IBD & Intestinal Disorders

An increase of patients presenting with the complex combination of hypermobile Ehlers-Danlos syndrome (hEDS) with co-existing gastrointestinal (GI) symptoms, postural orthostatic tachycardia syndrome (POTS), and/or mast cell activation syndrome (MCAS), has prompted the issuance of clinical practice guidance from AGA to help clinicians comprehend such cases.

“Recognizing and treating GI symptoms in patients with hEDS or hypermobility spectrum disorders and comorbid POTS or MCAS present major challenges for clinicians, who often feel under equipped to address their needs,” AGA reported in the update, published in Clinical Gastroenterology and Hepatology.

Importantly, “the poor understanding of these overlapping syndromes can lead to nonstandardized approaches to diagnostic evaluation and management,” the authors noted.

“Gastroenterology providers should be aware of the features of [these syndromes] to recognize the full complexity of patients presenting with multisystemic symptoms.”

Hypermobility spectrum disorders, which include hEDS, are typically genetic, and patients experience pain along with joint hypermobility, or extreme flexibility of joints beyond the normal range of motion.

With research showing that most of those patients — up to 98% — also experience GI symptoms, gastroenterologists may be encountering them more commonly than realized, Lucinda A. Harris, MD, AGAF, of the Mayo Clinic School of Medicine, in Scottsdale, Arizona, explained to GI & Hepatology News.

“As our knowledge in gastroenterology has progressed, we realize that hypermobility itself predisposes individuals to disorders of brain-gut interaction,” she said. “We may only be seeing the tip of the iceberg when it comes to diagnosing patients with hypermobility.”

Additionally, “many of these patients have POTS, which has also been increasingly diagnosed,” Harris added. “The strong overlap of these conditions prompted us to present this data.”

With a lack of evidence-based understanding of the overlapping syndromes, AGA’s guidance does not carry formal ratings but is drawn from a review of the published literature and expert opinion.

In addition to the key recommendation of being aware of the observed combination of syndromes, their recommendations include:

• Regarding testing: Testing for POTS/MCAS should be targeted to patients presenting with clinical manifestations of the disorders, but universal testing for POTS/MCAS in all patients with hEDS or hypermobility spectrum disorders is not currently supported by the evidence, the guidance advises.
• Gastroenterologists seeing patients with disorders of gut-brain interaction should inquire about joint hypermobility and strongly consider incorporating the Beighton score for assessing joint hypermobility into their practice as a screening tool; if the screen is positive, gastroenterologists may consider applying 2017 diagnostic criteria to diagnose hEDS or offer appropriate referral to a specialist where resources are available, the AGA recommends.
• Medical management: Management of GI symptoms in hEDS or hypermobility spectrum disorders and POTS/MCAS should focus on treating the most prominent GI symptoms and abnormal GI function test results.
• In addition to general disorders of gut-brain interactions and GI motility disorder treatment, management should also include treating any symptoms attributable to POTS and/or MCAS.

Treatment of POTS may include increasing fluid and salt intake, exercise training, and use of compression garments. Special pharmacological treatments for volume expansion, heart rate control, and vasoconstriction with integrated care from multiple specialties (eg, cardiology, neurology) should be considered in patients who do not respond to conservative lifestyle measures.

In patients presenting to gastroenterology providers, testing for mast cell disorders including MCAS should be considered in patients with hEDS or hypermobility spectrum disorders and disorders of gut-brain interaction with episodic symptoms that suggest a more generalized mast cell disorder involving two or more physiological systems. However, current data does not support the use of these tests for routine evaluation of GI symptoms in all patients with hEDS or hypermobility spectrum disorders without clinical or laboratory evidence of a primary or secondary mast cell disorder, the authors noted.

Harris explained that patients presenting with gut-brain disorders are often mistakenly classified as having irritable bowel syndrome or dyspepsia, whereas these conditions may be affecting the GI disorders they have.

“For example, a patient with Ehlers-Danlos syndrome might have problems with constipation, which is impacted by pelvic floor dysfunction,” she said. “Due to their hypermobility, they may experience more pelvic floor descent than usual.”

“If we do not recognize this, the patient risks developing rectal prolapse or not effectively addressing their constipation.”

Regarding patient characteristics, Harris said that those with hEDS and POTS appear to more likely be women and tend to present in younger patients, aged 18-50 years. Of note, there is no genetic test for hEDS.

“The take-home point for clinicians should be to consider POTS and Ehlers-Danlos syndrome when encountering young female patients with symptoms of palpitations, hypermobility, and orthostatic intolerance,” she said.

“Recognizing hypermobility is crucial, not only for GI symptoms but also to prevent joint dislocations, tendon ruptures, and other connective tissue issues.”

Clinicians are further urged to “offer informed counseling, and guide patients away from unreliable sources or fragmented care to foster therapeutic relationships and evidence-based care,” the authors added.

 

Deciphering Gut-Brain Disorder Challenges

Commenting to GI & Hepatology News, Clair Francomano, MD, a professor of medical and molecular genetics at the Indiana University School of Medicine, in Indianapolis, said the new guidance sheds important light on the syndromes.

“I’m delighted to see this guidance offered through the AGA as it will encourage gastroenterologists to think of EDS, POTS and MCAS when they are evaluating patients with disorders of gut-brain interaction,” Francomano said.

“This should allow patients to receive more accurate and timely diagnoses and appropriate management.”

Francomano noted that the Ehlers-Danlos Society, which provides information for clinicians and patients alike on the syndromes, and where she serves on the medical scientific board, has also been active in raising awareness.

“While co-occurrence of POTS and MCAS with EDS has in fact been recognized for many years, I do think awareness is increasing, in large part due to the advocacy and educational efforts of the Ehlers-Danlos Society,” she said.

The take-home message? “When clinicians see disorders of the gut-brain axis, POTS or MCAS, they should be thinking, ‘Could this be related to joint hypermobility or Ehlers-Danlos syndrome?’” Francomano said.

Harris reported serving as a consultant for AbbVie, Ardelyx, Salix, and Gemelli Biotech and reported receiving research support from Takeda and Anyx. Francomano did not report any relevant disclosures.

A version of this article appeared on Medscape.com.

An increase of patients presenting with the complex combination of hypermobile Ehlers-Danlos syndrome (hEDS) with co-existing gastrointestinal (GI) symptoms, postural orthostatic tachycardia syndrome (POTS), and/or mast cell activation syndrome (MCAS), has prompted the issuance of clinical practice guidance from AGA to help clinicians comprehend such cases.

“Recognizing and treating GI symptoms in patients with hEDS or hypermobility spectrum disorders and comorbid POTS or MCAS present major challenges for clinicians, who often feel under equipped to address their needs,” AGA reported in the update, published in Clinical Gastroenterology and Hepatology.

Importantly, “the poor understanding of these overlapping syndromes can lead to nonstandardized approaches to diagnostic evaluation and management,” the authors noted.

“Gastroenterology providers should be aware of the features of [these syndromes] to recognize the full complexity of patients presenting with multisystemic symptoms.”

Hypermobility spectrum disorders, which include hEDS, are typically genetic, and patients experience pain along with joint hypermobility, or extreme flexibility of joints beyond the normal range of motion.

With research showing that most of those patients — up to 98% — also experience GI symptoms, gastroenterologists may be encountering them more commonly than realized, Lucinda A. Harris, MD, AGAF, of the Mayo Clinic School of Medicine, in Scottsdale, Arizona, explained to GI & Hepatology News.

“As our knowledge in gastroenterology has progressed, we realize that hypermobility itself predisposes individuals to disorders of brain-gut interaction,” she said. “We may only be seeing the tip of the iceberg when it comes to diagnosing patients with hypermobility.”

Additionally, “many of these patients have POTS, which has also been increasingly diagnosed,” Harris added. “The strong overlap of these conditions prompted us to present this data.”

With a lack of evidence-based understanding of the overlapping syndromes, AGA’s guidance does not carry formal ratings but is drawn from a review of the published literature and expert opinion.

In addition to the key recommendation of being aware of the observed combination of syndromes, their recommendations include:

• Regarding testing: Testing for POTS/MCAS should be targeted to patients presenting with clinical manifestations of the disorders, but universal testing for POTS/MCAS in all patients with hEDS or hypermobility spectrum disorders is not currently supported by the evidence, the guidance advises.
• Gastroenterologists seeing patients with disorders of gut-brain interaction should inquire about joint hypermobility and strongly consider incorporating the Beighton score for assessing joint hypermobility into their practice as a screening tool; if the screen is positive, gastroenterologists may consider applying 2017 diagnostic criteria to diagnose hEDS or offer appropriate referral to a specialist where resources are available, the AGA recommends.
• Medical management: Management of GI symptoms in hEDS or hypermobility spectrum disorders and POTS/MCAS should focus on treating the most prominent GI symptoms and abnormal GI function test results.
• In addition to general disorders of gut-brain interactions and GI motility disorder treatment, management should also include treating any symptoms attributable to POTS and/or MCAS.

Treatment of POTS may include increasing fluid and salt intake, exercise training, and use of compression garments. Special pharmacological treatments for volume expansion, heart rate control, and vasoconstriction with integrated care from multiple specialties (eg, cardiology, neurology) should be considered in patients who do not respond to conservative lifestyle measures.

In patients presenting to gastroenterology providers, testing for mast cell disorders including MCAS should be considered in patients with hEDS or hypermobility spectrum disorders and disorders of gut-brain interaction with episodic symptoms that suggest a more generalized mast cell disorder involving two or more physiological systems. However, current data does not support the use of these tests for routine evaluation of GI symptoms in all patients with hEDS or hypermobility spectrum disorders without clinical or laboratory evidence of a primary or secondary mast cell disorder, the authors noted.

Harris explained that patients presenting with gut-brain disorders are often mistakenly classified as having irritable bowel syndrome or dyspepsia, whereas these conditions may be affecting the GI disorders they have.

“For example, a patient with Ehlers-Danlos syndrome might have problems with constipation, which is impacted by pelvic floor dysfunction,” she said. “Due to their hypermobility, they may experience more pelvic floor descent than usual.”

“If we do not recognize this, the patient risks developing rectal prolapse or not effectively addressing their constipation.”

Regarding patient characteristics, Harris said that those with hEDS and POTS appear to more likely be women and tend to present in younger patients, aged 18-50 years. Of note, there is no genetic test for hEDS.

“The take-home point for clinicians should be to consider POTS and Ehlers-Danlos syndrome when encountering young female patients with symptoms of palpitations, hypermobility, and orthostatic intolerance,” she said.

“Recognizing hypermobility is crucial, not only for GI symptoms but also to prevent joint dislocations, tendon ruptures, and other connective tissue issues.”

Clinicians are further urged to “offer informed counseling, and guide patients away from unreliable sources or fragmented care to foster therapeutic relationships and evidence-based care,” the authors added.

 

Deciphering Gut-Brain Disorder Challenges

Commenting to GI & Hepatology News, Clair Francomano, MD, a professor of medical and molecular genetics at the Indiana University School of Medicine, in Indianapolis, said the new guidance sheds important light on the syndromes.

“I’m delighted to see this guidance offered through the AGA as it will encourage gastroenterologists to think of EDS, POTS and MCAS when they are evaluating patients with disorders of gut-brain interaction,” Francomano said.

“This should allow patients to receive more accurate and timely diagnoses and appropriate management.”

Francomano noted that the Ehlers-Danlos Society, which provides information for clinicians and patients alike on the syndromes, and where she serves on the medical scientific board, has also been active in raising awareness.

“While co-occurrence of POTS and MCAS with EDS has in fact been recognized for many years, I do think awareness is increasing, in large part due to the advocacy and educational efforts of the Ehlers-Danlos Society,” she said.

The take-home message? “When clinicians see disorders of the gut-brain axis, POTS or MCAS, they should be thinking, ‘Could this be related to joint hypermobility or Ehlers-Danlos syndrome?’” Francomano said.

Harris reported serving as a consultant for AbbVie, Ardelyx, Salix, and Gemelli Biotech and reported receiving research support from Takeda and Anyx. Francomano did not report any relevant disclosures.

A version of this article appeared on Medscape.com.

An increase of patients presenting with the complex combination of hypermobile Ehlers-Danlos syndrome (hEDS) with co-existing gastrointestinal (GI) symptoms, postural orthostatic tachycardia syndrome (POTS), and/or mast cell activation syndrome (MCAS), has prompted the issuance of clinical practice guidance from AGA to help clinicians comprehend such cases.

“Recognizing and treating GI symptoms in patients with hEDS or hypermobility spectrum disorders and comorbid POTS or MCAS present major challenges for clinicians, who often feel under equipped to address their needs,” AGA reported in the update, published in Clinical Gastroenterology and Hepatology.

Importantly, “the poor understanding of these overlapping syndromes can lead to nonstandardized approaches to diagnostic evaluation and management,” the authors noted.

“Gastroenterology providers should be aware of the features of [these syndromes] to recognize the full complexity of patients presenting with multisystemic symptoms.”

Hypermobility spectrum disorders, which include hEDS, are typically genetic, and patients experience pain along with joint hypermobility, or extreme flexibility of joints beyond the normal range of motion.

With research showing that most of those patients — up to 98% — also experience GI symptoms, gastroenterologists may be encountering them more commonly than realized, Lucinda A. Harris, MD, AGAF, of the Mayo Clinic School of Medicine, in Scottsdale, Arizona, explained to GI & Hepatology News.

“As our knowledge in gastroenterology has progressed, we realize that hypermobility itself predisposes individuals to disorders of brain-gut interaction,” she said. “We may only be seeing the tip of the iceberg when it comes to diagnosing patients with hypermobility.”

Additionally, “many of these patients have POTS, which has also been increasingly diagnosed,” Harris added. “The strong overlap of these conditions prompted us to present this data.”

With a lack of evidence-based understanding of the overlapping syndromes, AGA’s guidance does not carry formal ratings but is drawn from a review of the published literature and expert opinion.

In addition to the key recommendation of being aware of the observed combination of syndromes, their recommendations include:

• Regarding testing: Testing for POTS/MCAS should be targeted to patients presenting with clinical manifestations of the disorders, but universal testing for POTS/MCAS in all patients with hEDS or hypermobility spectrum disorders is not currently supported by the evidence, the guidance advises.
• Gastroenterologists seeing patients with disorders of gut-brain interaction should inquire about joint hypermobility and strongly consider incorporating the Beighton score for assessing joint hypermobility into their practice as a screening tool; if the screen is positive, gastroenterologists may consider applying 2017 diagnostic criteria to diagnose hEDS or offer appropriate referral to a specialist where resources are available, the AGA recommends.
• Medical management: Management of GI symptoms in hEDS or hypermobility spectrum disorders and POTS/MCAS should focus on treating the most prominent GI symptoms and abnormal GI function test results.
• In addition to general disorders of gut-brain interactions and GI motility disorder treatment, management should also include treating any symptoms attributable to POTS and/or MCAS.

Treatment of POTS may include increasing fluid and salt intake, exercise training, and use of compression garments. Special pharmacological treatments for volume expansion, heart rate control, and vasoconstriction with integrated care from multiple specialties (eg, cardiology, neurology) should be considered in patients who do not respond to conservative lifestyle measures.

In patients presenting to gastroenterology providers, testing for mast cell disorders including MCAS should be considered in patients with hEDS or hypermobility spectrum disorders and disorders of gut-brain interaction with episodic symptoms that suggest a more generalized mast cell disorder involving two or more physiological systems. However, current data does not support the use of these tests for routine evaluation of GI symptoms in all patients with hEDS or hypermobility spectrum disorders without clinical or laboratory evidence of a primary or secondary mast cell disorder, the authors noted.

Harris explained that patients presenting with gut-brain disorders are often mistakenly classified as having irritable bowel syndrome or dyspepsia, whereas these conditions may be affecting the GI disorders they have.

“For example, a patient with Ehlers-Danlos syndrome might have problems with constipation, which is impacted by pelvic floor dysfunction,” she said. “Due to their hypermobility, they may experience more pelvic floor descent than usual.”

“If we do not recognize this, the patient risks developing rectal prolapse or not effectively addressing their constipation.”

Regarding patient characteristics, Harris said that those with hEDS and POTS appear to more likely be women and tend to present in younger patients, aged 18-50 years. Of note, there is no genetic test for hEDS.

