increases the amount of air swallowed.
  5. Many foods with carbohydrates can cause gas. Fats and proteins cause little gas.
  6. Foods more likely to cause gas include:
    • Beans (Presoaking reduces the gas-producing potential of beans if you discard the soaking water and cook using fresh water)
    • Vegetables such as artichokes, asparagus, broccoli, cabbage, Brussels sprouts, cauliflower, cucumbers, green peppers, onions, radishes, celery, carrots
    • Fruits such as apples, peaches, raisins, bananas, apricots, prune juice, pears
    • Whole grains and bran (Adding them slowly to your diet can help reduce gas forming potential)
    • Carbonated drinks (Allowing carbonated drinks, which contain a great deal of gas, to stand open for several hours allows the carbonation/gas to escape)
    • Milk and milk products, such as cheese and ice cream
    • Packaged foods prepared with lactose, such as bread, cereal, and salad dressing
    • Foods containing sorbitol, such as dietetic foods and sugarfree candies and gums
    • Beverages such as wine and dark beer
  7. Odor forming foods may include: alcohol, asparagus, beans, cabbage, chicken, coffee, cucumbers, dairy products, eggs, fish, garlic, nuts, onions, prunes, radishes, and highly seasoned foods.
  8. Foods less likely to cause gas include:
    • Meat, poultry, fish
    • Eggs
    • Vegetables such as lettuce, tomatoes, zucchini, okra,
    • Fruits such as cantaloupe, grapes, berries, cherries, avocado, olives
    • Carbohydrates such as gluten-free bread, rice bread, rice
  9. The most common symptoms of gas are belching, flatulence, bloating, and abdominal pain. However, an intestinal disorder, such as irritable bowel syndrome, rather than too much gas often cause some of these symptoms.
  10. The most common ways to reduce the discomfort of gas are changing diet, taking nonprescription or prescription medicines, and reducing the amount of air swallowed.
  11. Digestive enzymes, such as lactase supplements, actually help digest carbohydrates and may allow people to eat foods that normally cause gas.
  12. How we respond to dietary components varies from person to person. For one week try eliminating foods or beverages in your diet that you suspect most likely are causing you gas or odor problems. Then gradually reintroduce them one at a time to help identify the offenders.

Colon Gas & Flatus Prevention

Home > GI Health Resources > Colon Gas & Flatus Prevention
Updated 09/19/2018
Category: Diet 
The thriving healthy mix of bacteria within the colon does not happen without the production of some gases. Most of these gases are odorless – hydrogen, oxygen, carbon dioxide and methane. Nitrogen is also present from swallowed air, which then moves down into the colon. So, bacteria produce most of the gases that are passed as flatus. The tiny amount of the remaining gases are the sulfide ones. These are the smelly gases that are made by just a few species of bacteria specialized for this process. These rascals rely on sulfur in the water, food, beverages, and indeed, some medications we swallow to make these sulfide gases, including hydrogen sulfide.

What Is Normal?

Believe it or not, there is really a limited amount of information in the medical literature on this socially important question. Everyone will have her or his own idea of what normal is. Here is some general information that medical texts provide.
  • The amount of colon gas produced per day ranges from one pint to several quarts.
  • The number of flatus passages per day may be as low as 7 in females and up to 20 or more in males. An average is probably 10-13 flatus passages per day.
  • Men create more colon gas than females.
  • So do smokers. Don’t ask why. We don’t know.
  • Beer drinkers have smellier flatus, probably because most beer contains significant amounts of sulfur.

