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Among adults who consumed a proinflammatory diet, switching to a diet with lower inflammatory potential was associated with a significant subsequent decrease in risk for Crohn’s disease, according to a study of three longitudinal observational cohorts.
Researchers calculated empirical dietary inflammatory pattern (EDIP) scores based on food-frequency questionnaires completed by 166,903 women and 41,931 men who participated in the Nurses’ Health Study, the Nurses’ Health Study II, and the Health Professionals Follow-up Study. Questionnaires were completed at two time points, separated by 8 years. Overall, adults whose cumulative average EDIP scores fell within the highest quartile – meaning their diets had the highest inflammatory potential – were at 51% greater risk for developing Crohn’s disease than were adults whose diets fell within the lowest EDIP quartile (hazard ratio, 1.51; 95% confidence interval, 1.19-2.07; P = .01).
Strikingly, however, adults who initially consumed a proinflammatory diet (which is high in calories, red meat, high-fat dairy, and refined grains) and then switched to a low-inflammatory diet (one based around fruit, vegetables, legumes, whole grains, fish, and lean protein) had a statistically similar risk for Crohn’s disease as adults who consumed a low-inflammatory diet at both time points. The 95% confidence interval for the hazard ratio crossed 1.0 (HR, 1.51; 95% CI, 0.76-3.00). In contrast, adults who initially consumed a low-inflammatory diet and later changed to a proinflammatory diet were at twofold greater risk for Crohn’s disease than were those who remained on a low-inflammatory diet (HR, 2.05; 95% CI, 1.10-3.79).
These findings accounted for potential confounders, such as age, study cohort, time period, race, smoking, physical activity, and use of oral contraceptives and hormone replacement therapy, wrote Chun-Han Lo, MD, of the Harvard T.H. Chan School of Public Health, Boston, together with his associates in Gastroenterology.
The EDIP score is a weighted sum of 18 food groups that characterizes the potential for dietary inflammation based on circulating concentrations of inflammatory biomarkers. A proinflammatory diet may “trigger the onset of intestinal inflammation by inducing changes in [the] gut microbiome, altering host homeostasis, and regulating T-cell immune response,” the investigators noted.
In this study, which included nearly 5 million person-years of follow-up, 328 individuals were diagnosed with Crohn’s disease and 428 individuals developed ulcerative colitis. Median age at inflammatory bowel disease diagnosis was 55 years, with a range of 29-85 years. Notably, change in EDIP score was not linked to ulcerative colitis risk. Diet may be more relevant in Crohn’s disease than ulcerative colitis, and dietary factors linked to ulcerative colitis were not associated with inflammatory markers in the cohorts and, thus, were not factored into EDIP score, the researchers wrote.
The link between EDIP score and Crohn’s disease in this study did not change after controlling for fiber intake. Red wine (which contains anti-inflammatory resveratrol) might be a protective factor, the researchers hypothesized. They also found that pizza – a processed, calorie-dense food – was significantly inversely linked to inflammatory markers, perhaps because pizza contains abundant lycopene (from tomato paste) and fat (which facilitate lycopene absorption).
Prior studies on diet and inflammatory bowel disease assessed diets at only one time point and categorized dietary habits based on food groups, rather than linking foods with inflammatory markers, the researchers wrote. “Here, by identifying a combination of food groups predictive of circulating markers of inflammation, we provide a more robust evidence base behind the association of these foods with inflammation and inflammatory bowel disease.”
Most study participants were white health professionals. The researchers noted that “studies of dietary risk factors have not revealed a strong ethnicity-specific association, [but] extrapolating our findings to individuals of other ethnicity should be performed with caution.”
The National Institutes of Health, the Beker Foundation, the Chleck Family Foundation, and the Crohn’s and Colitis Foundation provided funding. Three coinvestigators disclosed ties to AbbVie, Bayer Pharma AG, Boehringer Ingelheim, Gilead, Janssen, Kyn Therapeutics, Merck Pfizer, Policy Analysis Inc., and Takeda.
SOURCE: Lo C-H et al. Gastroenterology. 2020 May 1. doi: 10.1053/j.gastro.2020.05.011.
Diet is the single most modifiable risk factor influencing inflammatory bowel disease (IBD) development. Accordingly, animal studies show that specific nutrients and food additives impact gut barrier function and/or microbiota, thereby influencing disease development. However, using these studies to provide humans practical dietary advice has been difficult, in part because effects of isolated food components can be quite different from those of complex foods. The complex nature of human foods has also stymied epidemiologic approaches to determine how diet influences IBD risk. This difficulty is exacerbated by the potential of IBD itself to influence diet, likely beginning long before disease diagnosis.
Andrew T. Gewirtz, PhD, is a professor at Georgia State University’s Institute for Biomedical Sciences, Atlanta. He has no conflicts.
