TBD Meeting (5232-19)

CHICAGO – Evidence suggests that diet may cause incident inflammatory bowel disease (IBD) and induce associated symptoms, according to a lecture delivered at Freston Conference 2019, sponsored by the American Gastroenterological Association.

Although the literature is highly consistent, it contains discordant findings, and many questions remain unanswered. “We need more rigorous studies, and particularly more interventions, to truly understand the role diet may play in patients with IBD,” said Ashwin N. Ananthakrishnan, MD, MPH, associate professor of medicine at Massachusetts General Hospital in Boston.
 

Food can cause symptoms in IBD

Many patients with IBD are convinced that their diet caused their disease. A relevant point for physicians to consider is that these patients are at least as likely as is the general population to have intolerance or sensitivity to food components such as lactose and gluten. In a prospective questionnaire of 400 consecutive patients with IBD in the United Kingdom, 48% expressed the belief that diet could initiate IBD, and 57% said that diet could trigger a flare-up. In addition, 60% of respondents reported worsening of symptoms after eating certain foods, and about two-thirds deprived themselves of their favorite foods to prevent relapses (Inflamm Bowel Dis. 2016;22[1]:164-70). A French study found similar results. “Clearly there’s something there,” said Dr. Ananthakrishnan. Patients’ beliefs about the relationship between food and their symptoms are not simply misconceptions, he added.

A Canadian study published in 2016 found that almost one-third of patients with IBD avoid many food groups. “But there is significant heterogeneity in the foods that are avoided, and sometimes we mistake this heterogeneity for a lack of association between diet and symptoms in IBD,” said Dr. Ananthakrishnan. A larger number of patients avoid certain foods during periods of active disease, which suggests that food exacerbates their symptoms, he added. The same study showed that patients with IBD have more restrictive diets than do community controls. Patients eat fewer fruits and vegetables and generally consume less iron-rich food and less protein-rich food than healthy controls. GI intolerance, rather than professional advice, is the most common reason that patients with IBD restrict their diets (JPEN J Parenter Enteral Nutr. 2016;40[3]:405-11.).

A cross-sectional survey of 130 patients with IBD and 70 controls yielded similar results. Among patients, GI symptoms that resulted from consuming foods were not related to disease activity, disease location, or prior surgery. Patients with IBD tended to have greater frequency of GI intolerance to foods than did controls (Scand J Gastroenterol. 1997;32[6]:569-71.).
 

Diet may cause intestinal inflammation

International research has recorded increases in the consumption of sugar and fat (particularly saturated fat) and concomitant decreases in fiber consumption during the past several decades. The incidence of IBD has increased in parallel with these dietary changes with a remarkably similar trajectory, said Dr. Ananthakrishnan. The correlation between dietary changes and IBD incidence “holds true even more strikingly in countries that are now experiencing Westernization,” he added. These countries have undergone more rapid dietary changes, and their IBD incidence has doubled or tripled. The transition to “less traditional diets” appears to promote intestinal inflammation, said Dr. Ananthakrishnan.

An analysis of data from the European Prospective Investigation into Cancer (EPIC) study found an association between high consumption of sugar and soft drinks, together with low consumption of vegetables, and risk of ulcerative colitis (Inflamm Bowel Dis. 2016;22[2]:345-54.). A subsequent analysis of data from two prospective Swedish cohorts, however, found no association between consumption of sugary beverages and risk of Crohn’s disease or ulcerative colitis (Clin Gastroenterol Hepatol. 2019;17[1]:123-9.).

Although the data on sugar are mixed, data on the association between other macronutrient groups and risk of IBD are more consistent. When Dr. Ananthakrishnan and colleagues examined data from the Nurses’ Health Study, they found that the highest quintile of dietary fiber intake was associated with a 40% reduction in risk of Crohn’s disease, compared with the lowest quintile. The observed reduction of risk seemed to be greatest for fiber derived from fruits. Fiber from cereals, whole grains, or legumes, however, did not affect risk of Crohn’s disease (Gastroenterology. 2013;145[5]:970-7.).

A separate analysis of the Nurses’ Health Study suggested that high intake of n-3 polyunsaturated fatty acids (PUFAs) and low intake of n-6 PUFAs was associated with a 31% reduction in risk of ulcerative colitis and a 15% reduction in the risk of Crohn’s disease. These data were consistent with a previous analysis of EPIC data that found that high intake of n-6 PUFAs was associated with increased risk of ulcerative colitis (Gut. 2009;58[12]:1606-11.). Other analyses indicate that genetic polymorphisms likely modify the association between PUFAs and risk of ulcerative colitis, said Dr. Ananthakrishnan. “There may be an additional layer of complexity beyond just measuring your dietary intake.”

In addition to macronutrients, micronutrients can modify a patient’s risk of ulcerative colitis or Crohn’s disease. When Dr. Ananthakrishnan and colleagues examined the Nurses’ Health Study, they found an inverse association between vitamin D intake and risk of Crohn’s disease (Gastroenterology. 2012;142[3]:482-9.). In a separate study, they found that a zinc intake greater than 16 mg/day was associated with reduced risk of Crohn’s disease (Int J Epidemiol. 2015;44[6]:1995-2005.).

Patients aged older than 40 years and patients of European ancestry tend to be overrepresented in cohort studies, which reduces the generalizability of their conclusions, said Dr. Ananthakrishnan. Furthermore, cohort studies have not produced consistent findings regarding the relationship between various dietary components and risk of IBD. Nevertheless, the data suggest that dietary patterns may be associated with incident Crohn’s disease or ulcerative colitis.

 

An influence of diet on IBD risk is plausible

One mechanism through which diet may exercise a causal influence on the risk of IBD is by affecting the microbiome. In 2011, investigators studied 98 healthy volunteers who answered questionnaires about their diet. The researchers also used 16s rDNA sequencing to characterize the population’s stool samples. A diet high in animal protein, amino acids, and saturated fats was associated with large populations of Bacteroides. A diet low in fat and in animal protein, but high in carbohydrates and simple sugars was associated with large populations of Prevotella. When the investigators conducted a controlled-feeding study of 10 patients, microbiome composition changed within 1 day of initiating a high-fat-and-low-fiber or a low-fat-and-high-fiber diet (Science. 2011;334[6052]:105-8.). A more recent study showed that the diversity of the microbiome increased with the adoption of an animal-based diet (Nature. 2014;505[7484]:559-63.).

Diet also may exert a causal influence on IBD risk by altering the intestinal barrier. In an experimental model, 5-mg/mL concentrations of fiber from plantain and broccoli significantly reduced the translocation of Escherichia coli through a human intestinal epithelial barrier (Gut. 2010;59[10]:1331-9.). Increased fiber intake may thus result in reduced intestinal inflammation, said Dr. Ananthakrishnan.

Observational and experimental evidence thus support an effect of diet on the risk of IBD, and experimental evidence indicates that this effect is biologically plausible. Nevertheless, “there are many missing links,” and further study will clarify the role of diet in IBD incidence, said Dr. Ananthakrishnan.

AGA offers education for your patients about IBD, including lifestyle and nutrition management, in the AGA GI Patient Center at https://www.gastro.org/practice-guidance/gi-patient-center/topic/inflammatory-bowel-disease-ibd.

[email protected]

CHICAGO – Evidence suggests that diet may cause incident inflammatory bowel disease (IBD) and induce associated symptoms, according to a lecture delivered at Freston Conference 2019, sponsored by the American Gastroenterological Association.

Although the literature is highly consistent, it contains discordant findings, and many questions remain unanswered. “We need more rigorous studies, and particularly more interventions, to truly understand the role diet may play in patients with IBD,” said Ashwin N. Ananthakrishnan, MD, MPH, associate professor of medicine at Massachusetts General Hospital in Boston.
 

Food can cause symptoms in IBD

Many patients with IBD are convinced that their diet caused their disease. A relevant point for physicians to consider is that these patients are at least as likely as is the general population to have intolerance or sensitivity to food components such as lactose and gluten. In a prospective questionnaire of 400 consecutive patients with IBD in the United Kingdom, 48% expressed the belief that diet could initiate IBD, and 57% said that diet could trigger a flare-up. In addition, 60% of respondents reported worsening of symptoms after eating certain foods, and about two-thirds deprived themselves of their favorite foods to prevent relapses (Inflamm Bowel Dis. 2016;22[1]:164-70). A French study found similar results. “Clearly there’s something there,” said Dr. Ananthakrishnan. Patients’ beliefs about the relationship between food and their symptoms are not simply misconceptions, he added.

A Canadian study published in 2016 found that almost one-third of patients with IBD avoid many food groups. “But there is significant heterogeneity in the foods that are avoided, and sometimes we mistake this heterogeneity for a lack of association between diet and symptoms in IBD,” said Dr. Ananthakrishnan. A larger number of patients avoid certain foods during periods of active disease, which suggests that food exacerbates their symptoms, he added. The same study showed that patients with IBD have more restrictive diets than do community controls. Patients eat fewer fruits and vegetables and generally consume less iron-rich food and less protein-rich food than healthy controls. GI intolerance, rather than professional advice, is the most common reason that patients with IBD restrict their diets (JPEN J Parenter Enteral Nutr. 2016;40[3]:405-11.).

A cross-sectional survey of 130 patients with IBD and 70 controls yielded similar results. Among patients, GI symptoms that resulted from consuming foods were not related to disease activity, disease location, or prior surgery. Patients with IBD tended to have greater frequency of GI intolerance to foods than did controls (Scand J Gastroenterol. 1997;32[6]:569-71.).
 

Diet may cause intestinal inflammation

International research has recorded increases in the consumption of sugar and fat (particularly saturated fat) and concomitant decreases in fiber consumption during the past several decades. The incidence of IBD has increased in parallel with these dietary changes with a remarkably similar trajectory, said Dr. Ananthakrishnan. The correlation between dietary changes and IBD incidence “holds true even more strikingly in countries that are now experiencing Westernization,” he added. These countries have undergone more rapid dietary changes, and their IBD incidence has doubled or tripled. The transition to “less traditional diets” appears to promote intestinal inflammation, said Dr. Ananthakrishnan.

An analysis of data from the European Prospective Investigation into Cancer (EPIC) study found an association between high consumption of sugar and soft drinks, together with low consumption of vegetables, and risk of ulcerative colitis (Inflamm Bowel Dis. 2016;22[2]:345-54.). A subsequent analysis of data from two prospective Swedish cohorts, however, found no association between consumption of sugary beverages and risk of Crohn’s disease or ulcerative colitis (Clin Gastroenterol Hepatol. 2019;17[1]:123-9.).

Although the data on sugar are mixed, data on the association between other macronutrient groups and risk of IBD are more consistent. When Dr. Ananthakrishnan and colleagues examined data from the Nurses’ Health Study, they found that the highest quintile of dietary fiber intake was associated with a 40% reduction in risk of Crohn’s disease, compared with the lowest quintile. The observed reduction of risk seemed to be greatest for fiber derived from fruits. Fiber from cereals, whole grains, or legumes, however, did not affect risk of Crohn’s disease (Gastroenterology. 2013;145[5]:970-7.).

A separate analysis of the Nurses’ Health Study suggested that high intake of n-3 polyunsaturated fatty acids (PUFAs) and low intake of n-6 PUFAs was associated with a 31% reduction in risk of ulcerative colitis and a 15% reduction in the risk of Crohn’s disease. These data were consistent with a previous analysis of EPIC data that found that high intake of n-6 PUFAs was associated with increased risk of ulcerative colitis (Gut. 2009;58[12]:1606-11.). Other analyses indicate that genetic polymorphisms likely modify the association between PUFAs and risk of ulcerative colitis, said Dr. Ananthakrishnan. “There may be an additional layer of complexity beyond just measuring your dietary intake.”

In addition to macronutrients, micronutrients can modify a patient’s risk of ulcerative colitis or Crohn’s disease. When Dr. Ananthakrishnan and colleagues examined the Nurses’ Health Study, they found an inverse association between vitamin D intake and risk of Crohn’s disease (Gastroenterology. 2012;142[3]:482-9.). In a separate study, they found that a zinc intake greater than 16 mg/day was associated with reduced risk of Crohn’s disease (Int J Epidemiol. 2015;44[6]:1995-2005.).

Patients aged older than 40 years and patients of European ancestry tend to be overrepresented in cohort studies, which reduces the generalizability of their conclusions, said Dr. Ananthakrishnan. Furthermore, cohort studies have not produced consistent findings regarding the relationship between various dietary components and risk of IBD. Nevertheless, the data suggest that dietary patterns may be associated with incident Crohn’s disease or ulcerative colitis.

 

An influence of diet on IBD risk is plausible

One mechanism through which diet may exercise a causal influence on the risk of IBD is by affecting the microbiome. In 2011, investigators studied 98 healthy volunteers who answered questionnaires about their diet. The researchers also used 16s rDNA sequencing to characterize the population’s stool samples. A diet high in animal protein, amino acids, and saturated fats was associated with large populations of Bacteroides. A diet low in fat and in animal protein, but high in carbohydrates and simple sugars was associated with large populations of Prevotella. When the investigators conducted a controlled-feeding study of 10 patients, microbiome composition changed within 1 day of initiating a high-fat-and-low-fiber or a low-fat-and-high-fiber diet (Science. 2011;334[6052]:105-8.). A more recent study showed that the diversity of the microbiome increased with the adoption of an animal-based diet (Nature. 2014;505[7484]:559-63.).

Diet also may exert a causal influence on IBD risk by altering the intestinal barrier. In an experimental model, 5-mg/mL concentrations of fiber from plantain and broccoli significantly reduced the translocation of Escherichia coli through a human intestinal epithelial barrier (Gut. 2010;59[10]:1331-9.). Increased fiber intake may thus result in reduced intestinal inflammation, said Dr. Ananthakrishnan.

Observational and experimental evidence thus support an effect of diet on the risk of IBD, and experimental evidence indicates that this effect is biologically plausible. Nevertheless, “there are many missing links,” and further study will clarify the role of diet in IBD incidence, said Dr. Ananthakrishnan.

AGA offers education for your patients about IBD, including lifestyle and nutrition management, in the AGA GI Patient Center at https://www.gastro.org/practice-guidance/gi-patient-center/topic/inflammatory-bowel-disease-ibd.

[email protected]

CHICAGO – Evidence suggests that diet may cause incident inflammatory bowel disease (IBD) and induce associated symptoms, according to a lecture delivered at Freston Conference 2019, sponsored by the American Gastroenterological Association.

Although the literature is highly consistent, it contains discordant findings, and many questions remain unanswered. “We need more rigorous studies, and particularly more interventions, to truly understand the role diet may play in patients with IBD,” said Ashwin N. Ananthakrishnan, MD, MPH, associate professor of medicine at Massachusetts General Hospital in Boston.
 

Food can cause symptoms in IBD

Many patients with IBD are convinced that their diet caused their disease. A relevant point for physicians to consider is that these patients are at least as likely as is the general population to have intolerance or sensitivity to food components such as lactose and gluten. In a prospective questionnaire of 400 consecutive patients with IBD in the United Kingdom, 48% expressed the belief that diet could initiate IBD, and 57% said that diet could trigger a flare-up. In addition, 60% of respondents reported worsening of symptoms after eating certain foods, and about two-thirds deprived themselves of their favorite foods to prevent relapses (Inflamm Bowel Dis. 2016;22[1]:164-70). A French study found similar results. “Clearly there’s something there,” said Dr. Ananthakrishnan. Patients’ beliefs about the relationship between food and their symptoms are not simply misconceptions, he added.

A Canadian study published in 2016 found that almost one-third of patients with IBD avoid many food groups. “But there is significant heterogeneity in the foods that are avoided, and sometimes we mistake this heterogeneity for a lack of association between diet and symptoms in IBD,” said Dr. Ananthakrishnan. A larger number of patients avoid certain foods during periods of active disease, which suggests that food exacerbates their symptoms, he added. The same study showed that patients with IBD have more restrictive diets than do community controls. Patients eat fewer fruits and vegetables and generally consume less iron-rich food and less protein-rich food than healthy controls. GI intolerance, rather than professional advice, is the most common reason that patients with IBD restrict their diets (JPEN J Parenter Enteral Nutr. 2016;40[3]:405-11.).