Plant Fiber

There are two main types of fiber, insoluble and soluble, and almost every plant will have some of each. Insoluble fiber does not dissolve in water, is not acted on by colon bacteria and so does not create colon gas. It is an important fiber, however, in that it hangs on to water within the colon, promoting a larger, bulkier stool and improved regularity. The second type of fiber is soluble, meaning it does dissolve in water and is fermented by colon bacteria. Some of these bacteria, then, create colon gas.
Most plants have both fibers to varying degrees. As examples, the fiber in wheat is mostly insoluble while those in oats and beans are mostly soluble. A special type of recently discovered soluble fibers are the prebiotic ones, especially inulin and oligofructose. These fibers have had a great deal of research done on them lately and multiple, very significant health benefits have been found to occur with them. Still, they are soluble and, as such, do produce colon gas just like all soluble fibers will if too much is taken.
The key is to get a good balance of these fibers. The recommended total fiber intake per day is 25-35 grams, depending on your sex, age and weight. At this level, multiple health benefits occur. However, if excess colon gas and flatus is the problem, then cutting back on soluble fiber should be done first.

Insoluble Fiber

As noted, this fiber, also known as roughage and bulk, does not dissolve in water but paradoxically does hang onto water in the large bowel. This creates a larger, softer and bulkier stool. It promotes regularity and seems to be associated with reduced chance of getting colon polyps and cancer, as cancer inciting agents such as carcinogens are swept through the bowel in a more rapid manner. In addition, it may promote weight loss and enhances diabetic control. These fibers are not fermented by colon bacteria and so do not produce colon gas. Foods that are particularly high in insoluble fiber are:
  • whole wheat bread and baked goods
  • wheat bran
  • whole grain breads
  • vegetables and fruit, especially the skins
  • peanuts
  • Brazil nuts
  • popcorn
  • brown rice
The section on Fiber Content of Food, provides the insoluble fiber content of many foods.

Soluble Fiber

This plant fiber does dissolve in water. In the colon, it provides food for the enormous numbers of bacteria that thrive there and, in so doing, provide many health benefits. Those fibers also promote regularity by increasing the growth of the colon bacteria. However, soluble fibers are the ones that some coon bacteria metabolize and so produce some colon gas. Foods that are particularly high in soluble fiber are:
  • oats in any form – cereal, muffins, etc.
  • apples, oranges, grapefruit, peaches, concord grapes
  • prunes, pears, cranberries
  • beans
  • beets
  • carrots
  • psyllium (found in supplements and some cereals)
The section on Fiber Content of Food, provides the insoluble fiber content of many foods.

Flatus Odor and Sulfate

Sulfate is the culprit. It is also a very necessary element in the diets as our body needs it for many functions. The problem with noxious flatus odor is that certain bacteria in the colon make sulfide gases in very tiny amounts, but certainly enough to be noticeable. It is pretty simple. The more sulfate you ingest, the more of it is available for colon bacteria to make sulfide gases. So where is the sulfate we ingest?
  • Drinking water – up to 20% or more may come from drinking water, depending on where yours comes from. City water is monitored so there won’t be too much, but well water can vary significantly.
  • Beverages – beer, red and white wine, cider, apple, grape and tomato juice, and even cow’s milk have significant amounts of sulfate.
  • Foods – the following have moderate amounts of sulfate
o    almonds
o    breads
o    cruciferous vegetables – broccoli, cauliflower, Brussels sprouts, cabbage
o    dates
o    dried apples, apricots – dried fruits are very high in sulfate
o    wheat pasta
o    peanuts
o    prunes
o    raisins
  • Animal Protein – There are only two amino acids, methionine and cystine, that contain sulfate but these are present in all animal products. The more meat, fish, and poultry you eat, the more sulfate enters your colon.
  • Supplements – chondroitin sulfate, glucosamine sulfate and MSM (methylsulfonylmethane) are used by many people for bone and joint disorders. These have significant amounts of sulfate. So does carrageenan, used as a thickening agent in many prepared foods. Read the labels.
So the first step to controlling flatus smell is to moderate the amount of sulfate containing foods and supplements you take. The second step is to acidify your colon.