Diet is the single most modifiable risk factor influencing inflammatory bowel disease (IBD) development. Accordingly, animal studies show that specific nutrients and food additives impact gut barrier function and/or microbiota, thereby influencing disease development. However, using these studies to provide humans practical dietary advice has been difficult, in part because effects of isolated food components can be quite different from those of complex foods. The complex nature of human foods has also stymied epidemiologic approaches to determine how diet influences IBD risk. This difficulty is exacerbated by the potential of IBD itself to influence diet, likely beginning long before disease diagnosis.
Andrew T. Gewirtz, PhD, is a professor at Georgia State University’s Institute for Biomedical Sciences, Atlanta. He has no conflicts.
Diet is the single most modifiable risk factor influencing inflammatory bowel disease (IBD) development. Accordingly, animal studies show that specific nutrients and food additives impact gut barrier function and/or microbiota, thereby influencing disease development. However, using these studies to provide humans practical dietary advice has been difficult, in part because effects of isolated food components can be quite different from those of complex foods. The complex nature of human foods has also stymied epidemiologic approaches to determine how diet influences IBD risk. This difficulty is exacerbated by the potential of IBD itself to influence diet, likely beginning long before disease diagnosis.
Andrew T. Gewirtz, PhD, is a professor at Georgia State University’s Institute for Biomedical Sciences, Atlanta. He has no conflicts.
Among adults who consumed a proinflammatory diet, switching to a diet with lower inflammatory potential was associated with a significant subsequent decrease in risk for Crohn’s disease, according to a study of three longitudinal observational cohorts.
Researchers calculated empirical dietary inflammatory pattern (EDIP) scores based on food-frequency questionnaires completed by 166,903 women and 41,931 men who participated in the Nurses’ Health Study, the Nurses’ Health Study II, and the Health Professionals Follow-up Study. Questionnaires were completed at two time points, separated by 8 years. Overall, adults whose cumulative average EDIP scores fell within the highest quartile – meaning their diets had the highest inflammatory potential – were at 51% greater risk for developing Crohn’s disease than were adults whose diets fell within the lowest EDIP quartile (hazard ratio, 1.51; 95% confidence interval, 1.19-2.07; P = .01).
Strikingly, however, adults who initially consumed a proinflammatory diet (which is high in calories, red meat, high-fat dairy, and refined grains) and then switched to a low-inflammatory diet (one based around fruit, vegetables, legumes, whole grains, fish, and lean protein) had a statistically similar risk for Crohn’s disease as adults who consumed a low-inflammatory diet at both time points. The 95% confidence interval for the hazard ratio crossed 1.0 (HR, 1.51; 95% CI, 0.76-3.00). In contrast, adults who initially consumed a low-inflammatory diet and later changed to a proinflammatory diet were at twofold greater risk for Crohn’s disease than were those who remained on a low-inflammatory diet (HR, 2.05; 95% CI, 1.10-3.79).
These findings accounted for potential confounders, such as age, study cohort, time period, race, smoking, physical activity, and use of oral contraceptives and hormone replacement therapy, wrote Chun-Han Lo, MD, of the Harvard T.H. Chan School of Public Health, Boston, together with his associates in Gastroenterology.
The EDIP score is a weighted sum of 18 food groups that characterizes the potential for dietary inflammation based on circulating concentrations of inflammatory biomarkers. A proinflammatory diet may “trigger the onset of intestinal inflammation by inducing changes in [the] gut microbiome, altering host homeostasis, and regulating T-cell immune response,” the investigators noted.
In this study, which included nearly 5 million person-years of follow-up, 328 individuals were diagnosed with Crohn’s disease and 428 individuals developed ulcerative colitis. Median age at inflammatory bowel disease diagnosis was 55 years, with a range of 29-85 years. Notably, change in EDIP score was not linked to ulcerative colitis risk. Diet may be more relevant in Crohn’s disease than ulcerative colitis, and dietary factors linked to ulcerative colitis were not associated with inflammatory markers in the cohorts and, thus, were not factored into EDIP score, the researchers wrote.
The link between EDIP score and Crohn’s disease in this study did not change after controlling for fiber intake. Red wine (which contains anti-inflammatory resveratrol) might be a protective factor, the researchers hypothesized. They also found that pizza – a processed, calorie-dense food – was significantly inversely linked to inflammatory markers, perhaps because pizza contains abundant lycopene (from tomato paste) and fat (which facilitate lycopene absorption).
Prior studies on diet and inflammatory bowel disease assessed diets at only one time point and categorized dietary habits based on food groups, rather than linking foods with inflammatory markers, the researchers wrote. “Here, by identifying a combination of food groups predictive of circulating markers of inflammation, we provide a more robust evidence base behind the association of these foods with inflammation and inflammatory bowel disease.”
