Martin Neimöller, the German theologian, summarized the slippery march of evil in his often-quoted statement: First they came for the Socialists, and I did not speak out— Because I was not a Socialist. Then they came for the Trade Unionists, and I did not speak out— Because I was not a Trade Unionist. Then they came for the Jews, and I did not speak out— Because I was not a Jew. Then they came for me—and there was no one left to speak out for me. Could this happen In India in the future?
I came to this book not entirely ignorant of America's shameful role in eugenics, but before reading this book, I was unaware of the extent of that role. Essentially, the U.S. provided Hitler the blueprints for the final solution.
Here in the U.S., thousands of Americans were sterilized against their will. No less a jurist that Oliver Wendell Holmes ruled that involuntary sterilization was a proper remedy to preventing these so-called inferiors from contaminating the gene stock. He famously wrote that "three generations of imbeciles are enough” in Buck v. Bell, a 1927 Supreme court case upholding a Virginia law that authorized the state to surgically sterilize certain “mental defectives” without their consent.
The people identified as defective were invariably poor and usually of color or of immigrant stock. My own forebears who lived in the Blue Ridge Mountains of West Virginia would have been prime candidates, being poor and uneducated.
I do have one criticism in that Black should have maintained a bit more emotional distance to his subject, though I understand his deep anger and outrage over these injustices.
After reading this book, I wonder what it was about America that provided such a fertile breeding ground for hate? ( )
I came to this book not entirely ignorant of America's shameful role in eugenics, but before reading this book, I was unaware of the extent of that role. Essentially, the U.S. provided Hitler the blueprints for the final solution.
Here in the U.S., thousands of Americans were sterilized against their will. No less a jurist that Oliver Wendell Holmes ruled that involuntary sterilization was a proper remedy to preventing these so-called inferiors from contaminating the gene stock. He famously wrote that "three generations of imbeciles are enough” in Buck v. Bell, a 1927 Supreme court case upholding a Virginia law that authorized the state to surgically sterilize certain “mental defectives” without their consent.
The people identified as defective were invariably poor and usually of color or of immigrant stock. My own forebears who lived in the Blue Ridge Mountains of West Virginia would have been prime candidates, being poor and uneducated.
I do have one criticism in that Black should have maintained a bit more emotional distance to his subject, though I understand his deep anger and outrage over these injustices.
After reading this book, I wonder what it was about America that provided such a fertile breeding ground for hate? ( )
A difficult book to read. Not because it is poorly written. But because it is so disappointing to read about the American history of oppressing the weak.
The pseudo-science of eugenics is the application of evolutionistic natural selection to humankind. If humans are descended from animals and still evolving then some portion of humankind could conceivably be further ahead than others. And if this is true, should not the human race be bettered by encouraging the propagation of this portion of our race and discouraging the continued breeding of those that may be further down the evolutionary ladder? Especially those that carry hereditary diseases, deformities, a high probability of mental defect, or propensity to engage in criminal misconduct. Or so eugenic theory would have you believe.
Some of the research backing this idea followed families through multiple generations and tracked the fact that most member's of this family were criminals. If these people were sterilized so they could not continue to have children the state and society would be safer and see a significant savings in the criminal justice arena. The same argument was presented for families with a history of expensive medical issues.
This "reasonable" view of evolution and society was cloaked in the blessing of science and used to create sterilization laws and laws prohibiting interracial marriages. These views and the corresponding laws were not the result of a groundswell of public sentiment calling for sterilizations to be accomplished on those found unfit or laws prohibiting interracial marriages. Rather, these laws were promulgated, lobbied for, and supported by a highly educated portion of the American scientific community funded by major philanthropic monies.
Part of the basis of this philanthropy was the idea of some that charity rewards people for failure and that human kind should mirror nature in letting the weak die off and the strong continue. Charity was viewed as unnatural meddling in the natural way of life. Eugenics was viewed as a way of restoring balance. Margaret Sanger, founder of planned parenthood believed in this view of charity as well as well as the importance of eugenics.
There were several doctors that performed uncalled for sterilizations on people they thought were unfit prior to laws being passed allowing the procedure. Indiana was the first state to legalize sterilization of the unfit. At least 29 other states followed that lead. California by far completed the most recorded sterilizations. And the funding to start the process was provided by New Englands wealthy. A victory showing what a small group of educated people with a vision and funding can accomplish while the majority of people are not really paying attention.
