GI and Hepatology News

US counties with limited access to healthy food (food deserts) or a high density of unhealthy food outlets (food swamps) have higher mortality rates from metabolic dysfunction–associated steatotic liver disease (MASLD), according to investigators.

These findings highlight the importance of addressing disparities in food environments and social determinants of health to help reduce MASLD-related mortality, lead author Annette Paik, MD, of Inova Health System, Falls Church, Virginia, and colleagues reported.

“Recent studies indicate that food swamps and deserts, as surrogates for food insecurity, are linked to poor glycemic control and higher adult obesity rates,” the investigators wrote in Clinical Gastroenterology and Hepatology. “Understanding the intersection of these factors with sociodemographic and clinical variables offers insights into MASLD-related outcomes, including mortality.”

To this end, the present study examined the association between food environments and MASLD-related mortality across more than 2,195 US counties. County-level mortality data were obtained from the CDC WONDER database (2016-2020) and linked to food environment data from the US Department of Agriculture Food Environment Atlas using Federal Information Processing Standards (FIPS) codes. Food deserts were defined as low-income areas with limited access to grocery stores, while food swamps were characterized by a predominance of unhealthy food outlets relative to healthy ones.

Additional data on obesity, type 2 diabetes (T2D), and nine social determinants of health were obtained from CDC PLACES and other publicly available datasets. Counties were stratified into quartiles based on MASLD-related mortality rates. Population-weighted mixed-effects linear regression models were used to evaluate associations between food environment exposures and MASLD mortality, adjusting for region, rural-urban status, age, sex, race, insurance coverage, chronic dis-ease prevalence, SNAP participation, and access to exercise facilities.

Counties with the worst food environments had significantly higher MASLD-related mortality, even after adjusting for clinical and sociodemographic factors. Compared with counties in the lowest quartile of MASLD mortality, those in the highest quartile had a greater proportion of food deserts (22.3% vs 14.9%; P < .001) and food swamps (73.1% vs 65.7%; P < .001). They also had a significantly higher prevalence of obesity (40.5% vs 32.5%), type 2 diabetes (15.8% vs 11.4%), and physical inactivity (33.7% vs 24.9%).

Demographically, counties with higher MASLD mortality had significantly larger proportions of Black and Hispanic residents, and were more likely to be rural and located in the South. These counties also had significantly lower median household incomes, higher poverty rates, fewer adults with a college education, lower access to exercise opportunities, greater SNAP participation, less broadband access, and more uninsured adults.

In multivariable regression models, both food deserts and food swamps remained independently associated with MASLD mortality. Counties in the highest quartile of food desert exposure had a 14.5% higher MASLD mortality rate, compared with the lowest quartile (P = .001), and those in the highest quartile for food swamp exposure had a 13.9% higher mortality rate (P = .005).

Type 2 diabetes, physical inactivity, and lack of health insurance were also independently associated with increased MASLD-related mortality. 

“Implementing public health interventions that address the specific environmental factors of each county can help US policymakers promote access to healthy, culturally appropriate food choices at affordable prices and reduce the consumption of poor-quality food,” the investigators wrote. “Moreover, improving access to parks and exercise facilities can further enhance the impact of healthy nutrition. These strategies could help curb the growing epidemic of metabolic diseases, including MASLD and related mortality.”

This study was supported by King Faisal Specialist Hospital & Research Center, the Global NASH Council, Center for Outcomes Research in Liver Diseases, and the Beatty Liver and Obesity Research Fund, Inova Health System. The investigators disclosed no conflicts of interest.
 

US counties with limited access to healthy food (food deserts) or a high density of unhealthy food outlets (food swamps) have higher mortality rates from metabolic dysfunction–associated steatotic liver disease (MASLD), according to investigators.

These findings highlight the importance of addressing disparities in food environments and social determinants of health to help reduce MASLD-related mortality, lead author Annette Paik, MD, of Inova Health System, Falls Church, Virginia, and colleagues reported.

“Recent studies indicate that food swamps and deserts, as surrogates for food insecurity, are linked to poor glycemic control and higher adult obesity rates,” the investigators wrote in Clinical Gastroenterology and Hepatology. “Understanding the intersection of these factors with sociodemographic and clinical variables offers insights into MASLD-related outcomes, including mortality.”

To this end, the present study examined the association between food environments and MASLD-related mortality across more than 2,195 US counties. County-level mortality data were obtained from the CDC WONDER database (2016-2020) and linked to food environment data from the US Department of Agriculture Food Environment Atlas using Federal Information Processing Standards (FIPS) codes. Food deserts were defined as low-income areas with limited access to grocery stores, while food swamps were characterized by a predominance of unhealthy food outlets relative to healthy ones.

Additional data on obesity, type 2 diabetes (T2D), and nine social determinants of health were obtained from CDC PLACES and other publicly available datasets. Counties were stratified into quartiles based on MASLD-related mortality rates. Population-weighted mixed-effects linear regression models were used to evaluate associations between food environment exposures and MASLD mortality, adjusting for region, rural-urban status, age, sex, race, insurance coverage, chronic dis-ease prevalence, SNAP participation, and access to exercise facilities.

Counties with the worst food environments had significantly higher MASLD-related mortality, even after adjusting for clinical and sociodemographic factors. Compared with counties in the lowest quartile of MASLD mortality, those in the highest quartile had a greater proportion of food deserts (22.3% vs 14.9%; P < .001) and food swamps (73.1% vs 65.7%; P < .001). They also had a significantly higher prevalence of obesity (40.5% vs 32.5%), type 2 diabetes (15.8% vs 11.4%), and physical inactivity (33.7% vs 24.9%).

Demographically, counties with higher MASLD mortality had significantly larger proportions of Black and Hispanic residents, and were more likely to be rural and located in the South. These counties also had significantly lower median household incomes, higher poverty rates, fewer adults with a college education, lower access to exercise opportunities, greater SNAP participation, less broadband access, and more uninsured adults.

In multivariable regression models, both food deserts and food swamps remained independently associated with MASLD mortality. Counties in the highest quartile of food desert exposure had a 14.5% higher MASLD mortality rate, compared with the lowest quartile (P = .001), and those in the highest quartile for food swamp exposure had a 13.9% higher mortality rate (P = .005).

Type 2 diabetes, physical inactivity, and lack of health insurance were also independently associated with increased MASLD-related mortality. 

“Implementing public health interventions that address the specific environmental factors of each county can help US policymakers promote access to healthy, culturally appropriate food choices at affordable prices and reduce the consumption of poor-quality food,” the investigators wrote. “Moreover, improving access to parks and exercise facilities can further enhance the impact of healthy nutrition. These strategies could help curb the growing epidemic of metabolic diseases, including MASLD and related mortality.”

This study was supported by King Faisal Specialist Hospital & Research Center, the Global NASH Council, Center for Outcomes Research in Liver Diseases, and the Beatty Liver and Obesity Research Fund, Inova Health System. The investigators disclosed no conflicts of interest.
 

US counties with limited access to healthy food (food deserts) or a high density of unhealthy food outlets (food swamps) have higher mortality rates from metabolic dysfunction–associated steatotic liver disease (MASLD), according to investigators.

These findings highlight the importance of addressing disparities in food environments and social determinants of health to help reduce MASLD-related mortality, lead author Annette Paik, MD, of Inova Health System, Falls Church, Virginia, and colleagues reported.

“Recent studies indicate that food swamps and deserts, as surrogates for food insecurity, are linked to poor glycemic control and higher adult obesity rates,” the investigators wrote in Clinical Gastroenterology and Hepatology. “Understanding the intersection of these factors with sociodemographic and clinical variables offers insights into MASLD-related outcomes, including mortality.”

To this end, the present study examined the association between food environments and MASLD-related mortality across more than 2,195 US counties. County-level mortality data were obtained from the CDC WONDER database (2016-2020) and linked to food environment data from the US Department of Agriculture Food Environment Atlas using Federal Information Processing Standards (FIPS) codes. Food deserts were defined as low-income areas with limited access to grocery stores, while food swamps were characterized by a predominance of unhealthy food outlets relative to healthy ones.

