Researchers at UCLA Health uncovered new information about the role inflammation plays in mitigating liver fibrosis, which is associated with metabolic-associated fatty liver disease (MAFLD). While inflammation in the liver has long been considered a prerequisite to developing liver fibrosis, the scarring and thickening of tissue that can impair the liver’s ability to function, this new research, published in the Journal of Clinical Investigation, suggests that reducing inflammation may not influence the extent of fibrosis.
“Liver fibrosis is the critical feature that creates chronic liver disease and liver cancer. If we can keep fibrosis in check then we can meaningfully impact liver disease,” said Tamer Sallam, MD, corresponding author of the study and vice chair and associate professor in the department of medicine at the David Geffen School of Medicine at UCLA.
“For decades we have believed that targeting inflammation is one of the most important ways to reduce MAFLD. But this new research indicates that inflammation, while still important, may not be the main driver of fibrosis.”
The studylooked specifically at a protein called lipopolysaccharide binding protein (LBP), which is involved in the body’s immune response, and how LBP functions in mice. Findings showed that mice without LBP in their liver cells had lower levels of liver inflammation and better liver function but no change in fibrosis.
In addition to mouse models, the researchers also studied genetic analyses from large human datasets and human tissue samples from MAFLD patients at different stages in the disease, to examine the consequence of loss of LBP function. The evidence combined showed that the LBP does not alter scar tissue markers.
Sallam indicated a need to further explore how LBP influences inflammation and whether other factors can offer a more potent reduction in inflammation and have an impact on reducing fibrosis.
“Reducing scar burden is one of the holy grails in the treatment of advanced liver diseases,” Sallam said. “These results suggest that certain ways of targeting inflammation may not be a viable option and that more directed therapies against other pathways could help us better target fibrosis and improve outcomes for patients.”
Cirrhosis is chronic, progressive end-stage liver disease that occurs when scar tissue prevents the liver from functioning normally. Studies have shown that two of the leading causes of cirrhosis – alcohol use disorder and viral hepatitis – occur more frequently in transgender individuals, but there has been little research examining if these risk factors translate into greater incidences of cirrhosis among transgender patients.
A new study from Keck Medicine of USC published in The American Journal of Gastroenterologyfinds that transgender adults have double the prevalence of cirrhosis compared to cisgender adults (people whose gender identity matches the sex they were assigned at birth), suggesting a need for more supportive, preventive care.
“Our study reveals that cirrhosis disproportionately affects transgender individuals and highlights a pressing health issue that needs addressing,” said Brian P. Lee, MD, MAS, a hepatologist and liver transplant specialist with Keck Medicine and principal investigator of the study.
Lee and his colleagues launched the study to provide scientifically backed liver health guidance for physicians so they could offer transgender patients a higher level of care.
Besides discovering that transgender cirrhosis rates are double that of the cisgender population, the study authors also learned that the majority of transgender adults with cirrhosis (60%) have a diagnosis of anxiety and/or depression, compared to 40% of the cisgender patients with cirrhosis.
They also found that alcohol was the leading cause of cirrhosis in the transgender group, accounting for some 60% of cases while the percentage of cisgender adults with alcohol-associated cirrhosis was approximately 50%.
In other findings, transgender patients with cirrhosis also tended to be younger (a larger portion were 44 or younger), had higher rates of viral hepatitis and were five times more likely to have HIV/AIDS than their cisgender counterparts.
Possible reasons behind the disparity
Lee hypothesises that the increased rates of depression and anxiety may be driving higher rates of alcohol use among transgender patients, which in turn, may result in greater cases of cirrhosis.
The increased rate of HIV/AIDS among transgender patients may also be a factor in that both conditions are known to be associated with liver disease progression, according to Lee.
Lack of access to quality health care could also play a role, hypothesises Jeffrey Kahn, MD, a hepatologist and liver transplant physician with Keck Medicine and co-author of the study.
Similar outcomes
Researchers also studied the five-year outcomes among all transgender and cisgender patients with cirrhosis. Interestingly, despite the differences in the two groups, the number of possible negative outcomes of cirrhosis – liver failure, liver transplant and liver cancer, as well as death, by any cause – was the same.
“This finding suggests that the transgender community is underserved in the initial stages of liver disease, but individuals are able to secure the care they need once cirrhosis is diagnosed,” said Kahn. “Early prevention is key because if liver disease is caught in time, there is less of a chance it will progress to cirrhosis.”