A cross-sectional survey of 130 patients with IBD and 70 controls yielded similar results. Among patients, GI symptoms that resulted from consuming foods were not related to disease activity, disease location, or prior surgery. Patients with IBD tended to have greater frequency of GI intolerance to foods than did controls (Scand J Gastroenterol. 1997;32[6]:569-71.).
 

Diet may cause intestinal inflammation

International research has recorded increases in the consumption of sugar and fat (particularly saturated fat) and concomitant decreases in fiber consumption during the past several decades. The incidence of IBD has increased in parallel with these dietary changes with a remarkably similar trajectory, said Dr. Ananthakrishnan. The correlation between dietary changes and IBD incidence “holds true even more strikingly in countries that are now experiencing Westernization,” he added. These countries have undergone more rapid dietary changes, and their IBD incidence has doubled or tripled. The transition to “less traditional diets” appears to promote intestinal inflammation, said Dr. Ananthakrishnan.

An analysis of data from the European Prospective Investigation into Cancer (EPIC) study found an association between high consumption of sugar and soft drinks, together with low consumption of vegetables, and risk of ulcerative colitis (Inflamm Bowel Dis. 2016;22[2]:345-54.). A subsequent analysis of data from two prospective Swedish cohorts, however, found no association between consumption of sugary beverages and risk of Crohn’s disease or ulcerative colitis (Clin Gastroenterol Hepatol. 2019;17[1]:123-9.).

Although the data on sugar are mixed, data on the association between other macronutrient groups and risk of IBD are more consistent. When Dr. Ananthakrishnan and colleagues examined data from the Nurses’ Health Study, they found that the highest quintile of dietary fiber intake was associated with a 40% reduction in risk of Crohn’s disease, compared with the lowest quintile. The observed reduction of risk seemed to be greatest for fiber derived from fruits. Fiber from cereals, whole grains, or legumes, however, did not affect risk of Crohn’s disease (Gastroenterology. 2013;145[5]:970-7.).

A separate analysis of the Nurses’ Health Study suggested that high intake of n-3 polyunsaturated fatty acids (PUFAs) and low intake of n-6 PUFAs was associated with a 31% reduction in risk of ulcerative colitis and a 15% reduction in the risk of Crohn’s disease. These data were consistent with a previous analysis of EPIC data that found that high intake of n-6 PUFAs was associated with increased risk of ulcerative colitis (Gut. 2009;58[12]:1606-11.). Other analyses indicate that genetic polymorphisms likely modify the association between PUFAs and risk of ulcerative colitis, said Dr. Ananthakrishnan. “There may be an additional layer of complexity beyond just measuring your dietary intake.”

In addition to macronutrients, micronutrients can modify a patient’s risk of ulcerative colitis or Crohn’s disease. When Dr. Ananthakrishnan and colleagues examined the Nurses’ Health Study, they found an inverse association between vitamin D intake and risk of Crohn’s disease (Gastroenterology. 2012;142[3]:482-9.). In a separate study, they found that a zinc intake greater than 16 mg/day was associated with reduced risk of Crohn’s disease (Int J Epidemiol. 2015;44[6]:1995-2005.).

Patients aged older than 40 years and patients of European ancestry tend to be overrepresented in cohort studies, which reduces the generalizability of their conclusions, said Dr. Ananthakrishnan. Furthermore, cohort studies have not produced consistent findings regarding the relationship between various dietary components and risk of IBD. Nevertheless, the data suggest that dietary patterns may be associated with incident Crohn’s disease or ulcerative colitis.

 

An influence of diet on IBD risk is plausible

One mechanism through which diet may exercise a causal influence on the risk of IBD is by affecting the microbiome. In 2011, investigators studied 98 healthy volunteers who answered questionnaires about their diet. The researchers also used 16s rDNA sequencing to characterize the population’s stool samples. A diet high in animal protein, amino acids, and saturated fats was associated with large populations of Bacteroides. A diet low in fat and in animal protein, but high in carbohydrates and simple sugars was associated with large populations of Prevotella. When the investigators conducted a controlled-feeding study of 10 patients, microbiome composition changed within 1 day of initiating a high-fat-and-low-fiber or a low-fat-and-high-fiber diet (Science. 2011;334[6052]:105-8.). A more recent study showed that the diversity of the microbiome increased with the adoption of an animal-based diet (Nature. 2014;505[7484]:559-63.).

Diet also may exert a causal influence on IBD risk by altering the intestinal barrier. In an experimental model, 5-mg/mL concentrations of fiber from plantain and broccoli significantly reduced the translocation of Escherichia coli through a human intestinal epithelial barrier (Gut. 2010;59[10]:1331-9.). Increased fiber intake may thus result in reduced intestinal inflammation, said Dr. Ananthakrishnan.

Observational and experimental evidence thus support an effect of diet on the risk of IBD, and experimental evidence indicates that this effect is biologically plausible. Nevertheless, “there are many missing links,” and further study will clarify the role of diet in IBD incidence, said Dr. Ananthakrishnan.

AGA offers education for your patients about IBD, including lifestyle and nutrition management, in the AGA GI Patient Center at https://www.gastro.org/practice-guidance/gi-patient-center/topic/inflammatory-bowel-disease-ibd.

[email protected]

CHICAGO – Evidence suggests that diet may cause incident inflammatory bowel disease (IBD) and induce associated symptoms, according to a lecture delivered at Freston Conference 2019, sponsored by the American Gastroenterological Association.

Although the literature is highly consistent, it contains discordant findings, and many questions remain unanswered. “We need more rigorous studies, and particularly more interventions, to truly understand the role diet may play in patients with IBD,” said Ashwin N. Ananthakrishnan, MD, MPH, associate professor of medicine at Massachusetts General Hospital in Boston.
 

Food can cause symptoms in IBD

Many patients with IBD are convinced that their diet caused their disease. A relevant point for physicians to consider is that these patients are at least as likely as is the general population to have intolerance or sensitivity to food components such as lactose and gluten. In a prospective questionnaire of 400 consecutive patients with IBD in the United Kingdom, 48% expressed the belief that diet could initiate IBD, and 57% said that diet could trigger a flare-up. In addition, 60% of respondents reported worsening of symptoms after eating certain foods, and about two-thirds deprived themselves of their favorite foods to prevent relapses (Inflamm Bowel Dis. 2016;22[1]:164-70). A French study found similar results. “Clearly there’s something there,” said Dr. Ananthakrishnan. Patients’ beliefs about the relationship between food and their symptoms are not simply misconceptions, he added.

A Canadian study published in 2016 found that almost one-third of patients with IBD avoid many food groups. “But there is significant heterogeneity in the foods that are avoided, and sometimes we mistake this heterogeneity for a lack of association between diet and symptoms in IBD,” said Dr. Ananthakrishnan. A larger number of patients avoid certain foods during periods of active disease, which suggests that food exacerbates their symptoms, he added. The same study showed that patients with IBD have more restrictive diets than do community controls. Patients eat fewer fruits and vegetables and generally consume less iron-rich food and less protein-rich food than healthy controls. GI intolerance, rather than professional advice, is the most common reason that patients with IBD restrict their diets (JPEN J Parenter Enteral Nutr. 2016;40[3]:405-11.).

A cross-sectional survey of 130 patients with IBD and 70 controls yielded similar results. Among patients, GI symptoms that resulted from consuming foods were not related to disease activity, disease location, or prior surgery. Patients with IBD tended to have greater frequency of GI intolerance to foods than did controls (Scand J Gastroenterol. 1997;32[6]:569-71.).

Diet may cause intestinal inflammation

International research has recorded increases in the consumption of sugar and fat (particularly saturated fat) and concomitant decreases in fiber consumption during the past several decades. The incidence of IBD has increased in parallel with these dietary changes with a remarkably similar trajectory, said Dr. Ananthakrishnan. The correlation between dietary changes and IBD incidence “holds true even more strikingly in countries that are now experiencing Westernization,” he added. These countries have undergone more rapid dietary changes, and their IBD incidence has doubled or tripled. The transition to “less traditional diets” appears to promote intestinal inflammation, said Dr. Ananthakrishnan.

An analysis of data from the European Prospective Investigation into Cancer (EPIC) study found an association between high consumption of sugar and soft drinks, together with low consumption of vegetables, and risk of ulcerative colitis (Inflamm Bowel Dis. 2016;22[2]:345-54.). A subsequent analysis of data from two prospective Swedish cohorts, however, found no association between consumption of sugary beverages and risk of Crohn’s disease or ulcerative colitis (Clin Gastroenterol Hepatol. 2019;17[1]:123-9.).

Although the data on sugar are mixed, data on the association between other macronutrient groups and risk of IBD are more consistent. When Dr. Ananthakrishnan and colleagues examined data from the Nurses’ Health Study, they found that the highest quintile of dietary fiber intake was associated with a 40% reduction in risk of Crohn’s disease, compared with the lowest quintile. The observed reduction of risk seemed to be greatest for fiber derived from fruits. Fiber from cereals, whole grains, or legumes, however, did not affect risk of Crohn’s disease (Gastroenterology. 2013;145[5]:970-7.).

A separate analysis of the Nurses’ Health Study suggested that high intake of n-3 polyunsaturated fatty acids (PUFAs) and low intake of n-6 PUFAs was associated with a 31% reduction in risk of ulcerative colitis and a 15% reduction in the risk of Crohn’s disease. These data were consistent with a previous analysis of EPIC data that found that high intake of n-6 PUFAs was associated with increased risk of ulcerative colitis (Gut. 2009;58[12]:1606-11.). Other analyses indicate that genetic polymorphisms likely modify the association between PUFAs and risk of ulcerative colitis, said Dr. Ananthakrishnan. “There may be an additional layer of complexity beyond just measuring your dietary intake.”

In addition to macronutrients, micronutrients can modify a patient’s risk of ulcerative colitis or Crohn’s disease. When Dr. Ananthakrishnan and colleagues examined the Nurses’ Health Study, they found an inverse association between vitamin D intake and risk of Crohn’s disease (Gastroenterology. 2012;142[3]:482-9.). In a separate study, they found that a zinc intake greater than 16 mg/day was associated with reduced risk of Crohn’s disease (Int J Epidemiol. 2015;44[6]:1995-2005.).

Patients aged older than 40 years and patients of European ancestry tend to be overrepresented in cohort studies, which reduces the generalizability of their conclusions, said Dr. Ananthakrishnan. Furthermore, cohort studies have not produced consistent findings regarding the relationship between various dietary components and risk of IBD. Nevertheless, the data suggest that dietary patterns may be associated with incident Crohn’s disease or ulcerative colitis.
 

An influence of diet on IBD risk is plausible

One mechanism through which diet may exercise a causal influence on the risk of IBD is by affecting the microbiome. In 2011, investigators studied 98 healthy volunteers who answered questionnaires about their diet. The researchers also used 16s rDNA sequencing to characterize the population’s stool samples. A diet high in animal protein, amino acids, and saturated fats was associated with large populations of Bacteroides. A diet low in fat and in animal protein, but high in carbohydrates and simple sugars was associated with large populations of Prevotella. When the investigators conducted a controlled-feeding study of 10 patients, microbiome composition changed within 1 day of initiating a high-fat-and-low-fiber or a low-fat-and-high-fiber diet (Science. 2011;334[6052]:105-8.). A more recent study showed that the diversity of the microbiome increased with the adoption of an animal-based diet (Nature. 2014;505[7484]:559-63.).

Diet also may exert a causal influence on IBD risk by altering the intestinal barrier. In an experimental model, 5-mg/mL concentrations of fiber from plantain and broccoli significantly reduced the translocation of Escherichia coli through a human intestinal epithelial barrier (Gut. 2010;59[10]:1331-9.). Increased fiber intake may thus result in reduced intestinal inflammation, said Dr. Ananthakrishnan.

Observational and experimental evidence thus support an effect of diet on the risk of IBD, and experimental evidence indicates that this effect is biologically plausible. Nevertheless, “there are many missing links,” and further study will clarify the role of diet in IBD incidence, said Dr. Ananthakrishnan.

[email protected]

CHICAGO – Evidence suggests that diet may cause incident inflammatory bowel disease (IBD) and induce associated symptoms, according to a lecture delivered at Freston Conference 2019, sponsored by the American Gastroenterological Association.

Although the literature is highly consistent, it contains discordant findings, and many questions remain unanswered. “We need more rigorous studies, and particularly more interventions, to truly understand the role diet may play in patients with IBD,” said Ashwin N. Ananthakrishnan, MD, MPH, associate professor of medicine at Massachusetts General Hospital in Boston.
 

Food can cause symptoms in IBD

Many patients with IBD are convinced that their diet caused their disease. A relevant point for physicians to consider is that these patients are at least as likely as is the general population to have intolerance or sensitivity to food components such as lactose and gluten. In a prospective questionnaire of 400 consecutive patients with IBD in the United Kingdom, 48% expressed the belief that diet could initiate IBD, and 57% said that diet could trigger a flare-up. In addition, 60% of respondents reported worsening of symptoms after eating certain foods, and about two-thirds deprived themselves of their favorite foods to prevent relapses (Inflamm Bowel Dis. 2016;22[1]:164-70). A French study found similar results. “Clearly there’s something there,” said Dr. Ananthakrishnan. Patients’ beliefs about the relationship between food and their symptoms are not simply misconceptions, he added.

A Canadian study published in 2016 found that almost one-third of patients with IBD avoid many food groups. “But there is significant heterogeneity in the foods that are avoided, and sometimes we mistake this heterogeneity for a lack of association between diet and symptoms in IBD,” said Dr. Ananthakrishnan. A larger number of patients avoid certain foods during periods of active disease, which suggests that food exacerbates their symptoms, he added. The same study showed that patients with IBD have more restrictive diets than do community controls. Patients eat fewer fruits and vegetables and generally consume less iron-rich food and less protein-rich food than healthy controls. GI intolerance, rather than professional advice, is the most common reason that patients with IBD restrict their diets (JPEN J Parenter Enteral Nutr. 2016;40[3]:405-11.).

A cross-sectional survey of 130 patients with IBD and 70 controls yielded similar results. Among patients, GI symptoms that resulted from consuming foods were not related to disease activity, disease location, or prior surgery. Patients with IBD tended to have greater frequency of GI intolerance to foods than did controls (Scand J Gastroenterol. 1997;32[6]:569-71.).

Diet may cause intestinal inflammation

International research has recorded increases in the consumption of sugar and fat (particularly saturated fat) and concomitant decreases in fiber consumption during the past several decades. The incidence of IBD has increased in parallel with these dietary changes with a remarkably similar trajectory, said Dr. Ananthakrishnan. The correlation between dietary changes and IBD incidence “holds true even more strikingly in countries that are now experiencing Westernization,” he added. These countries have undergone more rapid dietary changes, and their IBD incidence has doubled or tripled. The transition to “less traditional diets” appears to promote intestinal inflammation, said Dr. Ananthakrishnan.

An analysis of data from the European Prospective Investigation into Cancer (EPIC) study found an association between high consumption of sugar and soft drinks, together with low consumption of vegetables, and risk of ulcerative colitis (Inflamm Bowel Dis. 2016;22[2]:345-54.). A subsequent analysis of data from two prospective Swedish cohorts, however, found no association between consumption of sugary beverages and risk of Crohn’s disease or ulcerative colitis (Clin Gastroenterol Hepatol. 2019;17[1]:123-9.).

