User login
Ultraprocessed foods contain large amounts of artificial flavors, stabilizers, emulsifiers, sweeteners, or preservatives. Studies have linked higher consumption of them to cardiovascular disease, diabetes, obesity, and cancers.
For their research, published in Clinical Gastroenterology and Hepatology, Neeraj Nerula, MD of McMaster University, Hamilton, Ont., and colleagues pooled data from five recent cohort studies to assess whether their consumption was also linked to inflammatory bowel disease.
The included cohort studies together enrolled more than 1 million participants (mean age, 43-56; 55%-85% female). Of these, 916 developed Crohn’s disease, and 1,934 developed ulcerative colitis, during follow-up. None of the participants had IBD at baseline, and all were followed up at least 1 year. All the studies used the same food classification system, called NOVA, to assess foods eaten, and all were conducted between 2020 and 2022.
People who consumed more ultraprocessed foods saw higher Crohn’s risk, compared with those classed as consuming lower amounts of these foods (hazard ratio, 1.71; 95% confidence interval, 1.37-2.14). Also, lower risk of Crohn’s was observed among participants who consumed more unprocessed or minimally processed foods, such as vegetables, chicken, milk, and eggs (HR, 0.71; 95% CI, 0.53-0.94). The same associations were not seen for ulcerative colitis.
“Our findings support the hypothesis that consumption of [ultraprocessed foods] and low consumption of unprocessed/minimally processed foods may increase the risk for CD,” Dr. Nerula and colleagues wrote. The lack of association seen with ulcerative colitis might be explained by differences in the pathogenesis of each disease.
Ultraprocessed foods might contribute to Crohn’s by disrupting gut microbiota, the authors wrote. “For instance, emulsifiers have been shown to increase epithelial permeability, disruption of the intestinal barrier, and gut dysbiosis in mice. Carboxymethyl cellulose has been shown to facilitate bacterial adherence to gut epithelium, possibly leading to bacterial overgrowth and invasion of bacteria in between the intestinal villi. Furthermore, additives such as carrageenan, titanium dioxide, and maltodextrin have been shown to promote intestinal inflammation.”
Dr. Nerula and colleagues described as strengths of their study its large size, the low heterogenicity of the included studies, and the use of validated, standardized questionnaires to measure dietary intake in each study. Nonetheless, they cautioned, the results might not apply to younger age groups, and the majority of participants were White North Americans and Europeans, making it difficult to generalize results.
“Advancements in food processing and associated changes in dietary patterns could explain the rise of IBD incidence during the 20th and 21st centuries,” Dr. Narula and colleagues concluded. “Further investigations are needed to identify the specific potential culprits among processed foods that could account for the increased risk of CD observed.”
The study authors did not report outside funding. Dr. Narula disclosed receiving fees from pharmaceutical manufacturers including Janssen, AbbVie, Takeda, Pfizer, Merck, and others. Two of coauthors also disclosed receiving funds from industry, and five additional coauthors had no conflicts.
The causes of inflammatory bowel disease (IBD) are thought to be multifactorial and include genetic predisposition, dysregulated immune responses, imbalances in the intestinal microbiota, and environmental exposures.
Incidence and prevalence of IBD has increased over time, including in developing countries, and appear to parallel industrialization and “Westernization” of societies. One of the potential contributors to IBD risk is diet. Dietary changes associated with more modern or “Westernized” diets, including increases in processed foods, are some of the factors hypothesized to contribute to rising rates of IBD.
In the meta-analysis by Narula and colleagues, the authors observed a significant increase in the risk of CD, but not UC, in individuals who consumed significantly higher amounts of ultraprocessed foods (that is, frozen or long-shelf-life foods, products with thickeners/emulsifiers, etc.). Although there are limitations to the studies included in the meta-analysis, the association is intriguing and could point to potential lifestyle modifications that could form the basis of preventative interventions for individuals at higher risk for IBD, such as first-degree relatives.
More immediately, prospective research is needed to understand if restricting ultraprocessed foods (or increasing less-processed foods) can decrease disease activity or prevent flares in patients with IBD.
Understanding factors that predispose to or trigger IBD, such as specific dietary components, will lead to improved management strategies and ultimately preventative interventions.
Ryan Ungaro, MD, MS, is an associate professor of medicine in the division of gastroenterology at the Icahn School of Medicine at Mount Sinai, New York. He is director of the Comprehensive Care for the Recently Diagnosed IBD Patient (COMPASS-IBD). He has served as an advisory board member or consultant for AbbVie, Bristol-Myers Squibb, Celltrion, Lilly, Janssen, Pfizer, Roivant, and Takeda, and has received research support from AbbVie, Boehringer Ingelheim, Bristol-Myers Squibb, Lily, and Pfizer.