Additional data on obesity, type 2 diabetes (T2D), and nine social determinants of health were obtained from CDC PLACES and other publicly available datasets. Counties were stratified into quartiles based on MASLD-related mortality rates. Population-weighted mixed-effects linear regression models were used to evaluate associations between food environment exposures and MASLD mortality, adjusting for region, rural-urban status, age, sex, race, insurance coverage, chronic dis-ease prevalence, SNAP participation, and access to exercise facilities.

Counties with the worst food environments had significantly higher MASLD-related mortality, even after adjusting for clinical and sociodemographic factors. Compared with counties in the lowest quartile of MASLD mortality, those in the highest quartile had a greater proportion of food deserts (22.3% vs 14.9%; P < .001) and food swamps (73.1% vs 65.7%; P < .001). They also had a significantly higher prevalence of obesity (40.5% vs 32.5%), type 2 diabetes (15.8% vs 11.4%), and physical inactivity (33.7% vs 24.9%).

Demographically, counties with higher MASLD mortality had significantly larger proportions of Black and Hispanic residents, and were more likely to be rural and located in the South. These counties also had significantly lower median household incomes, higher poverty rates, fewer adults with a college education, lower access to exercise opportunities, greater SNAP participation, less broadband access, and more uninsured adults.

In multivariable regression models, both food deserts and food swamps remained independently associated with MASLD mortality. Counties in the highest quartile of food desert exposure had a 14.5% higher MASLD mortality rate, compared with the lowest quartile (P = .001), and those in the highest quartile for food swamp exposure had a 13.9% higher mortality rate (P = .005).

Type 2 diabetes, physical inactivity, and lack of health insurance were also independently associated with increased MASLD-related mortality. 

“Implementing public health interventions that address the specific environmental factors of each county can help US policymakers promote access to healthy, culturally appropriate food choices at affordable prices and reduce the consumption of poor-quality food,” the investigators wrote. “Moreover, improving access to parks and exercise facilities can further enhance the impact of healthy nutrition. These strategies could help curb the growing epidemic of metabolic diseases, including MASLD and related mortality.”

This study was supported by King Faisal Specialist Hospital & Research Center, the Global NASH Council, Center for Outcomes Research in Liver Diseases, and the Beatty Liver and Obesity Research Fund, Inova Health System. The investigators disclosed no conflicts of interest.
 

Only 1 in 6 US veterans with chronic hepatitis B (CHB) is tested for hepatitis D virus (HDV)—a coinfection associated with significantly higher risks of cirrhosis and hepatic decompensation—according to new findings.

The low testing rate suggests limited awareness of HDV-associated risks in patients with CHB, and underscores the need for earlier testing and diagnosis, lead author Robert J. Wong, MD, of Stanford University School of Medicine, Stanford, California, and colleagues, reported.

“Data among US populations are lacking to describe the epidemiology and long-term outcomes of patients with CHB and concurrent HDV infection,” the investigators wrote in Gastro Hep Advances (2025 Oct. doi: 10.1016/j.gastha.2024.10.015).

Prior studies have found that only 6% to 19% of patients with CHB get tested for HDV, and among those tested, the prevalence is relatively low—between 2% and 4.6%. Although relatively uncommon, HDV carries a substantial clinical and economic burden, Dr. Wong and colleagues noted, highlighting the importance of clinical awareness and accurate epidemiologic data.

The present study analyzed data from the Veterans Affairs (VA) Corporate Data Warehouse between 2010 and 2023. Adults with CHB were identified based on laboratory-confirmed markers and ICD-9/10 codes. HDV testing (anti-HDV antibody and HDV RNA) was assessed, and predictors of testing were evaluated using multivariable logistic regression.

To examine liver-related outcomes, patients who tested positive for HDV were propensity score–matched 1:2 with CHB patients who tested negative. Matching accounted for age, sex, race/ethnicity, HBeAg status, antiviral treatment, HCV and HIV coinfection, diabetes, and alcohol use. Patients with cirrhosis or hepatocellular carcinoma (HCC) at base-line were excluded. Incidence of cirrhosis, hepatic decompensation, and HCC was estimated using competing risks Nelson-Aalen methods.

Among 27,548 veterans with CHB, only 16.1% underwent HDV testing. Of those tested, 3.25% were HDV positive. Testing rates were higher among patients who were HBeAg positive, on antiviral therapy, or identified as Asian or Pacific Islander.

Conversely, testing was significantly less common among patients with high-risk alcohol use, past or current drug use, cirrhosis at diagnosis, or HCV coinfection. In contrast, HIV coinfection was associated with increased odds of being tested.

Among those tested, HDV positivity was more likely in patients with HCV coinfection, cirrhosis, or a history of drug use. On multivariable analysis, these factors were independent predictors of HDV positivity.

In the matched cohort of 71 HDV-positive patients and 140 HDV-negative controls, the incidence of cirrhosis was more than 3-fold higher in HDV-positive patients (4.39 vs 1.30 per 100,000 person-years; P less than .01), and hepatic decompensation was over 5 times more common (2.18 vs 0.41 per 100,000 person-years; P = .01). There was also a non-significant trend toward increased HCC risk in the HDV group.

“These findings align with existing studies and confirm that among a predominantly non-Asian US cohort of CHB patients, presence of concurrent HDV is associated with more severe liver disease progression,” the investigators wrote. “These observations, taken together with the low rates of HDV testing overall and particularly among high-risk individuals, emphasizes the need for greater awareness and novel strategies on how to improve HDV testing and diagnosis, particularly given that novel HDV therapies are on the near horizon.”

The study was supported by Gilead. The investigators disclosed additional relationships with Exact Sciences, GSK, Novo Nordisk, and others.

Only 1 in 6 US veterans with chronic hepatitis B (CHB) is tested for hepatitis D virus (HDV)—a coinfection associated with significantly higher risks of cirrhosis and hepatic decompensation—according to new findings.

The low testing rate suggests limited awareness of HDV-associated risks in patients with CHB, and underscores the need for earlier testing and diagnosis, lead author Robert J. Wong, MD, of Stanford University School of Medicine, Stanford, California, and colleagues, reported.

“Data among US populations are lacking to describe the epidemiology and long-term outcomes of patients with CHB and concurrent HDV infection,” the investigators wrote in Gastro Hep Advances (2025 Oct. doi: 10.1016/j.gastha.2024.10.015).

Prior studies have found that only 6% to 19% of patients with CHB get tested for HDV, and among those tested, the prevalence is relatively low—between 2% and 4.6%. Although relatively uncommon, HDV carries a substantial clinical and economic burden, Dr. Wong and colleagues noted, highlighting the importance of clinical awareness and accurate epidemiologic data.

The present study analyzed data from the Veterans Affairs (VA) Corporate Data Warehouse between 2010 and 2023. Adults with CHB were identified based on laboratory-confirmed markers and ICD-9/10 codes. HDV testing (anti-HDV antibody and HDV RNA) was assessed, and predictors of testing were evaluated using multivariable logistic regression.

To examine liver-related outcomes, patients who tested positive for HDV were propensity score–matched 1:2 with CHB patients who tested negative. Matching accounted for age, sex, race/ethnicity, HBeAg status, antiviral treatment, HCV and HIV coinfection, diabetes, and alcohol use. Patients with cirrhosis or hepatocellular carcinoma (HCC) at base-line were excluded. Incidence of cirrhosis, hepatic decompensation, and HCC was estimated using competing risks Nelson-Aalen methods.

Among 27,548 veterans with CHB, only 16.1% underwent HDV testing. Of those tested, 3.25% were HDV positive. Testing rates were higher among patients who were HBeAg positive, on antiviral therapy, or identified as Asian or Pacific Islander.

Conversely, testing was significantly less common among patients with high-risk alcohol use, past or current drug use, cirrhosis at diagnosis, or HCV coinfection. In contrast, HIV coinfection was associated with increased odds of being tested.

Among those tested, HDV positivity was more likely in patients with HCV coinfection, cirrhosis, or a history of drug use. On multivariable analysis, these factors were independent predictors of HDV positivity.

