In a nationwide Swedish study of more than 85 000 patients with biopsy-confirmed inflammatory bowel disease (IBD), researchers saw an increased risk of stroke, especially ischaemic stroke, compared to the general population. The results are published in Neurology.
IBD is a chronic intestinal disease with a relapsing-remitting manner, including Crohn’s disease (CD), ulcerative colitis (UC), and IBD-unclassified. Prior studies have suggested that IBD patients have a greater risk of thromboembolic events, but evidence for long-term risk of stroke remains scarce. A recent postmarketing safety study on tofacitinib, a new drug approved for IBD treatment, found an increased stroke risk.
The researchers, from Karolinska Institutet and Örebro University (Sweden), conducted a cohort study by linking a nationwide histopathology cohort (the ESPRESSO study) to national healthcare registers in Sweden to explore whether patients with a biopsy-confirmed IBD had an increased long-term risk of stroke compared to their IBD-free siblings or the general population.
During an average follow-up of 12 years, 3720 of IBD sufferers had a stroke (32.6/10 000 person years), compared with 15 599 of the IBD-free people (27.7/10 000 person-years). When accounting for other factors, such as heart disease, hypertension and obesity, they found that people with IBD were 13% more likely to have a stroke than those without IBD. The risk stayed elevated even 25 years after IBD diagnosis, equating to one additional stroke case per 93 IBD patients. The excess risk was mainly driven by ischaemic stroke rather than haemorrhagic stroke.
The risk for ischaemic stroke was significantly increased across all IBD subtypes (ie, CD, UC, and IBD-U). Sibling comparison analyses confirmed the main findings, suggesting the excess risk of stroke may be independent of familial factors.
Clinical implications
“Due to the excess risk of stroke in IBD patients, screening and management of traditional stroke risk factors in IBD patients could be more urgent to prevent fatal CVD complications”, says first author Jiangwei Sun, postdoc at the Department of Medical Epidemiology and Biostatistics.
“These findings highlight the need for clinical vigilance about the long-term excess risk of cerebrovascular events in IBD patients”, adds last author Jonas F Ludvigsson, professor at Karolinska Institutet and pediatrician at Örebro University Hospital.
Using parasites to treat disease may be the stuff of mediaeval medicinal horror stories, but for inflammatory bowel disease, it might actually be a worthwhile treatment. In a feasibility study published in Inflammatory Bowel Diseases, researchers from the Malaghan Institute found that hookworms were a safe and long-lasting treatment for participants with ulcerative colitis – paving the way for wider clinical studies.
For a number of years, Malaghan Institute researchers have been investigating therapeutic benefits of human hookworms for patients suffering allergic and inflammatory disease.
“This pilot study is the first controlled evidence in the use of hookworm as a therapy in ulcerative colitis,” says Malaghan Institute clinician and gastroenterologist Dr Tom Mules who led the study alongside Rutherford Clinic gastroenterologist Dr Stephen Inns. “Our study has shown this kind of therapy is well-tolerated, safe and feasible to take into a full-scale trial.”
In this pilot randomised controlled trial, patients currently in remission from ulcerative colitis were infected with a controlled dose of hookworm larvae or given placebo, and followed up over 12 months. Patients would provide regular feedback on any changes to their gut health or discomfort. Samples were collected throughout the year-long infection to test a range of scientific parameters such as gut inflammation, microbiome and immune cell composition.
“We deliberately chose to target patients with ulcerative colitis in remission,” says Dr Mules.
“We believe that the effect of hookworms may not be strong enough to push someone from an active disease state into disease remission. However, once someone is in remission hookworm could keep them there, prevent them from having disease flares and reduce the need to take medication, such as steroids, which suppresses the immune system and has adverse effects.”
Living in remission from an inflammatory disease typically means that patients experience less pain and discomfort associated with active disease. In order to stay in remission patients generally have to take daily medications to prevent flare ups. However, Dr.= Mules explains that there are significant barriers to taking daily medication, particularly when you do not have active symptoms to remind you to take pills morning and night. Importantly, not taking the medication increases the risk of having a flare. Disease flares impact quality of life, can lead to disease complications and need strong medications to bring under control.
“One of the key findings from this study was that a single dose of hookworm can reside in the body for several years, if not longer,” says Dr Mules. “This means that if hookworm is effective at preventing disease flares you can get infected and potentially no longer have to daily medicate. ‘Infect and forget’. The worms just sit there in the background and do their thing. I think that’s where the power of this therapy lies.”