Although the data on sugar are mixed, data on the association between other macronutrient groups and risk of IBD are more consistent. When Dr. Ananthakrishnan and colleagues examined data from the Nurses’ Health Study, they found that the highest quintile of dietary fiber intake was associated with a 40% reduction in risk of Crohn’s disease, compared with the lowest quintile. The observed reduction of risk seemed to be greatest for fiber derived from fruits. Fiber from cereals, whole grains, or legumes, however, did not affect risk of Crohn’s disease (Gastroenterology. 2013;145[5]:970-7.).

A separate analysis of the Nurses’ Health Study suggested that high intake of n-3 polyunsaturated fatty acids (PUFAs) and low intake of n-6 PUFAs was associated with a 31% reduction in risk of ulcerative colitis and a 15% reduction in the risk of Crohn’s disease. These data were consistent with a previous analysis of EPIC data that found that high intake of n-6 PUFAs was associated with increased risk of ulcerative colitis (Gut. 2009;58[12]:1606-11.). Other analyses indicate that genetic polymorphisms likely modify the association between PUFAs and risk of ulcerative colitis, said Dr. Ananthakrishnan. “There may be an additional layer of complexity beyond just measuring your dietary intake.”

In addition to macronutrients, micronutrients can modify a patient’s risk of ulcerative colitis or Crohn’s disease. When Dr. Ananthakrishnan and colleagues examined the Nurses’ Health Study, they found an inverse association between vitamin D intake and risk of Crohn’s disease (Gastroenterology. 2012;142[3]:482-9.). In a separate study, they found that a zinc intake greater than 16 mg/day was associated with reduced risk of Crohn’s disease (Int J Epidemiol. 2015;44[6]:1995-2005.).

Patients aged older than 40 years and patients of European ancestry tend to be overrepresented in cohort studies, which reduces the generalizability of their conclusions, said Dr. Ananthakrishnan. Furthermore, cohort studies have not produced consistent findings regarding the relationship between various dietary components and risk of IBD. Nevertheless, the data suggest that dietary patterns may be associated with incident Crohn’s disease or ulcerative colitis.
 

An influence of diet on IBD risk is plausible

One mechanism through which diet may exercise a causal influence on the risk of IBD is by affecting the microbiome. In 2011, investigators studied 98 healthy volunteers who answered questionnaires about their diet. The researchers also used 16s rDNA sequencing to characterize the population’s stool samples. A diet high in animal protein, amino acids, and saturated fats was associated with large populations of Bacteroides. A diet low in fat and in animal protein, but high in carbohydrates and simple sugars was associated with large populations of Prevotella. When the investigators conducted a controlled-feeding study of 10 patients, microbiome composition changed within 1 day of initiating a high-fat-and-low-fiber or a low-fat-and-high-fiber diet (Science. 2011;334[6052]:105-8.). A more recent study showed that the diversity of the microbiome increased with the adoption of an animal-based diet (Nature. 2014;505[7484]:559-63.).

Diet also may exert a causal influence on IBD risk by altering the intestinal barrier. In an experimental model, 5-mg/mL concentrations of fiber from plantain and broccoli significantly reduced the translocation of Escherichia coli through a human intestinal epithelial barrier (Gut. 2010;59[10]:1331-9.). Increased fiber intake may thus result in reduced intestinal inflammation, said Dr. Ananthakrishnan.

Observational and experimental evidence thus support an effect of diet on the risk of IBD, and experimental evidence indicates that this effect is biologically plausible. Nevertheless, “there are many missing links,” and further study will clarify the role of diet in IBD incidence, said Dr. Ananthakrishnan.

[email protected]

CHICAGO – Evidence suggests that diet may cause incident inflammatory bowel disease (IBD) and induce associated symptoms, according to a lecture delivered at Freston Conference 2019, sponsored by the American Gastroenterological Association.

Although the literature is highly consistent, it contains discordant findings, and many questions remain unanswered. “We need more rigorous studies, and particularly more interventions, to truly understand the role diet may play in patients with IBD,” said Ashwin N. Ananthakrishnan, MD, MPH, associate professor of medicine at Massachusetts General Hospital in Boston.
 

Food can cause symptoms in IBD

Many patients with IBD are convinced that their diet caused their disease. A relevant point for physicians to consider is that these patients are at least as likely as is the general population to have intolerance or sensitivity to food components such as lactose and gluten. In a prospective questionnaire of 400 consecutive patients with IBD in the United Kingdom, 48% expressed the belief that diet could initiate IBD, and 57% said that diet could trigger a flare-up. In addition, 60% of respondents reported worsening of symptoms after eating certain foods, and about two-thirds deprived themselves of their favorite foods to prevent relapses (Inflamm Bowel Dis. 2016;22[1]:164-70). A French study found similar results. “Clearly there’s something there,” said Dr. Ananthakrishnan. Patients’ beliefs about the relationship between food and their symptoms are not simply misconceptions, he added.

A Canadian study published in 2016 found that almost one-third of patients with IBD avoid many food groups. “But there is significant heterogeneity in the foods that are avoided, and sometimes we mistake this heterogeneity for a lack of association between diet and symptoms in IBD,” said Dr. Ananthakrishnan. A larger number of patients avoid certain foods during periods of active disease, which suggests that food exacerbates their symptoms, he added. The same study showed that patients with IBD have more restrictive diets than do community controls. Patients eat fewer fruits and vegetables and generally consume less iron-rich food and less protein-rich food than healthy controls. GI intolerance, rather than professional advice, is the most common reason that patients with IBD restrict their diets (JPEN J Parenter Enteral Nutr. 2016;40[3]:405-11.).

A cross-sectional survey of 130 patients with IBD and 70 controls yielded similar results. Among patients, GI symptoms that resulted from consuming foods were not related to disease activity, disease location, or prior surgery. Patients with IBD tended to have greater frequency of GI intolerance to foods than did controls (Scand J Gastroenterol. 1997;32[6]:569-71.).

Diet may cause intestinal inflammation

International research has recorded increases in the consumption of sugar and fat (particularly saturated fat) and concomitant decreases in fiber consumption during the past several decades. The incidence of IBD has increased in parallel with these dietary changes with a remarkably similar trajectory, said Dr. Ananthakrishnan. The correlation between dietary changes and IBD incidence “holds true even more strikingly in countries that are now experiencing Westernization,” he added. These countries have undergone more rapid dietary changes, and their IBD incidence has doubled or tripled. The transition to “less traditional diets” appears to promote intestinal inflammation, said Dr. Ananthakrishnan.

An analysis of data from the European Prospective Investigation into Cancer (EPIC) study found an association between high consumption of sugar and soft drinks, together with low consumption of vegetables, and risk of ulcerative colitis (Inflamm Bowel Dis. 2016;22[2]:345-54.). A subsequent analysis of data from two prospective Swedish cohorts, however, found no association between consumption of sugary beverages and risk of Crohn’s disease or ulcerative colitis (Clin Gastroenterol Hepatol. 2019;17[1]:123-9.).

Although the data on sugar are mixed, data on the association between other macronutrient groups and risk of IBD are more consistent. When Dr. Ananthakrishnan and colleagues examined data from the Nurses’ Health Study, they found that the highest quintile of dietary fiber intake was associated with a 40% reduction in risk of Crohn’s disease, compared with the lowest quintile. The observed reduction of risk seemed to be greatest for fiber derived from fruits. Fiber from cereals, whole grains, or legumes, however, did not affect risk of Crohn’s disease (Gastroenterology. 2013;145[5]:970-7.).

A separate analysis of the Nurses’ Health Study suggested that high intake of n-3 polyunsaturated fatty acids (PUFAs) and low intake of n-6 PUFAs was associated with a 31% reduction in risk of ulcerative colitis and a 15% reduction in the risk of Crohn’s disease. These data were consistent with a previous analysis of EPIC data that found that high intake of n-6 PUFAs was associated with increased risk of ulcerative colitis (Gut. 2009;58[12]:1606-11.). Other analyses indicate that genetic polymorphisms likely modify the association between PUFAs and risk of ulcerative colitis, said Dr. Ananthakrishnan. “There may be an additional layer of complexity beyond just measuring your dietary intake.”

In addition to macronutrients, micronutrients can modify a patient’s risk of ulcerative colitis or Crohn’s disease. When Dr. Ananthakrishnan and colleagues examined the Nurses’ Health Study, they found an inverse association between vitamin D intake and risk of Crohn’s disease (Gastroenterology. 2012;142[3]:482-9.). In a separate study, they found that a zinc intake greater than 16 mg/day was associated with reduced risk of Crohn’s disease (Int J Epidemiol. 2015;44[6]:1995-2005.).

Patients aged older than 40 years and patients of European ancestry tend to be overrepresented in cohort studies, which reduces the generalizability of their conclusions, said Dr. Ananthakrishnan. Furthermore, cohort studies have not produced consistent findings regarding the relationship between various dietary components and risk of IBD. Nevertheless, the data suggest that dietary patterns may be associated with incident Crohn’s disease or ulcerative colitis.
 

An influence of diet on IBD risk is plausible

One mechanism through which diet may exercise a causal influence on the risk of IBD is by affecting the microbiome. In 2011, investigators studied 98 healthy volunteers who answered questionnaires about their diet. The researchers also used 16s rDNA sequencing to characterize the population’s stool samples. A diet high in animal protein, amino acids, and saturated fats was associated with large populations of Bacteroides. A diet low in fat and in animal protein, but high in carbohydrates and simple sugars was associated with large populations of Prevotella. When the investigators conducted a controlled-feeding study of 10 patients, microbiome composition changed within 1 day of initiating a high-fat-and-low-fiber or a low-fat-and-high-fiber diet (Science. 2011;334[6052]:105-8.). A more recent study showed that the diversity of the microbiome increased with the adoption of an animal-based diet (Nature. 2014;505[7484]:559-63.).

Diet also may exert a causal influence on IBD risk by altering the intestinal barrier. In an experimental model, 5-mg/mL concentrations of fiber from plantain and broccoli significantly reduced the translocation of Escherichia coli through a human intestinal epithelial barrier (Gut. 2010;59[10]:1331-9.). Increased fiber intake may thus result in reduced intestinal inflammation, said Dr. Ananthakrishnan.

Observational and experimental evidence thus support an effect of diet on the risk of IBD, and experimental evidence indicates that this effect is biologically plausible. Nevertheless, “there are many missing links,” and further study will clarify the role of diet in IBD incidence, said Dr. Ananthakrishnan.

[email protected]

CHICAGO – Because gastroparesis and functional dyspepsia share several symptoms (e.g., upper abdominal pain, fullness, and bloating) and pathophysiological abnormalities (e.g., delayed gastric emptying, impaired gastric accommodation, and visceral hypersensitivity), it can be hard to distinguish the two conditions, according to a lecture presented at Freston Conference 2019, sponsored by the American Gastroenterological Association. Additional research into the role of diet in these conditions will improve the treatment of these patients, said Linda Nguyen, MD, director of neurogastroenterology and motility at Stanford (Calif.) University.

Distinguishing the disorders

The accepted definition of gastroparesis is abnormal gastric emptying in the absence of a mechanical obstruction. The condition’s symptoms include nausea, vomiting, bloating, early satiety, abdominal pain, and weight loss. A previous consensus held that if a patient had abdominal pain, he or she did not have gastroparesis. Yet studies indicate that up to 80% of patients with gastroparesis have pain.

Functional dyspepsia is defined as bothersome postprandial fullness, early satiety, and epigastric pain or burning in the absence of structural abnormality. The disorder can be subdivided into postprandial distress (i.e., meal-related symptomatology) and epigastric pain syndrome (i.e., pain or burning that may or may not be related to meals). Either of these alternatives may entail nausea and vomiting.

Comparing the pathophysiologies of gastroparesis and functional dyspepsia helps to distinguish these disorders from each other. A 2019 review described rapid gastric emptying and duodenal eosinophilia in patients with functional dyspepsia, but not in patients with gastroparesis. Patients with epigastric pain syndrome had sensitivity to acid, bile, and fats. Patients with idiopathic gastroparesis, which is the most common type, had a weak antral pump and abnormal duodenal feedback, but patients with functional dyspepsia did not have these characteristics (J Neurogastroenterol Motil. 2019;25[1]:27-35).
 

Examining symptoms and severity

One examination of patients with gastroparesis found that approximately 46% of them had a body mass index of 25 or greater. About 26% of patients had a BMI greater than 30. Yet these patients were eating less than 60% of their recommended daily allowances, based on their age, height, weight, and sex (Clin Gastroenterol Hepatol. 2011;9[12]:1056-64).

Accelerating gastric emptying may not relieve symptoms completely in a patient with gastroparesis, said Dr. Nguyen. A 2007 study of patients with gastroparesis found that 43% had impaired accommodation, and 29% had visceral hypersensitivity (Gut. 2007;56[1]:29-36). The same data indicated that gastric emptying time was not correlated with symptom severity. Impaired accommodation, however, was associated with early satiety and weight loss. Visceral hypersensitivity was associated with pain, early satiety, and weight loss. These data suggest that accommodation and visceral hypersensitivity may influence symptom severity in gastroparesis, said Dr. Nguyen.

Other researchers compared mild, moderate, and severe symptoms of early satiety in patients with gastroparesis. They found that patients with severe symptoms of early satiety have more delayed gastric emptying than do patients with mild or moderate symptoms of early satiety (Neurogastroenterol Motil. 2017;29[4].).

Dr. Nguyen and colleagues examined normal gastric emptying, compared with severely delayed gastric emptying, which they defined as greater than 35% retention at 4 hours. They found that severely delayed gastric emptying was associated with more severe symptoms, particularly nausea and vomiting, as measured by Gastroparesis Cardinal Symptom Index (GCSI). Extreme symptoms may help differentiate between gastroparesis and functional dyspepsia, said Dr. Nguyen.


 

Dietary and pharmacologic treatment

Although clinicians might consider recommending dietary modifications to treat gastroparesis or functional dyspepsia, the literature contains little evidence about their efficacy in these indications, said Dr. Nguyen. Based on a study by Tack and colleagues, some clinicians recommend small, frequent meals that are low in fat and low in fiber to patients with gastroparesis. Such a diet could be harmful, however, to patients with comorbid diabetes, irritable bowel syndrome, or renal failure.

Common dietary recommendations for functional dyspepsia include small, frequent meals; decreased fat consumption; and avoidance of citrus and spicy foods. These recommendations are based on small studies in which patients reported which foods tended to cause their symptoms. Trials of dietary modifications in functional dyspepsia, however, are lacking.

Nevertheless, the literature can guide the selection of pharmacotherapy for these disorders. Talley et al. examined the effects of neuromodulators such as amitriptyline, a tricyclic antidepressant, and escitalopram in functional dyspepsia. About 70% of the sample had postprandial distress syndrome, and 20% met criteria for idiopathic gastroparesis. Amitriptyline provided greater symptomatic relief to these patients than did placebo, but escitalopram did not. Patients who met criteria for idiopathic gastroparesis did not respond well to tricyclic antidepressants, but patients with epigastric pain syndrome did. Furthermore, compared with patients with normal gastric emptying, those with delayed emptying did not respond to tricyclic antidepressants. A separate study found that the tricyclic antidepressant nortriptyline did not improve symptoms of gastroparesis (JAMA. 2013;310[24]:2640-9).

Promotility agents may be beneficial for certain patients. A study published this year suggests that, compared with placebo, prucalopride is effective for nausea, vomiting, fullness, bloating, and gastric emptying in patients with idiopathic gastroparesis (Am J Gastroenterol. 2019;114[8]:1265-74.). A 2017 meta-analysis, however, found that proton pump inhibitors were more effective than promotility agents in patients with functional dyspepsia (Am J Gastroenterol. 2017;112[7]:988-1013.).

Pyloric dysfunction may accompany gastroparesis in some patients. Increased severity of gastric emptying delay is associated with increased pylorospasm. Endoscopists have gained experience in performing pyloric myotomy, and this treatment has become more popular. Uncontrolled studies indicate that the proportion of patients with decreased symptom severity after this procedure is higher than 70% and can be as high as 86% (Gastrointest Endosc. 2017;85[1]:123-8). The predictors of a good response include idiopathic etiology, male sex, moderate symptom severity, and greater delay in gastric emptying.