In the matched cohort of 71 HDV-positive patients and 140 HDV-negative controls, the incidence of cirrhosis was more than 3-fold higher in HDV-positive patients (4.39 vs 1.30 per 100,000 person-years; P less than .01), and hepatic decompensation was over 5 times more common (2.18 vs 0.41 per 100,000 person-years; P = .01). There was also a non-significant trend toward increased HCC risk in the HDV group.

“These findings align with existing studies and confirm that among a predominantly non-Asian US cohort of CHB patients, presence of concurrent HDV is associated with more severe liver disease progression,” the investigators wrote. “These observations, taken together with the low rates of HDV testing overall and particularly among high-risk individuals, emphasizes the need for greater awareness and novel strategies on how to improve HDV testing and diagnosis, particularly given that novel HDV therapies are on the near horizon.”

The study was supported by Gilead. The investigators disclosed additional relationships with Exact Sciences, GSK, Novo Nordisk, and others.

Only 1 in 6 US veterans with chronic hepatitis B (CHB) is tested for hepatitis D virus (HDV)—a coinfection associated with significantly higher risks of cirrhosis and hepatic decompensation—according to new findings.

The low testing rate suggests limited awareness of HDV-associated risks in patients with CHB, and underscores the need for earlier testing and diagnosis, lead author Robert J. Wong, MD, of Stanford University School of Medicine, Stanford, California, and colleagues, reported.

“Data among US populations are lacking to describe the epidemiology and long-term outcomes of patients with CHB and concurrent HDV infection,” the investigators wrote in Gastro Hep Advances (2025 Oct. doi: 10.1016/j.gastha.2024.10.015).

Prior studies have found that only 6% to 19% of patients with CHB get tested for HDV, and among those tested, the prevalence is relatively low—between 2% and 4.6%. Although relatively uncommon, HDV carries a substantial clinical and economic burden, Dr. Wong and colleagues noted, highlighting the importance of clinical awareness and accurate epidemiologic data.

The present study analyzed data from the Veterans Affairs (VA) Corporate Data Warehouse between 2010 and 2023. Adults with CHB were identified based on laboratory-confirmed markers and ICD-9/10 codes. HDV testing (anti-HDV antibody and HDV RNA) was assessed, and predictors of testing were evaluated using multivariable logistic regression.

To examine liver-related outcomes, patients who tested positive for HDV were propensity score–matched 1:2 with CHB patients who tested negative. Matching accounted for age, sex, race/ethnicity, HBeAg status, antiviral treatment, HCV and HIV coinfection, diabetes, and alcohol use. Patients with cirrhosis or hepatocellular carcinoma (HCC) at base-line were excluded. Incidence of cirrhosis, hepatic decompensation, and HCC was estimated using competing risks Nelson-Aalen methods.

Among 27,548 veterans with CHB, only 16.1% underwent HDV testing. Of those tested, 3.25% were HDV positive. Testing rates were higher among patients who were HBeAg positive, on antiviral therapy, or identified as Asian or Pacific Islander.

Conversely, testing was significantly less common among patients with high-risk alcohol use, past or current drug use, cirrhosis at diagnosis, or HCV coinfection. In contrast, HIV coinfection was associated with increased odds of being tested.

Among those tested, HDV positivity was more likely in patients with HCV coinfection, cirrhosis, or a history of drug use. On multivariable analysis, these factors were independent predictors of HDV positivity.

In the matched cohort of 71 HDV-positive patients and 140 HDV-negative controls, the incidence of cirrhosis was more than 3-fold higher in HDV-positive patients (4.39 vs 1.30 per 100,000 person-years; P less than .01), and hepatic decompensation was over 5 times more common (2.18 vs 0.41 per 100,000 person-years; P = .01). There was also a non-significant trend toward increased HCC risk in the HDV group.

“These findings align with existing studies and confirm that among a predominantly non-Asian US cohort of CHB patients, presence of concurrent HDV is associated with more severe liver disease progression,” the investigators wrote. “These observations, taken together with the low rates of HDV testing overall and particularly among high-risk individuals, emphasizes the need for greater awareness and novel strategies on how to improve HDV testing and diagnosis, particularly given that novel HDV therapies are on the near horizon.”

The study was supported by Gilead. The investigators disclosed additional relationships with Exact Sciences, GSK, Novo Nordisk, and others.

Long-term use of statins may delay or deflect the development of hepatocellular carcinoma in adults with chronic liver disease, as well as in the general population, emerging research, including several large cohort studies, suggested.

The most recent study, published in JAMA Internal Medicine, showed a lower incidence of hepatic decompensation among statin users in a registry for adults aged 40 years or older with baseline chronic liver disease.

“Our findings support the idea that statins may offer benefits beyond lipid-lowering in patients with [chronic liver disease], and clinicians may be more confident in prescribing statins when indicated,” even in these patients, said corresponding Co-author Raymond T. Chung, MD, gastroenterology investigator at Mass General Research Institute, Boston, in an interview. 

“While prior studies have suggested an association between statin use and reduced hepatocellular carcinoma risk, our study aimed to build on that evidence by using a large, real-world, hospital-based cohort inclusive of all etiologies of chronic liver disease,” Chung told GI & Hepatology News.

Chung, along with Jonggi Choi, MD, of the University of Ulsan College of Medicine, Seoul, South Korea, and colleagues, reviewed data from the Research Patient Data Registry from 2000 to 2023 for 16,501 participantsaged 40 years or older with baseline chronic liver disease and baseline Fibrosis-4 (FIB-4) scores ≥ 1.3.

The study population had a mean age of 59.7 years, and 40.9% were women. The researchers divided the population into statin users (n = 3610) and nonusers (n = 12,891). Statin use was defined as a cumulative defined daily dose ≥ 30 mg.

The primary outcome was the cumulative incidence of hepatocellular carcinoma and hepatic decompensation.

At 10 years follow-up, statin users showed a significantly reduced incidence of hepatocellular carcinoma vs nonusers (3.8% vs 8.0%; P < .001) as well as a significantly reduced incidence of hepatic decompensation (10.6% vs 19.5%; P < .001).

Incorporating FIB-4 scores, a surrogate marker for liver fibrosis, also showed that statin users were less likely to experience fibrosis progression, offering a potential mechanism of action for the observed reduction in adverse liver outcomes, Chung told GI & Hepatology News.

“Similar trends have been observed in prior observational studies, but our findings now support a real effect of statin use on fibrosis progression,” he said. “However, what strengthened our study was that the association remained consistent across multiple subgroups and sensitivity analyses.”

Another study published in Clinical Gastroenterology and Hepatology showed a reduced risk of developing severe liver disease in a Swedish cohort of noncirrhotic adults with chronic liver disease who used statins (n = 3862) compared with control patients with chronic liver disease (matched 1:1) and who did not use statins (hazard ratio [HR], 0.60). 

In that study, Rajani Sharma, MD, and colleagues found a protective association in both prefibrosis and fibrosis stages at diagnosis, and statin use was associated with reduced rates of progression to both cirrhosis and hepatocellular carcinoma (HR, 0.62 and 0.44, respectively).

 

Exciting and Necessary Research

The research by Choi and colleagues is “exciting,” said Bubu Banini, MD, PhD, an assistant professor in digestive diseases at Yale School of Medicine, New Haven, Connecticut, in an interview.

Liver cancer prevalence has risen over the past few decades in the United States and worldwide, and the 5-year overall survival rate of liver cancer is less than 20%, Banini told GI & Hepatology News.

Clinicians often withhold statins out of fear of liver injury in persons with chronic liver disease; however, a takeaway from this study is that for persons with chronic liver disease who have indications for statin use, the medication should not be withheld, she said.

Of course, prospective studies are needed to replicate the results, Banini added.

The study findings were limited by several factors, including the inability to adjust for all potential confounding variables, lack of data on post-index treatments, and the use of wide, cumulative, defined daily dose categories to ensure statistical power, the researchers noted.

“Moving forward, randomized controlled trials are essential to establish a causal relationship and clarify the molecular and clinical pathways through which statins exert hepatoprotective effects,” Chung added.

Randomized controlled trials are also needed to determine whether statins can actually reduce the risk for hepatocellular carcinoma and hepatic decompensation in patients with chronic liver disease, and cost-effectiveness analyses may be essential for translating this evidence into clinical guidelines, he added.