“The take-home point for clinicians should be to consider POTS and Ehlers-Danlos syndrome when encountering young female patients with symptoms of palpitations, hypermobility, and orthostatic intolerance,” she said.

“Recognizing hypermobility is crucial, not only for GI symptoms but also to prevent joint dislocations, tendon ruptures, and other connective tissue issues.”

Clinicians are further urged to “offer informed counseling, and guide patients away from unreliable sources or fragmented care to foster therapeutic relationships and evidence-based care,” the authors added.

 

Deciphering Gut-Brain Disorder Challenges

Commenting to GI & Hepatology News, Clair Francomano, MD, a professor of medical and molecular genetics at the Indiana University School of Medicine, in Indianapolis, said the new guidance sheds important light on the syndromes.

“I’m delighted to see this guidance offered through the AGA as it will encourage gastroenterologists to think of EDS, POTS and MCAS when they are evaluating patients with disorders of gut-brain interaction,” Francomano said.

“This should allow patients to receive more accurate and timely diagnoses and appropriate management.”

Francomano noted that the Ehlers-Danlos Society, which provides information for clinicians and patients alike on the syndromes, and where she serves on the medical scientific board, has also been active in raising awareness.

“While co-occurrence of POTS and MCAS with EDS has in fact been recognized for many years, I do think awareness is increasing, in large part due to the advocacy and educational efforts of the Ehlers-Danlos Society,” she said.

The take-home message? “When clinicians see disorders of the gut-brain axis, POTS or MCAS, they should be thinking, ‘Could this be related to joint hypermobility or Ehlers-Danlos syndrome?’” Francomano said.

Harris reported serving as a consultant for AbbVie, Ardelyx, Salix, and Gemelli Biotech and reported receiving research support from Takeda and Anyx. Francomano did not report any relevant disclosures.

A version of this article appeared on Medscape.com.

Diets high in packaged breads, cookies, and other highly processed grain products may raise the risk for inflammatory bowel disease (IBD), while minimally processed grain products may offer some protection, a large study has found.

The sweeping analysis of 124,590 adults from 21 countries found that those eating at least 19 g of ultraprocessed grains a day were about twice as likely to be diagnosed with IBD as peers eating less than 9 g daily.

“Our study adds robust evidence from a large, diverse global cohort that frequent consumption of ultraprocessed grains is associated with an increased risk of developing inflammatory bowel disease,” Neeraj Narula, MD, MPH, gastroenterologist and associate professor of medicine, McMaster University, Hamilton, Ontario, Canada, told GI & Hepatology News.

The study also “further clarifies that not all grains carry risk — minimally processed grains like fresh bread and rice were associated with lower risk even. These results build on and specify previous findings linking ultraprocessed foods more broadly to IBD,” Narula said.

The study was published in The American Journal of Gastroenterology.

 

Diet Matters to IBD Risk

According to the latest US data (2021-2023), ultraprocessed foods made up 62% of daily calories for young people and 53% for adults in 2021-2023.

The Prospective Urban Rural Epidemiology (PURE) study has followed participants aged 35-70 years for a median of nearly 13 years. At enrollment, volunteers completed country-specific food-frequency questionnaires, enabling researchers to quantify usual intake of more than 130 food items and track new cases of IBD reported at biennial follow-ups.

The researchers classified packaged breads, sweet breakfast cereals, crackers, pastries and ready-to-heat pizza or pasta as ultraprocessed grains because they are refined and typically contain additives such as emulsifiers and preservatives. Fresh bakery bread and plain rice were analyzed separately as minimally processed grain references.

During a median of 12.9 years, 605 participants developed IBD; 497 developed ulcerative colitis (UC) and 108 developed Crohn’s disease. 

Increased intake of ultraprocessed grains was associated with a higher risk for IBD, with hazard ratios (HR) of 2.08 for intake of ≥ 50 g/d and 1.37 for 19-50 g/d compared to intake of < 19 g/d. The increased risk was largely driven by a significantly increased risk for UC (HR, 2.46) and not Crohn’s disease (HR, 0.98).

Among the different ultraprocessed grain products, packaged bread stood out: Consuming ≥ 30 g/d of packaged bread (a little more than one slice) was associated with a greater than twofold increased risk for IBD (HR, 2.11) compared to no intake of packaged bread.

In contrast, greater consumption of fresh bread was associated with a reduced risk of developing IBD (HR, 0.61 for ≥ 65 g/d and 0.45 for 16-65 g/d compared to < 16 g/d).

Increased intake of rice was also associated with a lower risk of developing IBD (HR, 0.63 for ≥ 1 serving/d and 0.99 for < 1 serving/d).

When the researchers widened the lens to all ultraprocessed foods — from sodas to salty snacks — the risk for IBD climbed further.

Participants eating at least five servings a day had nearly a fourfold greater odds of IBD than those eating fewer than one serving (HR, 3.95) — a finding consistent with other data from the PURE study cohort.

 

What to Tell Patients?

The authors acknowledged in their paper that it’s difficult — if not impossible — to completely avoid ultraprocessed food in the Western diet.

They said their findings support “public health strategies to promote consumption of whole and minimally processed foods while reducing the consumption of highly processed alternatives.”

“I tell my patients that emerging literature shows an association between ultraprocessed food intake and IBD risk, but it’s not yet clear whether simply cutting out those foods will improve disease activity once IBD is established,” Narula told GI & Hepatology News.

“However, I still encourage patients to reduce ultraprocessed foods and to follow a Mediterranean-style diet — focusing on minimally processed grains, fruits, vegetables, healthy fats, and lean proteins — to support overall gut and general health,” Narula said.

Reached for comment, Ashwin Ananthakrishnan, MD, MPH, AGAF, associate professor of medicine, Massachusetts General Hospital, Boston, who wasn’t part of the study, said it “adds incrementally to the growing data on how ultraprocessed foods may affect the risk of IBD.”

“They (and others) have previously shown a link between general ultraprocessed food consumption and risk of IBD. Others have shown that some of this is mediated through refined grains. This study more specifically studies that question and demonstrates an association,” said Ananthkrishnan.

“This should not be used, however, to counsel patients. It does not study the impact of grain intake on patients with IBD. It may help inform population level preventive strategies (or in high-risk individuals) but requires more confirmation since there is significant heterogeneity between the various countries in this cohort. Countries that have high refined grain intake are also enriched in several other IBD risk factors (including genetics),” Ananthkrishnan told GI & Hepatology News.

The PURE study is an investigator-initiated study funded by the Population Health Research Institute, Hamilton Health Sciences Research Institute, Canadian Institutes of Health Research, and Heart and Stroke Foundation of Ontario. It received support from Canadian Institutes of Health Research’s Strategy for Patient Oriented Research, Ontario SPOR Support Unit, and Ontario Ministry of Health and Long-Term Care and unrestricted grants from several pharmaceutical companies. Narula declared receiving honoraria from Janssen, Abbvie, Takeda, Pfizer, Sandoz, Novartis, Iterative Health, Innomar Strategies, Fresinius Kabi, Amgen, Organon, Eli Lilly, and Ferring. Ananthkrishnan declared having no relevant disclosures.

A version of this article appeared on Medscape.com.

Diets high in packaged breads, cookies, and other highly processed grain products may raise the risk for inflammatory bowel disease (IBD), while minimally processed grain products may offer some protection, a large study has found.

The sweeping analysis of 124,590 adults from 21 countries found that those eating at least 19 g of ultraprocessed grains a day were about twice as likely to be diagnosed with IBD as peers eating less than 9 g daily.

“Our study adds robust evidence from a large, diverse global cohort that frequent consumption of ultraprocessed grains is associated with an increased risk of developing inflammatory bowel disease,” Neeraj Narula, MD, MPH, gastroenterologist and associate professor of medicine, McMaster University, Hamilton, Ontario, Canada, told GI & Hepatology News.

The study also “further clarifies that not all grains carry risk — minimally processed grains like fresh bread and rice were associated with lower risk even. These results build on and specify previous findings linking ultraprocessed foods more broadly to IBD,” Narula said.

The study was published in The American Journal of Gastroenterology.

 

Diet Matters to IBD Risk

According to the latest US data (2021-2023), ultraprocessed foods made up 62% of daily calories for young people and 53% for adults in 2021-2023.

The Prospective Urban Rural Epidemiology (PURE) study has followed participants aged 35-70 years for a median of nearly 13 years. At enrollment, volunteers completed country-specific food-frequency questionnaires, enabling researchers to quantify usual intake of more than 130 food items and track new cases of IBD reported at biennial follow-ups.

The researchers classified packaged breads, sweet breakfast cereals, crackers, pastries and ready-to-heat pizza or pasta as ultraprocessed grains because they are refined and typically contain additives such as emulsifiers and preservatives. Fresh bakery bread and plain rice were analyzed separately as minimally processed grain references.

During a median of 12.9 years, 605 participants developed IBD; 497 developed ulcerative colitis (UC) and 108 developed Crohn’s disease. 

Increased intake of ultraprocessed grains was associated with a higher risk for IBD, with hazard ratios (HR) of 2.08 for intake of ≥ 50 g/d and 1.37 for 19-50 g/d compared to intake of < 19 g/d. The increased risk was largely driven by a significantly increased risk for UC (HR, 2.46) and not Crohn’s disease (HR, 0.98).

Among the different ultraprocessed grain products, packaged bread stood out: Consuming ≥ 30 g/d of packaged bread (a little more than one slice) was associated with a greater than twofold increased risk for IBD (HR, 2.11) compared to no intake of packaged bread.

In contrast, greater consumption of fresh bread was associated with a reduced risk of developing IBD (HR, 0.61 for ≥ 65 g/d and 0.45 for 16-65 g/d compared to < 16 g/d).

Increased intake of rice was also associated with a lower risk of developing IBD (HR, 0.63 for ≥ 1 serving/d and 0.99 for < 1 serving/d).

When the researchers widened the lens to all ultraprocessed foods — from sodas to salty snacks — the risk for IBD climbed further.

Participants eating at least five servings a day had nearly a fourfold greater odds of IBD than those eating fewer than one serving (HR, 3.95) — a finding consistent with other data from the PURE study cohort.

 

What to Tell Patients?

The authors acknowledged in their paper that it’s difficult — if not impossible — to completely avoid ultraprocessed food in the Western diet.

They said their findings support “public health strategies to promote consumption of whole and minimally processed foods while reducing the consumption of highly processed alternatives.”

“I tell my patients that emerging literature shows an association between ultraprocessed food intake and IBD risk, but it’s not yet clear whether simply cutting out those foods will improve disease activity once IBD is established,” Narula told GI & Hepatology News.

“However, I still encourage patients to reduce ultraprocessed foods and to follow a Mediterranean-style diet — focusing on minimally processed grains, fruits, vegetables, healthy fats, and lean proteins — to support overall gut and general health,” Narula said.

Reached for comment, Ashwin Ananthakrishnan, MD, MPH, AGAF, associate professor of medicine, Massachusetts General Hospital, Boston, who wasn’t part of the study, said it “adds incrementally to the growing data on how ultraprocessed foods may affect the risk of IBD.”

“They (and others) have previously shown a link between general ultraprocessed food consumption and risk of IBD. Others have shown that some of this is mediated through refined grains. This study more specifically studies that question and demonstrates an association,” said Ananthkrishnan.

“This should not be used, however, to counsel patients. It does not study the impact of grain intake on patients with IBD. It may help inform population level preventive strategies (or in high-risk individuals) but requires more confirmation since there is significant heterogeneity between the various countries in this cohort. Countries that have high refined grain intake are also enriched in several other IBD risk factors (including genetics),” Ananthkrishnan told GI & Hepatology News.

The PURE study is an investigator-initiated study funded by the Population Health Research Institute, Hamilton Health Sciences Research Institute, Canadian Institutes of Health Research, and Heart and Stroke Foundation of Ontario. It received support from Canadian Institutes of Health Research’s Strategy for Patient Oriented Research, Ontario SPOR Support Unit, and Ontario Ministry of Health and Long-Term Care and unrestricted grants from several pharmaceutical companies. Narula declared receiving honoraria from Janssen, Abbvie, Takeda, Pfizer, Sandoz, Novartis, Iterative Health, Innomar Strategies, Fresinius Kabi, Amgen, Organon, Eli Lilly, and Ferring. Ananthkrishnan declared having no relevant disclosures.

A version of this article appeared on Medscape.com.

Diets high in packaged breads, cookies, and other highly processed grain products may raise the risk for inflammatory bowel disease (IBD), while minimally processed grain products may offer some protection, a large study has found.

The sweeping analysis of 124,590 adults from 21 countries found that those eating at least 19 g of ultraprocessed grains a day were about twice as likely to be diagnosed with IBD as peers eating less than 9 g daily.

“Our study adds robust evidence from a large, diverse global cohort that frequent consumption of ultraprocessed grains is associated with an increased risk of developing inflammatory bowel disease,” Neeraj Narula, MD, MPH, gastroenterologist and associate professor of medicine, McMaster University, Hamilton, Ontario, Canada, told GI & Hepatology News.

The study also “further clarifies that not all grains carry risk — minimally processed grains like fresh bread and rice were associated with lower risk even. These results build on and specify previous findings linking ultraprocessed foods more broadly to IBD,” Narula said.

The study was published in The American Journal of Gastroenterology.

 

Diet Matters to IBD Risk

According to the latest US data (2021-2023), ultraprocessed foods made up 62% of daily calories for young people and 53% for adults in 2021-2023.

The Prospective Urban Rural Epidemiology (PURE) study has followed participants aged 35-70 years for a median of nearly 13 years. At enrollment, volunteers completed country-specific food-frequency questionnaires, enabling researchers to quantify usual intake of more than 130 food items and track new cases of IBD reported at biennial follow-ups.

The researchers classified packaged breads, sweet breakfast cereals, crackers, pastries and ready-to-heat pizza or pasta as ultraprocessed grains because they are refined and typically contain additives such as emulsifiers and preservatives. Fresh bakery bread and plain rice were analyzed separately as minimally processed grain references.

During a median of 12.9 years, 605 participants developed IBD; 497 developed ulcerative colitis (UC) and 108 developed Crohn’s disease. 

Increased intake of ultraprocessed grains was associated with a higher risk for IBD, with hazard ratios (HR) of 2.08 for intake of ≥ 50 g/d and 1.37 for 19-50 g/d compared to intake of < 19 g/d. The increased risk was largely driven by a significantly increased risk for UC (HR, 2.46) and not Crohn’s disease (HR, 0.98).

Among the different ultraprocessed grain products, packaged bread stood out: Consuming ≥ 30 g/d of packaged bread (a little more than one slice) was associated with a greater than twofold increased risk for IBD (HR, 2.11) compared to no intake of packaged bread.

In contrast, greater consumption of fresh bread was associated with a reduced risk of developing IBD (HR, 0.61 for ≥ 65 g/d and 0.45 for 16-65 g/d compared to < 16 g/d).

Increased intake of rice was also associated with a lower risk of developing IBD (HR, 0.63 for ≥ 1 serving/d and 0.99 for < 1 serving/d).

When the researchers widened the lens to all ultraprocessed foods — from sodas to salty snacks — the risk for IBD climbed further.

Participants eating at least five servings a day had nearly a fourfold greater odds of IBD than those eating fewer than one serving (HR, 3.95) — a finding consistent with other data from the PURE study cohort.

 

What to Tell Patients?

The authors acknowledged in their paper that it’s difficult — if not impossible — to completely avoid ultraprocessed food in the Western diet.

They said their findings support “public health strategies to promote consumption of whole and minimally processed foods while reducing the consumption of highly processed alternatives.”

“I tell my patients that emerging literature shows an association between ultraprocessed food intake and IBD risk, but it’s not yet clear whether simply cutting out those foods will improve disease activity once IBD is established,” Narula told GI & Hepatology News.

“However, I still encourage patients to reduce ultraprocessed foods and to follow a Mediterranean-style diet — focusing on minimally processed grains, fruits, vegetables, healthy fats, and lean proteins — to support overall gut and general health,” Narula said.

Reached for comment, Ashwin Ananthakrishnan, MD, MPH, AGAF, associate professor of medicine, Massachusetts General Hospital, Boston, who wasn’t part of the study, said it “adds incrementally to the growing data on how ultraprocessed foods may affect the risk of IBD.”