To reach their conclusions, study authors culled data from a large national database, Optum, that contained medical claims for more than 60 million patients between 2007–2022. They first identified all transgender and cisgender adults (transgender patients accounted for 0.07%), and then compared the incidences of cirrhosis among each group as well as causes of the disease. Additionally, researchers tracked depression and anxiety in patients.
Lee and Kahn hope the study will spur more research and motivate health care practitioners to provide transgender patients with extra support, including liver screenings and access to mental health resources. “This population requires specific attention from clinicians and researchers alike,” said Lee.
While irritable bowel syndrome (IBS) is commonly associated with symptoms outside the intestine, it was not known whether these symptoms differed according to the subtypes of the condition. A new study published in Neurogastroenterology and Motility investigated the prevalence, and found that the IBS-M (mixed bowel habits) subtype had the highest prevalence of most extra-intestinal symptoms symptoms.
The researchers carried out a descriptive cross-sectional study patients with IBS according to Rome IV criteria. They were classified according to subtypes: IBS-D (diarrhoea-predominant), IBS-C (constipation-predominant), and IBS-M (mixed bowel habits). Of the 4862 patients included; there were 608 IBS-D (12.5%), 1978 IBS-C (40.7%), and 2276 IBS-M (46.8%).
Participants completed a patient health questionnaire-9 (PHQ-9) score for depressive symptoms, with IBS-M the highest at 12.7 compared to 11.1 for IBS-D and 10.5 for IBS-C. They also completed an IBS-severity scoring system (IBS-SSS) questionnaire.
Overall, the study found the following results:
IBS-M:
Overweight
High IBS-SSS of 320
Depressive symptoms (80.0%)
Multiple extra-intestinal symptoms
Arthralgia (62.4%)
Chronic cervicalgia (81.0%)
Extremity numbness (64.5%)
Atopic dermatitis (28.2%)
IBS-C:
Lower body mass index
Low BS-SSS of 290
IBS-D:
Overweight (30.9%)
Higher food intolerance perception (9.5%)
History of cholecystectomy (17.8%)
Faecal incontinence (36.2%)
The authors concluded that, “The prevalence of most extra-intestinal symptoms is higher among patients with IBS-M. Further research is needed to better characterize IBS subtypes, which could potentially help refining tailored therapeutic strategies.”
In Parkinson’s disease, a reduction in the gut bacteria of genes responsible for synthesising the essential B vitamins B2 and B7 was found. Credit: Reiko Matsushita
A study led by Nagoya University in Japan has revealed a link between gut microbiota and Parkinson’s disease (PD). The researchers found that the gut bacteria genes responsible for synthesising vitamins B2 and B7 were reduced. This gene reduction was also linked to low levels of agents that help maintain the integrity of the intestinal barrier, which when weakened causes the inflammation seen in PD. Their findings, published in npj Parkinson’s Disease, suggest that treatment with B vitamins to address these deficiencies can be used to treat PD.
PD is characterized by a variety of physical symptoms that hinder daily activities and mobility, such as shaking, slow movement, stiffness, and balance problems. While the frequency of PD may vary between different populations, it is estimated to affect approximately 1-2% of individuals aged 55 years or older.
Various physiological processes are heavily influenced by the microorganisms found in the gut, which are collectively known as gut microbiota. In ideal conditions, gut microbiota produce SCFAs and polyamines, which maintain the intestinal barrier that prevents toxins entering the bloodstream. Toxins in the blood can be carried to the brain where they cause inflammation and affect neurotransmission processes that are critical for maintaining mental health.
To better understand the relationship between the microbial characteristics of the gut in PD, Hiroshi Nishiwaki and Jun Ueyama from the Nagoya University Graduate School of Medicine conducted a metanalysis of stool samples from patients with PD from Japan, the United States, Germany, China, and Taiwan. They used shotgun sequencing, a technique that sequences all genetic material in a sample. This is an invaluable tool because it offers researchers a better understanding of the microbial community and genetic makeup of the sample.
They observed a decrease in the bacterial genes responsible for the synthesising of riboflavin (vitamin B2) and biotin (vitamin B7) in patients diagnosed with PD. Riboflavin and biotin, derived from both food and gut microbiota, have anti-inflammatory properties, which may counteract the neuroinflammation seen in diseases like PD.