 

Statins and HCC Risk in the General Population

A large cohort study, published in JAMA Network Open by Mara Sophie Vell, PhD, and colleagues, showed an association between reduced risk for hepatocellular carcinoma and statin use in the general population and in those at increased risk for liver disease.

The study, which included data for individuals aged 37-73 years from the UK Biobank, found a 15% reduced risk for new-onset liver disease and a 28% reduced risk for liver-related death among regular statin users than among nonusers (HR, 0.85 and 0.72, respectively). 

In addition, regular statin users showed a 74% reduced risk (P = .003) of developing hepatocellular carcinoma compared with those not using statins. The researchers identified a particular impact on liver disease risk reduction among men, individuals with diabetes, and patients with high levels of liver scarring at baseline based on the FIB-4 index.

A meta-analysis of 24 studies, previously published in the journal Cancers, showed a significant reduction of 46% in hepatocellular carcinoma risk among statins users compared with nonusers.

The researchers found this risk reduction was significant in subgroups of patients with diabetes, liver cirrhosis, and those on antiviral therapy, and they suggested that the antiangiogenic, immunomodulatory, antiproliferative, and antifibrotic properties of statins may contribute to their potential to reduce tumor growth or hepatocellular carcinoma development.

The meta-analysis authors noted that although most studies have reported a low risk for statin-induced hepatotoxicity, clinicians should proceed with caution in some patients with existing cirrhosis.

“If the patients are diagnosed with decompensated cirrhosis, then statins should be prescribed with caution at low doses,” they wrote.

Advocating statin use solely for chemoprevention may be premature based on observational data, Chung told GI & Hepatology News.

“However, in patients with [chronic liver disease] who already meet indications for statin therapy, the potential added benefit of reducing liver-related complications strengthens the rationale for their use,” he said. Future randomized clinical trials will be key to defining the risk-benefit profile in this context.

The study by Choi and colleagues was supported by the National Institutes of Health.

The study by Sharma and colleagues was supported by the Karolinska Institutet, Stockholm, Sweden, and the Columbia University Irving Medical Center, New York City; researchers were supported by grants from the Swedish Research Council, Center for Innovative Medicine, the Swedish Cancer Society, and the National Institutes of Health.

The study by Vell and colleagues had no outside funding.

The study by Mohaimenul Islam and colleagues was supported by the Ministry of Education and Ministry of Science and Technology, Taiwan.

Chung and Banini had no financial conflicts to disclose.

A version of this article appeared on Medscape.com.

Long-term use of statins may delay or deflect the development of hepatocellular carcinoma in adults with chronic liver disease, as well as in the general population, emerging research, including several large cohort studies, suggested.

The most recent study, published in JAMA Internal Medicine, showed a lower incidence of hepatic decompensation among statin users in a registry for adults aged 40 years or older with baseline chronic liver disease.

“Our findings support the idea that statins may offer benefits beyond lipid-lowering in patients with [chronic liver disease], and clinicians may be more confident in prescribing statins when indicated,” even in these patients, said corresponding Co-author Raymond T. Chung, MD, gastroenterology investigator at Mass General Research Institute, Boston, in an interview. 

“While prior studies have suggested an association between statin use and reduced hepatocellular carcinoma risk, our study aimed to build on that evidence by using a large, real-world, hospital-based cohort inclusive of all etiologies of chronic liver disease,” Chung told GI & Hepatology News.

Chung, along with Jonggi Choi, MD, of the University of Ulsan College of Medicine, Seoul, South Korea, and colleagues, reviewed data from the Research Patient Data Registry from 2000 to 2023 for 16,501 participantsaged 40 years or older with baseline chronic liver disease and baseline Fibrosis-4 (FIB-4) scores ≥ 1.3.

The study population had a mean age of 59.7 years, and 40.9% were women. The researchers divided the population into statin users (n = 3610) and nonusers (n = 12,891). Statin use was defined as a cumulative defined daily dose ≥ 30 mg.

The primary outcome was the cumulative incidence of hepatocellular carcinoma and hepatic decompensation.

At 10 years follow-up, statin users showed a significantly reduced incidence of hepatocellular carcinoma vs nonusers (3.8% vs 8.0%; P < .001) as well as a significantly reduced incidence of hepatic decompensation (10.6% vs 19.5%; P < .001).

Incorporating FIB-4 scores, a surrogate marker for liver fibrosis, also showed that statin users were less likely to experience fibrosis progression, offering a potential mechanism of action for the observed reduction in adverse liver outcomes, Chung told GI & Hepatology News.

“Similar trends have been observed in prior observational studies, but our findings now support a real effect of statin use on fibrosis progression,” he said. “However, what strengthened our study was that the association remained consistent across multiple subgroups and sensitivity analyses.”

Another study published in Clinical Gastroenterology and Hepatology showed a reduced risk of developing severe liver disease in a Swedish cohort of noncirrhotic adults with chronic liver disease who used statins (n = 3862) compared with control patients with chronic liver disease (matched 1:1) and who did not use statins (hazard ratio [HR], 0.60). 

In that study, Rajani Sharma, MD, and colleagues found a protective association in both prefibrosis and fibrosis stages at diagnosis, and statin use was associated with reduced rates of progression to both cirrhosis and hepatocellular carcinoma (HR, 0.62 and 0.44, respectively).

 

Exciting and Necessary Research

The research by Choi and colleagues is “exciting,” said Bubu Banini, MD, PhD, an assistant professor in digestive diseases at Yale School of Medicine, New Haven, Connecticut, in an interview.

Liver cancer prevalence has risen over the past few decades in the United States and worldwide, and the 5-year overall survival rate of liver cancer is less than 20%, Banini told GI & Hepatology News.

Clinicians often withhold statins out of fear of liver injury in persons with chronic liver disease; however, a takeaway from this study is that for persons with chronic liver disease who have indications for statin use, the medication should not be withheld, she said.

Of course, prospective studies are needed to replicate the results, Banini added.

The study findings were limited by several factors, including the inability to adjust for all potential confounding variables, lack of data on post-index treatments, and the use of wide, cumulative, defined daily dose categories to ensure statistical power, the researchers noted.

“Moving forward, randomized controlled trials are essential to establish a causal relationship and clarify the molecular and clinical pathways through which statins exert hepatoprotective effects,” Chung added.

Randomized controlled trials are also needed to determine whether statins can actually reduce the risk for hepatocellular carcinoma and hepatic decompensation in patients with chronic liver disease, and cost-effectiveness analyses may be essential for translating this evidence into clinical guidelines, he added.

 

Statins and HCC Risk in the General Population

A large cohort study, published in JAMA Network Open by Mara Sophie Vell, PhD, and colleagues, showed an association between reduced risk for hepatocellular carcinoma and statin use in the general population and in those at increased risk for liver disease.

The study, which included data for individuals aged 37-73 years from the UK Biobank, found a 15% reduced risk for new-onset liver disease and a 28% reduced risk for liver-related death among regular statin users than among nonusers (HR, 0.85 and 0.72, respectively). 

In addition, regular statin users showed a 74% reduced risk (P = .003) of developing hepatocellular carcinoma compared with those not using statins. The researchers identified a particular impact on liver disease risk reduction among men, individuals with diabetes, and patients with high levels of liver scarring at baseline based on the FIB-4 index.

A meta-analysis of 24 studies, previously published in the journal Cancers, showed a significant reduction of 46% in hepatocellular carcinoma risk among statins users compared with nonusers.

The researchers found this risk reduction was significant in subgroups of patients with diabetes, liver cirrhosis, and those on antiviral therapy, and they suggested that the antiangiogenic, immunomodulatory, antiproliferative, and antifibrotic properties of statins may contribute to their potential to reduce tumor growth or hepatocellular carcinoma development.

The meta-analysis authors noted that although most studies have reported a low risk for statin-induced hepatotoxicity, clinicians should proceed with caution in some patients with existing cirrhosis.

“If the patients are diagnosed with decompensated cirrhosis, then statins should be prescribed with caution at low doses,” they wrote.