“They (and others) have previously shown a link between general ultraprocessed food consumption and risk of IBD. Others have shown that some of this is mediated through refined grains. This study more specifically studies that question and demonstrates an association,” said Ananthkrishnan.

“This should not be used, however, to counsel patients. It does not study the impact of grain intake on patients with IBD. It may help inform population level preventive strategies (or in high-risk individuals) but requires more confirmation since there is significant heterogeneity between the various countries in this cohort. Countries that have high refined grain intake are also enriched in several other IBD risk factors (including genetics),” Ananthkrishnan told GI & Hepatology News.

The PURE study is an investigator-initiated study funded by the Population Health Research Institute, Hamilton Health Sciences Research Institute, Canadian Institutes of Health Research, and Heart and Stroke Foundation of Ontario. It received support from Canadian Institutes of Health Research’s Strategy for Patient Oriented Research, Ontario SPOR Support Unit, and Ontario Ministry of Health and Long-Term Care and unrestricted grants from several pharmaceutical companies. Narula declared receiving honoraria from Janssen, Abbvie, Takeda, Pfizer, Sandoz, Novartis, Iterative Health, Innomar Strategies, Fresinius Kabi, Amgen, Organon, Eli Lilly, and Ferring. Ananthkrishnan declared having no relevant disclosures.

A version of this article appeared on Medscape.com.

Medications for inflammatory bowel disease (IBD) appear to have no impact on risk of incident malignancies among patients with a history of breast cancer, according to investigators.

These findings diminish concerns that IBD therapy could theoretically reactivate dormant micrometastases, lead author Guillaume Le Cosquer, MD, of Toulouse University Hospital, Toulouse, France, and colleagues, reported.

“In patients with IBD, medical management of subjects with a history of breast cancer is a frequent and unresolved problem for clinicians,” the investigators wrote in Clinical Gastroenterology and Hepatology (2024 Nov. doi: 10.1016/j.cgh.2024.09.034).

Previous studies have reported that conventional immunosuppressants and biologics do not increase risk of incident cancer among IBD patients with a prior nondigestive malignancy; however, recent guidelines from the European Crohn’s and Colitis Organisation (ECCO) suggest that data are insufficient to make associated recommendations, prompting the present study.

“[T]he major strength of our work is that it is the first to focus on the most frequent cancer (breast cancer) in patients with IBD only, with the longest follow-up after breast cancer in patients with IBD ever published,” Dr. Le Cosquer and colleagues noted.

The dataset included 207 patients with IBD and a history of breast cancer, drawn from 7 tertiary centers across France. 

The index date was the time of breast cancer diagnosis, and patients were followed for a median of 71 months. The median time from cancer diagnosis to initiation of IBD treatment was 28 months. 

First-line post-cancer treatments included conventional immunosuppressants (19.3%), anti–tumor necrosis factor (anti-TNF) agents (19.8%), vedolizumab (7.2%), and ustekinumab (1.9%). Approximately half (51.6%) received no immunosuppressive therapy during follow-up.

Over the study period, 42 incident cancers were recorded (20.3%), among which 34 were breast cancer recurrences. Adjusted incidence rates per 1000 person-years were 10.2 (95% CI, 6.0–16.4) in the untreated group and 28.9 (95% CI, 11.6–59.6) in patients exposed to immunosuppressive or biologic therapies (P = .0519). Incident cancer–free survival did not differ significantly between treated and untreated groups (P = .4796).

On multivariable analysis, independent predictors of incident cancer included T4d stage (P = .036), triple-negative status (P = .016), and follow-up duration shorter than 71 months (P = .005).

“[I]mmunosuppressant and biologic use in selected patients with IBD with prior breast cancer does not seem to increase the risk of incident cancer,” the investigators wrote, noting that the main predictors of cancer recurrence were known poor prognostic features of breast cancer.

Dr. Le Cosquer and colleagues acknowledged a lack of prospective safety data for biologic therapies among patients with prior malignancy, as these individuals are often excluded from clinical trials. Still, they underscored alignment between their findings and earlier retrospective studies, including analyses from the SAPPHIRE registry and Medicare data, which also found no significant increase in breast cancer recurrence with anti-TNF agents or newer biologics such as vedolizumab and ustekinumab. 

“Our findings will help clinicians to make decisions in multidisciplinary meetings to start immunosuppressants or biologics in case of IBD flare-up in these patients,” they concluded.

The investigators disclosed relationships with AbbVie, Janssen, Takeda, and others.

Medications for inflammatory bowel disease (IBD) appear to have no impact on risk of incident malignancies among patients with a history of breast cancer, according to investigators.

These findings diminish concerns that IBD therapy could theoretically reactivate dormant micrometastases, lead author Guillaume Le Cosquer, MD, of Toulouse University Hospital, Toulouse, France, and colleagues, reported.

“In patients with IBD, medical management of subjects with a history of breast cancer is a frequent and unresolved problem for clinicians,” the investigators wrote in Clinical Gastroenterology and Hepatology (2024 Nov. doi: 10.1016/j.cgh.2024.09.034).

Previous studies have reported that conventional immunosuppressants and biologics do not increase risk of incident cancer among IBD patients with a prior nondigestive malignancy; however, recent guidelines from the European Crohn’s and Colitis Organisation (ECCO) suggest that data are insufficient to make associated recommendations, prompting the present study.

“[T]he major strength of our work is that it is the first to focus on the most frequent cancer (breast cancer) in patients with IBD only, with the longest follow-up after breast cancer in patients with IBD ever published,” Dr. Le Cosquer and colleagues noted.

The dataset included 207 patients with IBD and a history of breast cancer, drawn from 7 tertiary centers across France. 

The index date was the time of breast cancer diagnosis, and patients were followed for a median of 71 months. The median time from cancer diagnosis to initiation of IBD treatment was 28 months. 

First-line post-cancer treatments included conventional immunosuppressants (19.3%), anti–tumor necrosis factor (anti-TNF) agents (19.8%), vedolizumab (7.2%), and ustekinumab (1.9%). Approximately half (51.6%) received no immunosuppressive therapy during follow-up.

Over the study period, 42 incident cancers were recorded (20.3%), among which 34 were breast cancer recurrences. Adjusted incidence rates per 1000 person-years were 10.2 (95% CI, 6.0–16.4) in the untreated group and 28.9 (95% CI, 11.6–59.6) in patients exposed to immunosuppressive or biologic therapies (P = .0519). Incident cancer–free survival did not differ significantly between treated and untreated groups (P = .4796).

On multivariable analysis, independent predictors of incident cancer included T4d stage (P = .036), triple-negative status (P = .016), and follow-up duration shorter than 71 months (P = .005).

“[I]mmunosuppressant and biologic use in selected patients with IBD with prior breast cancer does not seem to increase the risk of incident cancer,” the investigators wrote, noting that the main predictors of cancer recurrence were known poor prognostic features of breast cancer.

Dr. Le Cosquer and colleagues acknowledged a lack of prospective safety data for biologic therapies among patients with prior malignancy, as these individuals are often excluded from clinical trials. Still, they underscored alignment between their findings and earlier retrospective studies, including analyses from the SAPPHIRE registry and Medicare data, which also found no significant increase in breast cancer recurrence with anti-TNF agents or newer biologics such as vedolizumab and ustekinumab. 

“Our findings will help clinicians to make decisions in multidisciplinary meetings to start immunosuppressants or biologics in case of IBD flare-up in these patients,” they concluded.

The investigators disclosed relationships with AbbVie, Janssen, Takeda, and others.

Medications for inflammatory bowel disease (IBD) appear to have no impact on risk of incident malignancies among patients with a history of breast cancer, according to investigators.

These findings diminish concerns that IBD therapy could theoretically reactivate dormant micrometastases, lead author Guillaume Le Cosquer, MD, of Toulouse University Hospital, Toulouse, France, and colleagues, reported.

“In patients with IBD, medical management of subjects with a history of breast cancer is a frequent and unresolved problem for clinicians,” the investigators wrote in Clinical Gastroenterology and Hepatology (2024 Nov. doi: 10.1016/j.cgh.2024.09.034).

Previous studies have reported that conventional immunosuppressants and biologics do not increase risk of incident cancer among IBD patients with a prior nondigestive malignancy; however, recent guidelines from the European Crohn’s and Colitis Organisation (ECCO) suggest that data are insufficient to make associated recommendations, prompting the present study.

“[T]he major strength of our work is that it is the first to focus on the most frequent cancer (breast cancer) in patients with IBD only, with the longest follow-up after breast cancer in patients with IBD ever published,” Dr. Le Cosquer and colleagues noted.

The dataset included 207 patients with IBD and a history of breast cancer, drawn from 7 tertiary centers across France. 

The index date was the time of breast cancer diagnosis, and patients were followed for a median of 71 months. The median time from cancer diagnosis to initiation of IBD treatment was 28 months. 

First-line post-cancer treatments included conventional immunosuppressants (19.3%), anti–tumor necrosis factor (anti-TNF) agents (19.8%), vedolizumab (7.2%), and ustekinumab (1.9%). Approximately half (51.6%) received no immunosuppressive therapy during follow-up.

Over the study period, 42 incident cancers were recorded (20.3%), among which 34 were breast cancer recurrences. Adjusted incidence rates per 1000 person-years were 10.2 (95% CI, 6.0–16.4) in the untreated group and 28.9 (95% CI, 11.6–59.6) in patients exposed to immunosuppressive or biologic therapies (P = .0519). Incident cancer–free survival did not differ significantly between treated and untreated groups (P = .4796).

On multivariable analysis, independent predictors of incident cancer included T4d stage (P = .036), triple-negative status (P = .016), and follow-up duration shorter than 71 months (P = .005).

“[I]mmunosuppressant and biologic use in selected patients with IBD with prior breast cancer does not seem to increase the risk of incident cancer,” the investigators wrote, noting that the main predictors of cancer recurrence were known poor prognostic features of breast cancer.

Dr. Le Cosquer and colleagues acknowledged a lack of prospective safety data for biologic therapies among patients with prior malignancy, as these individuals are often excluded from clinical trials. Still, they underscored alignment between their findings and earlier retrospective studies, including analyses from the SAPPHIRE registry and Medicare data, which also found no significant increase in breast cancer recurrence with anti-TNF agents or newer biologics such as vedolizumab and ustekinumab. 

“Our findings will help clinicians to make decisions in multidisciplinary meetings to start immunosuppressants or biologics in case of IBD flare-up in these patients,” they concluded.

The investigators disclosed relationships with AbbVie, Janssen, Takeda, and others.

Changes in sleep metrics detected with wearable technology could serve as an inflammation marker and potentially predict inflammatory bowel disease (IBD) flareups, regardless of whether a patient has symptoms, an observational study suggested.

Sleep data from 101 study participants over a mean duration of about 228 days revealed that altered sleep architecture was only apparent when inflammation was present — symptoms alone did not impact sleep cycles or signal inflammation.

“We thought symptoms might have an impact on sleep, but interestingly, our data showed that measurable changes like reduced rapid eye movement (REM) sleep and increased light sleep only occurred during periods of active inflammation,” Robert Hirten, MD, associate professor of Medicine (Gastroenterology), and Artificial Intelligence and Human Health, at the Icahn School of Medicine at Mount Sinai, New York City, told GI & Hepatology News.

“It was also interesting to see distinct patterns in sleep metrics begin to shift over the 45 days before a flare, suggesting the potential for sleep to serve as an early indicator of disease activity,” he added.

“Sleep is often overlooked in the management of IBD, but it may provide valuable insights into a patient’s underlying disease state,” he said. “While sleep monitoring isn’t yet a standard part of IBD care, this study highlights its potential as a noninvasive window into disease activity, and a promising area for future clinical integration.”

The study was published online in Clinical Gastroenterology and Hepatology.

 

Less REM Sleep, More Light Sleep

Researchers assessed the impact of inflammation and symptoms on sleep architecture in IBD by analyzing data from 101 individuals who answered daily disease activity surveys and wore a wearable device.

The mean age of participants was 41 years and 65.3% were women. Sixty-three participants (62.4%) had Crohn’s disease (CD) and 38 (37.6%) had ulcerative colitis (UC).

Almost 40 (39.6%) participants used an Apple Watch; 50 (49.5%) used a Fitbit; and 11 (10.9%) used an Oura ring. Sleep architecture, sleep efficiency, and total hours asleep were collected from the devices. Participants were encouraged to wear their devices for at least 4 days per week and 8 hours per day and were not required to wear them at night. Participants provided data by linking their devices to ehive, Mount Sinai’s custom app.

Daily clinical disease activity was assessed using the UC or CD Patient Reported Outcome-2 survey. Participants were asked to answer at least four daily surveys each week.

Associations between sleep metrics and periods of symptomatic and inflammatory flares, and combinations of symptomatic and inflammatory activity, were compared to periods of symptomatic and inflammatory remission.

Furthermore, researchers explored the rate of change in sleep metrics for 45 days before and after inflammatory and symptomatic flares.

Participants contributed a mean duration of 228.16 nights of wearable data. During active inflammation, they spent a lower percentage of sleep time in REM (20% vs 21.59%) and a greater percentage of sleep time in light sleep (62.23% vs 59.95%) than during inflammatory remission. No differences were observed in the mean percentage of time in deep sleep, sleep efficiency, or total time asleep.

During symptomatic flares, there were no differences in the percentage of sleep time in REM sleep, deep sleep, light sleep, or sleep efficiency compared with periods of inflammatory remission. However, participants slept less overall during symptomatic flares compared with during symptomatic remission.

Compared with during asymptomatic and uninflamed periods, during asymptomatic but inflamed periods, participants spent a lower percentage of time in REM sleep, and more time in light sleep; however, there were no differences in sleep efficiency or total time asleep.

Similarly, participants had more light sleep and less REM sleep during symptomatic and inflammatory flares than during asymptomatic and uninflamed periods — but there were no differences in the percentage of time spent in deep sleep, in sleep efficiency, and the total time asleep.

Symptomatic flares alone, without inflammation, did not impact sleep metrics, the researchers concluded. However, periods with active inflammation were associated with a significantly smaller percentage of sleep time in REM sleep and a greater percentage of sleep time in light sleep.

The team also performed longitudinal mapping of sleep patterns before, during, and after disease exacerbations by analyzing sleep data for 6 weeks before and 6 weeks after flare episodes.

They found that sleep disturbances significantly worsen leading up to inflammatory flares and improve afterward, suggesting that sleep changes may signal upcoming increased disease activity. Evaluating the intersection of inflammatory and symptomatic flares, altered sleep architecture was only evident when inflammation was present.

“These findings raise important questions about whether intervening on sleep can actually impact inflammation or disease trajectory in IBD,” Hirten said. “Next steps include studying whether targeted sleep interventions can improve both sleep and IBD outcomes.”

While this research is still in the early stages, he said, “it suggests that sleep may have a relationship with inflammatory activity in IBD. For patients, it reinforces the value of paying attention to sleep changes.”

The findings also show the potential of wearable devices to guide more personalized monitoring, he added. “More work is needed before sleep metrics can be used routinely in clinical decision-making.”

 

Validates the Use of Wearables

Commenting on the study for GI & Hepatology News, Michael Mintz, MD, a gastroenterologist at Weill Cornell Medicine and NewYork-Presbyterian in New York City, observed, “Gastrointestinal symptoms often do not correlate with objective disease activity in IBD, creating a diagnostic challenge for gastroenterologists. Burdensome, expensive, and/or invasive testing, such as colonoscopies, stool tests, or imaging, are frequently required to monitor disease activity.” 

“This study is a first step in objectively monitoring inflammation in a patient-centric way that does not create undue burden to our patients,” he said. “It also provides longitudinal data that suggests changes in sleep patterns can pre-date disease flares, which ideally can lead to earlier intervention to prevent disease complications.”

Like Hirten, he noted that clinical decisions, such as changing IBD therapy, should not be based on the results of this study. “Rather this provides validation that wearable technology can provide useful objective data that correlates with disease activity.”

Furthermore, he said, it is not clear whether analyzing sleep data is a cost-effective way of monitoring IBD disease activity, or whether that data should be used alone or in combination with other objective disease markers, to influence clinical decision-making.

“This study provides proof of concept that there is a relationship between sleep characteristics and objective inflammation, but further studies are needed,” he said. “I am hopeful that this technology will give us another tool that we can use in clinical practice to monitor disease activity and improve outcomes in a way that is comfortable and convenient for our patients.”