What did this movement cost America? The idea as a science and the word "eugenics" was British in origin (invented by Sir Francis Galton). However, it was in American where this idea became popular and applied in an active way. In the 20s and 30s these ideas accepted in America were globalized. American model legislation for sterilization was sent to many European countries and enacted there creating sterilization programs in Switzerland, Denmark, Norway, and Germany. German efforts to cleanse their race of those deemed unfit were highly admired in America. And it was because of successful eugenic efforts to restrict immigration into America of the unfit that many Jews were unable to escape Europe and holocaust to come.
American philanthropic efforts were not confined to the United States. Rockefeller and other wealthy New Englanders funded most of the eugenic scientist in Germany after WWI. The research and books that guided Hitler to understanding how the unfit made the German people weak were funded with American monies. Hitler even wrote an admiring thank you letter to one of the leading eugenics proponents in the United States.
We tend many time to tie up our righteous anger for the holocaust to the leader of the German people that led them into murdering millions and the SS who carried out his vision. We like to say Adolph Hitler was a racist, and that is true fact. But his racism was not merely some backwoods silly hatred based on people being different than he was. Rather, his hatred was based on the science of eugenics.
We should not forget that when Jews and other people that were considered unfit (not always based on race) got off the train at Auschwitz and other death camps it was not Hitler personally that decided who would be treated in what ways. Nor was it always the SS trooper. Rather usually there was someone there with medical credentials and eugenics training in their background making this decision. The SS were the trigger man. Hitler was the government leader that made the horrors of the holocaust possible politically. But it was the scientists and doctors, funded by American money that created the basis for all these horrors. How could ordinary people do such terrible things to other people in death camps and elsewhere? First, they were taught eugenics and that not all people are equal, and the unfit drag the rest of society down. Before they tried to kill off entire races they worked hard to cleanse their own race; sterilizing or killing the weaker parts of their society in nursing homes and insane asylums. It is clear that we cannot trust science alone to create a moral compass for society.
Much as I hate to admit it, America carries some moral responsibility for what happened in Europe with the holocaust. Because of the outrage and condemnation of the holocaust and Germany's eugenic actions the American eugenic community melted away into the background. Usually changing their names from eugenics to something with genetics. It still took many years to change all the laws that the American eugenic movement put into the books in the United States. It was not until the 1960s that laws against interracial marriages were set aside and people were being sterilized without their consent into the 1970s. Several states till have laws on the books for sterilization. But they have not been utilized for years.
This book is well written and researched. If anything there is probably much left unexamined for the sake of preserving a comprehensible narrative and story of a reasonable length. Clocking in at over 500 pages it's not a swift read. ( )
Bateson was acutely aware of the potential social and political impact of the newborn science. "What will happen when ... enlightenment actually comes to pass and the facts of heredity are ... commonly known?" he wrote, with striking prescience, in 1905. "One thing is certain: man- kind will begin to interfere; perhaps not in England, but in some country more ready to break with the past and eager for 'national efficiency.' ... Ignorance of the remoter consequences of interference has never long postponed such experiments." More than any scientist before him, Bateson also grasped the idea that the discontinuous nature of genetic information carried vast implications for the future of human genetics. If genes were, indeed, independent particles of information, then it should be possible to select, purify, and manipulate these particles independently from one another. Genes for "desirable" attributes might be selected or augmented, while undesirable genes might be eliminated from the gene pool. In principle, a scientist should be able to change the "composition of individuals," and of nations, and leave a permanent mark on human identity.
"When power is discovered, man always turns to it," Bateson wrote darkly. "The science of heredity will soon provide power on a stupendous scale; and in some country, at some time not, perhaps, far distant, that power will be applied to control the composition of a nation. Whether the institution of such control will ultimately be good or bad for that na- tion, or for humanity at large, is a separate question." He had preempted the century of the gene. Improved environment and education may better the generation already born. Improved blood will better every generation to come. —Herbert Walter, Genetics Most Eugenists are Euphemists. I mean merely that short words startle them, while long words soothe them. And they are utterly incapable of translating the one into the other.... Say to them "The ... citizen should... make sure that the burden of longevity in the previous generations does not become disproportionate and intolerable, especially to the females"; say this to them and they sway slightly to and fro.. Say to them "Murder your mother," and they sit up quite suddenly. —G. K. Chesterton, Eugenics and Other Evils In 1883, one year after Charles Darwin's death, Darwin's cousin Francis Galton published a provocative book—lnquiries into Human Faculty and Its Development—in which he laid out a strategic plan for the improve- ment of the human race. Galton's idea was simple: he would mimic the mechanism of natural selection. If nature could achieve such remark- able effects on animal populations through survival and selection, Gal- ton imagined accelerating the process of refining humans via human intervention. The selective breeding of the strongest, smartest, "fittest" humans—unnatural selection—Galton imagined, could achieve over just a few decades what nature had been attempting for eons. Galton needed a word for this strategy. "We greatly want a brief word to express the science of improving stock," he wrote, "to give the more suitable
"what if we learned to change our genetic code intentionally? If such technologies were available, who would control them, and who would ensure their safety? Who would be the masters, and who the victims, of this technology? How would the acquisition and control of this knowledge—and its inevitable invasion of our private and public lives—alter the way we imagine our societies, our children, and our- selves?"