Advocating statin use solely for chemoprevention may be premature based on observational data, Chung told GI & Hepatology News.

“However, in patients with [chronic liver disease] who already meet indications for statin therapy, the potential added benefit of reducing liver-related complications strengthens the rationale for their use,” he said. Future randomized clinical trials will be key to defining the risk-benefit profile in this context.

The study by Choi and colleagues was supported by the National Institutes of Health.

The study by Sharma and colleagues was supported by the Karolinska Institutet, Stockholm, Sweden, and the Columbia University Irving Medical Center, New York City; researchers were supported by grants from the Swedish Research Council, Center for Innovative Medicine, the Swedish Cancer Society, and the National Institutes of Health.

The study by Vell and colleagues had no outside funding.

The study by Mohaimenul Islam and colleagues was supported by the Ministry of Education and Ministry of Science and Technology, Taiwan.

Chung and Banini had no financial conflicts to disclose.

A version of this article appeared on Medscape.com.

Long-term use of statins may delay or deflect the development of hepatocellular carcinoma in adults with chronic liver disease, as well as in the general population, emerging research, including several large cohort studies, suggested.

The most recent study, published in JAMA Internal Medicine, showed a lower incidence of hepatic decompensation among statin users in a registry for adults aged 40 years or older with baseline chronic liver disease.

“Our findings support the idea that statins may offer benefits beyond lipid-lowering in patients with [chronic liver disease], and clinicians may be more confident in prescribing statins when indicated,” even in these patients, said corresponding Co-author Raymond T. Chung, MD, gastroenterology investigator at Mass General Research Institute, Boston, in an interview. 

“While prior studies have suggested an association between statin use and reduced hepatocellular carcinoma risk, our study aimed to build on that evidence by using a large, real-world, hospital-based cohort inclusive of all etiologies of chronic liver disease,” Chung told GI & Hepatology News.

Chung, along with Jonggi Choi, MD, of the University of Ulsan College of Medicine, Seoul, South Korea, and colleagues, reviewed data from the Research Patient Data Registry from 2000 to 2023 for 16,501 participantsaged 40 years or older with baseline chronic liver disease and baseline Fibrosis-4 (FIB-4) scores ≥ 1.3.

The study population had a mean age of 59.7 years, and 40.9% were women. The researchers divided the population into statin users (n = 3610) and nonusers (n = 12,891). Statin use was defined as a cumulative defined daily dose ≥ 30 mg.

The primary outcome was the cumulative incidence of hepatocellular carcinoma and hepatic decompensation.

At 10 years follow-up, statin users showed a significantly reduced incidence of hepatocellular carcinoma vs nonusers (3.8% vs 8.0%; P < .001) as well as a significantly reduced incidence of hepatic decompensation (10.6% vs 19.5%; P < .001).

Incorporating FIB-4 scores, a surrogate marker for liver fibrosis, also showed that statin users were less likely to experience fibrosis progression, offering a potential mechanism of action for the observed reduction in adverse liver outcomes, Chung told GI & Hepatology News.

“Similar trends have been observed in prior observational studies, but our findings now support a real effect of statin use on fibrosis progression,” he said. “However, what strengthened our study was that the association remained consistent across multiple subgroups and sensitivity analyses.”

Another study published in Clinical Gastroenterology and Hepatology showed a reduced risk of developing severe liver disease in a Swedish cohort of noncirrhotic adults with chronic liver disease who used statins (n = 3862) compared with control patients with chronic liver disease (matched 1:1) and who did not use statins (hazard ratio [HR], 0.60). 

In that study, Rajani Sharma, MD, and colleagues found a protective association in both prefibrosis and fibrosis stages at diagnosis, and statin use was associated with reduced rates of progression to both cirrhosis and hepatocellular carcinoma (HR, 0.62 and 0.44, respectively).

 

Exciting and Necessary Research

The research by Choi and colleagues is “exciting,” said Bubu Banini, MD, PhD, an assistant professor in digestive diseases at Yale School of Medicine, New Haven, Connecticut, in an interview.

Liver cancer prevalence has risen over the past few decades in the United States and worldwide, and the 5-year overall survival rate of liver cancer is less than 20%, Banini told GI & Hepatology News.

Clinicians often withhold statins out of fear of liver injury in persons with chronic liver disease; however, a takeaway from this study is that for persons with chronic liver disease who have indications for statin use, the medication should not be withheld, she said.

Of course, prospective studies are needed to replicate the results, Banini added.

The study findings were limited by several factors, including the inability to adjust for all potential confounding variables, lack of data on post-index treatments, and the use of wide, cumulative, defined daily dose categories to ensure statistical power, the researchers noted.

“Moving forward, randomized controlled trials are essential to establish a causal relationship and clarify the molecular and clinical pathways through which statins exert hepatoprotective effects,” Chung added.

Randomized controlled trials are also needed to determine whether statins can actually reduce the risk for hepatocellular carcinoma and hepatic decompensation in patients with chronic liver disease, and cost-effectiveness analyses may be essential for translating this evidence into clinical guidelines, he added.

 

Statins and HCC Risk in the General Population

A large cohort study, published in JAMA Network Open by Mara Sophie Vell, PhD, and colleagues, showed an association between reduced risk for hepatocellular carcinoma and statin use in the general population and in those at increased risk for liver disease.

The study, which included data for individuals aged 37-73 years from the UK Biobank, found a 15% reduced risk for new-onset liver disease and a 28% reduced risk for liver-related death among regular statin users than among nonusers (HR, 0.85 and 0.72, respectively). 

In addition, regular statin users showed a 74% reduced risk (P = .003) of developing hepatocellular carcinoma compared with those not using statins. The researchers identified a particular impact on liver disease risk reduction among men, individuals with diabetes, and patients with high levels of liver scarring at baseline based on the FIB-4 index.

A meta-analysis of 24 studies, previously published in the journal Cancers, showed a significant reduction of 46% in hepatocellular carcinoma risk among statins users compared with nonusers.

The researchers found this risk reduction was significant in subgroups of patients with diabetes, liver cirrhosis, and those on antiviral therapy, and they suggested that the antiangiogenic, immunomodulatory, antiproliferative, and antifibrotic properties of statins may contribute to their potential to reduce tumor growth or hepatocellular carcinoma development.

The meta-analysis authors noted that although most studies have reported a low risk for statin-induced hepatotoxicity, clinicians should proceed with caution in some patients with existing cirrhosis.

“If the patients are diagnosed with decompensated cirrhosis, then statins should be prescribed with caution at low doses,” they wrote.

Advocating statin use solely for chemoprevention may be premature based on observational data, Chung told GI & Hepatology News.

“However, in patients with [chronic liver disease] who already meet indications for statin therapy, the potential added benefit of reducing liver-related complications strengthens the rationale for their use,” he said. Future randomized clinical trials will be key to defining the risk-benefit profile in this context.

The study by Choi and colleagues was supported by the National Institutes of Health.

The study by Sharma and colleagues was supported by the Karolinska Institutet, Stockholm, Sweden, and the Columbia University Irving Medical Center, New York City; researchers were supported by grants from the Swedish Research Council, Center for Innovative Medicine, the Swedish Cancer Society, and the National Institutes of Health.

The study by Vell and colleagues had no outside funding.

The study by Mohaimenul Islam and colleagues was supported by the Ministry of Education and Ministry of Science and Technology, Taiwan.

Chung and Banini had no financial conflicts to disclose.

A version of this article appeared on Medscape.com.

WASHINGTON, DC — Age-related neurodegenerative disorders — motor neuron diseases, demyelinating diseases, Alzheimer’s disease, and other proteinopathies — are at an “inflection point,” said researcher Andrea R. Merchak, PhD, with a fuller understanding of disease pathophysiology but an overall dearth of effective disease-modifying treatments.

And this, Merchak said at the Gut Microbiota for Health (GMFH) World Summit 2025, is where the gut microbiome comes in. “The gut-brain axis is important to take into consideration,” she urged, both for gut microbiome researchers — whose collaboration with neurologists and neuroscientists is essential — and for practicing gastroenterologists.