B vitamins play crucial roles in the metabolic processes that influence the production and functions of short-chain fatty acids (SCFAs) and polyamines, two agents that help maintain the integrity of the intestinal barrier, preventing toxins entering the bloodstream. An examination of fecal metabolites revealed decreases of both in patients with PD.
The findings indicate a potential explanation for the progression of PD. “Deficiencies in polyamines and SCFAs could lead to thinning of the intestinal mucus layer, increasing intestinal permeability, both of which have been observed in PD,” Nishiwaki explained. “This higher permeability exposes nerves to toxins, contributing to abnormal aggregation of alpha-synuclein, activating the immune cells in the brain, and leading to long-term inflammation.”
He added, “Supplementation therapy targeting riboflavin and biotin holds promise as a potential therapeutic avenue for alleviating PD symptoms and slowing disease progression.”
The results of the study highlight the importance of understanding the complex relationship among gut microbiota, metabolic pathways, and neurodegeneration. In the coming years, customised therapy could potentially be based on patients’ unique microbiome profiles. By altering bacterial levels in the microbiome, doctors can potentially delay the onset of symptoms associated with diseases like PD.
“We could perform gut microbiota analysis on patients or conduct faecal metabolite analysis,” Nishiwaki said. “Using these findings, we could identify individuals with specific deficiencies and administer oral riboflavin and biotin supplements to those with decreased levels, potentially creating an effective treatment.”
The study, “Meta-analysis of shotgun sequencing of gut microbiota in Parkinson’s disease,” was published in npj Parkinson’s Disease on May 21, 2024, at DOI:10.1038/s41531-024-00724-z.
Gut Microbiome. Credit Darryl Leja National Human Genome Research Institute National Institutes Of Health
A study conducted by researcher Juan Du’s research group at the Karolinska Institutet sheds light on the capabilities of our gut microbes and their metabolites. The findings reveal potent inhibitory effects on the growth of antibiotic-resistant bacteria and suggest interactions and signaling between gut microbes and pathogens.
The study,published in the journal Gut Microbes, focuses on identifying key microbes within the gut microbiome that inhibit the growth of pathogens, particularly antibiotic-resistant strains.
Strains from Clostridium perfringens, Clostridium butyricum, and Enterobacter maltosivorans and their metabolites were found to directly inhibit the growth of pathogens, including multi-drug-resistant ones. The study also reveals novel dipeptide features, suggesting interactions and signaling between gut microbes and pathogens.
“Multidrug-resistant microorganisms pose a global threat, and understanding the role of gut microbiota is crucial. Metabolites derived from these microbial communities play a significant role in regulating biochemical processes in the human body. Despite this, only a limited number of gut microbes and their bioactive metabolites have been explored so far”, explains author Juan Du. She continues:
“We plan to expand our screening to include a broader collection of commensal bacteria from various body sites. We’ll conduct mechanism studies to understand how these compounds function on pathogens, especially antibiotic-resistant strains”, says Juan Du.
Inflammatory bowel disease (IBD) is associated with a slightly increased risk of heart failure up to 20 years after diagnosis, according to a comprehensive registry study from Karolinska Institutet published in the European Heart Journal.
The researchers analysed the risk of heart failure in over 80 000 patients with inflammatory bowel disease, that is, Crohn’s disease, ulcerative colitis or unclassified IBD, compared with 400 000 people from the general population, as part of the ESPRESSO study.
The results show that people with IBD have a 19% increased risk of developing heart failure up to 20 years after diagnosis. This corresponds to one extra heart failure case per 130 IBD patients in those 20 years, and the risk increase was seen regardless of the type of IBD. The highest risk of heart failure was seen in older patients, people with lower education and people with pre-existing cardiovascular-related disease at IBD diagnosis.
Contribute to new guidelines
“Both healthcare providers and patients should be aware of this increased risk, and it’s important that cardiovascular health is properly monitored,” says the study’s first author Jiangwei Sun, researcher at the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet. “We hope the results will raise the awareness of health workers as to the increased risk of heart failure in individuals with IBD and contribute to new guidelines for cardiovascular disease management in IBD patients.”