The Gene: An Intimate History
By Siddhartha Mukherjee When the poet Wallace Stevens writes, "In the sum of the parts, there are only the parts," he is referring to the deep structural mystery that runs through language: you can only decipher the meaning of a sentence by deciphering every individual word—yet a sentence carries more meaning than any of the individual words. And so it is with genes. An organism is much more than its genes, ofcourse, but to understand an organism, you must first understand its genes. When the Dutch biologist Hugo de Vries encountered the concept of the gene in the 1890s, he quickly intuited that the idea would reorganize our understanding of the natural world. "The whole or anic world is the result of innumerable different
The Gene: An Intimate History
By Siddhartha Mukherjee The atom, the byte, and the gene provide fundamentally new scientific and technological understandings of their respective systems. You cannot explain the behavior Of matter—why gold gleams; why hydrogen combusts with oxygen—without invoking the atomic nature of matter. Nor can you understand the complexities of computing—the nature of algorithms, or the storage or corruption of data—without comprehending the structural anatomy of digitized information. "Alchemy could not become chemistry until its fundamental units were discovered," "That the fundamental aspects of heredity should have turned out to be so extraordinarily simple supports us in the hope that nature may, after all, be entirely approachable," Thomas Morgan, the influential geneticist, wrote. "Her much-advertised inscrutability has once more been found to be an illusion." The atom provides an organizing principle for modern physics—and it tantalizes us with the prospect of controlling matter and energy. The gene provides an organizing principle for modern biology—and it tantalizes us with the prospect of controlling our bodies and fates. Embedded in the history of the gene is "the quest for eternal youth, the Faustian myth of abrupt reversal of fortune, and our own century's flirtation with the perfectibility of man." Embedded, equally, is the desire to decipher our manual of instructions. Most important, I owe a debt to my grandmother. She did not—she could not—outlive the grief of her inheritance, but she embraced and de- fended the most fragile of her children from the will of the strong. She weathered the buffets of history with resilience—but she weathered the buffets of heredity with something more than resilience: a grace that we, as her descendants, can only hope to emulate. It is to her that this book is dedicated.
How Pharma Companies Game the System to Keep Drugs Expensive
Erin Fox
APRIL 06, 2017
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I help the University of Utah hospital system manage its drug budgets and medication use policies, and in 2015 I got sticker shock. Our annual inpatient pharmacy cost for a single drug skyrocketed from $300,000 to $1.9 million. That’s because the drug maker Valeant suddenly increased the price of isoproterenol from $440 to roughly $2,700 a dose.
Isoproterenol is a heart drug. It helps with heart attacks and shock and works to keep up a patient’s blood pressure. With the sudden price increase, we were forced to remove isoproterenol from our 100 emergency crash carts. Instead, we stocked our pharmacy backup boxes, located on each floor of our hospitals, to have the vital drug on hand if needed. We had to minimize costs without impacting patient care.
This type of arbitrary and unpredictable inflation is not sustainable. And it’s not the way things are supposed to work in the United States. Isoproterenol is a drug that is no longer protected by a patent. Theoretically, any drug company should be able to make a generic version and sell it at a competitive cost. We should have had other options to buy a competitors’ copy for $440 or less. But that’s not happening like it should. The promise of generic medications is getting further from reality each day. As the U.S. Senate considers President Donald Trump’s choice to head the Food and Drug Administration, now is the time refocus efforts on generic drugs.
How generics are supposed to work
The 1984 Drug Price Competition and Patent Term Restoration Act gave pharmaceutical companies exclusive protections for innovating a new drug. If they brought a new therapy to life, they enjoyed patent protection to effectively monopolize the market. That was the payoff for shouldering the high risk and high costs of developing new drugs.