“We are the sum of our environmental exposures,” said Merchak, assistant research professor of neurology at the Indiana University School of Medicine, in Indianapolis. “So for your patient populations, remember you’re not only treating the diseases they’re coming to you with, you’re also treating them for a lifetime of healthy [brain] aging.”

At the center of a healthy aging brain are the brain-residing microglia and peripheral monocytes, she said. These immune cell populations are directly influenced by blood-brain barrier breakdown, inflammation, and gut permeability — and indirectly influenced by microbial products, gastrointestinal (GI) function, and bacterial diversity, Merchak said at the meeting, which was convened by AGA and the European Society of Neurogastroenterology and Motility.

“Many of us grew up learning that the brain is an immune-privileged site, but we’ve been establishing that this is fundamentally not true,” she said. “While the brain does have a privileged status, there are interactions with the blood, with the peripheral immune cells.”

Merchak coauthored a 2024 review in Neurotherapeutics in which she and her colleagues explained that the brain is “heavily connected with peripheral immune dynamics,” and that the gut — as the largest immune organ in the body — is a critical place for peripheral immune development, “thus influencing brain health.”

Gut microbiota interact with the brain via several mechanisms including microbiota-derived metabolites that enter circulation, direct communication via the vagus nerve, and modulation of the immune system, Merchak and her coauthors wrote. Leaky gut, they noted, can lead to an accumulation of inflammatory signals and cells that can exacerbate or induce the onset of neurodegenerative conditions.

As researchers better understand the role that GI dysfunction plays in neurodegenerative disease — as they identify microbiome signatures for predicting risk, for instance — there will be “opportunities to target the microbiome to prevent or reverse dysbiosis as a way to delay, arrest or prevent the onset and progression of neurodegenerative diseases,” they wrote.

At the GMFH meeting, Merchak described both ongoing preclinical research that is dissecting gut-brain communication, and preliminary clinical evidence for the use of gut microbiota-modulating therapies in neurodegenerative disease.

 

Support for a Gut-Focused Approach

Research on bile acid metabolism in multiple sclerosis (MS) and on peripheral inflammation in dementia exemplify the ongoing preclinical research uncovering the mechanisms of gut-brain communication, Merchak said.

The finding that bile acid metabolism modulates MS autoimmunity comes from research done by Merchak and a team at the University of Virginia, Charlottesville, Virginia, several years ago in which mice with experimental autoimmune encephalomyelitis (EAE) — an animal model of MS — were engineered for T cell specific knockout of the aryl hydrocarbon receptor (AHR). The AHR has been directly tied to MS, and T lymphocytes are known to play a central role in MS pathophysiology.

Blocking the activity of AHR in CD4-positive T cells significantly affected the production of bile acids and other metabolites in the microbiome — and the outcome of central nervous system autoimmunity. “Mice with high levels of bile acids, both primary and secondary, actually recovered from this EAE” and regained motor function, Merchak said at the GMFH meeting.

The potential impact of genetic manipulation on recovery was ruled out — and the role of bile acids confirmed — when, using the EAE model, gut bacteria from mice without AHR were transplanted into mice with AHR. The mice with AHR were able to recover, confirming that AHR can reprogram the gut microbiome and that “high levels of bile acid can lead to reduced autoimmunity in an MS model,” she said.

Other elements and stages of the research, which was published in PLOS Biology in 2023, showed increased apoptosis of CD4-positive immune cells in AHR-deficient mice and the ability of oral taurocholic acid — a bile acid that was especially high in mice without AHR — to reduce the severity of EAE, Merchak said.

Evidence for the role of gut and peripheral inflammation on neurodegeneration is building on numerous fronts, Merchak said. Unpublished research using spatial transcriptomics of colon biopsies from patients with inflammatory bowel disease (IBD), patients with Parkinson’s disease (PD), and neurologically healthy control individuals, for instance, showed similar cell communication patterns in patients with IBD or PD (and no history of IBD) compared with healthy control individuals.

And in research using a single-cell genomics approach and a mouse model of lipopolysaccharide (LPS)-induced system neuroinflammation, microglia were found to preferentially communicate with peripheral myeloid cells rather than other microglia after peripheral LPS exposure.

“In saline-treated mice, the microglia are talking primarily to microglia, but in LPS-treated mice, microglia spend more time communicating with monocytes and T cells,” Merchak explained. “We see communication going from inside the brain to cells coming in from the periphery.”

In another experiment, 2 months of a high-fat, high-sugar diet in mice with an engineered predisposition to frontotemporal dementia led to significant upregulation of major histocompatibility complex class II (MHC II) expression on monocytes in the brain, she said, describing unpublished research. Because MHC II handles antigen presentation in the brain, the change signals increased central-peripheral immune crosstalk and increased brain inflammation.

 

State of Clinical Research

On the clinical side, Merchak said studies of gut microbiome-modulating therapies are currently not longitudinal enough to accurately study neurodegenerative diseases that may develop over decades. Still, her review of the literature — part of her 2024 article — suggests there is at least some preliminary clinical evidence for the use of probiotics/prebiotics/diet and fecal microbiota transplant (FMT) in several diseases.

• Parkinson’s Disease: “There has been some evidence,” Merchak said at the meeting, “for the treatment [with probiotics, prebiotics and diet] of nonmotor symptoms — things like gastrointestinal distress and mood changes — but no real evidence that such treatments can help with the motor symptoms we see in Parkinson’s.” Over 60 patients with PD have been treated with FMT, she said, with reduced GI distress and mixed results with motor symptoms.
• Alzheimer’s and related dementias: “Diet shows promise for cognitive outcomes, but there hasn’t been much evidence for probiotics,” she said. Her review found 17 patients diagnosed with dementia who were treated with FMT, “and for many of them, maintenance of cognitive function was reported — so no further decline — which is excellent.”
• Multiple Sclerosis: “We see higher quality-of-life measures in patients getting probiotics, prebiotics, and changes in diet,” Merchak said. “Again, most of this [relates to] mood and digestion, but some studies show a slowing of neurological damage as measured by MRI.” 

There are reports of 15 patients treated with FMT, and “three of these document full functional recovery,” she said, noting that longer follow-up is necessary as MS is characterized by relapsed and periods of recovery.

Merchak reported no financial disclosures.

A version of this article appeared on Medscape.com.

WASHINGTON, DC — Age-related neurodegenerative disorders — motor neuron diseases, demyelinating diseases, Alzheimer’s disease, and other proteinopathies — are at an “inflection point,” said researcher Andrea R. Merchak, PhD, with a fuller understanding of disease pathophysiology but an overall dearth of effective disease-modifying treatments.

And this, Merchak said at the Gut Microbiota for Health (GMFH) World Summit 2025, is where the gut microbiome comes in. “The gut-brain axis is important to take into consideration,” she urged, both for gut microbiome researchers — whose collaboration with neurologists and neuroscientists is essential — and for practicing gastroenterologists.

“We are the sum of our environmental exposures,” said Merchak, assistant research professor of neurology at the Indiana University School of Medicine, in Indianapolis. “So for your patient populations, remember you’re not only treating the diseases they’re coming to you with, you’re also treating them for a lifetime of healthy [brain] aging.”

At the center of a healthy aging brain are the brain-residing microglia and peripheral monocytes, she said. These immune cell populations are directly influenced by blood-brain barrier breakdown, inflammation, and gut permeability — and indirectly influenced by microbial products, gastrointestinal (GI) function, and bacterial diversity, Merchak said at the meeting, which was convened by AGA and the European Society of Neurogastroenterology and Motility.

“Many of us grew up learning that the brain is an immune-privileged site, but we’ve been establishing that this is fundamentally not true,” she said. “While the brain does have a privileged status, there are interactions with the blood, with the peripheral immune cells.”

Merchak coauthored a 2024 review in Neurotherapeutics in which she and her colleagues explained that the brain is “heavily connected with peripheral immune dynamics,” and that the gut — as the largest immune organ in the body — is a critical place for peripheral immune development, “thus influencing brain health.”

Gut microbiota interact with the brain via several mechanisms including microbiota-derived metabolites that enter circulation, direct communication via the vagus nerve, and modulation of the immune system, Merchak and her coauthors wrote. Leaky gut, they noted, can lead to an accumulation of inflammatory signals and cells that can exacerbate or induce the onset of neurodegenerative conditions.