This study was supported by a grant to Hirten from the US National Institutes of Health. Hirten reported receiving consulting fees from Bristol Meyers Squibb, AbbVie; stock options from Salvo Health; and research support from Janssen, Intralytix, EnLiSense, Crohn’s and Colitis Foundation. Mintz declared no competing interests.

A version of this article appeared on Medscape.com.

Changes in sleep metrics detected with wearable technology could serve as an inflammation marker and potentially predict inflammatory bowel disease (IBD) flareups, regardless of whether a patient has symptoms, an observational study suggested.

Sleep data from 101 study participants over a mean duration of about 228 days revealed that altered sleep architecture was only apparent when inflammation was present — symptoms alone did not impact sleep cycles or signal inflammation.

“We thought symptoms might have an impact on sleep, but interestingly, our data showed that measurable changes like reduced rapid eye movement (REM) sleep and increased light sleep only occurred during periods of active inflammation,” Robert Hirten, MD, associate professor of Medicine (Gastroenterology), and Artificial Intelligence and Human Health, at the Icahn School of Medicine at Mount Sinai, New York City, told GI & Hepatology News.

“It was also interesting to see distinct patterns in sleep metrics begin to shift over the 45 days before a flare, suggesting the potential for sleep to serve as an early indicator of disease activity,” he added.

“Sleep is often overlooked in the management of IBD, but it may provide valuable insights into a patient’s underlying disease state,” he said. “While sleep monitoring isn’t yet a standard part of IBD care, this study highlights its potential as a noninvasive window into disease activity, and a promising area for future clinical integration.”

The study was published online in Clinical Gastroenterology and Hepatology.

 

Less REM Sleep, More Light Sleep

Researchers assessed the impact of inflammation and symptoms on sleep architecture in IBD by analyzing data from 101 individuals who answered daily disease activity surveys and wore a wearable device.

The mean age of participants was 41 years and 65.3% were women. Sixty-three participants (62.4%) had Crohn’s disease (CD) and 38 (37.6%) had ulcerative colitis (UC).

Almost 40 (39.6%) participants used an Apple Watch; 50 (49.5%) used a Fitbit; and 11 (10.9%) used an Oura ring. Sleep architecture, sleep efficiency, and total hours asleep were collected from the devices. Participants were encouraged to wear their devices for at least 4 days per week and 8 hours per day and were not required to wear them at night. Participants provided data by linking their devices to ehive, Mount Sinai’s custom app.

Daily clinical disease activity was assessed using the UC or CD Patient Reported Outcome-2 survey. Participants were asked to answer at least four daily surveys each week.

Associations between sleep metrics and periods of symptomatic and inflammatory flares, and combinations of symptomatic and inflammatory activity, were compared to periods of symptomatic and inflammatory remission.

Furthermore, researchers explored the rate of change in sleep metrics for 45 days before and after inflammatory and symptomatic flares.

Participants contributed a mean duration of 228.16 nights of wearable data. During active inflammation, they spent a lower percentage of sleep time in REM (20% vs 21.59%) and a greater percentage of sleep time in light sleep (62.23% vs 59.95%) than during inflammatory remission. No differences were observed in the mean percentage of time in deep sleep, sleep efficiency, or total time asleep.

During symptomatic flares, there were no differences in the percentage of sleep time in REM sleep, deep sleep, light sleep, or sleep efficiency compared with periods of inflammatory remission. However, participants slept less overall during symptomatic flares compared with during symptomatic remission.

Compared with during asymptomatic and uninflamed periods, during asymptomatic but inflamed periods, participants spent a lower percentage of time in REM sleep, and more time in light sleep; however, there were no differences in sleep efficiency or total time asleep.

Similarly, participants had more light sleep and less REM sleep during symptomatic and inflammatory flares than during asymptomatic and uninflamed periods — but there were no differences in the percentage of time spent in deep sleep, in sleep efficiency, and the total time asleep.

Symptomatic flares alone, without inflammation, did not impact sleep metrics, the researchers concluded. However, periods with active inflammation were associated with a significantly smaller percentage of sleep time in REM sleep and a greater percentage of sleep time in light sleep.

The team also performed longitudinal mapping of sleep patterns before, during, and after disease exacerbations by analyzing sleep data for 6 weeks before and 6 weeks after flare episodes.

They found that sleep disturbances significantly worsen leading up to inflammatory flares and improve afterward, suggesting that sleep changes may signal upcoming increased disease activity. Evaluating the intersection of inflammatory and symptomatic flares, altered sleep architecture was only evident when inflammation was present.

“These findings raise important questions about whether intervening on sleep can actually impact inflammation or disease trajectory in IBD,” Hirten said. “Next steps include studying whether targeted sleep interventions can improve both sleep and IBD outcomes.”

While this research is still in the early stages, he said, “it suggests that sleep may have a relationship with inflammatory activity in IBD. For patients, it reinforces the value of paying attention to sleep changes.”

The findings also show the potential of wearable devices to guide more personalized monitoring, he added. “More work is needed before sleep metrics can be used routinely in clinical decision-making.”

 

Validates the Use of Wearables

Commenting on the study for GI & Hepatology News, Michael Mintz, MD, a gastroenterologist at Weill Cornell Medicine and NewYork-Presbyterian in New York City, observed, “Gastrointestinal symptoms often do not correlate with objective disease activity in IBD, creating a diagnostic challenge for gastroenterologists. Burdensome, expensive, and/or invasive testing, such as colonoscopies, stool tests, or imaging, are frequently required to monitor disease activity.” 

“This study is a first step in objectively monitoring inflammation in a patient-centric way that does not create undue burden to our patients,” he said. “It also provides longitudinal data that suggests changes in sleep patterns can pre-date disease flares, which ideally can lead to earlier intervention to prevent disease complications.”

Like Hirten, he noted that clinical decisions, such as changing IBD therapy, should not be based on the results of this study. “Rather this provides validation that wearable technology can provide useful objective data that correlates with disease activity.”

Furthermore, he said, it is not clear whether analyzing sleep data is a cost-effective way of monitoring IBD disease activity, or whether that data should be used alone or in combination with other objective disease markers, to influence clinical decision-making.

“This study provides proof of concept that there is a relationship between sleep characteristics and objective inflammation, but further studies are needed,” he said. “I am hopeful that this technology will give us another tool that we can use in clinical practice to monitor disease activity and improve outcomes in a way that is comfortable and convenient for our patients.”

This study was supported by a grant to Hirten from the US National Institutes of Health. Hirten reported receiving consulting fees from Bristol Meyers Squibb, AbbVie; stock options from Salvo Health; and research support from Janssen, Intralytix, EnLiSense, Crohn’s and Colitis Foundation. Mintz declared no competing interests.

A version of this article appeared on Medscape.com.

Changes in sleep metrics detected with wearable technology could serve as an inflammation marker and potentially predict inflammatory bowel disease (IBD) flareups, regardless of whether a patient has symptoms, an observational study suggested.

Sleep data from 101 study participants over a mean duration of about 228 days revealed that altered sleep architecture was only apparent when inflammation was present — symptoms alone did not impact sleep cycles or signal inflammation.

“We thought symptoms might have an impact on sleep, but interestingly, our data showed that measurable changes like reduced rapid eye movement (REM) sleep and increased light sleep only occurred during periods of active inflammation,” Robert Hirten, MD, associate professor of Medicine (Gastroenterology), and Artificial Intelligence and Human Health, at the Icahn School of Medicine at Mount Sinai, New York City, told GI & Hepatology News.

“It was also interesting to see distinct patterns in sleep metrics begin to shift over the 45 days before a flare, suggesting the potential for sleep to serve as an early indicator of disease activity,” he added.

“Sleep is often overlooked in the management of IBD, but it may provide valuable insights into a patient’s underlying disease state,” he said. “While sleep monitoring isn’t yet a standard part of IBD care, this study highlights its potential as a noninvasive window into disease activity, and a promising area for future clinical integration.”

The study was published online in Clinical Gastroenterology and Hepatology.

 

Less REM Sleep, More Light Sleep

Researchers assessed the impact of inflammation and symptoms on sleep architecture in IBD by analyzing data from 101 individuals who answered daily disease activity surveys and wore a wearable device.

The mean age of participants was 41 years and 65.3% were women. Sixty-three participants (62.4%) had Crohn’s disease (CD) and 38 (37.6%) had ulcerative colitis (UC).

Almost 40 (39.6%) participants used an Apple Watch; 50 (49.5%) used a Fitbit; and 11 (10.9%) used an Oura ring. Sleep architecture, sleep efficiency, and total hours asleep were collected from the devices. Participants were encouraged to wear their devices for at least 4 days per week and 8 hours per day and were not required to wear them at night. Participants provided data by linking their devices to ehive, Mount Sinai’s custom app.

Daily clinical disease activity was assessed using the UC or CD Patient Reported Outcome-2 survey. Participants were asked to answer at least four daily surveys each week.

Associations between sleep metrics and periods of symptomatic and inflammatory flares, and combinations of symptomatic and inflammatory activity, were compared to periods of symptomatic and inflammatory remission.

Furthermore, researchers explored the rate of change in sleep metrics for 45 days before and after inflammatory and symptomatic flares.

Participants contributed a mean duration of 228.16 nights of wearable data. During active inflammation, they spent a lower percentage of sleep time in REM (20% vs 21.59%) and a greater percentage of sleep time in light sleep (62.23% vs 59.95%) than during inflammatory remission. No differences were observed in the mean percentage of time in deep sleep, sleep efficiency, or total time asleep.

During symptomatic flares, there were no differences in the percentage of sleep time in REM sleep, deep sleep, light sleep, or sleep efficiency compared with periods of inflammatory remission. However, participants slept less overall during symptomatic flares compared with during symptomatic remission.

Compared with during asymptomatic and uninflamed periods, during asymptomatic but inflamed periods, participants spent a lower percentage of time in REM sleep, and more time in light sleep; however, there were no differences in sleep efficiency or total time asleep.

Similarly, participants had more light sleep and less REM sleep during symptomatic and inflammatory flares than during asymptomatic and uninflamed periods — but there were no differences in the percentage of time spent in deep sleep, in sleep efficiency, and the total time asleep.

Symptomatic flares alone, without inflammation, did not impact sleep metrics, the researchers concluded. However, periods with active inflammation were associated with a significantly smaller percentage of sleep time in REM sleep and a greater percentage of sleep time in light sleep.

The team also performed longitudinal mapping of sleep patterns before, during, and after disease exacerbations by analyzing sleep data for 6 weeks before and 6 weeks after flare episodes.

They found that sleep disturbances significantly worsen leading up to inflammatory flares and improve afterward, suggesting that sleep changes may signal upcoming increased disease activity. Evaluating the intersection of inflammatory and symptomatic flares, altered sleep architecture was only evident when inflammation was present.

“These findings raise important questions about whether intervening on sleep can actually impact inflammation or disease trajectory in IBD,” Hirten said. “Next steps include studying whether targeted sleep interventions can improve both sleep and IBD outcomes.”

While this research is still in the early stages, he said, “it suggests that sleep may have a relationship with inflammatory activity in IBD. For patients, it reinforces the value of paying attention to sleep changes.”

The findings also show the potential of wearable devices to guide more personalized monitoring, he added. “More work is needed before sleep metrics can be used routinely in clinical decision-making.”

 

Validates the Use of Wearables

Commenting on the study for GI & Hepatology News, Michael Mintz, MD, a gastroenterologist at Weill Cornell Medicine and NewYork-Presbyterian in New York City, observed, “Gastrointestinal symptoms often do not correlate with objective disease activity in IBD, creating a diagnostic challenge for gastroenterologists. Burdensome, expensive, and/or invasive testing, such as colonoscopies, stool tests, or imaging, are frequently required to monitor disease activity.” 

“This study is a first step in objectively monitoring inflammation in a patient-centric way that does not create undue burden to our patients,” he said. “It also provides longitudinal data that suggests changes in sleep patterns can pre-date disease flares, which ideally can lead to earlier intervention to prevent disease complications.”

Like Hirten, he noted that clinical decisions, such as changing IBD therapy, should not be based on the results of this study. “Rather this provides validation that wearable technology can provide useful objective data that correlates with disease activity.”

Furthermore, he said, it is not clear whether analyzing sleep data is a cost-effective way of monitoring IBD disease activity, or whether that data should be used alone or in combination with other objective disease markers, to influence clinical decision-making.

“This study provides proof of concept that there is a relationship between sleep characteristics and objective inflammation, but further studies are needed,” he said. “I am hopeful that this technology will give us another tool that we can use in clinical practice to monitor disease activity and improve outcomes in a way that is comfortable and convenient for our patients.”

This study was supported by a grant to Hirten from the US National Institutes of Health. Hirten reported receiving consulting fees from Bristol Meyers Squibb, AbbVie; stock options from Salvo Health; and research support from Janssen, Intralytix, EnLiSense, Crohn’s and Colitis Foundation. Mintz declared no competing interests.

A version of this article appeared on Medscape.com.

WASHINGTON, DC — A low-emulsifier-containing diet led to a threefold increased likelihood of improvement in symptoms of Crohn’s disease compared with an emulsifier-containing diet in a randomized double-blind dietary trial involving 154 patients with mildly active disease living across the United Kingdom.

The findings were reported at Gut Microbiota for Health (GMFH) World Summit 2025 by Benoit Chassaing, PhD, of the Institut Pasteur, Paris, France, whose research leading up to the trial has demonstrated that food additive emulsifiers —ubiquitous in processed foods — alter microbiota composition and lead to microbiota encroachment into the mucus layer of the gut and subsequent chronic gut inflammation.

Patients in the ADDapt trial, which was also reported in an abstract earlier this year at the European Crohn’s and Colitis Organization (ECCO) 2025 Congress, had a Crohn’s disease activity index (CDAI) of 150-250 and evidence of inflammation (faecal calprotectin (FCP) ≥ 150 µg/g or endoscopy/radiology). All “had been exposed in their regular diets to emulsifiers,” said Chassaing, a co-investigator, during a GMFH session on “Dietary Drivers of Health and Disease.”

They were randomized to either a low-emulsifier diet or to a low-emulsifier diet followed by emulsifier “resupplementation” — a design meant to “account for the very strong placebo effect that is always observed with dietary studies,” he said.

All patients received dietary counseling, a smart phone app and barcode scan to support shopping, and weekly support. They also received supermarket foods for 25% of their needs that were either free of emulsifiers or contained emulsifiers, and they were provided three snacks per day that were emulsifier-free or contained carrageenan, carboxymethycellulse (CMC), and polysorbate-80 (P80) — dietary emulsifiers that are commonly added to processed foods to enhance texture and extend shelf-life.

In the intention-to-treat (ITT) analysis, 49% of patients in the intervention group reached the primary endpoint of a 70-point reduction or more in CDAI response after 8 weeks compared with 31% of those in the control group (P = .019), with an adjusted relative risk of response of 3.1 (P = .003), Chassaing shared at the GMFH meeting, convened by the American Gastroenterological Association and the European Society of Neurogastroenterology and Motility.

In the per-protocol analysis (n = 119), 61% and 47% of patients in the intervention and control groups, respectively, reached the primary outcome of CDAI response, with an adjusted relative risk of response of 3.0 (P = .018), he said.

Secondary endpoints included CDAI remission at 24 weeks, and according to the abstract for the ECCO Congress, in the ITT analysis, patients in the intervention group were more than twice as likely to experience remission.

Chassaing noted at the GMFH meeting that as part of the study, he and coinvestigators have been investigating the participants’ gut microbiota with metagenomic analyses. The study was led by Kevin Whelan, PhD, head of the Department of Nutritional Sciences at King’s College London, London, England.

 

Can Emulsifier-Sensitive Individuals Be Identified?

In murine model research 10 years ago, Chassaing showed that the administration of CMC and P80 results in microbiota encroachment into the mucus layer of the gut, alterations in microbiota composition — including an increase in bacteria that produce pro-inflammatory flagellin — and development of chronic inflammation.

Wild-type mice treated with these compounds developed metabolic disease, and mice that were modified to be predisposed to colitis had a higher incidence of robust colitis. Moreover, fecal transplantation from emulsifier-treated mice to germ-free mice reproduced these changes, “clearly suggesting that the microbiome itself is sufficient to drive chronic inflammation,” he said.