But once the patent and the exclusive hold on the market expires, the legislation encouraged competition to benefit consumers. Any drug company would be able to manufacture non-brand name versions of the very same drug, so-called “generics.” And for a while, the system worked well.
Not anymore. The system intended to reward drug companies for their innovations, but eventually protect consumers, is systematically being broken. Drug companies are thwarting competition through a number of tactics, and the result is high prices, little to no competition, and drug quality problems.
The ways companies stop generics
One of the ways branded drug manufacturers prevent competition is simple: cash. In so-called “pay for delay” agreements, a brand drug company simply pays a generic company not to launch a version of a drug. The Federal Trade Commission estimates these pacts cost U.S. consumers and taxpayers $3.5 billion in higher drug costs each year.
“Citizen petitions” offer drug companies another way to delay generics from being approved. These ask the Food and Drug Administration to delay action on a pending generic drug application. By law, the FDA is required to prioritize these petitions. However, the citizens filing concerns are not individuals, they’re corporations. The FDA recently said branded drug manufacturers submitted 92% of all citizen petitions. Many of these petitions are filed near the date of patent expiration, effectively limiting potential competition for another 150 days.
“Authorized generics” are another tactic to limit competition. These aren’t really generic products at all; they are the same product sold under a generic name by the company that sells the branded drug. Why? By law, the first generic company to market a drug gets an exclusivity period of 180 days. During this time, no other companies can market a generic product. But the company with the expiring patent is not barred from launching an “authorized generic.” By selling a drug they’re already making under a different name, pharmaceutical firms are effectively extending their monopoly for another six months.
Another way pharmaceutical firms are thwarting generics is by restricting access to samples for testing. Generic drug makers need to be able to purchase a sample of a brand-name product to conduct bioequivalence testing. That’s because they have to prove they can make a bioequivalent product following the current good manufacturing practices (CGMP) standard. These manufacturers don’t need to conduct clinical trials like the original drug company did.
But the original drug developer often declines to sell drug samples to generics manufacturers by citing “FDA requirements,” by which they mean the agency’s Risk Evaluation and Mitigation Strategies program. The idea behind this program is a good one: give access to patients who will benefit from these personalized medicines, and bar access for patients who won’t benefit and could be seriously harmed. However, brand drug makers are citing these requirements for the sole purpose of keeping generics from coming to market.
Problems with generic drug makers
Although makers of a branded drug are using a variety of tactics to create barriers to healthy competition, generic drug companies are often not helping their own case. In 2015, there were 267 recalls of generic drug products—more than one every other day. These recalls are for quality issues such as products not dissolving properly, becoming contaminated, or even being outright counterfeits.
A few high-profile recalls have shaken the belief that generic drugs are truly the same. In 2014, the FDA withdrew approval of Budeprion XL 300 — Teva’s generic version of GlaxoSmithKline’s Wellbutrin XL. Testing showed the drug did not properly release its key ingredient, substantiating consumers’ claims that the generic was not equivalent. In addition, concerns about contaminated generic Lipitor caused the FDA to launch a $20 million initiative to test generic products to ensure they are truly therapeutically equivalent.
In some cases, patent law also collides with the FDA’s manufacturing rules. For example, the Novartis patent for Diovan expired in 2012. Ranbaxy received exclusivity for 180 days for the first generic product. However, due to poor quality manufacturing, Ranbaxy couldn’t obtain final FDA approval for its generic version. The FDA banned shipments of Ranbaxy products to the United States. Ranbaxy ended up paying a $500 million fine, the largest penalty paid by a generic firm for violations.
Due to these protracted problems with the company that had won exclusivity, a generic product did not become available until 2014. The two-year delay cost Medicare and Medicaid at least $900 million. Ranbaxy’s poor-quality manufacturing also delayed other key generic products like Valcyte and Nexium. Ironically, it was Mylan—involved in its own drug pricing scandal over its EpiPen allergy-reaction injector—that filed the first lawsuit to have the FDA strip Ranbaxy of its exclusivity. Mylan made multiple attempts to produce generic products but was overruled in the courts.
Ways to Fix the System
Pharmaceutical firms are currently using a set of tactics to make their temporary monopolies semi-permanent. Eliminating these tactics will not be easy. Still, doing so will fulfill the deal that policy makers offered to drug makers and consumers: a temporary monopoly on sales to help pay for drug development.