Most study participants were white health professionals. The researchers noted that “studies of dietary risk factors have not revealed a strong ethnicity-specific association, [but] extrapolating our findings to individuals of other ethnicity should be performed with caution.”
The National Institutes of Health, the Beker Foundation, the Chleck Family Foundation, and the Crohn’s and Colitis Foundation provided funding. Three coinvestigators disclosed ties to AbbVie, Bayer Pharma AG, Boehringer Ingelheim, Gilead, Janssen, Kyn Therapeutics, Merck Pfizer, Policy Analysis Inc., and Takeda.
SOURCE: Lo C-H et al. Gastroenterology. 2020 May 1. doi: 10.1053/j.gastro.2020.05.011.
Among adults who consumed a proinflammatory diet, switching to a diet with lower inflammatory potential was associated with a significant subsequent decrease in risk for Crohn’s disease, according to a study of three longitudinal observational cohorts.
Researchers calculated empirical dietary inflammatory pattern (EDIP) scores based on food-frequency questionnaires completed by 166,903 women and 41,931 men who participated in the Nurses’ Health Study, the Nurses’ Health Study II, and the Health Professionals Follow-up Study. Questionnaires were completed at two time points, separated by 8 years. Overall, adults whose cumulative average EDIP scores fell within the highest quartile – meaning their diets had the highest inflammatory potential – were at 51% greater risk for developing Crohn’s disease than were adults whose diets fell within the lowest EDIP quartile (hazard ratio, 1.51; 95% confidence interval, 1.19-2.07; P = .01).
Strikingly, however, adults who initially consumed a proinflammatory diet (which is high in calories, red meat, high-fat dairy, and refined grains) and then switched to a low-inflammatory diet (one based around fruit, vegetables, legumes, whole grains, fish, and lean protein) had a statistically similar risk for Crohn’s disease as adults who consumed a low-inflammatory diet at both time points. The 95% confidence interval for the hazard ratio crossed 1.0 (HR, 1.51; 95% CI, 0.76-3.00). In contrast, adults who initially consumed a low-inflammatory diet and later changed to a proinflammatory diet were at twofold greater risk for Crohn’s disease than were those who remained on a low-inflammatory diet (HR, 2.05; 95% CI, 1.10-3.79).
These findings accounted for potential confounders, such as age, study cohort, time period, race, smoking, physical activity, and use of oral contraceptives and hormone replacement therapy, wrote Chun-Han Lo, MD, of the Harvard T.H. Chan School of Public Health, Boston, together with his associates in Gastroenterology.
The EDIP score is a weighted sum of 18 food groups that characterizes the potential for dietary inflammation based on circulating concentrations of inflammatory biomarkers. A proinflammatory diet may “trigger the onset of intestinal inflammation by inducing changes in [the] gut microbiome, altering host homeostasis, and regulating T-cell immune response,” the investigators noted.
In this study, which included nearly 5 million person-years of follow-up, 328 individuals were diagnosed with Crohn’s disease and 428 individuals developed ulcerative colitis. Median age at inflammatory bowel disease diagnosis was 55 years, with a range of 29-85 years. Notably, change in EDIP score was not linked to ulcerative colitis risk. Diet may be more relevant in Crohn’s disease than ulcerative colitis, and dietary factors linked to ulcerative colitis were not associated with inflammatory markers in the cohorts and, thus, were not factored into EDIP score, the researchers wrote.
The link between EDIP score and Crohn’s disease in this study did not change after controlling for fiber intake. Red wine (which contains anti-inflammatory resveratrol) might be a protective factor, the researchers hypothesized. They also found that pizza – a processed, calorie-dense food – was significantly inversely linked to inflammatory markers, perhaps because pizza contains abundant lycopene (from tomato paste) and fat (which facilitate lycopene absorption).
Prior studies on diet and inflammatory bowel disease assessed diets at only one time point and categorized dietary habits based on food groups, rather than linking foods with inflammatory markers, the researchers wrote. “Here, by identifying a combination of food groups predictive of circulating markers of inflammation, we provide a more robust evidence base behind the association of these foods with inflammation and inflammatory bowel disease.”
Most study participants were white health professionals. The researchers noted that “studies of dietary risk factors have not revealed a strong ethnicity-specific association, [but] extrapolating our findings to individuals of other ethnicity should be performed with caution.”
The National Institutes of Health, the Beker Foundation, the Chleck Family Foundation, and the Crohn’s and Colitis Foundation provided funding. Three coinvestigators disclosed ties to AbbVie, Bayer Pharma AG, Boehringer Ingelheim, Gilead, Janssen, Kyn Therapeutics, Merck Pfizer, Policy Analysis Inc., and Takeda.
SOURCE: Lo C-H et al. Gastroenterology. 2020 May 1. doi: 10.1053/j.gastro.2020.05.011.
FROM GASTROENTEROLOGY