In recent years, in humans, analyses from the large French NutriNet-Sante prospective cohort study have shown associations between exposure to food additive emulsifiers and the risk for cardiovascular disease, the risk for cancer (overall, breast, and prostate), and the risk for type 2 diabetes.

But to explore causality and better understand the mechanisms of emulsifier-driven changes on the microbiota, Chassaing and his colleagues also launched the FRESH study (Functional Research on Emulsifier in Humans), a double-blind randomized controlled-feeding study of the emulsifier CMC. For 11 days, nine healthy patients consumed an emulsifier-free diet and 11 consumed an identical diet enriched with 15 g/d of CMC.

Patients on the CMC-containing diet had reduced microbiota diversity and depletions of an array of microbiota-related metabolites, but only a small subset had profound alterations in microbiota composition and increased microbiota encroachment into the mucus layer. “Some seemed to be resistant to CMC-induced microbiota encroachment, while some were highly susceptible,” Chassaing said.

The pilot study raised the question, he said, of whether there is an “infectivity component” — some kind of “sensitive” gut microbiota composition — that may be associated with dietary emulsifier-driven inflammation and disease.

In other murine research, Chassaing and his team found that germ-free mice colonized with Crohn’s disease-associated adherent-invasive E coli (AIEC) and subsequently given CMC or P80 developed chronic inflammation and metabolic dysregulation, “clearly demonstrating that you can convert resistant mice to sensitive mice just by adding one bacteria to the ecosystem,” he said. “The presence of AIEC alone was sufficient to drive the detrimental effects of dietary emulsifiers.”

(In vitro research with transcriptomic analysis then showed that the emulsifiers directly elicit AIEC virulence gene expression, Chassaing and his coauthors wrote in their 2020 paper, facilitating AIEC’s “penetration of the mucus layer and adherence to epithelial cells and resulting in activation of host pro-inflammatory signaling.”)

“We don’t think it’s solely the AIEC bacteria that will drive emulsifier sensitivity, though…we think it’s more complex,” Chassaing said at the meeting. Overall, the findings raise the question of whether emulsifier-sensitive individuals can be identified.

This, he said, is one of his most recent research questions. His lab has led the development of an in vitro microbiota model built to predict an individual’s sensitivity to emulsifiers. In a study published in April, the model recapitulated the differential CMC sensitivity observed in the earlier FRESH study, suggesting that an individual’s sensitivity to emulsifiers can indeed be predicted by examining their baseline microbiota.

 

Interpreting the Epidemiology

Chassaing’s research arch illustrates the synergy between epidemiological research, basic/translational research, and clinical interventional research that’s needed to understand the diet-microbiome intersection in inflammatory bowel disease, said Ashwin Ananthakrishnan, MBBS, MPH, AGAF, associate professor of medicine at Massachusetts General Hospital, Boston, in an interview at the meeting.

“It’s a good example of how to really span the spectrum, starting from the big picture and going deeper to understand mechanisms, and starting from mechanisms and expanding it out,” Ananthakrishnan said.

In his own talk about research on IBD, Ananthakrishnan said that epidemiological data have shown over the past 10-15 years that total dietary fiber is inversely associated with the risk for Crohn’s disease (with the strongest associations with fiber from fruits and vegetables). Studies have also shown that a higher intake of polyunsaturated fatty acids is associated with a lower risk for ulcerative colitis, whereas “an n-6-fatty acid-rich diet is associated with a higher risk of ulcerative colitis,” he said.

Dietary cohort studies, meanwhile, have shed light on the influence of dietary patterns — such as the Mediterranean diet and diets with high inflammatory potential—on IBD. A diet rich in ultra-processed foods has also been shown in a prospective cohort study to be associated with a higher risk for Crohn’s disease, with certain categories of ultra-processed foods (eg, breads and breakfast foods) having the strongest associations.

Such studies are limited in part, however, by inadequate assessment of potentially relevant variables such as emulsifiers, preservatives, and how the food is processed, he said.

And in interpreting the epidemiological research on fiber and IBD, for instance, one must appreciate that “there are a number of mechanisms by which fiber is impactful…there’s a big picture to look at,” Ananthakrishnan said. Fiber “can affect the microbiome, clearly, it can affect the gut barrier, and it can affect bile acids, and there are detailed translational studies in support of each of these.”

But there are other constituents of fruits and vegetables “that could potentially influence disease risk, such as AhR ligands and polyphenols,” he said. “And importantly, people not eating a lot of fiber may be eating a lot of ultra-processed foods.”

Most interventional studies of fiber have not shown a benefit of a high-fiber diet, Ananthakrishnan said, but there are multiple possible reasons and factors at play, including potential population differences (eg, in inflammatory status or baseline microbiota), shortcomings of the interventions, and potentially inaccurate outcomes.

Abigail Johnson, PhD, RDN, associate director of the Nutrition Coordinating Center, University of Minnesota Twin Cities, which supports dietary analysis, said during the session that the focus of dietary research is “moving toward understanding overall dietary patterns” as opposed to focusing more narrowly on vitamins, minerals, and macronutrients such as proteins, fats, and carbohydrates.

This is an improvement, though “we still don’t have good approaches for understanding [the contributions of] things like additives and emulsifiers, food preparation and cooking, and food processing,” said Johnson, assistant professor in the Division of Epidemiology and Community Health at University of Minnesota Twin Cities. “Perhaps by looking at things at the food level we can overcome some of these limitations.”

Ananthakrishnan reported being a consultant for Geneoscopy and receiving a research grant from Takeda. Chassaing did not report any financial disclosures. Johnson reported that she had no financial disclosures.

A version of this article appeared on Medscape.com.

WASHINGTON, DC — A low-emulsifier-containing diet led to a threefold increased likelihood of improvement in symptoms of Crohn’s disease compared with an emulsifier-containing diet in a randomized double-blind dietary trial involving 154 patients with mildly active disease living across the United Kingdom.

The findings were reported at Gut Microbiota for Health (GMFH) World Summit 2025 by Benoit Chassaing, PhD, of the Institut Pasteur, Paris, France, whose research leading up to the trial has demonstrated that food additive emulsifiers —ubiquitous in processed foods — alter microbiota composition and lead to microbiota encroachment into the mucus layer of the gut and subsequent chronic gut inflammation.

Patients in the ADDapt trial, which was also reported in an abstract earlier this year at the European Crohn’s and Colitis Organization (ECCO) 2025 Congress, had a Crohn’s disease activity index (CDAI) of 150-250 and evidence of inflammation (faecal calprotectin (FCP) ≥ 150 µg/g or endoscopy/radiology). All “had been exposed in their regular diets to emulsifiers,” said Chassaing, a co-investigator, during a GMFH session on “Dietary Drivers of Health and Disease.”

They were randomized to either a low-emulsifier diet or to a low-emulsifier diet followed by emulsifier “resupplementation” — a design meant to “account for the very strong placebo effect that is always observed with dietary studies,” he said.

All patients received dietary counseling, a smart phone app and barcode scan to support shopping, and weekly support. They also received supermarket foods for 25% of their needs that were either free of emulsifiers or contained emulsifiers, and they were provided three snacks per day that were emulsifier-free or contained carrageenan, carboxymethycellulse (CMC), and polysorbate-80 (P80) — dietary emulsifiers that are commonly added to processed foods to enhance texture and extend shelf-life.

In the intention-to-treat (ITT) analysis, 49% of patients in the intervention group reached the primary endpoint of a 70-point reduction or more in CDAI response after 8 weeks compared with 31% of those in the control group (P = .019), with an adjusted relative risk of response of 3.1 (P = .003), Chassaing shared at the GMFH meeting, convened by the American Gastroenterological Association and the European Society of Neurogastroenterology and Motility.

In the per-protocol analysis (n = 119), 61% and 47% of patients in the intervention and control groups, respectively, reached the primary outcome of CDAI response, with an adjusted relative risk of response of 3.0 (P = .018), he said.

Secondary endpoints included CDAI remission at 24 weeks, and according to the abstract for the ECCO Congress, in the ITT analysis, patients in the intervention group were more than twice as likely to experience remission.

Chassaing noted at the GMFH meeting that as part of the study, he and coinvestigators have been investigating the participants’ gut microbiota with metagenomic analyses. The study was led by Kevin Whelan, PhD, head of the Department of Nutritional Sciences at King’s College London, London, England.

 

Can Emulsifier-Sensitive Individuals Be Identified?

In murine model research 10 years ago, Chassaing showed that the administration of CMC and P80 results in microbiota encroachment into the mucus layer of the gut, alterations in microbiota composition — including an increase in bacteria that produce pro-inflammatory flagellin — and development of chronic inflammation.

Wild-type mice treated with these compounds developed metabolic disease, and mice that were modified to be predisposed to colitis had a higher incidence of robust colitis. Moreover, fecal transplantation from emulsifier-treated mice to germ-free mice reproduced these changes, “clearly suggesting that the microbiome itself is sufficient to drive chronic inflammation,” he said.

In recent years, in humans, analyses from the large French NutriNet-Sante prospective cohort study have shown associations between exposure to food additive emulsifiers and the risk for cardiovascular disease, the risk for cancer (overall, breast, and prostate), and the risk for type 2 diabetes.

But to explore causality and better understand the mechanisms of emulsifier-driven changes on the microbiota, Chassaing and his colleagues also launched the FRESH study (Functional Research on Emulsifier in Humans), a double-blind randomized controlled-feeding study of the emulsifier CMC. For 11 days, nine healthy patients consumed an emulsifier-free diet and 11 consumed an identical diet enriched with 15 g/d of CMC.

Patients on the CMC-containing diet had reduced microbiota diversity and depletions of an array of microbiota-related metabolites, but only a small subset had profound alterations in microbiota composition and increased microbiota encroachment into the mucus layer. “Some seemed to be resistant to CMC-induced microbiota encroachment, while some were highly susceptible,” Chassaing said.

The pilot study raised the question, he said, of whether there is an “infectivity component” — some kind of “sensitive” gut microbiota composition — that may be associated with dietary emulsifier-driven inflammation and disease.

In other murine research, Chassaing and his team found that germ-free mice colonized with Crohn’s disease-associated adherent-invasive E coli (AIEC) and subsequently given CMC or P80 developed chronic inflammation and metabolic dysregulation, “clearly demonstrating that you can convert resistant mice to sensitive mice just by adding one bacteria to the ecosystem,” he said. “The presence of AIEC alone was sufficient to drive the detrimental effects of dietary emulsifiers.”

(In vitro research with transcriptomic analysis then showed that the emulsifiers directly elicit AIEC virulence gene expression, Chassaing and his coauthors wrote in their 2020 paper, facilitating AIEC’s “penetration of the mucus layer and adherence to epithelial cells and resulting in activation of host pro-inflammatory signaling.”)

“We don’t think it’s solely the AIEC bacteria that will drive emulsifier sensitivity, though…we think it’s more complex,” Chassaing said at the meeting. Overall, the findings raise the question of whether emulsifier-sensitive individuals can be identified.

This, he said, is one of his most recent research questions. His lab has led the development of an in vitro microbiota model built to predict an individual’s sensitivity to emulsifiers. In a study published in April, the model recapitulated the differential CMC sensitivity observed in the earlier FRESH study, suggesting that an individual’s sensitivity to emulsifiers can indeed be predicted by examining their baseline microbiota.

 

Interpreting the Epidemiology

Chassaing’s research arch illustrates the synergy between epidemiological research, basic/translational research, and clinical interventional research that’s needed to understand the diet-microbiome intersection in inflammatory bowel disease, said Ashwin Ananthakrishnan, MBBS, MPH, AGAF, associate professor of medicine at Massachusetts General Hospital, Boston, in an interview at the meeting.

“It’s a good example of how to really span the spectrum, starting from the big picture and going deeper to understand mechanisms, and starting from mechanisms and expanding it out,” Ananthakrishnan said.

In his own talk about research on IBD, Ananthakrishnan said that epidemiological data have shown over the past 10-15 years that total dietary fiber is inversely associated with the risk for Crohn’s disease (with the strongest associations with fiber from fruits and vegetables). Studies have also shown that a higher intake of polyunsaturated fatty acids is associated with a lower risk for ulcerative colitis, whereas “an n-6-fatty acid-rich diet is associated with a higher risk of ulcerative colitis,” he said.

Dietary cohort studies, meanwhile, have shed light on the influence of dietary patterns — such as the Mediterranean diet and diets with high inflammatory potential—on IBD. A diet rich in ultra-processed foods has also been shown in a prospective cohort study to be associated with a higher risk for Crohn’s disease, with certain categories of ultra-processed foods (eg, breads and breakfast foods) having the strongest associations.

Such studies are limited in part, however, by inadequate assessment of potentially relevant variables such as emulsifiers, preservatives, and how the food is processed, he said.

And in interpreting the epidemiological research on fiber and IBD, for instance, one must appreciate that “there are a number of mechanisms by which fiber is impactful…there’s a big picture to look at,” Ananthakrishnan said. Fiber “can affect the microbiome, clearly, it can affect the gut barrier, and it can affect bile acids, and there are detailed translational studies in support of each of these.”

But there are other constituents of fruits and vegetables “that could potentially influence disease risk, such as AhR ligands and polyphenols,” he said. “And importantly, people not eating a lot of fiber may be eating a lot of ultra-processed foods.”

Most interventional studies of fiber have not shown a benefit of a high-fiber diet, Ananthakrishnan said, but there are multiple possible reasons and factors at play, including potential population differences (eg, in inflammatory status or baseline microbiota), shortcomings of the interventions, and potentially inaccurate outcomes.

Abigail Johnson, PhD, RDN, associate director of the Nutrition Coordinating Center, University of Minnesota Twin Cities, which supports dietary analysis, said during the session that the focus of dietary research is “moving toward understanding overall dietary patterns” as opposed to focusing more narrowly on vitamins, minerals, and macronutrients such as proteins, fats, and carbohydrates.

This is an improvement, though “we still don’t have good approaches for understanding [the contributions of] things like additives and emulsifiers, food preparation and cooking, and food processing,” said Johnson, assistant professor in the Division of Epidemiology and Community Health at University of Minnesota Twin Cities. “Perhaps by looking at things at the food level we can overcome some of these limitations.”

Ananthakrishnan reported being a consultant for Geneoscopy and receiving a research grant from Takeda. Chassaing did not report any financial disclosures. Johnson reported that she had no financial disclosures.

A version of this article appeared on Medscape.com.

WASHINGTON, DC — A low-emulsifier-containing diet led to a threefold increased likelihood of improvement in symptoms of Crohn’s disease compared with an emulsifier-containing diet in a randomized double-blind dietary trial involving 154 patients with mildly active disease living across the United Kingdom.

The findings were reported at Gut Microbiota for Health (GMFH) World Summit 2025 by Benoit Chassaing, PhD, of the Institut Pasteur, Paris, France, whose research leading up to the trial has demonstrated that food additive emulsifiers —ubiquitous in processed foods — alter microbiota composition and lead to microbiota encroachment into the mucus layer of the gut and subsequent chronic gut inflammation.

Patients in the ADDapt trial, which was also reported in an abstract earlier this year at the European Crohn’s and Colitis Organization (ECCO) 2025 Congress, had a Crohn’s disease activity index (CDAI) of 150-250 and evidence of inflammation (faecal calprotectin (FCP) ≥ 150 µg/g or endoscopy/radiology). All “had been exposed in their regular diets to emulsifiers,” said Chassaing, a co-investigator, during a GMFH session on “Dietary Drivers of Health and Disease.”

They were randomized to either a low-emulsifier diet or to a low-emulsifier diet followed by emulsifier “resupplementation” — a design meant to “account for the very strong placebo effect that is always observed with dietary studies,” he said.

All patients received dietary counseling, a smart phone app and barcode scan to support shopping, and weekly support. They also received supermarket foods for 25% of their needs that were either free of emulsifiers or contained emulsifiers, and they were provided three snacks per day that were emulsifier-free or contained carrageenan, carboxymethycellulse (CMC), and polysorbate-80 (P80) — dietary emulsifiers that are commonly added to processed foods to enhance texture and extend shelf-life.

In the intention-to-treat (ITT) analysis, 49% of patients in the intervention group reached the primary endpoint of a 70-point reduction or more in CDAI response after 8 weeks compared with 31% of those in the control group (P = .019), with an adjusted relative risk of response of 3.1 (P = .003), Chassaing shared at the GMFH meeting, convened by the American Gastroenterological Association and the European Society of Neurogastroenterology and Motility.