The causes of inflammatory bowel disease (IBD) are thought to be multifactorial and include genetic predisposition, dysregulated immune responses, imbalances in the intestinal microbiota, and environmental exposures.
Incidence and prevalence of IBD has increased over time, including in developing countries, and appear to parallel industrialization and “Westernization” of societies. One of the potential contributors to IBD risk is diet. Dietary changes associated with more modern or “Westernized” diets, including increases in processed foods, are some of the factors hypothesized to contribute to rising rates of IBD.
In the meta-analysis by Narula and colleagues, the authors observed a significant increase in the risk of CD, but not UC, in individuals who consumed significantly higher amounts of ultraprocessed foods (that is, frozen or long-shelf-life foods, products with thickeners/emulsifiers, etc.). Although there are limitations to the studies included in the meta-analysis, the association is intriguing and could point to potential lifestyle modifications that could form the basis of preventative interventions for individuals at higher risk for IBD, such as first-degree relatives.
More immediately, prospective research is needed to understand if restricting ultraprocessed foods (or increasing less-processed foods) can decrease disease activity or prevent flares in patients with IBD.
Understanding factors that predispose to or trigger IBD, such as specific dietary components, will lead to improved management strategies and ultimately preventative interventions.
Ryan Ungaro, MD, MS, is an associate professor of medicine in the division of gastroenterology at the Icahn School of Medicine at Mount Sinai, New York. He is director of the Comprehensive Care for the Recently Diagnosed IBD Patient (COMPASS-IBD). He has served as an advisory board member or consultant for AbbVie, Bristol-Myers Squibb, Celltrion, Lilly, Janssen, Pfizer, Roivant, and Takeda, and has received research support from AbbVie, Boehringer Ingelheim, Bristol-Myers Squibb, Lily, and Pfizer.
The causes of inflammatory bowel disease (IBD) are thought to be multifactorial and include genetic predisposition, dysregulated immune responses, imbalances in the intestinal microbiota, and environmental exposures.
Incidence and prevalence of IBD has increased over time, including in developing countries, and appear to parallel industrialization and “Westernization” of societies. One of the potential contributors to IBD risk is diet. Dietary changes associated with more modern or “Westernized” diets, including increases in processed foods, are some of the factors hypothesized to contribute to rising rates of IBD.
In the meta-analysis by Narula and colleagues, the authors observed a significant increase in the risk of CD, but not UC, in individuals who consumed significantly higher amounts of ultraprocessed foods (that is, frozen or long-shelf-life foods, products with thickeners/emulsifiers, etc.). Although there are limitations to the studies included in the meta-analysis, the association is intriguing and could point to potential lifestyle modifications that could form the basis of preventative interventions for individuals at higher risk for IBD, such as first-degree relatives.
More immediately, prospective research is needed to understand if restricting ultraprocessed foods (or increasing less-processed foods) can decrease disease activity or prevent flares in patients with IBD.
Understanding factors that predispose to or trigger IBD, such as specific dietary components, will lead to improved management strategies and ultimately preventative interventions.
Ryan Ungaro, MD, MS, is an associate professor of medicine in the division of gastroenterology at the Icahn School of Medicine at Mount Sinai, New York. He is director of the Comprehensive Care for the Recently Diagnosed IBD Patient (COMPASS-IBD). He has served as an advisory board member or consultant for AbbVie, Bristol-Myers Squibb, Celltrion, Lilly, Janssen, Pfizer, Roivant, and Takeda, and has received research support from AbbVie, Boehringer Ingelheim, Bristol-Myers Squibb, Lily, and Pfizer.
Ultraprocessed foods contain large amounts of artificial flavors, stabilizers, emulsifiers, sweeteners, or preservatives. Studies have linked higher consumption of them to cardiovascular disease, diabetes, obesity, and cancers.
For their research, published in Clinical Gastroenterology and Hepatology, Neeraj Nerula, MD of McMaster University, Hamilton, Ont., and colleagues pooled data from five recent cohort studies to assess whether their consumption was also linked to inflammatory bowel disease.
The included cohort studies together enrolled more than 1 million participants (mean age, 43-56; 55%-85% female). Of these, 916 developed Crohn’s disease, and 1,934 developed ulcerative colitis, during follow-up. None of the participants had IBD at baseline, and all were followed up at least 1 year. All the studies used the same food classification system, called NOVA, to assess foods eaten, and all were conducted between 2020 and 2022.
People who consumed more ultraprocessed foods saw higher Crohn’s risk, compared with those classed as consuming lower amounts of these foods (hazard ratio, 1.71; 95% confidence interval, 1.37-2.14). Also, lower risk of Crohn’s was observed among participants who consumed more unprocessed or minimally processed foods, such as vegetables, chicken, milk, and eggs (HR, 0.71; 95% CI, 0.53-0.94). The same associations were not seen for ulcerative colitis.