Functional dyspepsia should perhaps be understood as normal gastric emptying and symptoms of epigastric pain syndrome, said Dr. Nguyen. Those patients may respond to neuromodulators, she added. Idiopathic gastroparesis appears to be characterized by severe delay in gastric emptying, postprandial symptoms, nausea, and vomiting. “In the middle is the gray zone, where you have these patients with postprandial distress with or without delayed gastric emptying,” said Dr. Nguyen. Functional dyspepsia and gastroparesis could be two ends of a spectrum, and the best management for patients with symptoms that occur in both disorders is unclear.

Help educate your patients about gastroparesis, its symptoms and causes, as well as testing and treatment using AGA patient education, which can be found in the GI Patient Center at https://www.gastro.org/practice-guidance/gi-patient-center/topic/gastroparesis.

[email protected]

CHICAGO – Because gastroparesis and functional dyspepsia share several symptoms (e.g., upper abdominal pain, fullness, and bloating) and pathophysiological abnormalities (e.g., delayed gastric emptying, impaired gastric accommodation, and visceral hypersensitivity), it can be hard to distinguish the two conditions, according to a lecture presented at Freston Conference 2019, sponsored by the American Gastroenterological Association. Additional research into the role of diet in these conditions will improve the treatment of these patients, said Linda Nguyen, MD, director of neurogastroenterology and motility at Stanford (Calif.) University.

Distinguishing the disorders

The accepted definition of gastroparesis is abnormal gastric emptying in the absence of a mechanical obstruction. The condition’s symptoms include nausea, vomiting, bloating, early satiety, abdominal pain, and weight loss. A previous consensus held that if a patient had abdominal pain, he or she did not have gastroparesis. Yet studies indicate that up to 80% of patients with gastroparesis have pain.

Functional dyspepsia is defined as bothersome postprandial fullness, early satiety, and epigastric pain or burning in the absence of structural abnormality. The disorder can be subdivided into postprandial distress (i.e., meal-related symptomatology) and epigastric pain syndrome (i.e., pain or burning that may or may not be related to meals). Either of these alternatives may entail nausea and vomiting.

Comparing the pathophysiologies of gastroparesis and functional dyspepsia helps to distinguish these disorders from each other. A 2019 review described rapid gastric emptying and duodenal eosinophilia in patients with functional dyspepsia, but not in patients with gastroparesis. Patients with epigastric pain syndrome had sensitivity to acid, bile, and fats. Patients with idiopathic gastroparesis, which is the most common type, had a weak antral pump and abnormal duodenal feedback, but patients with functional dyspepsia did not have these characteristics (J Neurogastroenterol Motil. 2019;25[1]:27-35).
 

Examining symptoms and severity

One examination of patients with gastroparesis found that approximately 46% of them had a body mass index of 25 or greater. About 26% of patients had a BMI greater than 30. Yet these patients were eating less than 60% of their recommended daily allowances, based on their age, height, weight, and sex (Clin Gastroenterol Hepatol. 2011;9[12]:1056-64).

Accelerating gastric emptying may not relieve symptoms completely in a patient with gastroparesis, said Dr. Nguyen. A 2007 study of patients with gastroparesis found that 43% had impaired accommodation, and 29% had visceral hypersensitivity (Gut. 2007;56[1]:29-36). The same data indicated that gastric emptying time was not correlated with symptom severity. Impaired accommodation, however, was associated with early satiety and weight loss. Visceral hypersensitivity was associated with pain, early satiety, and weight loss. These data suggest that accommodation and visceral hypersensitivity may influence symptom severity in gastroparesis, said Dr. Nguyen.

Other researchers compared mild, moderate, and severe symptoms of early satiety in patients with gastroparesis. They found that patients with severe symptoms of early satiety have more delayed gastric emptying than do patients with mild or moderate symptoms of early satiety (Neurogastroenterol Motil. 2017;29[4].).

Dr. Nguyen and colleagues examined normal gastric emptying, compared with severely delayed gastric emptying, which they defined as greater than 35% retention at 4 hours. They found that severely delayed gastric emptying was associated with more severe symptoms, particularly nausea and vomiting, as measured by Gastroparesis Cardinal Symptom Index (GCSI). Extreme symptoms may help differentiate between gastroparesis and functional dyspepsia, said Dr. Nguyen.


 

Dietary and pharmacologic treatment

Although clinicians might consider recommending dietary modifications to treat gastroparesis or functional dyspepsia, the literature contains little evidence about their efficacy in these indications, said Dr. Nguyen. Based on a study by Tack and colleagues, some clinicians recommend small, frequent meals that are low in fat and low in fiber to patients with gastroparesis. Such a diet could be harmful, however, to patients with comorbid diabetes, irritable bowel syndrome, or renal failure.

Common dietary recommendations for functional dyspepsia include small, frequent meals; decreased fat consumption; and avoidance of citrus and spicy foods. These recommendations are based on small studies in which patients reported which foods tended to cause their symptoms. Trials of dietary modifications in functional dyspepsia, however, are lacking.

Nevertheless, the literature can guide the selection of pharmacotherapy for these disorders. Talley et al. examined the effects of neuromodulators such as amitriptyline, a tricyclic antidepressant, and escitalopram in functional dyspepsia. About 70% of the sample had postprandial distress syndrome, and 20% met criteria for idiopathic gastroparesis. Amitriptyline provided greater symptomatic relief to these patients than did placebo, but escitalopram did not. Patients who met criteria for idiopathic gastroparesis did not respond well to tricyclic antidepressants, but patients with epigastric pain syndrome did. Furthermore, compared with patients with normal gastric emptying, those with delayed emptying did not respond to tricyclic antidepressants. A separate study found that the tricyclic antidepressant nortriptyline did not improve symptoms of gastroparesis (JAMA. 2013;310[24]:2640-9).

Promotility agents may be beneficial for certain patients. A study published this year suggests that, compared with placebo, prucalopride is effective for nausea, vomiting, fullness, bloating, and gastric emptying in patients with idiopathic gastroparesis (Am J Gastroenterol. 2019;114[8]:1265-74.). A 2017 meta-analysis, however, found that proton pump inhibitors were more effective than promotility agents in patients with functional dyspepsia (Am J Gastroenterol. 2017;112[7]:988-1013.).

Pyloric dysfunction may accompany gastroparesis in some patients. Increased severity of gastric emptying delay is associated with increased pylorospasm. Endoscopists have gained experience in performing pyloric myotomy, and this treatment has become more popular. Uncontrolled studies indicate that the proportion of patients with decreased symptom severity after this procedure is higher than 70% and can be as high as 86% (Gastrointest Endosc. 2017;85[1]:123-8). The predictors of a good response include idiopathic etiology, male sex, moderate symptom severity, and greater delay in gastric emptying.

Functional dyspepsia should perhaps be understood as normal gastric emptying and symptoms of epigastric pain syndrome, said Dr. Nguyen. Those patients may respond to neuromodulators, she added. Idiopathic gastroparesis appears to be characterized by severe delay in gastric emptying, postprandial symptoms, nausea, and vomiting. “In the middle is the gray zone, where you have these patients with postprandial distress with or without delayed gastric emptying,” said Dr. Nguyen. Functional dyspepsia and gastroparesis could be two ends of a spectrum, and the best management for patients with symptoms that occur in both disorders is unclear.

Help educate your patients about gastroparesis, its symptoms and causes, as well as testing and treatment using AGA patient education, which can be found in the GI Patient Center at https://www.gastro.org/practice-guidance/gi-patient-center/topic/gastroparesis.

[email protected]

CHICAGO – Because gastroparesis and functional dyspepsia share several symptoms (e.g., upper abdominal pain, fullness, and bloating) and pathophysiological abnormalities (e.g., delayed gastric emptying, impaired gastric accommodation, and visceral hypersensitivity), it can be hard to distinguish the two conditions, according to a lecture presented at Freston Conference 2019, sponsored by the American Gastroenterological Association. Additional research into the role of diet in these conditions will improve the treatment of these patients, said Linda Nguyen, MD, director of neurogastroenterology and motility at Stanford (Calif.) University.

Distinguishing the disorders

The accepted definition of gastroparesis is abnormal gastric emptying in the absence of a mechanical obstruction. The condition’s symptoms include nausea, vomiting, bloating, early satiety, abdominal pain, and weight loss. A previous consensus held that if a patient had abdominal pain, he or she did not have gastroparesis. Yet studies indicate that up to 80% of patients with gastroparesis have pain.

Functional dyspepsia is defined as bothersome postprandial fullness, early satiety, and epigastric pain or burning in the absence of structural abnormality. The disorder can be subdivided into postprandial distress (i.e., meal-related symptomatology) and epigastric pain syndrome (i.e., pain or burning that may or may not be related to meals). Either of these alternatives may entail nausea and vomiting.

Comparing the pathophysiologies of gastroparesis and functional dyspepsia helps to distinguish these disorders from each other. A 2019 review described rapid gastric emptying and duodenal eosinophilia in patients with functional dyspepsia, but not in patients with gastroparesis. Patients with epigastric pain syndrome had sensitivity to acid, bile, and fats. Patients with idiopathic gastroparesis, which is the most common type, had a weak antral pump and abnormal duodenal feedback, but patients with functional dyspepsia did not have these characteristics (J Neurogastroenterol Motil. 2019;25[1]:27-35).
 

Examining symptoms and severity

One examination of patients with gastroparesis found that approximately 46% of them had a body mass index of 25 or greater. About 26% of patients had a BMI greater than 30. Yet these patients were eating less than 60% of their recommended daily allowances, based on their age, height, weight, and sex (Clin Gastroenterol Hepatol. 2011;9[12]:1056-64).

Accelerating gastric emptying may not relieve symptoms completely in a patient with gastroparesis, said Dr. Nguyen. A 2007 study of patients with gastroparesis found that 43% had impaired accommodation, and 29% had visceral hypersensitivity (Gut. 2007;56[1]:29-36). The same data indicated that gastric emptying time was not correlated with symptom severity. Impaired accommodation, however, was associated with early satiety and weight loss. Visceral hypersensitivity was associated with pain, early satiety, and weight loss. These data suggest that accommodation and visceral hypersensitivity may influence symptom severity in gastroparesis, said Dr. Nguyen.

Other researchers compared mild, moderate, and severe symptoms of early satiety in patients with gastroparesis. They found that patients with severe symptoms of early satiety have more delayed gastric emptying than do patients with mild or moderate symptoms of early satiety (Neurogastroenterol Motil. 2017;29[4].).

Dr. Nguyen and colleagues examined normal gastric emptying, compared with severely delayed gastric emptying, which they defined as greater than 35% retention at 4 hours. They found that severely delayed gastric emptying was associated with more severe symptoms, particularly nausea and vomiting, as measured by Gastroparesis Cardinal Symptom Index (GCSI). Extreme symptoms may help differentiate between gastroparesis and functional dyspepsia, said Dr. Nguyen.


 

Dietary and pharmacologic treatment

Although clinicians might consider recommending dietary modifications to treat gastroparesis or functional dyspepsia, the literature contains little evidence about their efficacy in these indications, said Dr. Nguyen. Based on a study by Tack and colleagues, some clinicians recommend small, frequent meals that are low in fat and low in fiber to patients with gastroparesis. Such a diet could be harmful, however, to patients with comorbid diabetes, irritable bowel syndrome, or renal failure.

Common dietary recommendations for functional dyspepsia include small, frequent meals; decreased fat consumption; and avoidance of citrus and spicy foods. These recommendations are based on small studies in which patients reported which foods tended to cause their symptoms. Trials of dietary modifications in functional dyspepsia, however, are lacking.

Nevertheless, the literature can guide the selection of pharmacotherapy for these disorders. Talley et al. examined the effects of neuromodulators such as amitriptyline, a tricyclic antidepressant, and escitalopram in functional dyspepsia. About 70% of the sample had postprandial distress syndrome, and 20% met criteria for idiopathic gastroparesis. Amitriptyline provided greater symptomatic relief to these patients than did placebo, but escitalopram did not. Patients who met criteria for idiopathic gastroparesis did not respond well to tricyclic antidepressants, but patients with epigastric pain syndrome did. Furthermore, compared with patients with normal gastric emptying, those with delayed emptying did not respond to tricyclic antidepressants. A separate study found that the tricyclic antidepressant nortriptyline did not improve symptoms of gastroparesis (JAMA. 2013;310[24]:2640-9).

Promotility agents may be beneficial for certain patients. A study published this year suggests that, compared with placebo, prucalopride is effective for nausea, vomiting, fullness, bloating, and gastric emptying in patients with idiopathic gastroparesis (Am J Gastroenterol. 2019;114[8]:1265-74.). A 2017 meta-analysis, however, found that proton pump inhibitors were more effective than promotility agents in patients with functional dyspepsia (Am J Gastroenterol. 2017;112[7]:988-1013.).

Pyloric dysfunction may accompany gastroparesis in some patients. Increased severity of gastric emptying delay is associated with increased pylorospasm. Endoscopists have gained experience in performing pyloric myotomy, and this treatment has become more popular. Uncontrolled studies indicate that the proportion of patients with decreased symptom severity after this procedure is higher than 70% and can be as high as 86% (Gastrointest Endosc. 2017;85[1]:123-8). The predictors of a good response include idiopathic etiology, male sex, moderate symptom severity, and greater delay in gastric emptying.

Functional dyspepsia should perhaps be understood as normal gastric emptying and symptoms of epigastric pain syndrome, said Dr. Nguyen. Those patients may respond to neuromodulators, she added. Idiopathic gastroparesis appears to be characterized by severe delay in gastric emptying, postprandial symptoms, nausea, and vomiting. “In the middle is the gray zone, where you have these patients with postprandial distress with or without delayed gastric emptying,” said Dr. Nguyen. Functional dyspepsia and gastroparesis could be two ends of a spectrum, and the best management for patients with symptoms that occur in both disorders is unclear.

Help educate your patients about gastroparesis, its symptoms and causes, as well as testing and treatment using AGA patient education, which can be found in the GI Patient Center at https://www.gastro.org/practice-guidance/gi-patient-center/topic/gastroparesis.

[email protected]

CHICAGO – Because gastroparesis and functional dyspepsia share several symptoms (e.g., upper abdominal pain, fullness, and bloating) and pathophysiological abnormalities (e.g., delayed gastric emptying, impaired gastric accommodation, and visceral hypersensitivity), it can be hard to distinguish the two conditions, according to a lecture presented at Freston Conference 2019, sponsored by the American Gastroenterological Association. Additional research into the role of diet in these conditions will improve the treatment of these patients, said Linda Nguyen, MD, director of neurogastroenterology and motility at Stanford (Calif.) University.

Distinguishing the disorders

The accepted definition of gastroparesis is abnormal gastric emptying in the absence of a mechanical obstruction. The condition’s symptoms include nausea, vomiting, bloating, early satiety, abdominal pain, and weight loss. A previous consensus held that if a patient had abdominal pain, he or she did not have gastroparesis. Yet studies indicate that up to 80% of patients with gastroparesis have pain.

Functional dyspepsia is defined as bothersome postprandial fullness, early satiety, and epigastric pain or burning in the absence of structural abnormality. The disorder can be subdivided into postprandial distress (i.e., meal-related symptomatology) and epigastric pain syndrome (i.e., pain or burning that may or may not be related to meals). Either of these alternatives may entail nausea and vomiting.

Comparing the pathophysiologies of gastroparesis and functional dyspepsia helps to distinguish these disorders from each other. A 2019 review described rapid gastric emptying and duodenal eosinophilia in patients with functional dyspepsia, but not in patients with gastroparesis. Patients with epigastric pain syndrome had sensitivity to acid, bile, and fats. Patients with idiopathic gastroparesis, which is the most common type, had a weak antral pump and abnormal duodenal feedback, but patients with functional dyspepsia did not have these characteristics (J Neurogastroenterol Motil. 2019;25[1]:27-35).
 