Colon Acidity and Prebiotics

A little known fact, even to those in the medical field, is that the sulfide producing bacteria in the colon can’t grow in an acid environment. So, the trick is to acidify the colon by providing certain plant fibers that other good bacteria use to make acidic substances called short chain fatty acids. These fatty acids are a food source for the colon’s own cells. The plant fibers that do this best are the prebiotics. These can and should be obtained in certain foods as listed in prebiotics. These can also be obtained in our prebiotic supplements. My own research on family and friends shows that while these prebiotic fibers will not change the amount of colon gas, they will reduce and even eliminate the malodorous flatus smell. You should use enough to reduce or stop the smell but not so much as to get too gassy. So, to reduce noxious flatus smell:
So, to reduce noxious flatus smell
  • Reduce sulfates in beverages, food, dietary supplements and pills
  • Use prebiotic foods or our supplement prebiotic products to acidify the colon.

Final Flatus Factoids

The following are common sense tips on flatus. They may not work for everyone but perhaps a few might.
  • If you have no or little flatus, then you likely are not getting an adequate amount of soluble prebiotic fiber in your diet. The good benefits of these fibers can’t be obtained without a minimal amount of gas production.
  • Chewing gum – When you chew gum, you swallow more often and some air goes down into your stomach with each swallow. What you don’t belch up goes into the colon, where it can contribute to flatus.
  • Beans contain special types of carbohydrates that some colon gas forming bacteria love. These carbs are not part of the prebiotic family that are so good for the colon and for general health. However, beans are a great source of protein and other fiber, so it can be dilemma for some people. Soaking and/or overcooking beans may help reduce gas formation. Do the experiment and see.
  • Beano is an over-the-counter product touted for helping reduce flatus. It is an enzyme that works only on the carbohydrate in beans and only if it mixes with the chewed up beans in the stomach. So, you need to take the pills, and usually a lot of them, while you are eating beans. You can try taking the pills after eating but the results may not be as good.
  • Gulping food or eating fast may result in more air being swallowed, which results in more of this air in the colon. So, slow down and chew your food well.
  • Over-the-counter remedies – Gas-X and other similar preparations are simethicone, which is a chemical that breaks down small intestinal bubbles into big ones. I m not sure of the benefit as it does not get rid of gas. Charcoal tablets are reputed to absorb the bad sulfide smell. It has never been proven very well. Reducing sulfur in food and acidifying the colon with prebiotics foods and supplements makes more sense.
  • Odor eating underwear – Yes, you can get these online. They seem a bit of a stretch and inconvenience for a physiologic event that can be controlled in other, more natural ways.

Summary

The amount of colon gas and flatus can be controlled by modifying the amount of soluble fiber in the diet. You should not eliminate soluble fiber entirely because it provides so many health benefits to the colon and body.
The smell of flatus can be controlled by reducing the amount of sulfur containing foods and beverages and by making the colon more acidic using an adequate amount of prebiotic soluble fiber.
So, it is a balance. It is recommended to use enough soluble fiber so that your colon gas and flatus is tolerable to you. When the noxious smell of flatus is gone, then that is the right dose.

13 Foods That Cause Bloating (and What to Eat Instead)
 Written by Adda Bjarnadottir, MS on June 4, 2017
Bloating is when your belly feels swollen or enlarged after eating.

It is usually caused by gas or other digestive issues (1Trusted Source).

Bloating is very common. About 16–30% of people say they experience it regularly (2Trusted Source, 3Trusted Source).

Although bloating may be a symptom of a serious medical condition, it is usually caused by something in the diet (4Trusted Source).

Here are 13 foods that can cause bloating, along with suggestions on what to eat instead.

(People often confuse "bloating" with "water retention," which involves increased amounts of fluid in the body. Here are 6 simple ways to reduce water retention.)


1. Beans
Beans are a type of legume.

They contain high amounts of protein and healthy carbs. Beans are also very rich in fiber, as well as several vitamins and minerals ( 5Trusted Source).