In the per-protocol analysis (n = 119), 61% and 47% of patients in the intervention and control groups, respectively, reached the primary outcome of CDAI response, with an adjusted relative risk of response of 3.0 (P = .018), he said.

Secondary endpoints included CDAI remission at 24 weeks, and according to the abstract for the ECCO Congress, in the ITT analysis, patients in the intervention group were more than twice as likely to experience remission.

Chassaing noted at the GMFH meeting that as part of the study, he and coinvestigators have been investigating the participants’ gut microbiota with metagenomic analyses. The study was led by Kevin Whelan, PhD, head of the Department of Nutritional Sciences at King’s College London, London, England.

 

Can Emulsifier-Sensitive Individuals Be Identified?

In murine model research 10 years ago, Chassaing showed that the administration of CMC and P80 results in microbiota encroachment into the mucus layer of the gut, alterations in microbiota composition — including an increase in bacteria that produce pro-inflammatory flagellin — and development of chronic inflammation.

Wild-type mice treated with these compounds developed metabolic disease, and mice that were modified to be predisposed to colitis had a higher incidence of robust colitis. Moreover, fecal transplantation from emulsifier-treated mice to germ-free mice reproduced these changes, “clearly suggesting that the microbiome itself is sufficient to drive chronic inflammation,” he said.

In recent years, in humans, analyses from the large French NutriNet-Sante prospective cohort study have shown associations between exposure to food additive emulsifiers and the risk for cardiovascular disease, the risk for cancer (overall, breast, and prostate), and the risk for type 2 diabetes.

But to explore causality and better understand the mechanisms of emulsifier-driven changes on the microbiota, Chassaing and his colleagues also launched the FRESH study (Functional Research on Emulsifier in Humans), a double-blind randomized controlled-feeding study of the emulsifier CMC. For 11 days, nine healthy patients consumed an emulsifier-free diet and 11 consumed an identical diet enriched with 15 g/d of CMC.

Patients on the CMC-containing diet had reduced microbiota diversity and depletions of an array of microbiota-related metabolites, but only a small subset had profound alterations in microbiota composition and increased microbiota encroachment into the mucus layer. “Some seemed to be resistant to CMC-induced microbiota encroachment, while some were highly susceptible,” Chassaing said.

The pilot study raised the question, he said, of whether there is an “infectivity component” — some kind of “sensitive” gut microbiota composition — that may be associated with dietary emulsifier-driven inflammation and disease.

In other murine research, Chassaing and his team found that germ-free mice colonized with Crohn’s disease-associated adherent-invasive E coli (AIEC) and subsequently given CMC or P80 developed chronic inflammation and metabolic dysregulation, “clearly demonstrating that you can convert resistant mice to sensitive mice just by adding one bacteria to the ecosystem,” he said. “The presence of AIEC alone was sufficient to drive the detrimental effects of dietary emulsifiers.”

(In vitro research with transcriptomic analysis then showed that the emulsifiers directly elicit AIEC virulence gene expression, Chassaing and his coauthors wrote in their 2020 paper, facilitating AIEC’s “penetration of the mucus layer and adherence to epithelial cells and resulting in activation of host pro-inflammatory signaling.”)

“We don’t think it’s solely the AIEC bacteria that will drive emulsifier sensitivity, though…we think it’s more complex,” Chassaing said at the meeting. Overall, the findings raise the question of whether emulsifier-sensitive individuals can be identified.

This, he said, is one of his most recent research questions. His lab has led the development of an in vitro microbiota model built to predict an individual’s sensitivity to emulsifiers. In a study published in April, the model recapitulated the differential CMC sensitivity observed in the earlier FRESH study, suggesting that an individual’s sensitivity to emulsifiers can indeed be predicted by examining their baseline microbiota.

 

Interpreting the Epidemiology

Chassaing’s research arch illustrates the synergy between epidemiological research, basic/translational research, and clinical interventional research that’s needed to understand the diet-microbiome intersection in inflammatory bowel disease, said Ashwin Ananthakrishnan, MBBS, MPH, AGAF, associate professor of medicine at Massachusetts General Hospital, Boston, in an interview at the meeting.

“It’s a good example of how to really span the spectrum, starting from the big picture and going deeper to understand mechanisms, and starting from mechanisms and expanding it out,” Ananthakrishnan said.

In his own talk about research on IBD, Ananthakrishnan said that epidemiological data have shown over the past 10-15 years that total dietary fiber is inversely associated with the risk for Crohn’s disease (with the strongest associations with fiber from fruits and vegetables). Studies have also shown that a higher intake of polyunsaturated fatty acids is associated with a lower risk for ulcerative colitis, whereas “an n-6-fatty acid-rich diet is associated with a higher risk of ulcerative colitis,” he said.

Dietary cohort studies, meanwhile, have shed light on the influence of dietary patterns — such as the Mediterranean diet and diets with high inflammatory potential—on IBD. A diet rich in ultra-processed foods has also been shown in a prospective cohort study to be associated with a higher risk for Crohn’s disease, with certain categories of ultra-processed foods (eg, breads and breakfast foods) having the strongest associations.

Such studies are limited in part, however, by inadequate assessment of potentially relevant variables such as emulsifiers, preservatives, and how the food is processed, he said.

And in interpreting the epidemiological research on fiber and IBD, for instance, one must appreciate that “there are a number of mechanisms by which fiber is impactful…there’s a big picture to look at,” Ananthakrishnan said. Fiber “can affect the microbiome, clearly, it can affect the gut barrier, and it can affect bile acids, and there are detailed translational studies in support of each of these.”

But there are other constituents of fruits and vegetables “that could potentially influence disease risk, such as AhR ligands and polyphenols,” he said. “And importantly, people not eating a lot of fiber may be eating a lot of ultra-processed foods.”

Most interventional studies of fiber have not shown a benefit of a high-fiber diet, Ananthakrishnan said, but there are multiple possible reasons and factors at play, including potential population differences (eg, in inflammatory status or baseline microbiota), shortcomings of the interventions, and potentially inaccurate outcomes.

Abigail Johnson, PhD, RDN, associate director of the Nutrition Coordinating Center, University of Minnesota Twin Cities, which supports dietary analysis, said during the session that the focus of dietary research is “moving toward understanding overall dietary patterns” as opposed to focusing more narrowly on vitamins, minerals, and macronutrients such as proteins, fats, and carbohydrates.

This is an improvement, though “we still don’t have good approaches for understanding [the contributions of] things like additives and emulsifiers, food preparation and cooking, and food processing,” said Johnson, assistant professor in the Division of Epidemiology and Community Health at University of Minnesota Twin Cities. “Perhaps by looking at things at the food level we can overcome some of these limitations.”

Ananthakrishnan reported being a consultant for Geneoscopy and receiving a research grant from Takeda. Chassaing did not report any financial disclosures. Johnson reported that she had no financial disclosures.

A version of this article appeared on Medscape.com.

A head-to-head comparison of the JAK inhibitor drug tofacitinib and chimeric monoclonal antibody infliximab in the treatment of acute severe ulcerative colitis (ASUC) shows that, contrary to concerns, tofacitinib is not associated with worse postoperative complications and in fact may reduce the risk of the need for colectomy.

“Tofacitinib has shown efficacy in managing ASUC, but concerns about postoperative complications have limited its adoption,” reported the authors in research published in Clinical Gastroenterology and Hepatology.“This study shows that tofacitinib is safe and doesn’t impair wound healing or lead to more infections if the patient needs an urgent colectomy, which is unfortunately common in this population,” senior author Jeffrey A. Berinstein, MD, of the Division of Gastroenterology and Hepatology, Michigan Medicine, Ann Arbor, Michigan, told GI & Hepatology News. 

Recent treatment advances for UC have provided significant benefits in reducing the severity of symptoms; however, about a quarter of patients go on to experience flares, with fecal urgency, rectal bleeding, and severe abdominal pain of ASUC potentially requiring hospitalization.

The standard of care for those patients is rapid induction with intravenous (IV) corticosteroids; however, up to 30% of patients don’t respond to those interventions, and even with subsequent treatment of cyclosporine and infliximab helping to reduce the risk for an urgent colectomy, patients often don’t respond, and ultimately, up to a third of patients with ASUC end up having to receive a colectomy.

While JAK inhibitor therapies, including tofacitinib and upadacitinib, have recently emerged as potentially important treatment options in such cases, showing reductions in the risk for colectomy, concerns about the drugs’ downstream biologic effects have given many clinicians reservations about their use.

“Anecdotally, gastroenterologists and surgeons have expressed concern about JAK inhibitors leading to poor wound healing, as well as increasing both intraoperative and postoperative complications, despite limited data to support these claims,” the authors wrote.

To better understand those possible risks, first author Charlotte Larson, MD, of the Department of Internal Medicine, Michigan Medicine, and colleagues conducted a multicenter, retrospective, case-control study of 109 patients hospitalized with ASUC at two centers in the US and 14 in France.

Of the patients, 41 were treated with tofacitinib and 68 with infliximab prior to colectomy. 

Among patients treated with tofacitinib, five (12.2%) received infliximab and four (9.8%) received cyclosporine rescue immediately prior to receiving tofacitinib during the index admission. In the infliximab group, one (1.5%) received rescue cyclosporine.

In a univariate analysis, the tofacitinib-treated patients showed significantly lower overall rates of postoperative complications than infliximab-treated patients (31.7% vs 64.7%; odds ratio [OR], 0.33; P = .006).

The tofacitinib-treated group also had lower rates of serious postoperative complications (12% vs 28.9; OR, 0.20; P = .016).

After adjusting for multivariate factors including age, inflammatory burden, nutrition status, 90-day cumulative corticosteroid exposure and open surgery, there was a trend favoring tofacitinib but no statistically significant difference between the two treatments in terms of serious postoperative complications (P = .061). 

However, a significantly lower rate of overall postoperative complications with tofacitinib was observed after the adjustment (odds ratio, 0.38; P = .023).

Importantly, a subanalysis showed that the 63.4% of tofacitinib-treated patients receiving the standard FDA-approved induction dose of 10 mg twice daily did indeed have significantly lower rates than infliximab-treated patients in terms of serious postoperative complications (OR, .10; P = .031), as well as overall postoperative complications (OR, 0.23; P = .003), whereas neither of the outcomes were significantly improved among the 36.6% of patients who received the higher-intensity thrice-daily tofacitinib dose (P = .3 and P = .4, respectively).

Further complicating the matter, in a previous case-control study that the research team conducted, it was the off-label, 10 mg thrice-daily dose of tofacitinib that performed favorably and was associated with a significantly lower risk for colectomy than the twice-daily dose (hazard ratio 0.28; P = .018); the twice-daily dose was not protective.

Berinstein added that a hypothesis for the benefits overall, with either dose, is that tofacitinib’s anti-inflammatory properties are key.

“We believe that lowering inflammation as much as possible, with the colon less inflamed, could be providing the benefit in lowering complications rate in surgery,” he explained.

Regarding the dosing, “it’s a careful trade-off,” Berinstein added. “Obviously, we want to avoid the need for a colectomy in the first place, as it is a life-changing surgery, but we don’t want to increase the risk of infections.” 

In other findings, the tofacitinib group had no increased risk for postoperative venous thrombotic embolisms (VTEs), which is important as tofacitinib exposure has previously been associated with an increased risk for VTEs independent of other prothrombotic factors common to patients with ASUC, including decreased ambulation, active inflammation, corticosteroid use, and major colorectal surgery.

“This observed absence of an increased VTE risk may alleviate some of the hypothetical postoperative safety concern attributed to JAK inhibitor therapy in this high-risk population,” the authors wrote.

Overall, the results underscore that “providers should feel comfortable using this medication if they need it and if they think it’s most likely to help their patients avoid colectomy,” Berinstein said.

“They should not give pause over concerns of postoperative complications because we didn’t show that,” he said.

Commenting on the study, Joseph D. Feuerstein, MD, AGAF, of the Department of Medicine and Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, noted that, in general, in patients with ASUC who fail on IV steroids, “the main treatments are infliximab, cyclosporine, or a JAK inhibitor like tofacitinib or upadacitinib, [and] knowing that if someone needs surgery, the complication rates are similar and that pre-operative use is okay is reassuring.”

Regarding the protective effect observed with some circumstances, “I don’t put too much weight into that,” he noted. “[One] could speculate that it is somehow related to faster half-life of the drug, and it might not sit around as long,” he said.

Feuerstein added that “the study design being retrospective is a limitation, but this is the best data we have to date.”

Berinstein and Feuerstein had no disclosures to report.

A version of this article appeared on Medscape.com . 

A head-to-head comparison of the JAK inhibitor drug tofacitinib and chimeric monoclonal antibody infliximab in the treatment of acute severe ulcerative colitis (ASUC) shows that, contrary to concerns, tofacitinib is not associated with worse postoperative complications and in fact may reduce the risk of the need for colectomy.

“Tofacitinib has shown efficacy in managing ASUC, but concerns about postoperative complications have limited its adoption,” reported the authors in research published in Clinical Gastroenterology and Hepatology.“This study shows that tofacitinib is safe and doesn’t impair wound healing or lead to more infections if the patient needs an urgent colectomy, which is unfortunately common in this population,” senior author Jeffrey A. Berinstein, MD, of the Division of Gastroenterology and Hepatology, Michigan Medicine, Ann Arbor, Michigan, told GI & Hepatology News. 

Recent treatment advances for UC have provided significant benefits in reducing the severity of symptoms; however, about a quarter of patients go on to experience flares, with fecal urgency, rectal bleeding, and severe abdominal pain of ASUC potentially requiring hospitalization.

The standard of care for those patients is rapid induction with intravenous (IV) corticosteroids; however, up to 30% of patients don’t respond to those interventions, and even with subsequent treatment of cyclosporine and infliximab helping to reduce the risk for an urgent colectomy, patients often don’t respond, and ultimately, up to a third of patients with ASUC end up having to receive a colectomy.

While JAK inhibitor therapies, including tofacitinib and upadacitinib, have recently emerged as potentially important treatment options in such cases, showing reductions in the risk for colectomy, concerns about the drugs’ downstream biologic effects have given many clinicians reservations about their use.

“Anecdotally, gastroenterologists and surgeons have expressed concern about JAK inhibitors leading to poor wound healing, as well as increasing both intraoperative and postoperative complications, despite limited data to support these claims,” the authors wrote.

To better understand those possible risks, first author Charlotte Larson, MD, of the Department of Internal Medicine, Michigan Medicine, and colleagues conducted a multicenter, retrospective, case-control study of 109 patients hospitalized with ASUC at two centers in the US and 14 in France.

Of the patients, 41 were treated with tofacitinib and 68 with infliximab prior to colectomy. 

Among patients treated with tofacitinib, five (12.2%) received infliximab and four (9.8%) received cyclosporine rescue immediately prior to receiving tofacitinib during the index admission. In the infliximab group, one (1.5%) received rescue cyclosporine.

In a univariate analysis, the tofacitinib-treated patients showed significantly lower overall rates of postoperative complications than infliximab-treated patients (31.7% vs 64.7%; odds ratio [OR], 0.33; P = .006).

The tofacitinib-treated group also had lower rates of serious postoperative complications (12% vs 28.9; OR, 0.20; P = .016).

After adjusting for multivariate factors including age, inflammatory burden, nutrition status, 90-day cumulative corticosteroid exposure and open surgery, there was a trend favoring tofacitinib but no statistically significant difference between the two treatments in terms of serious postoperative complications (P = .061). 

However, a significantly lower rate of overall postoperative complications with tofacitinib was observed after the adjustment (odds ratio, 0.38; P = .023).

Importantly, a subanalysis showed that the 63.4% of tofacitinib-treated patients receiving the standard FDA-approved induction dose of 10 mg twice daily did indeed have significantly lower rates than infliximab-treated patients in terms of serious postoperative complications (OR, .10; P = .031), as well as overall postoperative complications (OR, 0.23; P = .003), whereas neither of the outcomes were significantly improved among the 36.6% of patients who received the higher-intensity thrice-daily tofacitinib dose (P = .3 and P = .4, respectively).