Examining symptoms and severity

One examination of patients with gastroparesis found that approximately 46% of them had a body mass index of 25 or greater. About 26% of patients had a BMI greater than 30. Yet these patients were eating less than 60% of their recommended daily allowances, based on their age, height, weight, and sex (Clin Gastroenterol Hepatol. 2011;9[12]:1056-64).

Accelerating gastric emptying may not relieve symptoms completely in a patient with gastroparesis, said Dr. Nguyen. A 2007 study of patients with gastroparesis found that 43% had impaired accommodation, and 29% had visceral hypersensitivity (Gut. 2007;56[1]:29-36). The same data indicated that gastric emptying time was not correlated with symptom severity. Impaired accommodation, however, was associated with early satiety and weight loss. Visceral hypersensitivity was associated with pain, early satiety, and weight loss. These data suggest that accommodation and visceral hypersensitivity may influence symptom severity in gastroparesis, said Dr. Nguyen.

Other researchers compared mild, moderate, and severe symptoms of early satiety in patients with gastroparesis. They found that patients with severe symptoms of early satiety have more delayed gastric emptying than do patients with mild or moderate symptoms of early satiety (Neurogastroenterol Motil. 2017;29[4].).

Dr. Nguyen and colleagues examined normal gastric emptying, compared with severely delayed gastric emptying, which they defined as greater than 35% retention at 4 hours. They found that severely delayed gastric emptying was associated with more severe symptoms, particularly nausea and vomiting, as measured by Gastroparesis Cardinal Symptom Index (GCSI). Extreme symptoms may help differentiate between gastroparesis and functional dyspepsia, said Dr. Nguyen.
 

Dietary and pharmacologic treatment

Although clinicians might consider recommending dietary modifications to treat gastroparesis or functional dyspepsia, the literature contains little evidence about their efficacy in these indications, said Dr. Nguyen. Based on a study by Tack and colleagues, some clinicians recommend small, frequent meals that are low in fat and low in fiber to patients with gastroparesis. Such a diet could be harmful, however, to patients with comorbid diabetes, irritable bowel syndrome, or renal failure.

Common dietary recommendations for functional dyspepsia include small, frequent meals; decreased fat consumption; and avoidance of citrus and spicy foods. These recommendations are based on small studies in which patients reported which foods tended to cause their symptoms. Trials of dietary modifications in functional dyspepsia, however, are lacking.

Nevertheless, the literature can guide the selection of pharmacotherapy for these disorders. Talley et al. examined the effects of neuromodulators such as amitriptyline, a tricyclic antidepressant, and escitalopram in functional dyspepsia. About 70% of the sample had postprandial distress syndrome, and 20% met criteria for idiopathic gastroparesis. Amitriptyline provided greater symptomatic relief to these patients than did placebo, but escitalopram did not. Patients who met criteria for idiopathic gastroparesis did not respond well to tricyclic antidepressants, but patients with epigastric pain syndrome did. Furthermore, compared with patients with normal gastric emptying, those with delayed emptying did not respond to tricyclic antidepressants. A separate study found that the tricyclic antidepressant nortriptyline did not improve symptoms of gastroparesis (JAMA. 2013;310[24]:2640-9).

Promotility agents may be beneficial for certain patients. A study published this year suggests that, compared with placebo, prucalopride is effective for nausea, vomiting, fullness, bloating, and gastric emptying in patients with idiopathic gastroparesis (Am J Gastroenterol. 2019;114[8]:1265-74.). A 2017 meta-analysis, however, found that proton pump inhibitors were more effective than promotility agents in patients with functional dyspepsia (Am J Gastroenterol. 2017;112[7]:988-1013.).

Pyloric dysfunction may accompany gastroparesis in some patients. Increased severity of gastric emptying delay is associated with increased pylorospasm. Endoscopists have gained experience in performing pyloric myotomy, and this treatment has become more popular. Uncontrolled studies indicate that the proportion of patients with decreased symptom severity after this procedure is higher than 70% and can be as high as 86% (Gastrointest Endosc. 2017;85[1]:123-8). The predictors of a good response include idiopathic etiology, male sex, moderate symptom severity, and greater delay in gastric emptying.

Functional dyspepsia should perhaps be understood as normal gastric emptying and symptoms of epigastric pain syndrome, said Dr. Nguyen. Those patients may respond to neuromodulators, she added. Idiopathic gastroparesis appears to be characterized by severe delay in gastric emptying, postprandial symptoms, nausea, and vomiting. “In the middle is the gray zone, where you have these patients with postprandial distress with or without delayed gastric emptying,” said Dr. Nguyen. Functional dyspepsia and gastroparesis could be two ends of a spectrum, and the best management for patients with symptoms that occur in both disorders is unclear.

[email protected]

CHICAGO – Because gastroparesis and functional dyspepsia share several symptoms (e.g., upper abdominal pain, fullness, and bloating) and pathophysiological abnormalities (e.g., delayed gastric emptying, impaired gastric accommodation, and visceral hypersensitivity), it can be hard to distinguish the two conditions, according to a lecture presented at Freston Conference 2019, sponsored by the American Gastroenterological Association. Additional research into the role of diet in these conditions will improve the treatment of these patients, said Linda Nguyen, MD, director of neurogastroenterology and motility at Stanford (Calif.) University.

Distinguishing the disorders

The accepted definition of gastroparesis is abnormal gastric emptying in the absence of a mechanical obstruction. The condition’s symptoms include nausea, vomiting, bloating, early satiety, abdominal pain, and weight loss. A previous consensus held that if a patient had abdominal pain, he or she did not have gastroparesis. Yet studies indicate that up to 80% of patients with gastroparesis have pain.

Functional dyspepsia is defined as bothersome postprandial fullness, early satiety, and epigastric pain or burning in the absence of structural abnormality. The disorder can be subdivided into postprandial distress (i.e., meal-related symptomatology) and epigastric pain syndrome (i.e., pain or burning that may or may not be related to meals). Either of these alternatives may entail nausea and vomiting.

Comparing the pathophysiologies of gastroparesis and functional dyspepsia helps to distinguish these disorders from each other. A 2019 review described rapid gastric emptying and duodenal eosinophilia in patients with functional dyspepsia, but not in patients with gastroparesis. Patients with epigastric pain syndrome had sensitivity to acid, bile, and fats. Patients with idiopathic gastroparesis, which is the most common type, had a weak antral pump and abnormal duodenal feedback, but patients with functional dyspepsia did not have these characteristics (J Neurogastroenterol Motil. 2019;25[1]:27-35).
 

Examining symptoms and severity

One examination of patients with gastroparesis found that approximately 46% of them had a body mass index of 25 or greater. About 26% of patients had a BMI greater than 30. Yet these patients were eating less than 60% of their recommended daily allowances, based on their age, height, weight, and sex (Clin Gastroenterol Hepatol. 2011;9[12]:1056-64).

Accelerating gastric emptying may not relieve symptoms completely in a patient with gastroparesis, said Dr. Nguyen. A 2007 study of patients with gastroparesis found that 43% had impaired accommodation, and 29% had visceral hypersensitivity (Gut. 2007;56[1]:29-36). The same data indicated that gastric emptying time was not correlated with symptom severity. Impaired accommodation, however, was associated with early satiety and weight loss. Visceral hypersensitivity was associated with pain, early satiety, and weight loss. These data suggest that accommodation and visceral hypersensitivity may influence symptom severity in gastroparesis, said Dr. Nguyen.

Other researchers compared mild, moderate, and severe symptoms of early satiety in patients with gastroparesis. They found that patients with severe symptoms of early satiety have more delayed gastric emptying than do patients with mild or moderate symptoms of early satiety (Neurogastroenterol Motil. 2017;29[4].).

Dr. Nguyen and colleagues examined normal gastric emptying, compared with severely delayed gastric emptying, which they defined as greater than 35% retention at 4 hours. They found that severely delayed gastric emptying was associated with more severe symptoms, particularly nausea and vomiting, as measured by Gastroparesis Cardinal Symptom Index (GCSI). Extreme symptoms may help differentiate between gastroparesis and functional dyspepsia, said Dr. Nguyen.
 

Dietary and pharmacologic treatment

Although clinicians might consider recommending dietary modifications to treat gastroparesis or functional dyspepsia, the literature contains little evidence about their efficacy in these indications, said Dr. Nguyen. Based on a study by Tack and colleagues, some clinicians recommend small, frequent meals that are low in fat and low in fiber to patients with gastroparesis. Such a diet could be harmful, however, to patients with comorbid diabetes, irritable bowel syndrome, or renal failure.

Common dietary recommendations for functional dyspepsia include small, frequent meals; decreased fat consumption; and avoidance of citrus and spicy foods. These recommendations are based on small studies in which patients reported which foods tended to cause their symptoms. Trials of dietary modifications in functional dyspepsia, however, are lacking.

Nevertheless, the literature can guide the selection of pharmacotherapy for these disorders. Talley et al. examined the effects of neuromodulators such as amitriptyline, a tricyclic antidepressant, and escitalopram in functional dyspepsia. About 70% of the sample had postprandial distress syndrome, and 20% met criteria for idiopathic gastroparesis. Amitriptyline provided greater symptomatic relief to these patients than did placebo, but escitalopram did not. Patients who met criteria for idiopathic gastroparesis did not respond well to tricyclic antidepressants, but patients with epigastric pain syndrome did. Furthermore, compared with patients with normal gastric emptying, those with delayed emptying did not respond to tricyclic antidepressants. A separate study found that the tricyclic antidepressant nortriptyline did not improve symptoms of gastroparesis (JAMA. 2013;310[24]:2640-9).

Promotility agents may be beneficial for certain patients. A study published this year suggests that, compared with placebo, prucalopride is effective for nausea, vomiting, fullness, bloating, and gastric emptying in patients with idiopathic gastroparesis (Am J Gastroenterol. 2019;114[8]:1265-74.). A 2017 meta-analysis, however, found that proton pump inhibitors were more effective than promotility agents in patients with functional dyspepsia (Am J Gastroenterol. 2017;112[7]:988-1013.).

Pyloric dysfunction may accompany gastroparesis in some patients. Increased severity of gastric emptying delay is associated with increased pylorospasm. Endoscopists have gained experience in performing pyloric myotomy, and this treatment has become more popular. Uncontrolled studies indicate that the proportion of patients with decreased symptom severity after this procedure is higher than 70% and can be as high as 86% (Gastrointest Endosc. 2017;85[1]:123-8). The predictors of a good response include idiopathic etiology, male sex, moderate symptom severity, and greater delay in gastric emptying.

Functional dyspepsia should perhaps be understood as normal gastric emptying and symptoms of epigastric pain syndrome, said Dr. Nguyen. Those patients may respond to neuromodulators, she added. Idiopathic gastroparesis appears to be characterized by severe delay in gastric emptying, postprandial symptoms, nausea, and vomiting. “In the middle is the gray zone, where you have these patients with postprandial distress with or without delayed gastric emptying,” said Dr. Nguyen. Functional dyspepsia and gastroparesis could be two ends of a spectrum, and the best management for patients with symptoms that occur in both disorders is unclear.

[email protected]

CHICAGO – Because gastroparesis and functional dyspepsia share several symptoms (e.g., upper abdominal pain, fullness, and bloating) and pathophysiological abnormalities (e.g., delayed gastric emptying, impaired gastric accommodation, and visceral hypersensitivity), it can be hard to distinguish the two conditions, according to a lecture presented at Freston Conference 2019, sponsored by the American Gastroenterological Association. Additional research into the role of diet in these conditions will improve the treatment of these patients, said Linda Nguyen, MD, director of neurogastroenterology and motility at Stanford (Calif.) University.

Distinguishing the disorders

The accepted definition of gastroparesis is abnormal gastric emptying in the absence of a mechanical obstruction. The condition’s symptoms include nausea, vomiting, bloating, early satiety, abdominal pain, and weight loss. A previous consensus held that if a patient had abdominal pain, he or she did not have gastroparesis. Yet studies indicate that up to 80% of patients with gastroparesis have pain.

Functional dyspepsia is defined as bothersome postprandial fullness, early satiety, and epigastric pain or burning in the absence of structural abnormality. The disorder can be subdivided into postprandial distress (i.e., meal-related symptomatology) and epigastric pain syndrome (i.e., pain or burning that may or may not be related to meals). Either of these alternatives may entail nausea and vomiting.

Comparing the pathophysiologies of gastroparesis and functional dyspepsia helps to distinguish these disorders from each other. A 2019 review described rapid gastric emptying and duodenal eosinophilia in patients with functional dyspepsia, but not in patients with gastroparesis. Patients with epigastric pain syndrome had sensitivity to acid, bile, and fats. Patients with idiopathic gastroparesis, which is the most common type, had a weak antral pump and abnormal duodenal feedback, but patients with functional dyspepsia did not have these characteristics (J Neurogastroenterol Motil. 2019;25[1]:27-35).
 

Examining symptoms and severity

One examination of patients with gastroparesis found that approximately 46% of them had a body mass index of 25 or greater. About 26% of patients had a BMI greater than 30. Yet these patients were eating less than 60% of their recommended daily allowances, based on their age, height, weight, and sex (Clin Gastroenterol Hepatol. 2011;9[12]:1056-64).

Accelerating gastric emptying may not relieve symptoms completely in a patient with gastroparesis, said Dr. Nguyen. A 2007 study of patients with gastroparesis found that 43% had impaired accommodation, and 29% had visceral hypersensitivity (Gut. 2007;56[1]:29-36). The same data indicated that gastric emptying time was not correlated with symptom severity. Impaired accommodation, however, was associated with early satiety and weight loss. Visceral hypersensitivity was associated with pain, early satiety, and weight loss. These data suggest that accommodation and visceral hypersensitivity may influence symptom severity in gastroparesis, said Dr. Nguyen.

Other researchers compared mild, moderate, and severe symptoms of early satiety in patients with gastroparesis. They found that patients with severe symptoms of early satiety have more delayed gastric emptying than do patients with mild or moderate symptoms of early satiety (Neurogastroenterol Motil. 2017;29[4].).

Dr. Nguyen and colleagues examined normal gastric emptying, compared with severely delayed gastric emptying, which they defined as greater than 35% retention at 4 hours. They found that severely delayed gastric emptying was associated with more severe symptoms, particularly nausea and vomiting, as measured by Gastroparesis Cardinal Symptom Index (GCSI). Extreme symptoms may help differentiate between gastroparesis and functional dyspepsia, said Dr. Nguyen.
 

Dietary and pharmacologic treatment

Although clinicians might consider recommending dietary modifications to treat gastroparesis or functional dyspepsia, the literature contains little evidence about their efficacy in these indications, said Dr. Nguyen. Based on a study by Tack and colleagues, some clinicians recommend small, frequent meals that are low in fat and low in fiber to patients with gastroparesis. Such a diet could be harmful, however, to patients with comorbid diabetes, irritable bowel syndrome, or renal failure.

Common dietary recommendations for functional dyspepsia include small, frequent meals; decreased fat consumption; and avoidance of citrus and spicy foods. These recommendations are based on small studies in which patients reported which foods tended to cause their symptoms. Trials of dietary modifications in functional dyspepsia, however, are lacking.

Nevertheless, the literature can guide the selection of pharmacotherapy for these disorders. Talley et al. examined the effects of neuromodulators such as amitriptyline, a tricyclic antidepressant, and escitalopram in functional dyspepsia. About 70% of the sample had postprandial distress syndrome, and 20% met criteria for idiopathic gastroparesis. Amitriptyline provided greater symptomatic relief to these patients than did placebo, but escitalopram did not. Patients who met criteria for idiopathic gastroparesis did not respond well to tricyclic antidepressants, but patients with epigastric pain syndrome did. Furthermore, compared with patients with normal gastric emptying, those with delayed emptying did not respond to tricyclic antidepressants. A separate study found that the tricyclic antidepressant nortriptyline did not improve symptoms of gastroparesis (JAMA. 2013;310[24]:2640-9).