However, most beans contain sugars called alpha-galactosides, which belong to a group of carbs called FODMAPs.

FODMAPs (fermentable oligo-, di-, mono-saccharides and polyols) are short-chain carbohydrates that escape digestion and are then fermented by gut bacteria in the colon. Gas is a byproduct of this process.

For healthy people, FODMAPs simply provide fuel for the beneficial digestive bacteria and should not cause any problems.

However, for individuals with irritable bowel syndrome, another type of gas is formed during the fermentation process. This may cause major discomfort, with symptoms like bloating, flatulence, cramping and diarrhea (6Trusted Source).

Soaking and sprouting the beans is a good way to reduce the FODMAPs in beans. Changing the soaking water several times can also help (7Trusted Source).

What to eat instead: Some beans are easier on the digestive system. Pinto beans and black beans may be more digestible, especially after soaking.

You can also replace beans with grains, meat or quinoa.

2. Lentils
Lentils are also legumes. They contain high amounts of protein, fiber and healthy carbs, as well as minerals such as iron, copper and manganese.

Because of their high fiber content, they can cause bloating in sensitive individuals. This is especially true for people who are not used to eating a lot of fiber.

Like beans, lentils also contain FODMAPs. These sugars may contribute to excessive gas production and bloating.

However, soaking or spouting the lentils before you eat them can make them much easier on the digestive system.

What to eat instead: Light colored lentils are generally lower in fiber than darker ones, and may therefore cause less bloating.


3. Carbonated Drinks
Carbonated drinks are another very common cause of bloating.

These drinks contain high amounts of carbon dioxide, a gas.

When you drink one of these beverages, you end up swallowing large amounts of this gas.

Some of the gas gets trapped in the digestive system, which can cause uncomfortable bloating and even cramping.

What to drink instead: Plain water is always best. Other healthy alternatives include coffee, tea and fruit-flavored still water.

4. Wheat
Wheat has been highly controversial in the past few years, mainly because it contains a protein called gluten.

Despite the controversy, wheat is still very widely consumed. It is an ingredient in most breads, pastas, tortillas and pizzas, as well as baked goods like cakes, biscuits, pancakes and waffles.

For people with celiac disease or gluten sensitivity, wheat causes major digestive problems. This includes bloating, gas, diarrhea and stomach pain (8Trusted Source, 9Trusted Source).

Wheat is also a major source of FODMAPs, which can cause digestive problems in many people (10Trusted Source, 11Trusted Source).

What to eat instead: There are many gluten-free alternatives to wheat, such as pure oats, quinoa, buckwheat, almond flour and coconut flour.

There are several alternatives to conventional wheat bread in this article.



5. Broccoli and Other Cruciferous Vegetables
The cruciferous vegetable family includes broccoli, cauliflower, cabbage, brussels sprouts and several others.

These are very healthy, containing many essential nutrients like fiber, vitamin C, vitamin K, iron and potassium.

However, they also contain FODMAPs, so they may cause bloating in some people (12Trusted Source).

Cooking cruciferous vegetables may make them easier to digest.

What to eat instead: There are many possible alternatives, including spinach, cucumbers, lettuce, sweet potatoes and zucchini.

6. Onions
Onions are underground bulb vegetables with a unique, powerful taste. They are rarely eaten whole, but are popular in cooked meals, side dishes and salads.

Even though they're usually eaten in small quantities, onions are one of the main dietary sources of fructans. These are soluble fibers that can cause bloating (13Trusted Source, 14).

Additionally, some people are sensitive or intolerant to other compounds in onions, especially raw onions (15Trusted Source).

Therefore, onions are a known cause of bloating and other digestive discomforts. Cooking the onions may reduce these digestive effects.

What to eat instead: Try using fresh herbs or spices as an alternative to onions.


7. Barley
Barley is a commonly consumed cereal grain.

It is very nutritious, since it is rich in fiber and contains high amounts of vitamins and minerals like molybdenum, manganese and selenium.