Comparing siblings with and without ABD, the risk increase was slightly lower, 10%, suggesting that genetics and early environmental factors shared within families may play a role.
“We don’t know if there is a causal relationship, but we will continue to explore genetic factors and the role of IBD medications and disease activities on the risk of heart failure,” says the study’s senior author Professor Jonas F. Ludvigsson from the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet.
In the stomach, so-called parietal cells are responsible for acid production. They react not only to the body’s own messenger molecules, but also to bitter-tasting food constituents such as caffeine. In a study published in the Journal of Agricultural and Food Chemistry, researchers tested bitter compounds on a human gastric cell line. Their results help to clarify the molecular regulatory mechanisms by which bitter substances influence gastric acid production.
It is known that taste receptors for bitter substances are not only found on the tongue, but also on the surface of other tissues and cells. These include the parietal cells of the stomach, which secrete protons into the stomach – ie, produce gastric acid. Recent studies have already shown that the bitter taste receptors found in parietal cells are involved in the regulation of gastric acid release. However, the underlying molecular signaling pathways are not yet fully understood.
Gastric cells as a test system
To further clarify the molecular interaction between bitter substances, bitter taste receptors, and gastric acid production, a research team led by Veronika Somoza, Director of the Leibniz Institute in Freising, has carried out a study on a cellular test system. This involves human parietal HGT-1 cells, which are able to secrete protons and, like taste cells, have bitter taste receptors.
Veronika Somoza’s team initially developed a working hypothesis based on the results of previous studies and the findings on signal transduction pathways in taste cells. According to this hypothesis, bitter tasting food constituents stimulate bitter taste receptors that are embedded in the cell membrane. This releases calcium ions inside the cells, leading to ion channel opening. This, in turn, allows sodium ions to flow into the gastric cells from the outside, ultimately contributing to the release of protons.
Hypothesis confirmed
First author Phil Richter explains: “We have successfully tested this mechanism with the two bitter substances caffeine and l-arginine. As expected from previous results, both food constituents were shown to stimulate gastric cell proton secretion in our test system.” The PhD student adds: “For the first time, we were able to demonstrate that the transient receptor potential channelsM4 and M5 are involved in the signaling cascade not only in taste cells but also in gastric cells and ensure an influx of sodium ions into the cells.”
Senior Scientist Gaby Andersen says: “By using knock-out experiments, in which we specifically switched off one type of bitter taste receptor in the cells, we were also able to show for the first time that there is a link between bitter taste receptors and the activation of the ion channels.” The scientist emphasizes that the results not only contribute to a better understanding of the role of taste receptors in the stomach but would also show that HGT-1 cells could be suitable as a replacement model for taste cells.
The research team agrees that the results will provide new insights into the regulation of gastric acid production and thus lead to innovative approaches in treating gastric diseases in the long term. However, further studies are needed to deepen knowledge of the molecular regulatory mechanisms and intracellular signaling pathways.
Fatty liver disease often leads to chronic liver inflammation and can even result in liver cancer. Scientists from the German Cancer Research Center (DKFZ) and the University of Tübingen have now shown in mice* that intermittent fasting on a five days on, two days off schedule can halt this development.
In mice with pre-existing liver inflammation, this fasting regime reduces the development of liver cancer . The researchers also identified two proteins in liver cells that are jointly responsible for the protective effect of fasting. An existing drug can partially mimic this effect.
The most common chronic liver condition is non-alcoholic fatty liver disease. If left untreated, it can lead to liver inflammation (metabolic dysfunction-associated steatohepatitis, MASH), liver cirrhosis and even liver cancer. Fatty liver disease is largely considered to be a direct consequence of obesity.
“The vicious circle of an unhealthy diet, obesity, liver inflammation and liver cancer is associated with major restrictions and suffering for those affected and also represents a considerable burden on healthcare systems,” says Mathias Heikenwälder, DKFZ and University of Tübingen. “We have therefore investigated whether simple dietary changes can specifically interrupt this fatal process.”
Intermittent fasting has already been shown in several studies to be an effective means of reducing weight and alleviating certain metabolic disorders. Heikenwälder’s team has now tested in mice whether this approach can also protect the liver from fatty degeneration and chronic inflammation. Their results are published in Cell Metabolism.