Further complicating the matter, in a previous case-control study that the research team conducted, it was the off-label, 10 mg thrice-daily dose of tofacitinib that performed favorably and was associated with a significantly lower risk for colectomy than the twice-daily dose (hazard ratio 0.28; P = .018); the twice-daily dose was not protective.

Berinstein added that a hypothesis for the benefits overall, with either dose, is that tofacitinib’s anti-inflammatory properties are key.

“We believe that lowering inflammation as much as possible, with the colon less inflamed, could be providing the benefit in lowering complications rate in surgery,” he explained.

Regarding the dosing, “it’s a careful trade-off,” Berinstein added. “Obviously, we want to avoid the need for a colectomy in the first place, as it is a life-changing surgery, but we don’t want to increase the risk of infections.” 

In other findings, the tofacitinib group had no increased risk for postoperative venous thrombotic embolisms (VTEs), which is important as tofacitinib exposure has previously been associated with an increased risk for VTEs independent of other prothrombotic factors common to patients with ASUC, including decreased ambulation, active inflammation, corticosteroid use, and major colorectal surgery.

“This observed absence of an increased VTE risk may alleviate some of the hypothetical postoperative safety concern attributed to JAK inhibitor therapy in this high-risk population,” the authors wrote.

Overall, the results underscore that “providers should feel comfortable using this medication if they need it and if they think it’s most likely to help their patients avoid colectomy,” Berinstein said.

“They should not give pause over concerns of postoperative complications because we didn’t show that,” he said.

Commenting on the study, Joseph D. Feuerstein, MD, AGAF, of the Department of Medicine and Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, noted that, in general, in patients with ASUC who fail on IV steroids, “the main treatments are infliximab, cyclosporine, or a JAK inhibitor like tofacitinib or upadacitinib, [and] knowing that if someone needs surgery, the complication rates are similar and that pre-operative use is okay is reassuring.”

Regarding the protective effect observed with some circumstances, “I don’t put too much weight into that,” he noted. “[One] could speculate that it is somehow related to faster half-life of the drug, and it might not sit around as long,” he said.

Feuerstein added that “the study design being retrospective is a limitation, but this is the best data we have to date.”

Berinstein and Feuerstein had no disclosures to report.

A version of this article appeared on Medscape.com . 

A head-to-head comparison of the JAK inhibitor drug tofacitinib and chimeric monoclonal antibody infliximab in the treatment of acute severe ulcerative colitis (ASUC) shows that, contrary to concerns, tofacitinib is not associated with worse postoperative complications and in fact may reduce the risk of the need for colectomy.

“Tofacitinib has shown efficacy in managing ASUC, but concerns about postoperative complications have limited its adoption,” reported the authors in research published in Clinical Gastroenterology and Hepatology.“This study shows that tofacitinib is safe and doesn’t impair wound healing or lead to more infections if the patient needs an urgent colectomy, which is unfortunately common in this population,” senior author Jeffrey A. Berinstein, MD, of the Division of Gastroenterology and Hepatology, Michigan Medicine, Ann Arbor, Michigan, told GI & Hepatology News. 

Recent treatment advances for UC have provided significant benefits in reducing the severity of symptoms; however, about a quarter of patients go on to experience flares, with fecal urgency, rectal bleeding, and severe abdominal pain of ASUC potentially requiring hospitalization.

The standard of care for those patients is rapid induction with intravenous (IV) corticosteroids; however, up to 30% of patients don’t respond to those interventions, and even with subsequent treatment of cyclosporine and infliximab helping to reduce the risk for an urgent colectomy, patients often don’t respond, and ultimately, up to a third of patients with ASUC end up having to receive a colectomy.

While JAK inhibitor therapies, including tofacitinib and upadacitinib, have recently emerged as potentially important treatment options in such cases, showing reductions in the risk for colectomy, concerns about the drugs’ downstream biologic effects have given many clinicians reservations about their use.

“Anecdotally, gastroenterologists and surgeons have expressed concern about JAK inhibitors leading to poor wound healing, as well as increasing both intraoperative and postoperative complications, despite limited data to support these claims,” the authors wrote.

To better understand those possible risks, first author Charlotte Larson, MD, of the Department of Internal Medicine, Michigan Medicine, and colleagues conducted a multicenter, retrospective, case-control study of 109 patients hospitalized with ASUC at two centers in the US and 14 in France.

Of the patients, 41 were treated with tofacitinib and 68 with infliximab prior to colectomy. 

Among patients treated with tofacitinib, five (12.2%) received infliximab and four (9.8%) received cyclosporine rescue immediately prior to receiving tofacitinib during the index admission. In the infliximab group, one (1.5%) received rescue cyclosporine.

In a univariate analysis, the tofacitinib-treated patients showed significantly lower overall rates of postoperative complications than infliximab-treated patients (31.7% vs 64.7%; odds ratio [OR], 0.33; P = .006).

The tofacitinib-treated group also had lower rates of serious postoperative complications (12% vs 28.9; OR, 0.20; P = .016).

After adjusting for multivariate factors including age, inflammatory burden, nutrition status, 90-day cumulative corticosteroid exposure and open surgery, there was a trend favoring tofacitinib but no statistically significant difference between the two treatments in terms of serious postoperative complications (P = .061). 

However, a significantly lower rate of overall postoperative complications with tofacitinib was observed after the adjustment (odds ratio, 0.38; P = .023).

Importantly, a subanalysis showed that the 63.4% of tofacitinib-treated patients receiving the standard FDA-approved induction dose of 10 mg twice daily did indeed have significantly lower rates than infliximab-treated patients in terms of serious postoperative complications (OR, .10; P = .031), as well as overall postoperative complications (OR, 0.23; P = .003), whereas neither of the outcomes were significantly improved among the 36.6% of patients who received the higher-intensity thrice-daily tofacitinib dose (P = .3 and P = .4, respectively).

Further complicating the matter, in a previous case-control study that the research team conducted, it was the off-label, 10 mg thrice-daily dose of tofacitinib that performed favorably and was associated with a significantly lower risk for colectomy than the twice-daily dose (hazard ratio 0.28; P = .018); the twice-daily dose was not protective.

Berinstein added that a hypothesis for the benefits overall, with either dose, is that tofacitinib’s anti-inflammatory properties are key.

“We believe that lowering inflammation as much as possible, with the colon less inflamed, could be providing the benefit in lowering complications rate in surgery,” he explained.

Regarding the dosing, “it’s a careful trade-off,” Berinstein added. “Obviously, we want to avoid the need for a colectomy in the first place, as it is a life-changing surgery, but we don’t want to increase the risk of infections.” 

In other findings, the tofacitinib group had no increased risk for postoperative venous thrombotic embolisms (VTEs), which is important as tofacitinib exposure has previously been associated with an increased risk for VTEs independent of other prothrombotic factors common to patients with ASUC, including decreased ambulation, active inflammation, corticosteroid use, and major colorectal surgery.

“This observed absence of an increased VTE risk may alleviate some of the hypothetical postoperative safety concern attributed to JAK inhibitor therapy in this high-risk population,” the authors wrote.

Overall, the results underscore that “providers should feel comfortable using this medication if they need it and if they think it’s most likely to help their patients avoid colectomy,” Berinstein said.

“They should not give pause over concerns of postoperative complications because we didn’t show that,” he said.

Commenting on the study, Joseph D. Feuerstein, MD, AGAF, of the Department of Medicine and Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, noted that, in general, in patients with ASUC who fail on IV steroids, “the main treatments are infliximab, cyclosporine, or a JAK inhibitor like tofacitinib or upadacitinib, [and] knowing that if someone needs surgery, the complication rates are similar and that pre-operative use is okay is reassuring.”

Regarding the protective effect observed with some circumstances, “I don’t put too much weight into that,” he noted. “[One] could speculate that it is somehow related to faster half-life of the drug, and it might not sit around as long,” he said.

Feuerstein added that “the study design being retrospective is a limitation, but this is the best data we have to date.”

Berinstein and Feuerstein had no disclosures to report.

A version of this article appeared on Medscape.com . 

The American Gastroenterological Association (AGA) has released a comprehensive clinical practice update on lifting agents for endoscopic surgery.

Published in Clinical Gastroenterology and Hepatology, the commentary reviews available agents and provides clinically relevant commentary on their indications and use — with the caveat that it is not a formal systematic review but rather empirical advice for endoscopists. No formal rating of the quality of evidence or strength of recommendations was performed.

Led by Tobias Zuchelli, MD, a clinical associate professor at Michigan State University and a gastroenterologist at the Henry Ford Health System in Detroit, the expert panel noted that endoscopists are increasingly resecting precancerous lesions and early cancers of the gastrointestinal tract.

“Although new endoscopic procedures have been developed, there had not been much in terms of high-quality guidance on lifting agents,” panelist Amit V. Patel, MD, a professor of medicine at Duke University and director of Endoscopy at Durham Veterans Affairs Medical Center in Durham, North Carolina, told GI & Hepatology News. “With our better understanding and use of techniques, this commentary was timely. It summarizes the available data on the topic and includes our clinical experiences.”

Filling that knowledge gap, the document reviews in detail the timing and methods of agent injection according to procedure type, including the dynamic needle approach, the empirical merits of different agents such as saline (with or without blue contrast) and viscous agents, as well as lift-enhancing assistive devices — for example, the ERBEJET 2 high-pressure water jet, an adjustable hydrosurgical device to facilitate lifting. A chart provides an at-a-glance summary of agents and their pros and cons.

“The feedback from gastroenterologists so far has been quite positive on social media and on GI channels,” Patel said.

Endoscopic resection has evolved from snare polypectomy to endoscopic mucosal resection (EMR) and now, endoscopic submucosal dissection (ESD). The primary benefit of submucosal lifting is the creation of a separating submucosal cushion between the lesion and muscularis propria (MP), which reduces the risk for immediate or delayed perforation of the muscle. Adding a contrast agent also demarcates lesion margins and stains the submucosa, which is fundamental to ESD and allows for assessment of MP injury during EMR.

For decades, homemade solutions were used to lift lesions before removal, with the sentinel agent being normal saline, later mixed with a blue contrast agent, usually indigo carmine or methylene blue. The authors noted that some endoscopists performing ESD start the submucosal injection and incision using a prepackaged viscous solution. “The endoscopist may continue with the viscous fluid or transition to saline or another less expensive solution,” they wrote.

Saline tends to dissipate more quickly than viscous solutions, however. In 2015, the polymer compound SIC-8000 became the first FDA-approved submucosal injection agent. Since then, several other fluids have come on the market, although homemade agents remain available.

Among the update’s recommendations, the fluid selected for EMR should be determined by lesion size, predicted histology, and endoscopist preference. Based on the US Multi-Society Task Force (USMSTF) on Colorectal Cancer, submucosal injection is optional for nonpedunculated colorectal lesions (NPCRLs) of intermediate size (10-19 mm).

Cold snare polypectomy without submucosal injection was later found to be non-inferior to other resection methods utilizing submucosal injection for NPCRLs ≤ 15 mm. 

The update noted that the USMSTF considers EMR first-line therapy for most NPCRLs ≥ 20 mm and advocates viscous solutions as preferred, while the use of lifting agents for pedunculated polyps is generally at the discretion of the endoscopist.

For Patel, the main “clinical pearls” in the update are adding a contrast agent to normal saline, using a viscous agent for cold EMR, and manipulating the injection needle first tangentially and then dynamically toward the lumen to maximize separation of the lesion.

In terms of the ideal, an optimal lifting solution would be readily available, inexpensive, and premixed, providing a sustained submucosal cushion. “However, this ideal solution currently does not exist. Injection fluids should, therefore, be selected based on planned resection method, predicted histology, local expertise and preferences, and cost,” the panelists wrote.

Added Patel, “A lot of the agents out there check most of these boxes, but we’re hoping for further development toward the ideal.”

Offering a nonparticipant’s perspective on the overview, Wasseem Skef, MD, a gastroenterologist at UTHealth Houston, found the update very useful. “It always helps to have the literature summarized,” he told GI & Hepatology News. “It’s a pretty balanced review that pulls together the various options but allows people to stick to their preferred practice.”

In his practice, the lifting agent selected depends on the type of resection. “Viscous agents are generally more popular for EMR-type resections,” Skef said. One unanswered question, he noted, is whether adding a hemostatic agent would be superior to a viscous agent alone. “But overall, this is a nice summary of available agents. Gastroenterologists should consider these different options if doing procedures like EMR.”

This review was sponsored by the AGA Institute. 

Zuchelli is a consultant for Boston Scientific. Patel consults for Medpace, Renexxion, and Sanofi. Skef reported having no relevant disclosures.

A version of this article appeared on Medscape.com . 

The American Gastroenterological Association (AGA) has released a comprehensive clinical practice update on lifting agents for endoscopic surgery.

Published in Clinical Gastroenterology and Hepatology, the commentary reviews available agents and provides clinically relevant commentary on their indications and use — with the caveat that it is not a formal systematic review but rather empirical advice for endoscopists. No formal rating of the quality of evidence or strength of recommendations was performed.

Led by Tobias Zuchelli, MD, a clinical associate professor at Michigan State University and a gastroenterologist at the Henry Ford Health System in Detroit, the expert panel noted that endoscopists are increasingly resecting precancerous lesions and early cancers of the gastrointestinal tract.

“Although new endoscopic procedures have been developed, there had not been much in terms of high-quality guidance on lifting agents,” panelist Amit V. Patel, MD, a professor of medicine at Duke University and director of Endoscopy at Durham Veterans Affairs Medical Center in Durham, North Carolina, told GI & Hepatology News. “With our better understanding and use of techniques, this commentary was timely. It summarizes the available data on the topic and includes our clinical experiences.”

Filling that knowledge gap, the document reviews in detail the timing and methods of agent injection according to procedure type, including the dynamic needle approach, the empirical merits of different agents such as saline (with or without blue contrast) and viscous agents, as well as lift-enhancing assistive devices — for example, the ERBEJET 2 high-pressure water jet, an adjustable hydrosurgical device to facilitate lifting. A chart provides an at-a-glance summary of agents and their pros and cons.

“The feedback from gastroenterologists so far has been quite positive on social media and on GI channels,” Patel said.

Endoscopic resection has evolved from snare polypectomy to endoscopic mucosal resection (EMR) and now, endoscopic submucosal dissection (ESD). The primary benefit of submucosal lifting is the creation of a separating submucosal cushion between the lesion and muscularis propria (MP), which reduces the risk for immediate or delayed perforation of the muscle. Adding a contrast agent also demarcates lesion margins and stains the submucosa, which is fundamental to ESD and allows for assessment of MP injury during EMR.

For decades, homemade solutions were used to lift lesions before removal, with the sentinel agent being normal saline, later mixed with a blue contrast agent, usually indigo carmine or methylene blue. The authors noted that some endoscopists performing ESD start the submucosal injection and incision using a prepackaged viscous solution. “The endoscopist may continue with the viscous fluid or transition to saline or another less expensive solution,” they wrote.

Saline tends to dissipate more quickly than viscous solutions, however. In 2015, the polymer compound SIC-8000 became the first FDA-approved submucosal injection agent. Since then, several other fluids have come on the market, although homemade agents remain available.

Among the update’s recommendations, the fluid selected for EMR should be determined by lesion size, predicted histology, and endoscopist preference. Based on the US Multi-Society Task Force (USMSTF) on Colorectal Cancer, submucosal injection is optional for nonpedunculated colorectal lesions (NPCRLs) of intermediate size (10-19 mm).

Cold snare polypectomy without submucosal injection was later found to be non-inferior to other resection methods utilizing submucosal injection for NPCRLs ≤ 15 mm. 

The update noted that the USMSTF considers EMR first-line therapy for most NPCRLs ≥ 20 mm and advocates viscous solutions as preferred, while the use of lifting agents for pedunculated polyps is generally at the discretion of the endoscopist.

For Patel, the main “clinical pearls” in the update are adding a contrast agent to normal saline, using a viscous agent for cold EMR, and manipulating the injection needle first tangentially and then dynamically toward the lumen to maximize separation of the lesion.

In terms of the ideal, an optimal lifting solution would be readily available, inexpensive, and premixed, providing a sustained submucosal cushion. “However, this ideal solution currently does not exist. Injection fluids should, therefore, be selected based on planned resection method, predicted histology, local expertise and preferences, and cost,” the panelists wrote.

Added Patel, “A lot of the agents out there check most of these boxes, but we’re hoping for further development toward the ideal.”