First, restrictive distribution programs need to be stopped. Generic companies must also be allowed to purchase samples of these medications to conduct bioequivalence studies. (One measure to close these loopholes already has bipartisan support.) Next, pay-for-delay agreements should be eliminated as well as a corporation’s ability to issue citizen petitions with the intent of delaying generic competition.
Encouraging and enforcing high-quality standards for medications must also be an industry imperative. To create transparency around drug quality, the FDA has proposed a system of letter grades for manufacturers. In an economic study, one official notes that lack of transparency “may have produced a market situation in which quality problems have become sufficiently common and severe to result in drug shortages.”
Another way to achieve greater transparency in medication quality is to change the product labeling laws. Labels should disclose the medication’s manufacturer. Currently, hospitals and pharmacies don’t always know which company actually made the product. This makes it difficult to base purchase decisions on quality.
Generic medications can provide great benefits for patients and health systems when there is adequate competition and quality. But their promise is unfulfilled, and it’s costing consumers. By eliminating restrictive distribution schemes, pay-for-delay, and citizen petitions as well as providing more transparency around quality, hospitals, clinicians, lawmakers, and the new leaders at the FDA have a clear opportunity. They can start to reverse rising health care costs and ensure quality medications are accessible to the American people.
Erin Fox is the director of Drug Information at University of Utah Health. A teaching pharmacist, she tracks drug shortages for the American Society of Health-System Pharmacists.
Do Companies Buy Competitors in Order to Shut Them Down?
FLORIAN EDERER, SONG MA
Large companies will sometimes buy smaller firms only to terminate those firms’ projects. A study co-authored by Yale SOM researchers Florian Ederer and Song Ma suggests that pharmaceutical companies frequently perform such “killer acquisitions” to eliminate competing therapies under development. They argue that the practice is potentially limiting the number of new treatments available.
Large companies often acquire other firms to benefit from their products, or to snap up their talent. But in some cases, it appears, an acquisition is made to destroy the potential competition presented by the smaller company. After such “killer acquisitions,” the larger firm simply shelves the competing innovative projects before they are marketed.
“It’s a little bit surprising, where you buy something in order to then shut it down,” says Florian Ederer, an economics professor at Yale SOM.
In a recent study, Ederer, Yale SOM finance professor Song Ma, and London Business School’s Colleen Cunningham looked at acquisitions in the pharmaceutical industry to see how often they eliminated potential competition. The team found that drugs under development acquired by other firms were more likely to be terminated than non-acquired drugs, particularly when the parent company already had a very similar product. The researchers estimated that 7% of the acquisitions were killer acquisitions; if such deals did not take place, the number of drugs continuing development each year would increase by 5%. In other words, killer acquisitions may be holding back a substantial number of medical treatments. “This phenomenon is pervasive and could be very detrimental to society,” Ma says
The researchers began by creating a theoretical model to study drug development decisions. The model predicted that when the two companies’ products were similar, the acquiring firm was more likely to terminate the acquired project compared to the case in which project was not acquired. But if the incumbent already faced a lot of competition from other companies or if future competition was likely to increase, killer acquisitions were less likely to take place.
The team then tested these ideas on a data set of more than 35,000 drug projects for the U.S. market from 1989 to 2011. The data included information on company acquisitions and drug development milestones, such as clinical trials, patent applications, steps toward commercialization, and termination.
Drugs acquired by another firm had a 92% chance of being discontinued, while non-acquired drugs had an 85% chance. If the therapy treated the same disease as one of the parent company’s products using a similar biological mechanism, the chances of termination were even higher. “Firms try to protect their market power,” Ma says. “Hence, they want to kill future competitors by terminating their innovation projects.” Out of about 750 drug acquisitions per year, the team estimates, an average of 54 were killer acquisitions.
The researchers also considered the effects of market competition on the likelihood of killer acquisitions. They found that killer acquisitions usually occurred in areas where existing competition for the disease treatment was scarce. And, if the incumbent firm’s patent on its drug was due to expire in the next five years—allowing generic competitors to enter the market—the chances of killer acquisitions decreased.
The team tried to determine if other factors could explain these patterns. For example, perhaps the acquiring firms had shelved some of the target company’s projects because they wanted to focus on the best remaining ones. But the data suggested that wasn’t the case: killer acquisitions were even more prevalent when the target company was developing only one drug.
Another possible explanation was that while a particular drug may have been terminated, the incumbent firm shifted the smaller company’s technology and people to more promising projects. But the team saw no evidence that the parent firms’ drugs became more chemically similar to the acquired drugs. Nor did the acquired staff seem to be redeployed more efficiently. Less than one-quarter of inventors stayed with the incumbent company, and those who did saw a 30% drop in their patenting rate over five years. “Even in the acquired firm, they do not seem to be really productive,” Ma says.