As researchers better understand the role that GI dysfunction plays in neurodegenerative disease — as they identify microbiome signatures for predicting risk, for instance — there will be “opportunities to target the microbiome to prevent or reverse dysbiosis as a way to delay, arrest or prevent the onset and progression of neurodegenerative diseases,” they wrote.

At the GMFH meeting, Merchak described both ongoing preclinical research that is dissecting gut-brain communication, and preliminary clinical evidence for the use of gut microbiota-modulating therapies in neurodegenerative disease.

 

Support for a Gut-Focused Approach

Research on bile acid metabolism in multiple sclerosis (MS) and on peripheral inflammation in dementia exemplify the ongoing preclinical research uncovering the mechanisms of gut-brain communication, Merchak said.

The finding that bile acid metabolism modulates MS autoimmunity comes from research done by Merchak and a team at the University of Virginia, Charlottesville, Virginia, several years ago in which mice with experimental autoimmune encephalomyelitis (EAE) — an animal model of MS — were engineered for T cell specific knockout of the aryl hydrocarbon receptor (AHR). The AHR has been directly tied to MS, and T lymphocytes are known to play a central role in MS pathophysiology.

Blocking the activity of AHR in CD4-positive T cells significantly affected the production of bile acids and other metabolites in the microbiome — and the outcome of central nervous system autoimmunity. “Mice with high levels of bile acids, both primary and secondary, actually recovered from this EAE” and regained motor function, Merchak said at the GMFH meeting.

The potential impact of genetic manipulation on recovery was ruled out — and the role of bile acids confirmed — when, using the EAE model, gut bacteria from mice without AHR were transplanted into mice with AHR. The mice with AHR were able to recover, confirming that AHR can reprogram the gut microbiome and that “high levels of bile acid can lead to reduced autoimmunity in an MS model,” she said.

Other elements and stages of the research, which was published in PLOS Biology in 2023, showed increased apoptosis of CD4-positive immune cells in AHR-deficient mice and the ability of oral taurocholic acid — a bile acid that was especially high in mice without AHR — to reduce the severity of EAE, Merchak said.

Evidence for the role of gut and peripheral inflammation on neurodegeneration is building on numerous fronts, Merchak said. Unpublished research using spatial transcriptomics of colon biopsies from patients with inflammatory bowel disease (IBD), patients with Parkinson’s disease (PD), and neurologically healthy control individuals, for instance, showed similar cell communication patterns in patients with IBD or PD (and no history of IBD) compared with healthy control individuals.

And in research using a single-cell genomics approach and a mouse model of lipopolysaccharide (LPS)-induced system neuroinflammation, microglia were found to preferentially communicate with peripheral myeloid cells rather than other microglia after peripheral LPS exposure.

“In saline-treated mice, the microglia are talking primarily to microglia, but in LPS-treated mice, microglia spend more time communicating with monocytes and T cells,” Merchak explained. “We see communication going from inside the brain to cells coming in from the periphery.”

In another experiment, 2 months of a high-fat, high-sugar diet in mice with an engineered predisposition to frontotemporal dementia led to significant upregulation of major histocompatibility complex class II (MHC II) expression on monocytes in the brain, she said, describing unpublished research. Because MHC II handles antigen presentation in the brain, the change signals increased central-peripheral immune crosstalk and increased brain inflammation.

 

State of Clinical Research

On the clinical side, Merchak said studies of gut microbiome-modulating therapies are currently not longitudinal enough to accurately study neurodegenerative diseases that may develop over decades. Still, her review of the literature — part of her 2024 article — suggests there is at least some preliminary clinical evidence for the use of probiotics/prebiotics/diet and fecal microbiota transplant (FMT) in several diseases.

• Parkinson’s Disease: “There has been some evidence,” Merchak said at the meeting, “for the treatment [with probiotics, prebiotics and diet] of nonmotor symptoms — things like gastrointestinal distress and mood changes — but no real evidence that such treatments can help with the motor symptoms we see in Parkinson’s.” Over 60 patients with PD have been treated with FMT, she said, with reduced GI distress and mixed results with motor symptoms.
• Alzheimer’s and related dementias: “Diet shows promise for cognitive outcomes, but there hasn’t been much evidence for probiotics,” she said. Her review found 17 patients diagnosed with dementia who were treated with FMT, “and for many of them, maintenance of cognitive function was reported — so no further decline — which is excellent.”
• Multiple Sclerosis: “We see higher quality-of-life measures in patients getting probiotics, prebiotics, and changes in diet,” Merchak said. “Again, most of this [relates to] mood and digestion, but some studies show a slowing of neurological damage as measured by MRI.” 

There are reports of 15 patients treated with FMT, and “three of these document full functional recovery,” she said, noting that longer follow-up is necessary as MS is characterized by relapsed and periods of recovery.

Merchak reported no financial disclosures.

A version of this article appeared on Medscape.com.

WASHINGTON, DC — Age-related neurodegenerative disorders — motor neuron diseases, demyelinating diseases, Alzheimer’s disease, and other proteinopathies — are at an “inflection point,” said researcher Andrea R. Merchak, PhD, with a fuller understanding of disease pathophysiology but an overall dearth of effective disease-modifying treatments.

And this, Merchak said at the Gut Microbiota for Health (GMFH) World Summit 2025, is where the gut microbiome comes in. “The gut-brain axis is important to take into consideration,” she urged, both for gut microbiome researchers — whose collaboration with neurologists and neuroscientists is essential — and for practicing gastroenterologists.

“We are the sum of our environmental exposures,” said Merchak, assistant research professor of neurology at the Indiana University School of Medicine, in Indianapolis. “So for your patient populations, remember you’re not only treating the diseases they’re coming to you with, you’re also treating them for a lifetime of healthy [brain] aging.”

At the center of a healthy aging brain are the brain-residing microglia and peripheral monocytes, she said. These immune cell populations are directly influenced by blood-brain barrier breakdown, inflammation, and gut permeability — and indirectly influenced by microbial products, gastrointestinal (GI) function, and bacterial diversity, Merchak said at the meeting, which was convened by AGA and the European Society of Neurogastroenterology and Motility.

“Many of us grew up learning that the brain is an immune-privileged site, but we’ve been establishing that this is fundamentally not true,” she said. “While the brain does have a privileged status, there are interactions with the blood, with the peripheral immune cells.”

Merchak coauthored a 2024 review in Neurotherapeutics in which she and her colleagues explained that the brain is “heavily connected with peripheral immune dynamics,” and that the gut — as the largest immune organ in the body — is a critical place for peripheral immune development, “thus influencing brain health.”

Gut microbiota interact with the brain via several mechanisms including microbiota-derived metabolites that enter circulation, direct communication via the vagus nerve, and modulation of the immune system, Merchak and her coauthors wrote. Leaky gut, they noted, can lead to an accumulation of inflammatory signals and cells that can exacerbate or induce the onset of neurodegenerative conditions.

As researchers better understand the role that GI dysfunction plays in neurodegenerative disease — as they identify microbiome signatures for predicting risk, for instance — there will be “opportunities to target the microbiome to prevent or reverse dysbiosis as a way to delay, arrest or prevent the onset and progression of neurodegenerative diseases,” they wrote.

At the GMFH meeting, Merchak described both ongoing preclinical research that is dissecting gut-brain communication, and preliminary clinical evidence for the use of gut microbiota-modulating therapies in neurodegenerative disease.

 

Support for a Gut-Focused Approach

Research on bile acid metabolism in multiple sclerosis (MS) and on peripheral inflammation in dementia exemplify the ongoing preclinical research uncovering the mechanisms of gut-brain communication, Merchak said.

The finding that bile acid metabolism modulates MS autoimmunity comes from research done by Merchak and a team at the University of Virginia, Charlottesville, Virginia, several years ago in which mice with experimental autoimmune encephalomyelitis (EAE) — an animal model of MS — were engineered for T cell specific knockout of the aryl hydrocarbon receptor (AHR). The AHR has been directly tied to MS, and T lymphocytes are known to play a central role in MS pathophysiology.