Because of its high fiber content, whole grain barley may cause bloating in individuals who are not used to eating a lot of fiber.

Furthermore, barley contains gluten. This may cause problems for people who are intolerant to gluten.

What to eat instead: Refined barley, like pearl or scotch barley, may be tolerated better. Barley can also be replaced with other grains or pseudocereals like oats, brown rice, quinoa or buckwheat.

8. Rye
Rye is a cereal grain that is related to wheat.

It is very nutritious and an excellent source of fiber, manganese, phosphorus, copper and B-vitamins.

However, rye also contains gluten, a protein that many people are sensitive or intolerant to.

Because of its high fiber and gluten content, rye may be a major cause of bloating in sensitive individuals.

What to eat instead: Other grains or pseudocereals, including oats, brown rice, buckwheat or quinoa.


9. Dairy Products
Dairy is highly nutritious, as well as an excellent source of protein and calcium.

There are many dairy products available, including milk, cheese, cream cheese, yogurt and butter.

However, about 75% of the world's population can't break down lactose, the sugar found in milk. This condition is known as lactose intolerance (16Trusted Source, 17Trusted Source).

If you're lactose intolerant, dairy can cause major digestive problems. Symptoms include bloating, gas, cramping and diarrhea.

What to eat instead: People who are lactose intolerant can sometimes handle cream and butter, or fermented dairy like yogurt (18Trusted Source).

Lactose-free milk products are also available. Other alternatives to regular milk include coconut, almond, soy or rice milk.

10. Apples
Apples are among the most popular fruits in the world.

They are high in fiber, vitamin C and antioxidants, and have been linked with a range of health benefits (19Trusted Source, 20).

However, apples have also been known to cause bloating and other digestive issues for some people.

The culprits are fructose (which is a FODMAP) and the high fiber content. Fructose and fiber can both be fermented in the large intestine, and may cause gas and bloating.

Cooked apples may be easier to digest than fresh ones.

What to eat instead: Other fruits, such as bananas, blueberries, grapefruit, mandarins, oranges or strawberries.

11. Garlic
Garlic is incredibly popular, both for flavoring and as a health remedy.

Like onions, garlic contains fructans, which are FODMAPs that can cause bloating (21Trusted Source).

Allergy or intolerance to other compounds found in garlic is also fairly common, with symptoms such as bloating, belching and gas (22Trusted Source).

However, cooking the garlic may reduce these effects.

What to eat instead: Try using other herbs and spices in your cooking, such as thyme, parsley, chives or basil.

12. Sugar Alcohols
Sugar alcohols are used to replace sugar in sugar-free foods and chewing gums.

Common types include xylitol, sorbitol and mannitol.

Sugar alcohols are also FODMAPs. They tend to cause digestive problems, since they reach the large intestine unchanged where the gut bacteria feed on them.

Consuming high amounts of sugar alcohols may cause digestive issues, such as bloating, gas and diarrhea.

What to eat instead: Erythritol is also a sugar alcohol, but it is easier on digestion than the ones mentioned above. Stevia is also a healthy alternative to sugar and sugar alcohols.

13. Beer
Everyone has probably heard the term "beer belly" used before.

It refers not only to increased belly fat, but also to the bloating caused by drinking beer.

Beer is a carbonated beverage made from sources of fermentable carbs like barley, maize, wheat and rice, along with some yeast and water.

Therefore, it contains both gas (carbon dioxide) and fermentable carbs, two well-known causes of bloating. The grains used to brew the beer also often contain gluten.

What to drink instead: Water is always the best beverage, but if you are looking for alcoholic alternatives then red wine, white wine or spirits may cause less bloating.

Other Ways to Reduce Bloating
Bloating is a very common problem, but can often be resolved with relatively simple changes.

There are several strategies that can help reduce bloating, outlined in this article.