The team needed to confirm safety before they could test their “infect and forget” theory in a full-scale trial.
“We did see that around the 6–8 week mark participants reported mild tummy symptoms, but those had all resolved by week 10–12,” says Dr Mules. “Otherwise, compared to the placebo group there was no significant differences in adverse events.
“The fact that these worms are well tolerated and safe to give to people with inflammatory disease is really important. One of the big safety questions was if the immune response triggered by the hookworm in the early stages of the infection could trigger a flare of ulcerative colitis. We did not see this, again highlighting that this therapy is safe in these patients.”
With no effective cure for severe inflammatory and allergic diseases the idea of using hookworms to manage harmful and aggressive symptoms is something many people have latched onto. There exists a thriving “underground” market of people self-medicating with hookworms, and significant anecdotal evidence indicating they are helpful in treating disease and managing symptoms, says Dr Mules.
“We know that people with inflammatory bowel disease, including ulcerative colitis, already use medically unsupervised hookworms to manage their symptoms and regain some semblance of quality of life, however the evidence needed to support this is lacking. The aim of this study was to provide some solid scientific groundwork, to hopefully one day make this a real, legitimate therapy to help people living with debilitating disease.”
The team now plans larger clinical trials and applying their findings to other diseases.
“The power of our study’s findings is that we can apply them to other diseases as well,” says Dr Mules. “We are in the process of deciding what the best disease target is. It could be ulcerative colitis but there are also early findings demonstrating hookworm therapy could be beneficial to a wide-range of autoimmune, allergic and metabolic diseases.
“We’re extremely grateful to the participants for taking part in this important study which will let us apply hookworm therapy where it will have the biggest impact.”
Gut Microbiome. Credit Darryl Leja National Human Genome Research Institute National Institutes Of Health
Diarrhoeal disease outbreaks are on the increase in South Africa owing to unsafe or unhygienic water sources, which is being compounded by the effects of loadshedding.1 Equally, the deadly floods that affected particularly the Eastern Cape and KwaZulu-Natal in April last year damaged an already ailing sewerage and water system, with millions of litres of untreated sewage spilling onto beaches, rivers, harbours and the ocean in and around Durban.2
This has resulted in an increased incidence of gastroenteritis, which is caused by intestinal infection owing to the contamination of food, water or hands.3 Acute-onset vomiting and diarrhoea is second only to respiratory illnesses as a cause of childhood deaths worldwide.3
Diarrhoea accounts for 19% of deaths of under-fives in South Africa and for 46% on the African continent.4 Acute diarrhoea has several risks and complications, and may lead to life-threatening dehydration and electrolyte disturbances.3 When diarrhoea is not halted, there is a risk of disturbed digestion and absorption of nutrients with nutritional deterioration.3
Guidelines published in the South African Medical Journal (SAMJ) state that acute diarrhoea is predominantly a problem of fluids and feeding – both being heavily dependent on the caregiver’s understanding and reactions.3
It is vital that healthcare practitioners and caregivers understand the ‘what’ and the ‘how’ of oral rehydration therapy (ORT) and re-feeding, and that they are given guidance on the need to seek further help in the event of the following:3
• Ongoing vomiting despite small fluid sips, especially if associated with abdominal distension or pain
• Persisting fever after 24 hours of ORT
• Increasing lethargy and failure to feed
• Deteriorating hydration and failure to pass urine
• Presence of blood in the stools
• Diarrhoea persisting for more than 1 week.
Momeena Omarjee, Consumer Healthcare Country Head: Scientific Affairs, at Sanofi South Africa, outlines an ambitious campaign by Sanofi in partnership with non-profit organisation (NPO), Save the Children, to impact over 2 000 000 lives by 2025, through education on hygiene and nutrition and improved access to water.
“Sanofi is committed to ensuring that no child dies of a preventable disease. Since October 2022, Sanofi has donated 15 water tanks and 14 hand-washing stations to Early Childhood Development centres in KwaZulu-Natal communities in need, to ensure access to clean, drinkable water. This will help to curb the prevalence of diarrhoea and diarrhoea-associated deaths in children under five, which are entirely avoidable,” says Omarjee.
“Children living in poverty-stricken environments are approximately 10 times more likely to die from diarrhoea than their more privileged counterparts.5 Providing adequate access to clean, drinkable water and quality early childcare and development will impact the lives and health of so many vulnerable children,” says Omarjee.