Are killer acquisitions hurting innovation enough that they should be subject to antitrust regulation? The overall effect on society isn’t clear, the authors say. On the one hand, the practice could prevent promising treatments from reaching patients and thereby allow prices on existing therapies to rise. On the other hand, perhaps the prospect of being acquired motivates smaller firms to be more innovative in their drug development, so on balance, the phenomenon is not negative.
Since healthy market competition seems to discourage killer acquisitions, regulation may not be needed, Ederer says: “Maybe it is enough just to encourage competition, and then this will settle out by itself.”
Amgen, Merck, and Eli Lilly sue over Trump administration policy to require drug prices in TV ads
By LEV FACHER @levfacher JUNE 14, 2019
TV yellow and blue
ADOBE
WASHINGTON — A trio of pharmaceutical manufacturers on Friday filed suit to overturn one of the most impactful drug pricing policies the Trump administration has enacted to date: a requirement that the companies include a medicine’s list price in direct-to-consumer advertising.
The drug makers — Amgen, Merck, and Eli Lilly — were joined by the Association of National Advertisers on the lawsuit. In a press release, Amgen said the rule raises “freedom of speech concerns” and that it “fails to account for differences among insurance, treatments, and patients themselves.”
The rule is set to go into effect this summer.
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“Americans deserve accurate information about the price they will pay for prescription drugs,” the lawsuit reads.
But while the rule “purports to further that objective,” the drug makers argue, it “will instead frustrate it by misleading patients about their out-of-pocket costs for prescription drugs in a manner that even HHS admits may ‘confuse’ and ‘intimidate’ patients.”
In a supporting legal analysis, Ravi Dhar, a Yale professor and paid consultant to the plaintiffs, argued that advertisements’ inclusion of wholesale acquisition cost — a common industry pricing benchmark — is “likely to mislead consumers into overestimating their actual out-of-pocket costs and is not likely to lead to more informed choices.”
Related: There’s a legal battle looming over Trump’s new proposal on drug ads. Here’s what’s at the heart of it
Almost immediately after the Trump administration first proposed the policy, drug makers began to question the federal government’s legal standing for requiring the price disclosures. They also argued that list prices are often not effective barometers of patient expense, given the variance between insurers, providers, and patient assistance programs, among other factors.
In the document rolling out the policy, the federal government included a lengthy legal justification, relying on the argument that the price disclosures will bolster the efficiency of federal health programs like Medicare and Medicaid.
“We are telling drug companies today: You’ve got to level with people [about] what your drugs cost,” Health and Human Services Secretary Alex Azar said when the Trump administration finalized the rule last month. “Put it in the TV ads. Patients have a right to know, and if you’re ashamed of your drug prices, change your drug prices. It’s that simple.”
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Legal scholars remain split on whether the policy violates the First Amendment. Arguments will likely center on the federal government’s rationale for requiring the price disclosures and whether they will help consumers and government programs — or whether they are focused on shaming companies making costly drugs.
The free speech issue has sunk Food and Drug Administration regulations in the past. The FDA’s previous proposal to require graphic warnings on cigarette cartons was struck down in 2012, because the court found the FDA couldn’t prove the graphic images it was requiring would actually lower smoking rates.
“If the drug companies are embarrassed by their prices or afraid that the prices will scare patients away, they should lower them,” Caitlin Oakley, a spokeswoman for the Department of Health and Human Services, said in a statement. “President Trump and Secretary Azar are committed to providing patients the information they need to make their own informed healthcare decisions.”
Nicholas Florko contributed reporting.
About the Author
Lev Facher
Washington Correspondent
Lev Facher covers the politics of health and life sciences.
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.
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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
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.
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.
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.
People often believe normal passage of gas to be
excessive.
Gas comes from two main sources: swallowed air and
normal breakdown of certain foods by harmless bacteria naturally present
in the large intestine.
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.
Many foods with carbohydrates can cause gas. Fats
and proteins cause little gas.
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
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
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.
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.
Digestive enzymes, such as lactase supplements,
actually help digest carbohydrates and may allow people to eat foods that
normally cause gas.
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.
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:
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
odried apples, apricots – dried fruits are very
high in sulfate
owheat pasta
opeanuts
oprunes
oraisins
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 problems. Peanutsin 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.
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.
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.
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
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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