Promotility agents may be beneficial for certain patients. A study published this year suggests that, compared with placebo, prucalopride is effective for nausea, vomiting, fullness, bloating, and gastric emptying in patients with idiopathic gastroparesis (Am J Gastroenterol. 2019;114[8]:1265-74.). A 2017 meta-analysis, however, found that proton pump inhibitors were more effective than promotility agents in patients with functional dyspepsia (Am J Gastroenterol. 2017;112[7]:988-1013.).

Pyloric dysfunction may accompany gastroparesis in some patients. Increased severity of gastric emptying delay is associated with increased pylorospasm. Endoscopists have gained experience in performing pyloric myotomy, and this treatment has become more popular. Uncontrolled studies indicate that the proportion of patients with decreased symptom severity after this procedure is higher than 70% and can be as high as 86% (Gastrointest Endosc. 2017;85[1]:123-8). The predictors of a good response include idiopathic etiology, male sex, moderate symptom severity, and greater delay in gastric emptying.

Functional dyspepsia should perhaps be understood as normal gastric emptying and symptoms of epigastric pain syndrome, said Dr. Nguyen. Those patients may respond to neuromodulators, she added. Idiopathic gastroparesis appears to be characterized by severe delay in gastric emptying, postprandial symptoms, nausea, and vomiting. “In the middle is the gray zone, where you have these patients with postprandial distress with or without delayed gastric emptying,” said Dr. Nguyen. Functional dyspepsia and gastroparesis could be two ends of a spectrum, and the best management for patients with symptoms that occur in both disorders is unclear.

[email protected]

CHICAGO – Physicians can recognize mast cell activation syndrome by learning its associated triggers and symptoms, which affect many organ systems. Patients have good outcomes when they receive the appropriate pharmaceutical and dietary therapies, according to an overview presented at Freston Conference 2019, sponsored by the American Gastroenterological Association.

Mast cells are immune cells that originate in bone marrow. They defend against pathogens and contribute to tissue homeostasis and repair, said Matthew J. Hamilton, MD, associate gastroenterologist at Brigham and Women’s Hospital and assistant professor of medicine at Harvard Medical School, Boston.

Aberrant regulation, which may be perpetuated by persistent stimuli, can cause unwanted mast cell activation. Symptoms affect many systems simultaneously, such as the cutaneous (e.g., flushing, pruritis, and urticaria), digestive (e.g., abdominal cramping, diarrhea, reflux, and bloat), cardiovascular (e.g., hypotension, syncope, light-headedness, and tachycardia), and others. “These patients have a lot of morbidity due to these symptoms,” said Dr. Hamilton. Symptoms are episodic and result from predictable triggers. Their severity fluctuates. Alcohol, stress, heat, hot water, strong smells, medications, and foods are typical triggers for patients with mast cell activation syndrome. The foods that trigger symptoms vary greatly between patients, said Dr. Hamilton.
 

Patients have a typical presentation

On physical examination, patients often have flushing and dermatographia. Patients also may have tachycardia when at rest or when standing. Sites of abdominal pain or bloat and problems with concentration or memory also are common. Few biomarkers for mast cell activation syndrome have been identified. A blood test for mast cell tryptase and a 24-hour urine test for metabolites of histamine and prostaglandin should be ordered for every patient suspected of having the syndrome. “Ideally, you do baseline levels of these studies, and then repeat them when patients are symptomatic,” said Dr. Hamilton. “The tryptase really has to be done within hours of a reaction. That can be a challenge.” A subset of patients with mast cell activation syndrome have a baseline serum tryptase level greater than 11.4 ng/mL.

In 2010, Akin et al. proposed criteria for mast cell activation syndrome (J Allergy Clin Immunol. 2010;126[6]:1099-104). A patient must have typical signs and symptoms of mast cell activation that affect two or more organ systems, as well as laboratory evidence of mast cell activation. A patient also must respond to medications that block mast cell mediators, and no other diagnosis should better explain his or her clinical profile.

As in the workup for other gastroenterological disorders, an endoscopy or colonoscopy is warranted to rule out other conditions such as inflammatory bowel disease, celiac disease, or disorders associated with intestinal eosinophilia. These procedures also can evaluate patients for systemic mastocytosis, the clonal form of mast cell disorders. In general, endoscopy is normal and reveals no specific features in patients with mast cell activation syndrome, said Dr. Hamilton. Histopathology generally is normal, as well. One study indicated that the mean number of mast cells did not differ between patients with mast cell activation syndrome, patients with irritable bowel syndrome (IBS), and healthy controls. Current studies are evaluating subsets of patients with mast cell activation syndrome who have increased numbers of mast cells noted per high power field to determine the utility of quantifying mast cells on histology in patients suspected of having this disorder.
 

A multifaceted approach to treatment

The best treatment for mast cell activation syndrome is multifaceted, said Dr. Hamilton. The first step is to recommend medications that target mast cells, which are exceptionally effective. These medications include type 1 and type 2 antihistamines, cromolyn, ketotifen, and leukotriene antagonists. Medications to alleviate symptoms are another component of treatment. Dietary modification is beneficial, and social and psychological support may be needed, as well.

Patients often will ask which foods they can eat without triggering symptoms. In a survey of 420 patients with a mast cell disorder, half of respondents reported having an “allergy” to a food or beverage (J Allergy Clin Immunol Pract. 2014;2[1]:70-6). Although not all of these patients have true allergies, they have symptoms in response to certain foods, said Dr. Hamilton. Milk, dairy products, red meat, and wheat are common triggers for these patients. But for some patients, a food may not cause symptoms consistently. “It has more to do with [the patient’s] state of reactivity at the time of eating than the actual foods [that he or she] eats,” said Dr. Hamilton.

Dietary modifications can relieve symptoms for patients with mast cell activation syndrome. Food diaries can be beneficial because they prompt patients to observe what they eat and which foods cause symptoms. An important principle is to eliminate triggers, allergies, and food sensitivities.

One way for patients to take the initiative in their treatment is for them to prepare their own food as often as possible. They should avoid restaurants and strive to eat a balanced, nutritious diet, said Dr. Hamilton. A nutritionist can provide guidance in this regard. “In general, I tell [patients] to avoid sugars, chemicals, processed foods, preservatives, and alcohol,” said Dr. Hamilton. “These things in our Western diet can be toxic to a lot of patients.” A diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs) can benefit patients with symptoms similar to those of IBS, he added.

Physicians who treat patients with mast cell activation syndrome still have unmet needs, however. Researchers need to identify additional objective biomarkers of the syndrome, said Dr. Hamilton. Research also should be directed toward recognizing disease subtypes such as familial hypertryptasemia, a subset of mast cell activation syndrome, he added. Finally, patients need more safe and effective therapies, as well as optimized diet therapy.

[email protected]

CHICAGO – Physicians can recognize mast cell activation syndrome by learning its associated triggers and symptoms, which affect many organ systems. Patients have good outcomes when they receive the appropriate pharmaceutical and dietary therapies, according to an overview presented at Freston Conference 2019, sponsored by the American Gastroenterological Association.

Mast cells are immune cells that originate in bone marrow. They defend against pathogens and contribute to tissue homeostasis and repair, said Matthew J. Hamilton, MD, associate gastroenterologist at Brigham and Women’s Hospital and assistant professor of medicine at Harvard Medical School, Boston.

Aberrant regulation, which may be perpetuated by persistent stimuli, can cause unwanted mast cell activation. Symptoms affect many systems simultaneously, such as the cutaneous (e.g., flushing, pruritis, and urticaria), digestive (e.g., abdominal cramping, diarrhea, reflux, and bloat), cardiovascular (e.g., hypotension, syncope, light-headedness, and tachycardia), and others. “These patients have a lot of morbidity due to these symptoms,” said Dr. Hamilton. Symptoms are episodic and result from predictable triggers. Their severity fluctuates. Alcohol, stress, heat, hot water, strong smells, medications, and foods are typical triggers for patients with mast cell activation syndrome. The foods that trigger symptoms vary greatly between patients, said Dr. Hamilton.
 

Patients have a typical presentation

On physical examination, patients often have flushing and dermatographia. Patients also may have tachycardia when at rest or when standing. Sites of abdominal pain or bloat and problems with concentration or memory also are common. Few biomarkers for mast cell activation syndrome have been identified. A blood test for mast cell tryptase and a 24-hour urine test for metabolites of histamine and prostaglandin should be ordered for every patient suspected of having the syndrome. “Ideally, you do baseline levels of these studies, and then repeat them when patients are symptomatic,” said Dr. Hamilton. “The tryptase really has to be done within hours of a reaction. That can be a challenge.” A subset of patients with mast cell activation syndrome have a baseline serum tryptase level greater than 11.4 ng/mL.

In 2010, Akin et al. proposed criteria for mast cell activation syndrome (J Allergy Clin Immunol. 2010;126[6]:1099-104). A patient must have typical signs and symptoms of mast cell activation that affect two or more organ systems, as well as laboratory evidence of mast cell activation. A patient also must respond to medications that block mast cell mediators, and no other diagnosis should better explain his or her clinical profile.

As in the workup for other gastroenterological disorders, an endoscopy or colonoscopy is warranted to rule out other conditions such as inflammatory bowel disease, celiac disease, or disorders associated with intestinal eosinophilia. These procedures also can evaluate patients for systemic mastocytosis, the clonal form of mast cell disorders. In general, endoscopy is normal and reveals no specific features in patients with mast cell activation syndrome, said Dr. Hamilton. Histopathology generally is normal, as well. One study indicated that the mean number of mast cells did not differ between patients with mast cell activation syndrome, patients with irritable bowel syndrome (IBS), and healthy controls. Current studies are evaluating subsets of patients with mast cell activation syndrome who have increased numbers of mast cells noted per high power field to determine the utility of quantifying mast cells on histology in patients suspected of having this disorder.
 

A multifaceted approach to treatment

The best treatment for mast cell activation syndrome is multifaceted, said Dr. Hamilton. The first step is to recommend medications that target mast cells, which are exceptionally effective. These medications include type 1 and type 2 antihistamines, cromolyn, ketotifen, and leukotriene antagonists. Medications to alleviate symptoms are another component of treatment. Dietary modification is beneficial, and social and psychological support may be needed, as well.

Patients often will ask which foods they can eat without triggering symptoms. In a survey of 420 patients with a mast cell disorder, half of respondents reported having an “allergy” to a food or beverage (J Allergy Clin Immunol Pract. 2014;2[1]:70-6). Although not all of these patients have true allergies, they have symptoms in response to certain foods, said Dr. Hamilton. Milk, dairy products, red meat, and wheat are common triggers for these patients. But for some patients, a food may not cause symptoms consistently. “It has more to do with [the patient’s] state of reactivity at the time of eating than the actual foods [that he or she] eats,” said Dr. Hamilton.

Dietary modifications can relieve symptoms for patients with mast cell activation syndrome. Food diaries can be beneficial because they prompt patients to observe what they eat and which foods cause symptoms. An important principle is to eliminate triggers, allergies, and food sensitivities.

One way for patients to take the initiative in their treatment is for them to prepare their own food as often as possible. They should avoid restaurants and strive to eat a balanced, nutritious diet, said Dr. Hamilton. A nutritionist can provide guidance in this regard. “In general, I tell [patients] to avoid sugars, chemicals, processed foods, preservatives, and alcohol,” said Dr. Hamilton. “These things in our Western diet can be toxic to a lot of patients.” A diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs) can benefit patients with symptoms similar to those of IBS, he added.

Physicians who treat patients with mast cell activation syndrome still have unmet needs, however. Researchers need to identify additional objective biomarkers of the syndrome, said Dr. Hamilton. Research also should be directed toward recognizing disease subtypes such as familial hypertryptasemia, a subset of mast cell activation syndrome, he added. Finally, patients need more safe and effective therapies, as well as optimized diet therapy.

[email protected]

CHICAGO – Physicians can recognize mast cell activation syndrome by learning its associated triggers and symptoms, which affect many organ systems. Patients have good outcomes when they receive the appropriate pharmaceutical and dietary therapies, according to an overview presented at Freston Conference 2019, sponsored by the American Gastroenterological Association.

Mast cells are immune cells that originate in bone marrow. They defend against pathogens and contribute to tissue homeostasis and repair, said Matthew J. Hamilton, MD, associate gastroenterologist at Brigham and Women’s Hospital and assistant professor of medicine at Harvard Medical School, Boston.

Aberrant regulation, which may be perpetuated by persistent stimuli, can cause unwanted mast cell activation. Symptoms affect many systems simultaneously, such as the cutaneous (e.g., flushing, pruritis, and urticaria), digestive (e.g., abdominal cramping, diarrhea, reflux, and bloat), cardiovascular (e.g., hypotension, syncope, light-headedness, and tachycardia), and others. “These patients have a lot of morbidity due to these symptoms,” said Dr. Hamilton. Symptoms are episodic and result from predictable triggers. Their severity fluctuates. Alcohol, stress, heat, hot water, strong smells, medications, and foods are typical triggers for patients with mast cell activation syndrome. The foods that trigger symptoms vary greatly between patients, said Dr. Hamilton.
 

Patients have a typical presentation

On physical examination, patients often have flushing and dermatographia. Patients also may have tachycardia when at rest or when standing. Sites of abdominal pain or bloat and problems with concentration or memory also are common. Few biomarkers for mast cell activation syndrome have been identified. A blood test for mast cell tryptase and a 24-hour urine test for metabolites of histamine and prostaglandin should be ordered for every patient suspected of having the syndrome. “Ideally, you do baseline levels of these studies, and then repeat them when patients are symptomatic,” said Dr. Hamilton. “The tryptase really has to be done within hours of a reaction. That can be a challenge.” A subset of patients with mast cell activation syndrome have a baseline serum tryptase level greater than 11.4 ng/mL.

In 2010, Akin et al. proposed criteria for mast cell activation syndrome (J Allergy Clin Immunol. 2010;126[6]:1099-104). A patient must have typical signs and symptoms of mast cell activation that affect two or more organ systems, as well as laboratory evidence of mast cell activation. A patient also must respond to medications that block mast cell mediators, and no other diagnosis should better explain his or her clinical profile.

As in the workup for other gastroenterological disorders, an endoscopy or colonoscopy is warranted to rule out other conditions such as inflammatory bowel disease, celiac disease, or disorders associated with intestinal eosinophilia. These procedures also can evaluate patients for systemic mastocytosis, the clonal form of mast cell disorders. In general, endoscopy is normal and reveals no specific features in patients with mast cell activation syndrome, said Dr. Hamilton. Histopathology generally is normal, as well. One study indicated that the mean number of mast cells did not differ between patients with mast cell activation syndrome, patients with irritable bowel syndrome (IBS), and healthy controls. Current studies are evaluating subsets of patients with mast cell activation syndrome who have increased numbers of mast cells noted per high power field to determine the utility of quantifying mast cells on histology in patients suspected of having this disorder.
 

A multifaceted approach to treatment

The best treatment for mast cell activation syndrome is multifaceted, said Dr. Hamilton. The first step is to recommend medications that target mast cells, which are exceptionally effective. These medications include type 1 and type 2 antihistamines, cromolyn, ketotifen, and leukotriene antagonists. Medications to alleviate symptoms are another component of treatment. Dietary modification is beneficial, and social and psychological support may be needed, as well.

Patients often will ask which foods they can eat without triggering symptoms. In a survey of 420 patients with a mast cell disorder, half of respondents reported having an “allergy” to a food or beverage (J Allergy Clin Immunol Pract. 2014;2[1]:70-6). Although not all of these patients have true allergies, they have symptoms in response to certain foods, said Dr. Hamilton. Milk, dairy products, red meat, and wheat are common triggers for these patients. But for some patients, a food may not cause symptoms consistently. “It has more to do with [the patient’s] state of reactivity at the time of eating than the actual foods [that he or she] eats,” said Dr. Hamilton.