Several studies have shown that probiotics shorten the duration of diarrhoea and prevent recurrence of other episodes.6 Furthermore, probiotics can prevent diarrhoea from infection in infants with malnutrition.6
The World Gastroenterology Organisation states that oral administration of probiotics shortens the duration of acute diarrheal illness in children by approximately 1 day.7 There is also evidence of efficacy in adults or children who are receiving antibiotic therapy, for prevention of antibiotic-associated diarrhoea.7
“Healthcare professionals should encourage parents to give children a daily, regular probiotic, which could go a long way in preventing diarrhoea and illness,” concludes Omarjee.
Wittenberg, DF. 2012. Management guidelines for acute infective diarrhoea/gastroenteritis in infants. SAMJ, vol. 102, No. 2.
Awotione, O.F., et al. 2016. Systematic review: Diarrhoea in children under five years of age in South Africa (1997-2014). Tropical Medicine and International Health, 21(9), 1060-1070.
Chola, L., et al. 2015. Reducing diarrhoea deaths in South Africa: costs and effects of scaling up essential interventions to prevent and treat diarrhoea in under five children. BMC Public Health, 15, 394.
Solis, B. et al. 2002. Probiotics as a help in children suffering from malnutrition and diarrhoea. European Journal of Clinical Nutrition, 56, S57-59.
A new study published in the Journal of Toxicology and Environmental Health, Part B, found that a chemical formed during the digestion of widely used sweetener is “genotoxic,” meaning it breaks up DNA. The chemical is also found in trace amounts in the sweetener itself, and the finding raises questions about how the sweetener may contribute to health problems.
At issue is sucralose, a widely used artificial sweetener. Previous work by the same research team established that several fat-soluble compounds are produced in the gut after sucralose ingestion. One of these compounds is sucralose-6-acetate.
“Our new work establishes that sucralose-6-acetate is genotoxic,” says Susan Schiffman, corresponding author of the study and an adjunct professor at North Carolina State University. “We also found that trace amounts of sucralose-6-acetate can be found in off-the-shelf sucralose, even before it is consumed and metabolised.
“To put this in context, the European Food Safety Authority has a threshold of toxicological concern for all genotoxic substances of 0.15 micrograms per person per day,” Schiffman says. “Our work suggests that the trace amounts of sucralose-6-acetate in a single, daily sucralose-sweetened drink exceed that threshold. And that’s not even accounting for the amount of sucralose-6-acetate produced as metabolites after people consume sucralose.”
For the study, researchers conducted a series of in vitro experiments exposing human blood cells to sucralose-6-acetate and monitoring for markers of genotoxicity.
“In short, we found that sucralose-6-acetate is genotoxic, and that it effectively broke up DNA in cells that were exposed to the chemical,” Schiffman says.
The researchers also conducted in vitro tests that exposed human gut tissues to sucralose-6-acetate.
“Other studies have found that sucralose can adversely affect gut health, so we wanted to see what might be happening there,” Schiffman says. “When we exposed sucralose and sucralose-6-acetate to gut epithelial tissues – the tissue that lines your gut wall – we found that both chemicals cause ‘leaky gut.’ Basically, they make the wall of the gut more permeable. The chemicals damage the ‘tight junctions,’ or interfaces, where cells in the gut wall connect to each other.
“A leaky gut is problematic, because it means that things that would normally be flushed out of the body in feces are instead leaking out of the gut and being absorbed into the bloodstream.”
The researchers also looked at the genetic activity of the gut cells to see how they responded to the presence of sucralose-6-acetate.
“We found that gut cells exposed to sucralose-6-acetate had increased activity in genes related to oxidative stress, inflammation and carcinogenicity,” Schiffman says.
“This work raises a host of concerns about the potential health effects associated with sucralose and its metabolites. It’s time to revisit the safety and regulatory status of sucralose, because the evidence is mounting that it carries significant risks. If nothing else, I encourage people to avoid products containing sucralose. It’s something you should not be eating.”
Karolinska Institutet researchers have found that the risk of developing lymphoma is slightly elevated in inflammatory bowel disease (IBD) and, in recent years has been on the rise in patients with Crohn’s disease. Publishing in Clinical Gastroenterology and Hepatology, the researchers also observed a risk increase in patients taking modern IBD drugs, which was less strong for those not taking them. Thus, the lymphoma risk could be affected by both the medication and the disease activity itself.