“Our findings support the hypothesis that consumption of [ultraprocessed foods] and low consumption of unprocessed/minimally processed foods may increase the risk for CD,” Dr. Nerula and colleagues wrote. The lack of association seen with ulcerative colitis might be explained by differences in the pathogenesis of each disease.
Ultraprocessed foods might contribute to Crohn’s by disrupting gut microbiota, the authors wrote. “For instance, emulsifiers have been shown to increase epithelial permeability, disruption of the intestinal barrier, and gut dysbiosis in mice. Carboxymethyl cellulose has been shown to facilitate bacterial adherence to gut epithelium, possibly leading to bacterial overgrowth and invasion of bacteria in between the intestinal villi. Furthermore, additives such as carrageenan, titanium dioxide, and maltodextrin have been shown to promote intestinal inflammation.”
Dr. Nerula and colleagues described as strengths of their study its large size, the low heterogenicity of the included studies, and the use of validated, standardized questionnaires to measure dietary intake in each study. Nonetheless, they cautioned, the results might not apply to younger age groups, and the majority of participants were White North Americans and Europeans, making it difficult to generalize results.
“Advancements in food processing and associated changes in dietary patterns could explain the rise of IBD incidence during the 20th and 21st centuries,” Dr. Narula and colleagues concluded. “Further investigations are needed to identify the specific potential culprits among processed foods that could account for the increased risk of CD observed.”
The study authors did not report outside funding. Dr. Narula disclosed receiving fees from pharmaceutical manufacturers including Janssen, AbbVie, Takeda, Pfizer, Merck, and others. Two of coauthors also disclosed receiving funds from industry, and five additional coauthors had no conflicts.
Ultraprocessed foods contain large amounts of artificial flavors, stabilizers, emulsifiers, sweeteners, or preservatives. Studies have linked higher consumption of them to cardiovascular disease, diabetes, obesity, and cancers.
For their research, published in Clinical Gastroenterology and Hepatology, Neeraj Nerula, MD of McMaster University, Hamilton, Ont., and colleagues pooled data from five recent cohort studies to assess whether their consumption was also linked to inflammatory bowel disease.
The included cohort studies together enrolled more than 1 million participants (mean age, 43-56; 55%-85% female). Of these, 916 developed Crohn’s disease, and 1,934 developed ulcerative colitis, during follow-up. None of the participants had IBD at baseline, and all were followed up at least 1 year. All the studies used the same food classification system, called NOVA, to assess foods eaten, and all were conducted between 2020 and 2022.
People who consumed more ultraprocessed foods saw higher Crohn’s risk, compared with those classed as consuming lower amounts of these foods (hazard ratio, 1.71; 95% confidence interval, 1.37-2.14). Also, lower risk of Crohn’s was observed among participants who consumed more unprocessed or minimally processed foods, such as vegetables, chicken, milk, and eggs (HR, 0.71; 95% CI, 0.53-0.94). The same associations were not seen for ulcerative colitis.
“Our findings support the hypothesis that consumption of [ultraprocessed foods] and low consumption of unprocessed/minimally processed foods may increase the risk for CD,” Dr. Nerula and colleagues wrote. The lack of association seen with ulcerative colitis might be explained by differences in the pathogenesis of each disease.
Ultraprocessed foods might contribute to Crohn’s by disrupting gut microbiota, the authors wrote. “For instance, emulsifiers have been shown to increase epithelial permeability, disruption of the intestinal barrier, and gut dysbiosis in mice. Carboxymethyl cellulose has been shown to facilitate bacterial adherence to gut epithelium, possibly leading to bacterial overgrowth and invasion of bacteria in between the intestinal villi. Furthermore, additives such as carrageenan, titanium dioxide, and maltodextrin have been shown to promote intestinal inflammation.”
Dr. Nerula and colleagues described as strengths of their study its large size, the low heterogenicity of the included studies, and the use of validated, standardized questionnaires to measure dietary intake in each study. Nonetheless, they cautioned, the results might not apply to younger age groups, and the majority of participants were White North Americans and Europeans, making it difficult to generalize results.
“Advancements in food processing and associated changes in dietary patterns could explain the rise of IBD incidence during the 20th and 21st centuries,” Dr. Narula and colleagues concluded. “Further investigations are needed to identify the specific potential culprits among processed foods that could account for the increased risk of CD observed.”
The study authors did not report outside funding. Dr. Narula disclosed receiving fees from pharmaceutical manufacturers including Janssen, AbbVie, Takeda, Pfizer, Merck, and others. Two of coauthors also disclosed receiving funds from industry, and five additional coauthors had no conflicts.
FROM CLINICAL GASTROENTEROLOGY AND HEPATOLOGY