If you have persistent digestive problems, then you may want to consider a low-FODMAP diet. It can be incredibly effective, not just for bloating but for other digestive issues as well.

However, make sure to also see a doctor to rule out a potentially serious medical condition.

Take Home Message
If you have problems with bloating, then chances are that a food on this list is the culprit.

That being said, there is no reason to avoid all of these foods, only the ones that cause you problems personally.

If you find that a certain food consistently makes you bloated, then simply avoid it. No food is worth suffering for.
Do Peanuts cause gas?
They contain high amounts of protein, fiber and healthy carbs, as well as minerals such as iron, copper and manganese. Because of their high fiber content, they can cause bloating in sensitive individuals. ... These sugars may contribute to excessivegas production and bloating.Jun 4, 2017


There are several reasons why legumes can cause digestive problemsPeanutsin particular contain aflatoxin (toxins produced by a mold) and lectins, while soy also contains phytoestrogens. All of these could irritate the digestive system.


Let's talk about something uncomfortable: gas and bloating. Most of us pass gas anywhere from 12 to 25 times a day, according to Brigham and Women's Hospital, and surveys show that abdominal bloating affects up to 30 percent of Americans. "Having a perfectly flat stomach all the time isn't normal," said Health contributing nutrition editor Cynthia Sass, MPH, RD."After you eat and drink, food and liquids take up space inside your stomach and intestines, and that means some expansion."
A ballooned belly doesn't necessarily indicate that something is wrong with what you eat, but if your abdomen is too swollen to squeeze into your jeans, you may want to identify the belly bloaters in your diet.
Worst: Broccoli, cabbage, kale
Kale, broccoli, and cabbage are cruciferous vegetables, which contain raffinose — a sugar that remains undigested until bacteria in your gut ferment it, which produces gas and, in turn, makes you bloat. But don't shun those healthful greens just yet. "Consistently eating nutrient-rich, high-fiber foods leads to having a stronger, healthier digestive system that's less prone to bloating," Sass said.
So keep eating the green stuff, but keep your portions in check. And if you absolutely can't part ways with even a gram of your kale, steam it: "Cooking any vegetable softens the fiber and shrinks the portion as some of the water cooks out, so it takes up less space in the GI tract," Sass said. It won't eliminate or prevent bloating altogether, but it may make your veggies easier to digest.
Worst: Legumes
It's probably not news to you, but beans, along with lentils, soybeans, and peas are gas-causing foods. These little guys are basically bursts of protein in a pod, but they also contain sugars and fibers that our bodies can't absorb. So when legumes reach the large intestine, your gut bacteria take the lead and feast on them. This process leads to gas and can balloon out your waist.
Combine legumes with easily digestible whole grains, like rice or quinoa. Your body will eventually get used to them. "If you eat fruits, veggies, nuts, whole grains, and beans often, they won't bother you as much as if you eat them sporadically," Sass said.
Worst: Dairy
If you feel gassy after a few slices of cheese or a bowl of cereal with milk, you may be lactose intolerant, which means your body lacks the necessary enzymes to break down lactose (the sugar found in dairy products). That can cause gas to form in the GI tract, which may trigger bloating.
So before all that gas gets to you, steer clear of dairy products and opt for the many lactose-free or nondairy alternatives out there. The American Gastroenterological Association (AGA) also suggests the use of lactase tablets like Lactaid, which help people digest foods that contain lactose.
Worst: Apples
An apple a day may save you a trip to the doctor's office, but it does not keep the bloat away. High in fiber, apples also contain fructose and sorbitol, sugars found in fruits that many people can't tolerate, Sass said. The result? You guessed it: gas and the inevitable puffy feeling.