Inflammatory bowel disease (IBD), which includes Crohn’s disease and ulcerative colitis, is a chronic intestinal inflammation that can increase the risk of developing lymph node cancer (lymphoma), a disease that affects the immune system.
“Previous studies of the lymphoma risk of IBD have been too small to draw reliable conclusions,” says the study’s first author Ola Olén, consultant and docent at the Department of Medicine (Solna), Karolinska Institutet. “The studies have not taken into account of important systematic errors or been representative of today’s IBD patients.”
The present study included almost 170 000 IBD patients identified in Swedish and Danish national registries between 1969 and 2019. Compared to patients with a matched population without IBD, patients with both Crohn’s disease and ulcerative colitis had a higher risk of lymphoma. The highest risk was in patients with Crohn’s disease, the increase being driven mainly by T-cell lymphoma and aggressive B-cell lymphoma.
“We found an elevated relative risk of different types of lymphoma in both Crohn’s disease and ulcerative colitis, but we need to point out that the absolute risk is very low,” says the study’s last author Jonas F Ludvigsson, consultant and professor at Karolinska Institutet.
“The increase in risk equates to only one extra case of lymphoma in 1000 people with IBD, who were followed for ten years.”
“Both inflammation and treatment play a part”
The risk of lymphoma has increased in patients with Crohn’s disease over the past two decades, which coincides with the increasing use of immunomodulating drugs for IBD. While the highest risk of developing the cancer was observed in patients who had received these drugs, the researchers found that patients who were not on such medication were also at a higher risk of lymphoma.
“This finding indicates that both the inflammation in itself and its treatment play a part,” says Dr Olén. “Since there’s a lot of talk about the lymphoma risk associated with immunomodulating drugs, it’s important to make it clear that also the disease and the inflammation per se seem to drive the development of lymphoma. One has to take account of this and discuss it when prescribing modern treatments where there might be a concern that they will increase the risk of lymphoma.”
Dr Olén says the teamaims to use more detailed data to determine whether the disease itself or its treatment is more important in terms of lymphoma risk.
There is a great deal of variation in the anatomy of the gastrointestinal system, with pronounced differences possible between healthy individuals, according to surprising new research published in PeerJ. Differences between males and females were also uncovered.
The finding has implications for understanding the role that the digestive tract’s anatomy can play in affecting human health, as well as providing potential insights into medical diagnoses and the microbial ecosystem of the gut.
“There was research more than a century ago that found variability in the relative lengths of human intestines, but this area has largely been ignored since then,” says Amanda Hale, study co-first author and a PhD candidate at North Carolina State University. “When we began exploring this issue, we were astonished at the extent of the variability we found.”
“If you’re talking to four different people, odds are good that all of them have different guts, in terms of the relative sizes of the organs that make up that system,” says Erin McKenney, corresponding author and an assistant professor of applied ecology at NC State. “For example, the cecum is an organ that’s found at the nexus of the large and small intestine. One person may have a cecum that is only a few centimeters long, while another may have a cecum the size of a coin purse. And we found similar variability for many digestive organs.”
In another striking example, the researchers found that women tend to have longer small intestines than men.
“Because having a longer small intestine helps you extract nutrients from your diet, this finding supports the canalisation hypothesis, which posits that women are better able to survive during periods of stress,” says Hale.
“Given that there is more variation in human gut anatomy than we thought, this could inform our understanding of what is driving a range of health-related issues and how we treat them,” says McKenney. “Basically, now that we know this variability exists, it raises a number of research questions that need to be explored.”
For this study, the researchers measured the digestive organs of 45 people who donated their remains to the Anatomical Gifts Program at the Duke University School of Medicine.
In addition to shedding light on the unexpected variability in human anatomy, this project also led to rediscovering the importance of teaching anatomical variation to medical students.
“It’s particularly important in medical training, because if students are only learning about a ‘normal’ or ‘average’ anatomy, that means they are not going to be familiar with the scope of human variation,” says Roxanne Larsen, co-author of the paper and an associate professor of veterinary and biomedical sciences at the University of Minnesota. “It’s increasingly clear that the medical field is moving toward individualized medicine to improve patient outcomes and overall health and well-being. Garnering experience in understanding anatomical variation can play a critical role in helping future doctors understand the importance of individualised medicine.”
“We’re excited about this discovery and future directions for the work,” McKenney says. “It underscores just how little we know about our own bodies.”