Dietary modifications can relieve symptoms for patients with mast cell activation syndrome. Food diaries can be beneficial because they prompt patients to observe what they eat and which foods cause symptoms. An important principle is to eliminate triggers, allergies, and food sensitivities.

One way for patients to take the initiative in their treatment is for them to prepare their own food as often as possible. They should avoid restaurants and strive to eat a balanced, nutritious diet, said Dr. Hamilton. A nutritionist can provide guidance in this regard. “In general, I tell [patients] to avoid sugars, chemicals, processed foods, preservatives, and alcohol,” said Dr. Hamilton. “These things in our Western diet can be toxic to a lot of patients.” A diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs) can benefit patients with symptoms similar to those of IBS, he added.

Physicians who treat patients with mast cell activation syndrome still have unmet needs, however. Researchers need to identify additional objective biomarkers of the syndrome, said Dr. Hamilton. Research also should be directed toward recognizing disease subtypes such as familial hypertryptasemia, a subset of mast cell activation syndrome, he added. Finally, patients need more safe and effective therapies, as well as optimized diet therapy.

[email protected]

CHICAGO – Dietary therapies can form a beneficial part of personalized treatment for gastroesophageal reflux disease (GERD), according to an overview presented at the meeting, sponsored by the American Gastroenterological Association. Modifying diet may reduce lower esophageal sphincter (LES) pressure and decrease the number of reflux events. Prescribing an overly restrictive diet, however, can promote hypervigilance and overwhelm patients. Successful dietary therapy requires balancing expectations and maintaining cognitive flexibility, said John E. Pandolfino, MD, Hans Popper Professor of Medicine at Northwestern University in Chicago.

When a patient presents with GERD and does not have warning signs such as dysphagia or odynophagia, the initial treatment typically is a proton pump inhibitor (PPI). This therapy effectively reduces the acidity of the gastric juice and improves acid clearance. It does not, however, change the number of reflux events or affect tissue permeability, said Dr. Pandolfino. Dietary therapy has the potential to address these outcomes.
 

Diets can facilitate weight loss

The first mechanism by which dietary therapies reduce GERD is by facilitating weight loss. “Obesity is associated with reflux. If you reduce that gastroesophageal pressure gradient that is generated by truncal obesity, you will improve reflux,” said Dr. Pandolfino. Second, reducing the intake of alcohol, coffee, or carbohydrates can decrease the acidity of the gastric juice. Certain foods can reduce the number of reflux events, and others can strengthen the LES.

The increasing incidence of obesity is associated with increasing incidence of GERD. Exacerbations of GERD increase the number of transient LES relaxations (TLESRs), increase the amount of liquid refluxate, and promote the formation of a hiatus hernia, said Dr. Pandolfino. One study found that moderate weight gain can cause or worsen reflux symptoms among patients of normal weight (N Engl J Med. 2006;354[22]:2340-8.). Weight loss was associated with a decreased risk of GERD symptoms. Another analysis found that reducing body mass index by 3.5 points is associated with “a dramatic reduction in overall symptoms,” said Dr. Pandolfino (Am J Gastroenterol. 2013;108[3]:376-82). Weight loss enhanced the effects of medication and reduced the gastroesophageal pressure gradient.

Dr. Pandolfino and colleagues developed and studied the Reflux Improvement and Monitoring (TRIM) program as a treatment for GERD. In this program, patients with GERD who had a BMI above 30 and were taking a PPI were referred to health coaches for weight loss treatment. Participants’ GERD Q scores decreased from 8.7 at baseline to 7.5 at 3 months and 7.4 at 6 months. Furthermore, percentage of excess body weight continued to decline for 12 months among patients who participated in TRIM, compared with controls (Am J Gastroenterol. 2018;113[1]:23-30.).

“These patients learn healthier habits [such as] walking a little bit more and watching the overall volume of food that they’re taking in,” said Dr. Pandolfino. “This was a simple thing to focus on, diet and exercise, that dramatically reduced overall severity of reflux. The interesting thing here is that we got 30% of people off their PPI therapy.”
 

Lifestyle changes may benefit patients

Several common lifestyle recommendations for patients with GERD relate to diet. Such recommendations include avoiding alcohol; eating smaller, more frequent meals; and avoiding food within 3 hours of bedtime. But data suggest that it is not effective to recommend the avoidance of acidic or irritative foods (e.g., citrus fruits, tomatoes, and carbonated beverages) or refluxogenic foods (e.g., fatty or fried foods, coffee, and chocolate) to all patients. Genetic predispositions may cause these foods to be irritants to certain patients, but “I don’t globally tell people to avoid things unless they irritate them,” said Dr. Pandolfino.

Understanding the mechanism by which certain foods trigger GERD can aid in appropriate therapy. For example, coffee can reduce LES pressure and increase gastric acid production. “If you have someone who already has low LES pressure, reducing coffee consumption might help that patient,” said Dr. Pandolfino. Data suggest that certain elimination diets are ineffective, however. Clinical trials do not suggest that eliminating carbonated beverages affects symptoms, and the data about eliminating alcohol, citrus, spicy foods, and chocolate are conflicting (Curr Gastroenterol Rep. 2017;19[8]:38.).

In a 2018 study, investigators gave patients with GERD 5 g of psyllium t.i.d. They performed physiologic testing on the patients at baseline and after 10 days of the diet. The intervention was associated with a significant increase in LES pressure and a reduction in overall reflux (World J Gastroenterol. 2018;24[21]:2291-9.). “This was one of the first studies that showed a dramatic improvement in physiology,” said Dr. Pandolfino. “Certainly, this is provocative, and I think that this is not an unreasonable thing to do in someone who’s not getting enough fiber.”

In addition to improving cardiovascular disease and diabetes, the Mediterranean diet reduces reflux symptoms and complications. When the researchers controlled for eating habits, the association persisted (Dis Esophagus. 2016;29[7]:794-800.).

Optimal GERD therapy follows from an analysis of patient-centered foci, such as obesity and triggers, and specific functional defects. In the quest for personalized therapy, a clinician should not discount the underlying pathogenesis, because some patients may require medications or surgery, said Dr. Pandolfino.

[email protected]

CHICAGO – Dietary therapies can form a beneficial part of personalized treatment for gastroesophageal reflux disease (GERD), according to an overview presented at the meeting, sponsored by the American Gastroenterological Association. Modifying diet may reduce lower esophageal sphincter (LES) pressure and decrease the number of reflux events. Prescribing an overly restrictive diet, however, can promote hypervigilance and overwhelm patients. Successful dietary therapy requires balancing expectations and maintaining cognitive flexibility, said John E. Pandolfino, MD, Hans Popper Professor of Medicine at Northwestern University in Chicago.

When a patient presents with GERD and does not have warning signs such as dysphagia or odynophagia, the initial treatment typically is a proton pump inhibitor (PPI). This therapy effectively reduces the acidity of the gastric juice and improves acid clearance. It does not, however, change the number of reflux events or affect tissue permeability, said Dr. Pandolfino. Dietary therapy has the potential to address these outcomes.
 

Diets can facilitate weight loss

The first mechanism by which dietary therapies reduce GERD is by facilitating weight loss. “Obesity is associated with reflux. If you reduce that gastroesophageal pressure gradient that is generated by truncal obesity, you will improve reflux,” said Dr. Pandolfino. Second, reducing the intake of alcohol, coffee, or carbohydrates can decrease the acidity of the gastric juice. Certain foods can reduce the number of reflux events, and others can strengthen the LES.

The increasing incidence of obesity is associated with increasing incidence of GERD. Exacerbations of GERD increase the number of transient LES relaxations (TLESRs), increase the amount of liquid refluxate, and promote the formation of a hiatus hernia, said Dr. Pandolfino. One study found that moderate weight gain can cause or worsen reflux symptoms among patients of normal weight (N Engl J Med. 2006;354[22]:2340-8.). Weight loss was associated with a decreased risk of GERD symptoms. Another analysis found that reducing body mass index by 3.5 points is associated with “a dramatic reduction in overall symptoms,” said Dr. Pandolfino (Am J Gastroenterol. 2013;108[3]:376-82). Weight loss enhanced the effects of medication and reduced the gastroesophageal pressure gradient.

Dr. Pandolfino and colleagues developed and studied the Reflux Improvement and Monitoring (TRIM) program as a treatment for GERD. In this program, patients with GERD who had a BMI above 30 and were taking a PPI were referred to health coaches for weight loss treatment. Participants’ GERD Q scores decreased from 8.7 at baseline to 7.5 at 3 months and 7.4 at 6 months. Furthermore, percentage of excess body weight continued to decline for 12 months among patients who participated in TRIM, compared with controls (Am J Gastroenterol. 2018;113[1]:23-30.).

“These patients learn healthier habits [such as] walking a little bit more and watching the overall volume of food that they’re taking in,” said Dr. Pandolfino. “This was a simple thing to focus on, diet and exercise, that dramatically reduced overall severity of reflux. The interesting thing here is that we got 30% of people off their PPI therapy.”
 

Lifestyle changes may benefit patients

Several common lifestyle recommendations for patients with GERD relate to diet. Such recommendations include avoiding alcohol; eating smaller, more frequent meals; and avoiding food within 3 hours of bedtime. But data suggest that it is not effective to recommend the avoidance of acidic or irritative foods (e.g., citrus fruits, tomatoes, and carbonated beverages) or refluxogenic foods (e.g., fatty or fried foods, coffee, and chocolate) to all patients. Genetic predispositions may cause these foods to be irritants to certain patients, but “I don’t globally tell people to avoid things unless they irritate them,” said Dr. Pandolfino.

Understanding the mechanism by which certain foods trigger GERD can aid in appropriate therapy. For example, coffee can reduce LES pressure and increase gastric acid production. “If you have someone who already has low LES pressure, reducing coffee consumption might help that patient,” said Dr. Pandolfino. Data suggest that certain elimination diets are ineffective, however. Clinical trials do not suggest that eliminating carbonated beverages affects symptoms, and the data about eliminating alcohol, citrus, spicy foods, and chocolate are conflicting (Curr Gastroenterol Rep. 2017;19[8]:38.).

In a 2018 study, investigators gave patients with GERD 5 g of psyllium t.i.d. They performed physiologic testing on the patients at baseline and after 10 days of the diet. The intervention was associated with a significant increase in LES pressure and a reduction in overall reflux (World J Gastroenterol. 2018;24[21]:2291-9.). “This was one of the first studies that showed a dramatic improvement in physiology,” said Dr. Pandolfino. “Certainly, this is provocative, and I think that this is not an unreasonable thing to do in someone who’s not getting enough fiber.”

In addition to improving cardiovascular disease and diabetes, the Mediterranean diet reduces reflux symptoms and complications. When the researchers controlled for eating habits, the association persisted (Dis Esophagus. 2016;29[7]:794-800.).

Optimal GERD therapy follows from an analysis of patient-centered foci, such as obesity and triggers, and specific functional defects. In the quest for personalized therapy, a clinician should not discount the underlying pathogenesis, because some patients may require medications or surgery, said Dr. Pandolfino.

[email protected]

CHICAGO – Dietary therapies can form a beneficial part of personalized treatment for gastroesophageal reflux disease (GERD), according to an overview presented at the meeting, sponsored by the American Gastroenterological Association. Modifying diet may reduce lower esophageal sphincter (LES) pressure and decrease the number of reflux events. Prescribing an overly restrictive diet, however, can promote hypervigilance and overwhelm patients. Successful dietary therapy requires balancing expectations and maintaining cognitive flexibility, said John E. Pandolfino, MD, Hans Popper Professor of Medicine at Northwestern University in Chicago.

When a patient presents with GERD and does not have warning signs such as dysphagia or odynophagia, the initial treatment typically is a proton pump inhibitor (PPI). This therapy effectively reduces the acidity of the gastric juice and improves acid clearance. It does not, however, change the number of reflux events or affect tissue permeability, said Dr. Pandolfino. Dietary therapy has the potential to address these outcomes.
 

Diets can facilitate weight loss

The first mechanism by which dietary therapies reduce GERD is by facilitating weight loss. “Obesity is associated with reflux. If you reduce that gastroesophageal pressure gradient that is generated by truncal obesity, you will improve reflux,” said Dr. Pandolfino. Second, reducing the intake of alcohol, coffee, or carbohydrates can decrease the acidity of the gastric juice. Certain foods can reduce the number of reflux events, and others can strengthen the LES.

The increasing incidence of obesity is associated with increasing incidence of GERD. Exacerbations of GERD increase the number of transient LES relaxations (TLESRs), increase the amount of liquid refluxate, and promote the formation of a hiatus hernia, said Dr. Pandolfino. One study found that moderate weight gain can cause or worsen reflux symptoms among patients of normal weight (N Engl J Med. 2006;354[22]:2340-8.). Weight loss was associated with a decreased risk of GERD symptoms. Another analysis found that reducing body mass index by 3.5 points is associated with “a dramatic reduction in overall symptoms,” said Dr. Pandolfino (Am J Gastroenterol. 2013;108[3]:376-82). Weight loss enhanced the effects of medication and reduced the gastroesophageal pressure gradient.

Dr. Pandolfino and colleagues developed and studied the Reflux Improvement and Monitoring (TRIM) program as a treatment for GERD. In this program, patients with GERD who had a BMI above 30 and were taking a PPI were referred to health coaches for weight loss treatment. Participants’ GERD Q scores decreased from 8.7 at baseline to 7.5 at 3 months and 7.4 at 6 months. Furthermore, percentage of excess body weight continued to decline for 12 months among patients who participated in TRIM, compared with controls (Am J Gastroenterol. 2018;113[1]:23-30.).

“These patients learn healthier habits [such as] walking a little bit more and watching the overall volume of food that they’re taking in,” said Dr. Pandolfino. “This was a simple thing to focus on, diet and exercise, that dramatically reduced overall severity of reflux. The interesting thing here is that we got 30% of people off their PPI therapy.”
 

Lifestyle changes may benefit patients

Several common lifestyle recommendations for patients with GERD relate to diet. Such recommendations include avoiding alcohol; eating smaller, more frequent meals; and avoiding food within 3 hours of bedtime. But data suggest that it is not effective to recommend the avoidance of acidic or irritative foods (e.g., citrus fruits, tomatoes, and carbonated beverages) or refluxogenic foods (e.g., fatty or fried foods, coffee, and chocolate) to all patients. Genetic predispositions may cause these foods to be irritants to certain patients, but “I don’t globally tell people to avoid things unless they irritate them,” said Dr. Pandolfino.

Understanding the mechanism by which certain foods trigger GERD can aid in appropriate therapy. For example, coffee can reduce LES pressure and increase gastric acid production. “If you have someone who already has low LES pressure, reducing coffee consumption might help that patient,” said Dr. Pandolfino. Data suggest that certain elimination diets are ineffective, however. Clinical trials do not suggest that eliminating carbonated beverages affects symptoms, and the data about eliminating alcohol, citrus, spicy foods, and chocolate are conflicting (Curr Gastroenterol Rep. 2017;19[8]:38.).

In a 2018 study, investigators gave patients with GERD 5 g of psyllium t.i.d. They performed physiologic testing on the patients at baseline and after 10 days of the diet. The intervention was associated with a significant increase in LES pressure and a reduction in overall reflux (World J Gastroenterol. 2018;24[21]:2291-9.). “This was one of the first studies that showed a dramatic improvement in physiology,” said Dr. Pandolfino. “Certainly, this is provocative, and I think that this is not an unreasonable thing to do in someone who’s not getting enough fiber.”

In addition to improving cardiovascular disease and diabetes, the Mediterranean diet reduces reflux symptoms and complications. When the researchers controlled for eating habits, the association persisted (Dis Esophagus. 2016;29[7]:794-800.).

Optimal GERD therapy follows from an analysis of patient-centered foci, such as obesity and triggers, and specific functional defects. In the quest for personalized therapy, a clinician should not discount the underlying pathogenesis, because some patients may require medications or surgery, said Dr. Pandolfino.