Apples are a great snack, however: One fruit provides an average of 4.5 grams of protein and around 10 percent of your daily vitamin C requirement, so don’t give up on them altogether. "Eating apples specifically has been linked to a lower risk of heart disease and respiratory problems, including asthma, bronchitis, and emphysema," Sass said. Eat them in moderation and separately from meals, and time your eating right: "If you'll be wearing a form-fitting outfit or bathing suit, you might not want to reach for an apple," Sass said. Other fruits that bloat: pear, peaches, and prunes.
Worst: Salty foods
Eating high-sodium foods can trigger water retention, which can balloon you up, Sass said. Avoiding sodium isn't as simple as steering clear of the saltshaker, however. The CDC reports that about 90 percent of Americans consume more sodium than is recommended for a healthy diet (2,300 mg per day for most people, and 1,500 mg for adults over 50, and people with diabetes, high blood pressure, and high risk of hypertension). Sodium sneaks its way into most processed and packaged foods, including soups, breads, and these other surprisingly salty foods. That makes it very difficult to avoid. When and if you do succumb to salt, drink a lot of water to help flush it out.
Best: Cucumber
People use cucumbers to reduce puffiness under their eyes—and you can eat them to do the same thing for your belly. The vegetable contains quercetin, a flavonoid antioxidant that helps reduce swelling, says Sass.
"Cucumbers have been shown to inhibit the activity of pro-inflammatory enzymes," she adds.
So slice it up and eat it as is, or swap sugary drinks with a glass of cucumber water.
Best: Bananas
Foods rich in potassium—like bananas, plus avocados, kiwis, oranges, and pistachios—prevent water retention by regulating sodium levels in your body and can thus reduce salt-induced bloating. Bananas also have soluble fiber, which can relieve or prevent constipation.
"Bloating can also be caused by constipation," Sass said. "If you’re not able to eliminate waste in the GI tract, you become 'backed up' so to speak, which can lead to a bloated look."
Best: Papaya
The enzyme contained in papaya (papain) helps break down proteins in your GI system, which makes digestion easier. Sass says that the tropical fruit also has anti-inflammatory properties, as well as fibers that support a strong digestive tract.
Eat papaya whole and fresh or blended into a smoothie
Best: Asparagus
Asparagus is an anti-bloating superfood. Sure, it makes your urine smell, but it also makes you pee, period—helping you flush all that excess water, thus relieving any discomfort and bloat.
It also contains prebiotics, which help support the growth of 'good' bacteria, according to Sass. This helps maintain a healthy balance in your digestive system to prevent and/or reduce gas.
Finally, the vegetable contains soluble and insoluble fibers, which helps promote overall digestive health.
Best: Yogurt with probiotics
Get some of those good bacteria into your gut! Called probiotics, they help regulate digestion and champion the overall health of your digestive tract. Sure, you can take probiotic supplements, but you may as well get a breakfast out of it.
So eat your bloat away with a yogurt that has active cultures. You can sweeten it with a little honey, jam, or granola.
Best: Fennel seeds
Fennel is a digestive tract savior. The seeds have a compound that relaxes GI spasms, which allows gas to pass and relieve bloating, says Sass.
You can find fennel and fennel seeds in breads, sausages, and other meat dishes. You can also chew on the seeds directly or sip on a fennel tea at the end of a meal.
Best: Ginger
Ginger is a go-to home remedy for colds, achy muscles, cramps, and seasickness. Add bloating to the list—ginger is a natural anti-inflammatory and an all-star digestive aid. It soothes the digestive system and relaxes the muscles of the digestive tract, which can relieve bloating, Sass said. It also contains an enzyme that absorbs proteins, thus reducing protein-induced puffiness and gas.
Fresh ginger can be added to smoothies and salad dressings, and it adds tons of flavor to recipes like these. You can also make homemade tea.
Best: Peppermint and chamomile tea
If you're feeling stretched out after dinner, you can sip on a hot cup of peppermint or chamomile tea. Both kinds relax GI muscles to help dissipate the gas that causes your stomach to bloat. Aside from improving digestion, chamomile can also soothe and relax, which can help ease any sort of stomach discomfort.


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