Offering a nonparticipant’s perspective on the overview, Wasseem Skef, MD, a gastroenterologist at UTHealth Houston, found the update very useful. “It always helps to have the literature summarized,” he told GI & Hepatology News. “It’s a pretty balanced review that pulls together the various options but allows people to stick to their preferred practice.”

In his practice, the lifting agent selected depends on the type of resection. “Viscous agents are generally more popular for EMR-type resections,” Skef said. One unanswered question, he noted, is whether adding a hemostatic agent would be superior to a viscous agent alone. “But overall, this is a nice summary of available agents. Gastroenterologists should consider these different options if doing procedures like EMR.”

This review was sponsored by the AGA Institute. 

Zuchelli is a consultant for Boston Scientific. Patel consults for Medpace, Renexxion, and Sanofi. Skef reported having no relevant disclosures.

A version of this article appeared on Medscape.com . 

The American Gastroenterological Association (AGA) has released a comprehensive clinical practice update on lifting agents for endoscopic surgery.

Published in Clinical Gastroenterology and Hepatology, the commentary reviews available agents and provides clinically relevant commentary on their indications and use — with the caveat that it is not a formal systematic review but rather empirical advice for endoscopists. No formal rating of the quality of evidence or strength of recommendations was performed.

Led by Tobias Zuchelli, MD, a clinical associate professor at Michigan State University and a gastroenterologist at the Henry Ford Health System in Detroit, the expert panel noted that endoscopists are increasingly resecting precancerous lesions and early cancers of the gastrointestinal tract.

“Although new endoscopic procedures have been developed, there had not been much in terms of high-quality guidance on lifting agents,” panelist Amit V. Patel, MD, a professor of medicine at Duke University and director of Endoscopy at Durham Veterans Affairs Medical Center in Durham, North Carolina, told GI & Hepatology News. “With our better understanding and use of techniques, this commentary was timely. It summarizes the available data on the topic and includes our clinical experiences.”

Filling that knowledge gap, the document reviews in detail the timing and methods of agent injection according to procedure type, including the dynamic needle approach, the empirical merits of different agents such as saline (with or without blue contrast) and viscous agents, as well as lift-enhancing assistive devices — for example, the ERBEJET 2 high-pressure water jet, an adjustable hydrosurgical device to facilitate lifting. A chart provides an at-a-glance summary of agents and their pros and cons.

“The feedback from gastroenterologists so far has been quite positive on social media and on GI channels,” Patel said.

Endoscopic resection has evolved from snare polypectomy to endoscopic mucosal resection (EMR) and now, endoscopic submucosal dissection (ESD). The primary benefit of submucosal lifting is the creation of a separating submucosal cushion between the lesion and muscularis propria (MP), which reduces the risk for immediate or delayed perforation of the muscle. Adding a contrast agent also demarcates lesion margins and stains the submucosa, which is fundamental to ESD and allows for assessment of MP injury during EMR.

For decades, homemade solutions were used to lift lesions before removal, with the sentinel agent being normal saline, later mixed with a blue contrast agent, usually indigo carmine or methylene blue. The authors noted that some endoscopists performing ESD start the submucosal injection and incision using a prepackaged viscous solution. “The endoscopist may continue with the viscous fluid or transition to saline or another less expensive solution,” they wrote.

Saline tends to dissipate more quickly than viscous solutions, however. In 2015, the polymer compound SIC-8000 became the first FDA-approved submucosal injection agent. Since then, several other fluids have come on the market, although homemade agents remain available.

Among the update’s recommendations, the fluid selected for EMR should be determined by lesion size, predicted histology, and endoscopist preference. Based on the US Multi-Society Task Force (USMSTF) on Colorectal Cancer, submucosal injection is optional for nonpedunculated colorectal lesions (NPCRLs) of intermediate size (10-19 mm).

Cold snare polypectomy without submucosal injection was later found to be non-inferior to other resection methods utilizing submucosal injection for NPCRLs ≤ 15 mm. 

The update noted that the USMSTF considers EMR first-line therapy for most NPCRLs ≥ 20 mm and advocates viscous solutions as preferred, while the use of lifting agents for pedunculated polyps is generally at the discretion of the endoscopist.

For Patel, the main “clinical pearls” in the update are adding a contrast agent to normal saline, using a viscous agent for cold EMR, and manipulating the injection needle first tangentially and then dynamically toward the lumen to maximize separation of the lesion.

In terms of the ideal, an optimal lifting solution would be readily available, inexpensive, and premixed, providing a sustained submucosal cushion. “However, this ideal solution currently does not exist. Injection fluids should, therefore, be selected based on planned resection method, predicted histology, local expertise and preferences, and cost,” the panelists wrote.

Added Patel, “A lot of the agents out there check most of these boxes, but we’re hoping for further development toward the ideal.”

Offering a nonparticipant’s perspective on the overview, Wasseem Skef, MD, a gastroenterologist at UTHealth Houston, found the update very useful. “It always helps to have the literature summarized,” he told GI & Hepatology News. “It’s a pretty balanced review that pulls together the various options but allows people to stick to their preferred practice.”

In his practice, the lifting agent selected depends on the type of resection. “Viscous agents are generally more popular for EMR-type resections,” Skef said. One unanswered question, he noted, is whether adding a hemostatic agent would be superior to a viscous agent alone. “But overall, this is a nice summary of available agents. Gastroenterologists should consider these different options if doing procedures like EMR.”

This review was sponsored by the AGA Institute. 

Zuchelli is a consultant for Boston Scientific. Patel consults for Medpace, Renexxion, and Sanofi. Skef reported having no relevant disclosures.

A version of this article appeared on Medscape.com . 

The prevalence of irritable bowel syndrome (IBS) and chronic idiopathic constipation among US adults rose significantly during the COVID-19 pandemic, with a near doubling of the national rate of IBS over 2 years, a study has found.

The uptick is probably due to not only the direct impact of SARS-CoV-2 infection on the gastrointestinal tract but also to the psychological stress associated with pandemic life, the study team said. 

“COVID infection itself can definitely cause gastrointestinal symptoms like diarrhea, nausea, and abdominal pain — and for some people, those symptoms can linger and lead to chronic conditions like IBS,” Christopher V. Almario, MD, MSHPM, lead author and gastroenterologist at Cedars-Sinai Medical Center, Los Angeles, California, told GI & Hepatology News. 

“But the stress of living through the pandemic — lockdowns, fear, isolation — also likely played a major role as well in the increased prevalence of digestive disorders. Both the infection itself and the psychological toll of the pandemic can disrupt the gut-brain axis and trigger chronic digestive disorders like IBS,” Almario said. 

The study was published in Neurogastroenterology & Motility.

 

Growing Burden of Gut Disorders 

Disorders of gut-brain interaction (DGBIs) are a heterogeneous group of conditions in which gastrointestinal symptoms occur without any detectable structural or biochemical abnormalities in the digestive tract. They include IBS, functional dyspepsia, and chronic idiopathic constipation, among others. 

DGBIs are highly prevalent. Research has shown that nearly 40% of people in the US meet Rome IV criteria for at least one DGBI. 

Almario and colleagues assessed trends in prevalence of these conditions during the COVID-19 pandemic. Starting in May 2020 through May 2022, they conducted a series of online surveys with more than 160,000 adults aged 18 or older using validated Rome IV diagnostic questionnaires. 

Results showed that during the pandemic, IBS prevalence rose from 6.1% in May 2020 to 11.0% by May 2022, an increase of 0.188% per month (adjusted P < .001). 

Chronic idiopathic constipation showed a smaller but statistically significant increase, from 6.0% to 6.4% (0.056% per month; adjusted P < .001). 

Within the IBS subtypes, mixed-type IBS showed the largest relative increase (0.085% per month), followed by IBS with constipation (0.041% per month) and IBS with diarrhea (0.037% per month). 

There were no significant changes in the prevalence of other DGBIs, such as functional bloating, functional diarrhea, or functional dyspepsia, during the study period. 

Almario told GI & Hepatology News only about 9% of those surveyed reported a positive COVID test at the time of the surveys, but that figure probably underrepresents actual infections, especially in the early months of the pandemic. “Most of the survey responses came in during the earlier phases of the pandemic, and the percentage reporting a positive test increased over time,” he explained. 

Almario also noted that this study did not directly compare digestive disorder rates between infected and uninfected individuals. However, a separate study by the Cedars-Sinai team currently undergoing peer review addresses that question more directly. “That study, along with several other studies, show that having COVID increases the risk of developing conditions like IBS and functional dyspepsia,” Almario said. 

Taken together, the findings “underscore the increasing healthcare and economic burden of DGBI in the post-pandemic era, emphasizing the need for targeted efforts to effectively diagnose and manage these complex conditions,” they wrote. 

“This will be especially challenging for healthcare systems to address, given the existing shortage of primary care physicians and gastroenterologists — clinicians who primarily manage individuals with DGBI,” they noted. 

Support for this study was received from Ironwood Pharmaceuticals and Salix Pharmaceuticals in the form of institutional research grants to Cedars-Sinai. Almario has consulted for Exact Sciences, Greenspace Labs, Owlstone Medical, Salix Pharmaceuticals, and Universal DX.

A version of this article appeared on Medscape.com.

The prevalence of irritable bowel syndrome (IBS) and chronic idiopathic constipation among US adults rose significantly during the COVID-19 pandemic, with a near doubling of the national rate of IBS over 2 years, a study has found.

The uptick is probably due to not only the direct impact of SARS-CoV-2 infection on the gastrointestinal tract but also to the psychological stress associated with pandemic life, the study team said. 

“COVID infection itself can definitely cause gastrointestinal symptoms like diarrhea, nausea, and abdominal pain — and for some people, those symptoms can linger and lead to chronic conditions like IBS,” Christopher V. Almario, MD, MSHPM, lead author and gastroenterologist at Cedars-Sinai Medical Center, Los Angeles, California, told GI & Hepatology News. 

“But the stress of living through the pandemic — lockdowns, fear, isolation — also likely played a major role as well in the increased prevalence of digestive disorders. Both the infection itself and the psychological toll of the pandemic can disrupt the gut-brain axis and trigger chronic digestive disorders like IBS,” Almario said. 

The study was published in Neurogastroenterology & Motility.

 

Growing Burden of Gut Disorders 

Disorders of gut-brain interaction (DGBIs) are a heterogeneous group of conditions in which gastrointestinal symptoms occur without any detectable structural or biochemical abnormalities in the digestive tract. They include IBS, functional dyspepsia, and chronic idiopathic constipation, among others. 

DGBIs are highly prevalent. Research has shown that nearly 40% of people in the US meet Rome IV criteria for at least one DGBI. 

Almario and colleagues assessed trends in prevalence of these conditions during the COVID-19 pandemic. Starting in May 2020 through May 2022, they conducted a series of online surveys with more than 160,000 adults aged 18 or older using validated Rome IV diagnostic questionnaires. 

Results showed that during the pandemic, IBS prevalence rose from 6.1% in May 2020 to 11.0% by May 2022, an increase of 0.188% per month (adjusted P < .001). 

Chronic idiopathic constipation showed a smaller but statistically significant increase, from 6.0% to 6.4% (0.056% per month; adjusted P < .001). 

Within the IBS subtypes, mixed-type IBS showed the largest relative increase (0.085% per month), followed by IBS with constipation (0.041% per month) and IBS with diarrhea (0.037% per month). 

There were no significant changes in the prevalence of other DGBIs, such as functional bloating, functional diarrhea, or functional dyspepsia, during the study period. 

Almario told GI & Hepatology News only about 9% of those surveyed reported a positive COVID test at the time of the surveys, but that figure probably underrepresents actual infections, especially in the early months of the pandemic. “Most of the survey responses came in during the earlier phases of the pandemic, and the percentage reporting a positive test increased over time,” he explained. 

Almario also noted that this study did not directly compare digestive disorder rates between infected and uninfected individuals. However, a separate study by the Cedars-Sinai team currently undergoing peer review addresses that question more directly. “That study, along with several other studies, show that having COVID increases the risk of developing conditions like IBS and functional dyspepsia,” Almario said. 

Taken together, the findings “underscore the increasing healthcare and economic burden of DGBI in the post-pandemic era, emphasizing the need for targeted efforts to effectively diagnose and manage these complex conditions,” they wrote. 

“This will be especially challenging for healthcare systems to address, given the existing shortage of primary care physicians and gastroenterologists — clinicians who primarily manage individuals with DGBI,” they noted. 

Support for this study was received from Ironwood Pharmaceuticals and Salix Pharmaceuticals in the form of institutional research grants to Cedars-Sinai. Almario has consulted for Exact Sciences, Greenspace Labs, Owlstone Medical, Salix Pharmaceuticals, and Universal DX.

A version of this article appeared on Medscape.com.

The prevalence of irritable bowel syndrome (IBS) and chronic idiopathic constipation among US adults rose significantly during the COVID-19 pandemic, with a near doubling of the national rate of IBS over 2 years, a study has found.

The uptick is probably due to not only the direct impact of SARS-CoV-2 infection on the gastrointestinal tract but also to the psychological stress associated with pandemic life, the study team said. 

“COVID infection itself can definitely cause gastrointestinal symptoms like diarrhea, nausea, and abdominal pain — and for some people, those symptoms can linger and lead to chronic conditions like IBS,” Christopher V. Almario, MD, MSHPM, lead author and gastroenterologist at Cedars-Sinai Medical Center, Los Angeles, California, told GI & Hepatology News. 

“But the stress of living through the pandemic — lockdowns, fear, isolation — also likely played a major role as well in the increased prevalence of digestive disorders. Both the infection itself and the psychological toll of the pandemic can disrupt the gut-brain axis and trigger chronic digestive disorders like IBS,” Almario said. 

The study was published in Neurogastroenterology & Motility.

 

Growing Burden of Gut Disorders 

Disorders of gut-brain interaction (DGBIs) are a heterogeneous group of conditions in which gastrointestinal symptoms occur without any detectable structural or biochemical abnormalities in the digestive tract. They include IBS, functional dyspepsia, and chronic idiopathic constipation, among others. 

DGBIs are highly prevalent. Research has shown that nearly 40% of people in the US meet Rome IV criteria for at least one DGBI. 

Almario and colleagues assessed trends in prevalence of these conditions during the COVID-19 pandemic. Starting in May 2020 through May 2022, they conducted a series of online surveys with more than 160,000 adults aged 18 or older using validated Rome IV diagnostic questionnaires. 

Results showed that during the pandemic, IBS prevalence rose from 6.1% in May 2020 to 11.0% by May 2022, an increase of 0.188% per month (adjusted P < .001). 

Chronic idiopathic constipation showed a smaller but statistically significant increase, from 6.0% to 6.4% (0.056% per month; adjusted P < .001). 

Within the IBS subtypes, mixed-type IBS showed the largest relative increase (0.085% per month), followed by IBS with constipation (0.041% per month) and IBS with diarrhea (0.037% per month). 

There were no significant changes in the prevalence of other DGBIs, such as functional bloating, functional diarrhea, or functional dyspepsia, during the study period. 

Almario told GI & Hepatology News only about 9% of those surveyed reported a positive COVID test at the time of the surveys, but that figure probably underrepresents actual infections, especially in the early months of the pandemic. “Most of the survey responses came in during the earlier phases of the pandemic, and the percentage reporting a positive test increased over time,” he explained. 

Almario also noted that this study did not directly compare digestive disorder rates between infected and uninfected individuals. However, a separate study by the Cedars-Sinai team currently undergoing peer review addresses that question more directly. “That study, along with several other studies, show that having COVID increases the risk of developing conditions like IBS and functional dyspepsia,” Almario said. 

Taken together, the findings “underscore the increasing healthcare and economic burden of DGBI in the post-pandemic era, emphasizing the need for targeted efforts to effectively diagnose and manage these complex conditions,” they wrote. 

“This will be especially challenging for healthcare systems to address, given the existing shortage of primary care physicians and gastroenterologists — clinicians who primarily manage individuals with DGBI,” they noted. 

Support for this study was received from Ironwood Pharmaceuticals and Salix Pharmaceuticals in the form of institutional research grants to Cedars-Sinai. Almario has consulted for Exact Sciences, Greenspace Labs, Owlstone Medical, Salix Pharmaceuticals, and Universal DX.

A version of this article appeared on Medscape.com.