Certain gut microorganisms are thought to contribute to the development of inflammatory conditions such as inflammatory bowel disease (IBD), but the sequence of events leading from microbes to immune cells to disease remains elusive. A new study published in Immunity explores exactly what leads to the generation of Th17 cells, an important subtype of cells in the intestine, and uncovers some of the underappreciated molecular players and events that lead to cell differentiation in the gut. One of those players is the purine metabolite xanthine – high levels of which are found in caffeinated foods such as coffee, tea and chocolate.
“One of the concepts in our field is that microbes are required for Th17 cell differentiation, but our study suggests that there may be exceptions,” said co-lead auhor Jinzhi Duan, PhD, of the Division of Gastroenterology, Hepatology and Endoscopy in the Department of Medicine at Brigham and Women’s Hospital,. “We studied the underlying mechanisms of Th17 cell generation in the gut and found some surprising results that may help us to better understand how and why diseases like IBD may develop.”
While illuminating the steps leading to Th17 cell differentiation, the researchers unexpectedly discovered a role for xanthine in the gut.
“Sometimes in research, we make these serendipitous discoveries – it’s not necessarily something you sought out, but it’s an interesting finding that opens up further areas of inquiry,” said senior author Richard Blumberg, MD, of the Division of Gastroenterology, Hepatology and Endoscopy in the Department of Medicine. “It’s too soon to speculate on whether the amount of xanthine in a cup of coffee leads to helpful or harmful effects in a person’s gut, but it gives us interesting leads to follow up on as we pursue ways to generate a protective response and stronger barrier in the intestine.”
Interleukin-17-producing T helper (Th17) cells are thought to play a key role in the intestine. The cells can help to build a protective barrier in the gut, and when a bacterial or fungal infection occurs, these cells may release signals that cause the body to produce more Th17 cells. But the cells have also been implicated in diseases such as multiple sclerosis, rheumatoid arthritis, psoriasis, and IBD.
Duan, co-lead author Juan Matute, MD, Blumberg and colleagues used several mouse models to study the molecular events that lead to the development of Th17 cells. Surprisingly, they found that Th17 cells could proliferate even in germ-free mice or mice that had been giving antibiotics wiping out bacteria. The team found that endoplasmic reticulum stress in intestinal epithelial cells drove Th17 cell differentiation through purine metabolites, such as xanthine, even in mice that did not carry microbes and with genetic signatures that suggested cells with protective properties.
The authors note that their study was limited to cells in the intestine. It’s possible that crosstalk between cells in the gut and other organs, such as the skin and lung, may have an important influence on outcomes. They also note that their study does not identify what causes Th17 cells to become pathogenic, and that further exploration is needed, including studies that focus on human-IBD Th17 cells.
“While we don’t yet know what’s causing pathogenesis, the tools we have developed here may take us a step closer to understanding what causes disease and what could help resolve or prevent it,” said Blumberg.
Scientists have discovered that a high-fat diet might actually have a benefit in some cases: it allows the immune system to eliminate a parasitic worm which is a major cause of death and illness in the developing world. Their findings appear in the journal Mucosal Immunology.
Parasitic worms affect up to a billion people, particularly in developing nations with poor sanitation. One of these parasites known as “whipworm” can cause long lasting infections in the large intestine.
Lead author Dr Evelyn Funjika, formerly at Manchester and now at the University of Zambia, said: “Just like the UK, the cheapest diets are often high in fat and at-risk communities to whipworm are increasingly utilising these cheap diets. Therefore, how worm infection and western diets interact is a key unknown for developing nations.
“In order to be able to study how nutrition affects parasite worm infection, we have been using a mouse model, Trichuris muris, closely related to the human whipworm Trichuris trichiura and seeing how a high-fat diet impacts immunity.”
It has been previously shown that immune responses which expel the parasite rely on white blood cells called T-helper 2 cells, specialised for eliminating gastrointestinal parasites.
The findings demonstrate how a high-fat diet, rather than obesity itself, increases a molecule on T-helper cells called ST2 and this allows an increased T-helper 2 response which expels the parasite from the large intestinal lining.
Dr John Worthington from the Department of Biomedical and Life Science at Lancaster University co-led the research.
“We were quite surprised by what we found during this study. High-fat diets are mostly associated with increased pathology during disease. However, in the case of whipworm infection this high fat diet licenses the T-helper cells to make the correct immune response to expel the worm.”