[email protected]

CHICAGO – Several new drugs for the treatment of celiac disease are in development, and existing treatments for other indications are being studied as treatments for celiac disease as well, according to a lecture delivered at the 2019 James W. Freston Conference: Food at the Intersection of Gut Health and Disease.

Home testing services and portable gluten-detection devices enable patients to diagnose and manage themselves without medical supervision, but these strategies raise concerns about accuracy and efficacy, said Benjamin Lebwohl, MD, director of clinical research at the Celiac Disease Center at Columbia University in New York.
 

Potential treatments on the horizon

The gluten-free diet is the only treatment proven effective for celiac disease, but it can be expensive or unpalatable for some patients. The diet also entails risks of bowel irregularity and weight gain. “The gluten-free diet remains an inadequate treatment for many people with celiac disease,” said Dr. Lebwohl.

Tennyson et al. found that 66% of patients with biopsy-proven celiac disease are interested in nondietary therapy (Therap Adv Gastroenterol. 2013;6[5]:358-64.). Such patients are more likely to be male and older than 50 years.

Latiglutenase, a gluten enzyme derived from bacteria and cereal, is among the pharmacotherapies being investigated as a treatment for nonresponsive celiac disease. It reduces or eliminates the toxicity of gluten. In a recent phase 2b trial, however, the treatment did not achieve the primary outcome measure of histologic improvement (Gastroenterology. 2017;152[4]:787-98.). Compared with placebo, the drug was not associated with significant improvements in histologic and symptom scores.

Another drug in development is the tight-junction modulator larazotide acetate. Studies of zonula occludens toxin and its mammalian analogue zonulin led to the development of larazotide acetate. Leffler et al. found that a 0.5-mg dose of the drug reduced symptoms of nonresponsive celiac disease in patients who were following a gluten-free diet, compared with patients treated with the diet alone (Gastroenterology. 2015;148[7]:1311-9.). Innovate Pharmaceuticals plans to study the drug in phase 3 trials, said Dr. Lebwohl.

ImmunosanT has studied Nexvax2, which promotes gluten peptide desensitization. A phase 2 study examined the drug’s efficacy in reducing symptoms during a masked food challenge. The company discontinued this study when an interim analysis showed that the drug provided no more protection from gluten exposure than placebo. Nexvax2 was safe and well tolerated, and the study revealed no new safety signals.

In addition to newly developed therapies, researchers are studying whether drugs marketed for other indications could be effective treatments for celiac disease. For example, budesonide, a treatment for asthma and chronic obstructive pulmonary disease, is being investigated for nonresponsive celiac disease and refractory celiac disease. Other research is examining whether budesonide could provide effective protection after inadvertent gluten exposure. Systemic steroids, immunosuppressants such as azathioprine, chemotherapeutics such as cladribine, and mesalamine, which is a treatment for inflammatory bowel disease, also are under investigation.

But several questions related to drug development for celiac disease remain unanswered. For example, whether researchers should choose clinical or histologic endpoints for their trials is a subject of debate. “Probably, we’re going to be looking for two endpoints,” said Dr. Lebwohl. No consensus has been established about whether trials should include patients for whom diagnosis is based on a test other than a biopsy. Also, the effect of nondietary therapy on adherence to the gluten-free diet remains to be clarified.
 

Self-management of celiac disease

“We’re in a new era” of self-monitoring and direct-to-consumer advertising aimed at patients with celiac disease, said Dr. Lebwohl. Products and services that enable patients to diagnose and manage themselves independently are broadly available. For example, 23andMe provides at-home testing for HLA-DQ2.5 and HLA-DQ8, which could support a diagnosis of celiac disease. The service does not, however, test for HLA-DQ2.2, which is present in about 5% of patients with celiac disease. This testing consequently has high negative-predictive value, but poor positive-predictive value, said Dr. Lebwohl.

Similarly, ImAware provides blood tests that patients can take at home and send to the company for results. The tests look for antibodies such as tissue transglutaminase immunoglobulin A/immunoglobulin G and deamidated gliadin peptide IgA/IgG. The company advises patients to share their results with a health care professional.

Furthermore, portable devices such as Nima are marketed as gluten detectors. One study of the device included 804 users from all 50 states. The device found gluten in 32% of all restaurant food tested advertised as gluten-free. The interpretation of these results should take into account the fact that the device may detect gluten levels lower than 20 ppm, which generally are safe for patients with celiac disease. Furthermore, the data were uploaded voluntarily by users, and thus are not a random sample (Am J Gastroenterol. 2019;114[5]:792-7.). The device cannot detect certain forms of gluten such as barley malt. Because of limitations like these, the Nima device has “vocal critics,” said Dr. Lebwohl.

A profusion of books that offer dietary advice for patients with celiac disease also has become available. Data from Google Trends indicate that the popularity of the gluten-free diet spread from small pockets of the country in 2006 to most of the states in 2015.

Yet this “do-it-yourself” approach to celiac disease raises several concerns, said Dr. Lebwohl. Patients are at risk of interpreting their test results incorrectly, for example. Failing to consult a dietitian or physician, each of whom could have expertise in the field, entails risks as well. “Knowledgeable and empathetic care-giving is more important than ever,” Dr. Lebwohl concluded.

Dr. Lebwohl is on the medical advisory board of Innovate Biopharmaceuticals, a consultant for Takeda, and an unpaid advisor for the Nima Sensor.

[email protected]

CHICAGO – Several new drugs for the treatment of celiac disease are in development, and existing treatments for other indications are being studied as treatments for celiac disease as well, according to a lecture delivered at the 2019 James W. Freston Conference: Food at the Intersection of Gut Health and Disease.

Home testing services and portable gluten-detection devices enable patients to diagnose and manage themselves without medical supervision, but these strategies raise concerns about accuracy and efficacy, said Benjamin Lebwohl, MD, director of clinical research at the Celiac Disease Center at Columbia University in New York.
 

Potential treatments on the horizon

The gluten-free diet is the only treatment proven effective for celiac disease, but it can be expensive or unpalatable for some patients. The diet also entails risks of bowel irregularity and weight gain. “The gluten-free diet remains an inadequate treatment for many people with celiac disease,” said Dr. Lebwohl.

Tennyson et al. found that 66% of patients with biopsy-proven celiac disease are interested in nondietary therapy (Therap Adv Gastroenterol. 2013;6[5]:358-64.). Such patients are more likely to be male and older than 50 years.

Latiglutenase, a gluten enzyme derived from bacteria and cereal, is among the pharmacotherapies being investigated as a treatment for nonresponsive celiac disease. It reduces or eliminates the toxicity of gluten. In a recent phase 2b trial, however, the treatment did not achieve the primary outcome measure of histologic improvement (Gastroenterology. 2017;152[4]:787-98.). Compared with placebo, the drug was not associated with significant improvements in histologic and symptom scores.

Another drug in development is the tight-junction modulator larazotide acetate. Studies of zonula occludens toxin and its mammalian analogue zonulin led to the development of larazotide acetate. Leffler et al. found that a 0.5-mg dose of the drug reduced symptoms of nonresponsive celiac disease in patients who were following a gluten-free diet, compared with patients treated with the diet alone (Gastroenterology. 2015;148[7]:1311-9.). Innovate Pharmaceuticals plans to study the drug in phase 3 trials, said Dr. Lebwohl.

ImmunosanT has studied Nexvax2, which promotes gluten peptide desensitization. A phase 2 study examined the drug’s efficacy in reducing symptoms during a masked food challenge. The company discontinued this study when an interim analysis showed that the drug provided no more protection from gluten exposure than placebo. Nexvax2 was safe and well tolerated, and the study revealed no new safety signals.

In addition to newly developed therapies, researchers are studying whether drugs marketed for other indications could be effective treatments for celiac disease. For example, budesonide, a treatment for asthma and chronic obstructive pulmonary disease, is being investigated for nonresponsive celiac disease and refractory celiac disease. Other research is examining whether budesonide could provide effective protection after inadvertent gluten exposure. Systemic steroids, immunosuppressants such as azathioprine, chemotherapeutics such as cladribine, and mesalamine, which is a treatment for inflammatory bowel disease, also are under investigation.

But several questions related to drug development for celiac disease remain unanswered. For example, whether researchers should choose clinical or histologic endpoints for their trials is a subject of debate. “Probably, we’re going to be looking for two endpoints,” said Dr. Lebwohl. No consensus has been established about whether trials should include patients for whom diagnosis is based on a test other than a biopsy. Also, the effect of nondietary therapy on adherence to the gluten-free diet remains to be clarified.
 

Self-management of celiac disease

“We’re in a new era” of self-monitoring and direct-to-consumer advertising aimed at patients with celiac disease, said Dr. Lebwohl. Products and services that enable patients to diagnose and manage themselves independently are broadly available. For example, 23andMe provides at-home testing for HLA-DQ2.5 and HLA-DQ8, which could support a diagnosis of celiac disease. The service does not, however, test for HLA-DQ2.2, which is present in about 5% of patients with celiac disease. This testing consequently has high negative-predictive value, but poor positive-predictive value, said Dr. Lebwohl.

Similarly, ImAware provides blood tests that patients can take at home and send to the company for results. The tests look for antibodies such as tissue transglutaminase immunoglobulin A/immunoglobulin G and deamidated gliadin peptide IgA/IgG. The company advises patients to share their results with a health care professional.

Furthermore, portable devices such as Nima are marketed as gluten detectors. One study of the device included 804 users from all 50 states. The device found gluten in 32% of all restaurant food tested advertised as gluten-free. The interpretation of these results should take into account the fact that the device may detect gluten levels lower than 20 ppm, which generally are safe for patients with celiac disease. Furthermore, the data were uploaded voluntarily by users, and thus are not a random sample (Am J Gastroenterol. 2019;114[5]:792-7.). The device cannot detect certain forms of gluten such as barley malt. Because of limitations like these, the Nima device has “vocal critics,” said Dr. Lebwohl.

A profusion of books that offer dietary advice for patients with celiac disease also has become available. Data from Google Trends indicate that the popularity of the gluten-free diet spread from small pockets of the country in 2006 to most of the states in 2015.

Yet this “do-it-yourself” approach to celiac disease raises several concerns, said Dr. Lebwohl. Patients are at risk of interpreting their test results incorrectly, for example. Failing to consult a dietitian or physician, each of whom could have expertise in the field, entails risks as well. “Knowledgeable and empathetic care-giving is more important than ever,” Dr. Lebwohl concluded.

Dr. Lebwohl is on the medical advisory board of Innovate Biopharmaceuticals, a consultant for Takeda, and an unpaid advisor for the Nima Sensor.

[email protected]

CHICAGO – Several new drugs for the treatment of celiac disease are in development, and existing treatments for other indications are being studied as treatments for celiac disease as well, according to a lecture delivered at the 2019 James W. Freston Conference: Food at the Intersection of Gut Health and Disease.

Home testing services and portable gluten-detection devices enable patients to diagnose and manage themselves without medical supervision, but these strategies raise concerns about accuracy and efficacy, said Benjamin Lebwohl, MD, director of clinical research at the Celiac Disease Center at Columbia University in New York.
 

Potential treatments on the horizon

The gluten-free diet is the only treatment proven effective for celiac disease, but it can be expensive or unpalatable for some patients. The diet also entails risks of bowel irregularity and weight gain. “The gluten-free diet remains an inadequate treatment for many people with celiac disease,” said Dr. Lebwohl.

Tennyson et al. found that 66% of patients with biopsy-proven celiac disease are interested in nondietary therapy (Therap Adv Gastroenterol. 2013;6[5]:358-64.). Such patients are more likely to be male and older than 50 years.

Latiglutenase, a gluten enzyme derived from bacteria and cereal, is among the pharmacotherapies being investigated as a treatment for nonresponsive celiac disease. It reduces or eliminates the toxicity of gluten. In a recent phase 2b trial, however, the treatment did not achieve the primary outcome measure of histologic improvement (Gastroenterology. 2017;152[4]:787-98.). Compared with placebo, the drug was not associated with significant improvements in histologic and symptom scores.

Another drug in development is the tight-junction modulator larazotide acetate. Studies of zonula occludens toxin and its mammalian analogue zonulin led to the development of larazotide acetate. Leffler et al. found that a 0.5-mg dose of the drug reduced symptoms of nonresponsive celiac disease in patients who were following a gluten-free diet, compared with patients treated with the diet alone (Gastroenterology. 2015;148[7]:1311-9.). Innovate Pharmaceuticals plans to study the drug in phase 3 trials, said Dr. Lebwohl.

ImmunosanT has studied Nexvax2, which promotes gluten peptide desensitization. A phase 2 study examined the drug’s efficacy in reducing symptoms during a masked food challenge. The company discontinued this study when an interim analysis showed that the drug provided no more protection from gluten exposure than placebo. Nexvax2 was safe and well tolerated, and the study revealed no new safety signals.

In addition to newly developed therapies, researchers are studying whether drugs marketed for other indications could be effective treatments for celiac disease. For example, budesonide, a treatment for asthma and chronic obstructive pulmonary disease, is being investigated for nonresponsive celiac disease and refractory celiac disease. Other research is examining whether budesonide could provide effective protection after inadvertent gluten exposure. Systemic steroids, immunosuppressants such as azathioprine, chemotherapeutics such as cladribine, and mesalamine, which is a treatment for inflammatory bowel disease, also are under investigation.

But several questions related to drug development for celiac disease remain unanswered. For example, whether researchers should choose clinical or histologic endpoints for their trials is a subject of debate. “Probably, we’re going to be looking for two endpoints,” said Dr. Lebwohl. No consensus has been established about whether trials should include patients for whom diagnosis is based on a test other than a biopsy. Also, the effect of nondietary therapy on adherence to the gluten-free diet remains to be clarified.
 

Self-management of celiac disease

“We’re in a new era” of self-monitoring and direct-to-consumer advertising aimed at patients with celiac disease, said Dr. Lebwohl. Products and services that enable patients to diagnose and manage themselves independently are broadly available. For example, 23andMe provides at-home testing for HLA-DQ2.5 and HLA-DQ8, which could support a diagnosis of celiac disease. The service does not, however, test for HLA-DQ2.2, which is present in about 5% of patients with celiac disease. This testing consequently has high negative-predictive value, but poor positive-predictive value, said Dr. Lebwohl.

Similarly, ImAware provides blood tests that patients can take at home and send to the company for results. The tests look for antibodies such as tissue transglutaminase immunoglobulin A/immunoglobulin G and deamidated gliadin peptide IgA/IgG. The company advises patients to share their results with a health care professional.

Furthermore, portable devices such as Nima are marketed as gluten detectors. One study of the device included 804 users from all 50 states. The device found gluten in 32% of all restaurant food tested advertised as gluten-free. The interpretation of these results should take into account the fact that the device may detect gluten levels lower than 20 ppm, which generally are safe for patients with celiac disease. Furthermore, the data were uploaded voluntarily by users, and thus are not a random sample (Am J Gastroenterol. 2019;114[5]:792-7.). The device cannot detect certain forms of gluten such as barley malt. Because of limitations like these, the Nima device has “vocal critics,” said Dr. Lebwohl.

A profusion of books that offer dietary advice for patients with celiac disease also has become available. Data from Google Trends indicate that the popularity of the gluten-free diet spread from small pockets of the country in 2006 to most of the states in 2015.

Yet this “do-it-yourself” approach to celiac disease raises several concerns, said Dr. Lebwohl. Patients are at risk of interpreting their test results incorrectly, for example. Failing to consult a dietitian or physician, each of whom could have expertise in the field, entails risks as well. “Knowledgeable and empathetic care-giving is more important than ever,” Dr. Lebwohl concluded.

Dr. Lebwohl is on the medical advisory board of Innovate Biopharmaceuticals, a consultant for Takeda, and an unpaid advisor for the Nima Sensor.

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