Resistance to liver inflammation is independent of calorie intake
The animals were fed with a high-sugar and high-fat diet corresponding to the typical Western diet. One group of mice had constant access to the food. As expected, these animals gained weight and body fat and developed chronic liver inflammation.
The mice in the other group were given nothing to eat on two days a week (5:2 intermittent fasting, or 5:2 IF for short), but were allowed to eat as much as they wished on the other days. Despite the high-calorie diet, these animals did not put on weight, showed fewer signs of liver disease and had lower levels of biomarkers that indicate liver damage. In short, they were resistant to the development of MASH.
Interestingly, resistance to the development of a fatty liver was independent of the total calorie intake, as the animals immediately made up for the lost rations after the end of the fasting periods.
When experimenting with different variants of intermittent fasting, it was found that several parameters determine protection against liver inflammation: The number and duration of fasting cycles play a role, as does the start of the fasting phase. A 5:2 dietary pattern works better than 6:1; 24-hour fasting phases better than 12-hour ones. A particularly unhealthy diet requires more frequent dieting cycles.
Heikenwälder’s team now wanted to find out the molecular background of the response to fasting. To this end, the researchers compared protein composition, metabolic pathways and gene activity in the liver of fasting and non-fasting mice. Two main players responsible for the protective fasting response emerged: the transcription factor PPARα and the enzyme PCK1. The two molecular players work together to increase the breakdown of fatty acids and gluconeogenesis and inhibit the build-up of fats.
“The fasting cycles lead to profound metabolic changes, which together act as beneficial detoxification mechanisms and help to combat MASH,” says Heikenwälder, summarizing the molecular details.
The fact that these correlations are not just a mouse phenomenon was shown when tissue samples from MASH patients were examined: Here, too, the researchers found the same molecular pattern with reduced PPAR α and PCK1. Are PPAR α and PCK1 actually responsible for the beneficial effects of fasting? When both proteins were genetically switched off simultaneously in the liver cells of the mice, intermittent fasting was unable to prevent either chronic inflammation or fibrosis.
The drug pemafibrate mimics the effects of PPARα in the cell. Can the substance also mimic the protective effect of fasting? The researchers investigated this question in mice. Pemafibrate induced some of the favourable metabolic changes that were observed with 5:2 fasting. However, it was only able to partially mimic the protective effects of fasting. “This is hardly surprising, as we can only influence one of the two key players with pemafibrate. Unfortunately, a drug that mimics the effects of PCK1 is not yet available,” explains Mathias Heikenwälder.
Intermittent fasting as liver therapy
While Heikenwälder and his team initially focused on the effects of intermittent fasting on MASH prevention, then investigated whether the 5:2 diet could also alleviate existing chronic liver inflammation.
To this end, the team examined mice that had developed MASH after months of being fed a high-sugar, high-fat diet. After a further four months of 5:2 intermittent fasting (on the same diet), these animals were compared with the non-fasting control group. The fasting mice had better blood values, less fatty liver and liver inflammation and above all: they developed less liver cancer and had fewer cancer foci in the liver.
“This shows us that 5:2 intermittent fasting has great potential – both in the prevention of MASH and liver cancer, as well as in the treatment of established chronic liver inflammation,” summarises principal investigator Heikenwälder. “The promising results justify studies in patients to find out whether intermittent fasting protects against chronic liver inflammation as well as in the mouse model.”
The 5:2 fasting regimen is popular. It is considered comparatively easy to integrate into everyday life, as the fasting days can be tailored to personal needs and no specific foods are prohibited. “Nevertheless, there will always be people who can’t stick to a strict diet in the long term,” says Heikenwälder. “That’s why we want to continue to investigate which combinations of drugs we can use to fully mimic the protective effects of fasting.”
People who take acid-reducing drugs may have a higher risk of migraine and other severe headache than people who do not take these medications, a new study has shown. The acid-reducing drugs include proton pump inhibitors such as omeprazole and esomeprazole, histamine H2-receptor antagonists, or H2 blockers, such as cimetidine and famotidine, and antacid supplements.
The study, study published in Neurology®Clinical Practice, an official journal of the American Academy of Neurology, does not prove causation; only an association.
In acid reflux, stomach acid flows into the oesophagus, usually after a meal or when lying down, causing heartburn and ulcers. People with frequent acid reflux may develop gastroesophageal reflux disease, or GORD, which can lead to cancer of the oesophagus.