Co-lead Professor Richard Grencis from the University of Manchester said: “Our studies in mice on a standard diet demonstrate that ST2 is not normally triggered when expelling the parasite, but the high-fat diet boosts the levels of ST2 and hence allows expulsion via an alternative pathway.”
Co-lead Professor David Thornton from the University of Manchester added: “It was really fascinating that simply altering the diet completely switched the immune response in the gut from one that fails to expel the parasite, to one that brings about all the correct mechanisms to eliminate it.”
However, Dr Worthington added caution to the findings.
“Before you order that extra take-away, we have previously published that weight loss can aid the expulsion of a different gut parasite worm. So these results may be context specific, but what is really exciting is the demonstration of how diet can profoundly alter the capacity to generate protective immunity and this may give us new clues for treatments for the millions who suffer from intestinal parasitic infections worldwide.”
People with irritable bowel syndrome (IBS) have lower bacterial diversity in the intestine than do healthy people, according to research appearing in Microbiology Spectrum. The investigators believe that theirs is the first analysis to find a clear association between IBS and reduced diversity in the microbiota of the gut. The an open-access journal of the American Society for Microbiology.
Normally, “More than 10 000 species of microorganism live in the human intestine,” said corresponding author Jung Ok Shim, MD, PhD, a professor at Korea University College of Medicine. Disruption of the microbiome of the human gastrointestinal tract can trigger IBS. Typically, IBS causes bloating, diarrhoea, and stomach pain or cramps.
Previous studies of gut bacteria in patients with IBS have been controversial, with inconsistent results, due to small sample size and lack of consistent analytical methods used among these studies, said Shim. The investigators combined their own dataset with 9 published, shared datasets, encompassing 576 IBS patients and 487 healthy controls, analysing them with a “unified data processing and analytical method.”
The researchers found that the gut bacterial community is less diverse in IBS patients than in healthy people, said Shim. Additionally, the abundance of 21 bacterial species differed between IBS patients and healthy controls. However, the findings were not statistically significant in the paediatric cohort due to small sample size.
The investigators proved that the disturbed gut bacterial community “is associated with IBS, though this does not mean that the relationship is causal,” said Shim. “Functional studies are needed to prove whether the change in gut micro-organisms contributes to development of IBS.”
Even though IBS is a common disorder, its pathogenesis remains unknown, and as yet there is no effective treatment strategy. “Based on the epidemiological studies of IBS patients, altered gut microbiota was proposed as one of the possible causes of IBS,” the researchers write. “Acute bacterial gastroenteritis can cause chronic, asymptomatic, low-grade intestinal wall inflammation sufficient to alter neuromuscular and epithelial cell function.”
Using a wearable device to record nerve activity, researchers in Japan have discovered that the sympathetic nervous system of patients with irritable bowel syndrome (IBS) activated a few minutes before defecation, and persisted for a few minutes afterwards. Their results are published in the journal PLoS ONE.
Irritable bowel syndrome (IBS) is a difficult disease to treat, characterised by chronic abdominal pain related to bowel movements, of which there are four types: diarrhoeal, constipation, mixed, and unclassifiable. Patients with IBS report a reduction in quality of life and experiences of social discomfort, as they are forced to restrict their activity, such as work or travel, because of the sudden and unpredictable need to use the toilet. While there have been studies of IBS-related abnormalities in the autonomic nervous system based on 24-hour electrocardiogram measurement, until now none of them examined changes in the autonomic nervous system during bowel movements.
Associate Professor Fumio Tanaka and his research group at the Osaka Metropolitan University Graduate School of Medicine recorded the autonomic nervous system activity of IBS patients and healthy subjects using a wearable device and tracked activities such as defecation and sleep. As a result, they found that unlike healthy subjects, the sympathetic nervous system of IBS patients was activated two minutes before defecation and persisted until 9 minutes after defecation. Furthermore, the activation of the sympathetic nervous system was found to be associated with greater abdominal pain and lower quality of life.
“This research is characterised by the fact that autonomic nervous system functions are measured using a clothing-type wearable device, and that lifestyle events such as defecation and abdominal symptoms are input simultaneously in real time, using a smartphone application originally developed by our group. As a result, autonomic nervous system activity during defecation was accurately evaluated. We hope that further research will improve the quality of life of IBS patients and help elucidate the pathophysiology,” Professor Tanaka concluded.