“Given the wide usage of acid-reducing drugs and these potential implications with migraine, these results warrant further investigation,” said study author Margaret Slavin, PhD, RDN, of the University of Maryland in College Park. “These drugs are often considered to be overprescribed, and new research has shown other risks tied to long-term use of proton pump inhibitors, such as an increased risk of dementia.”
For the study, researchers looked at data on 11,818 people who provided information on use of acid-reducing drugs and whether they had migraine or severe headache in the past three months.
A total of 25% of participants taking proton pump inhibitors had migraine or severe headache, compared to 19% of those who were not taking the drugs. A total of 25% of those taking H2 blockers had severe headache, compared to 20% of those who were not taking those drugs. And 22% of those taking antacid supplements had severe headache, compared to 20% of those not taking antacids.
When researchers adjusted for other factors that could affect the risk of migraine, such as age, sex and use of caffeine and alcohol, they found that people taking proton pump inhibitors were 70% more likely to have migraine than people not taking proton pump inhibitors. Those taking H2 blockers were 40% more likely and those taking antacid supplements were 30% more likely.
“It’s important to note that many people do need acid-reducing medications to manage acid reflux or other conditions, and people with migraine or severe headache who are taking these drugs or supplements should talk with their doctors about whether they should continue,” Slavin said.
Slavin noted that the study looked only at prescription drugs. Some of the drugs became available for over-the-counter use at non-prescription strength during the study period, but use of these over-the-counter drugs was not included in this study.
Other studies have shown that people with gastrointestinal conditions may be more likely to have migraine, but Slavin said that relationship is not likely to fully explain the tie between acid-reducing drugs and migraine found in the study.
A limitation of the study is that a small number of people were taking the drugs, especially the H2 blockers.
Dietary treatment is more effective than medications in irritable bowel syndrome (IBS), according to the results of a study conducted at the University of Gothenburg. With dietary adjustments, more than seven out of ten patients had significantly reduced symptoms.
Irritable bowel syndrome (IBS) is a common diagnosis that causes abdominal pain, gas and abdominal bloating, diarrhoea, and constipation, in various combinations and with varying degrees of severity.
Treatment often consists of dietary advice such as eating small and frequent meals and avoiding excessive intake of food triggers such as coffee, alcohol and fizzy drinks. Patients may also be given medications to improve specific symptoms, such as gas or constipation, diarrhoea, bloating or abdominal pain. Antidepressants are sometimes used to improve symptoms in IBS.
The current study, published in The Lancet Gastroenterology & Hepatology, compared three treatments: two dietary and one medication-based. The participants were adult patients with severe or moderate IBS symptoms at Sahlgrenska University Hospital in Gothenburg.
More symptom relief after dietary adjustment
The first group was given traditional IBS dietary advice, focusing on eating behaviour combined with low intake of fermentable carbohydrates (FODMAPs). These include products with lactose, legumes, onions, and grains, which ferment in the colon and can cause pain in IBS.
The second group received a dietary treatment low in carbohydrates and proportionally high in protein and fat. In the third group, the best possible medication was given based on the patient’s most troublesome IBS symptoms.
Each group included around 100 participants in four-week treatment periods. Treatment response was measure with an established IBS symptom scoring scale.
Of those who received traditional IBS dietary advice and low content of FODMAPs, 76% had significantly reduced symptoms. In the group receiving low carbohydrates and high protein and fat, the proportion was 71%, and in the medication group 58%.
All groups reported significantly better quality of life, less physical symptoms and less symptoms of anxiety and depression.
The importance of personalisation
At a six-month follow-up, when participants in the dietary groups had partially returned to their previous eating habits, a large proportion still had clinically significant symptom relief; 68% in the traditional dietary advice and low FODMAP group, and 60% in the low-carbohydrate diet group.
The study was led by Sanna Nybacka, Researcher and Dietician, Stine Störsrud, Associate Professor, and Magnus Simrén, Professor and Senior Consultant, all at Sahlgrenska Academy, University of Gothenburg.
“With this study, we can show that diet plays a central role in the treatment of IBS, but that there are several alternative treatments that are effective,” says Sanna Nybacka.
“We need more knowledge about how to best personalise the treatment of IBS in the future and we will further investigate whether there are certain factors that can predict whether individuals will respond better to different treatment options,” she concludes.