Blocking the activity of AHR in CD4-positive T cells significantly affected the production of bile acids and other metabolites in the microbiome — and the outcome of central nervous system autoimmunity. “Mice with high levels of bile acids, both primary and secondary, actually recovered from this EAE” and regained motor function, Merchak said at the GMFH meeting.

The potential impact of genetic manipulation on recovery was ruled out — and the role of bile acids confirmed — when, using the EAE model, gut bacteria from mice without AHR were transplanted into mice with AHR. The mice with AHR were able to recover, confirming that AHR can reprogram the gut microbiome and that “high levels of bile acid can lead to reduced autoimmunity in an MS model,” she said.

Other elements and stages of the research, which was published in PLOS Biology in 2023, showed increased apoptosis of CD4-positive immune cells in AHR-deficient mice and the ability of oral taurocholic acid — a bile acid that was especially high in mice without AHR — to reduce the severity of EAE, Merchak said.

Evidence for the role of gut and peripheral inflammation on neurodegeneration is building on numerous fronts, Merchak said. Unpublished research using spatial transcriptomics of colon biopsies from patients with inflammatory bowel disease (IBD), patients with Parkinson’s disease (PD), and neurologically healthy control individuals, for instance, showed similar cell communication patterns in patients with IBD or PD (and no history of IBD) compared with healthy control individuals.

And in research using a single-cell genomics approach and a mouse model of lipopolysaccharide (LPS)-induced system neuroinflammation, microglia were found to preferentially communicate with peripheral myeloid cells rather than other microglia after peripheral LPS exposure.

“In saline-treated mice, the microglia are talking primarily to microglia, but in LPS-treated mice, microglia spend more time communicating with monocytes and T cells,” Merchak explained. “We see communication going from inside the brain to cells coming in from the periphery.”

In another experiment, 2 months of a high-fat, high-sugar diet in mice with an engineered predisposition to frontotemporal dementia led to significant upregulation of major histocompatibility complex class II (MHC II) expression on monocytes in the brain, she said, describing unpublished research. Because MHC II handles antigen presentation in the brain, the change signals increased central-peripheral immune crosstalk and increased brain inflammation.

 

State of Clinical Research

On the clinical side, Merchak said studies of gut microbiome-modulating therapies are currently not longitudinal enough to accurately study neurodegenerative diseases that may develop over decades. Still, her review of the literature — part of her 2024 article — suggests there is at least some preliminary clinical evidence for the use of probiotics/prebiotics/diet and fecal microbiota transplant (FMT) in several diseases.

• Parkinson’s Disease: “There has been some evidence,” Merchak said at the meeting, “for the treatment [with probiotics, prebiotics and diet] of nonmotor symptoms — things like gastrointestinal distress and mood changes — but no real evidence that such treatments can help with the motor symptoms we see in Parkinson’s.” Over 60 patients with PD have been treated with FMT, she said, with reduced GI distress and mixed results with motor symptoms.
• Alzheimer’s and related dementias: “Diet shows promise for cognitive outcomes, but there hasn’t been much evidence for probiotics,” she said. Her review found 17 patients diagnosed with dementia who were treated with FMT, “and for many of them, maintenance of cognitive function was reported — so no further decline — which is excellent.”
• Multiple Sclerosis: “We see higher quality-of-life measures in patients getting probiotics, prebiotics, and changes in diet,” Merchak said. “Again, most of this [relates to] mood and digestion, but some studies show a slowing of neurological damage as measured by MRI.” 

There are reports of 15 patients treated with FMT, and “three of these document full functional recovery,” she said, noting that longer follow-up is necessary as MS is characterized by relapsed and periods of recovery.

Merchak reported no financial disclosures.

A version of this article appeared on Medscape.com.

You have a will, so you can rest easy, right? Not necessarily. If your will is outdated, it can cause more harm than good.

Even though it can provide for some contingencies, an old will can’t cover every change that may have occurred since it was first drawn. Professionals advise that you review your will every few years and more often if situations such as the following five have occurred since you last updated your will. 

 

1. Family Changes

If you’ve had any changes in your family situation, you will probably need to update your will. Events such as marriage, divorce, death, birth, adoption, or a falling out with a loved one may affect how your estate will be distributed, who should act as guardian for your dependents, and who should be named as executor of your estate.

2. Relocating to a New State

The laws among the states vary. Moving to a new state or purchasing property in another state can affect your estate plan and how property in that state will be taxed and distributed.

3. Tax Law Changes

Federal and state legislatures are continually tinkering with federal estate and state inheritance tax laws. An old will may fail to take advantage of strategies that will minimize estate taxes.

4. You Want to Support a Favorite Cause

If you have developed a connection to a cause, you may want to benefit a particular charity with a gift in your estate. Contact us for sample language you can share with your attorney to include a gift to us in your will.

5. Changes in Your Estate’s Value

When you made your will, your assets may have been relatively modest. Now the value may be larger and your will no longer reflects how you would like your estate divided.

Consider including a gift to the AGA Research Foundation in your will. You will help spark future discoveries in GI. Visit our website at https://gastro.planmylegacy.org or contact us at [email protected].

You have a will, so you can rest easy, right? Not necessarily. If your will is outdated, it can cause more harm than good.

Even though it can provide for some contingencies, an old will can’t cover every change that may have occurred since it was first drawn. Professionals advise that you review your will every few years and more often if situations such as the following five have occurred since you last updated your will. 

 

1. Family Changes

If you’ve had any changes in your family situation, you will probably need to update your will. Events such as marriage, divorce, death, birth, adoption, or a falling out with a loved one may affect how your estate will be distributed, who should act as guardian for your dependents, and who should be named as executor of your estate.

2. Relocating to a New State

The laws among the states vary. Moving to a new state or purchasing property in another state can affect your estate plan and how property in that state will be taxed and distributed.

3. Tax Law Changes

Federal and state legislatures are continually tinkering with federal estate and state inheritance tax laws. An old will may fail to take advantage of strategies that will minimize estate taxes.

4. You Want to Support a Favorite Cause

If you have developed a connection to a cause, you may want to benefit a particular charity with a gift in your estate. Contact us for sample language you can share with your attorney to include a gift to us in your will.

5. Changes in Your Estate’s Value

When you made your will, your assets may have been relatively modest. Now the value may be larger and your will no longer reflects how you would like your estate divided.

Consider including a gift to the AGA Research Foundation in your will. You will help spark future discoveries in GI. Visit our website at https://gastro.planmylegacy.org or contact us at [email protected].

You have a will, so you can rest easy, right? Not necessarily. If your will is outdated, it can cause more harm than good.

Even though it can provide for some contingencies, an old will can’t cover every change that may have occurred since it was first drawn. Professionals advise that you review your will every few years and more often if situations such as the following five have occurred since you last updated your will. 

 

1. Family Changes

If you’ve had any changes in your family situation, you will probably need to update your will. Events such as marriage, divorce, death, birth, adoption, or a falling out with a loved one may affect how your estate will be distributed, who should act as guardian for your dependents, and who should be named as executor of your estate.

2. Relocating to a New State

The laws among the states vary. Moving to a new state or purchasing property in another state can affect your estate plan and how property in that state will be taxed and distributed.

3. Tax Law Changes

Federal and state legislatures are continually tinkering with federal estate and state inheritance tax laws. An old will may fail to take advantage of strategies that will minimize estate taxes.

4. You Want to Support a Favorite Cause

If you have developed a connection to a cause, you may want to benefit a particular charity with a gift in your estate. Contact us for sample language you can share with your attorney to include a gift to us in your will.

5. Changes in Your Estate’s Value

When you made your will, your assets may have been relatively modest. Now the value may be larger and your will no longer reflects how you would like your estate divided.

Consider including a gift to the AGA Research Foundation in your will. You will help spark future discoveries in GI. Visit our website at https://gastro.planmylegacy.org or contact us at [email protected].

Researchers have developed and internally validated a simple score using clinical factors that can help estimate the likelihood of advanced colorectal neoplasia in adults younger than age 45 years.

While colorectal cancer (CRC) incidence has declined overall due to screening, early-onset CRC is on the rise, particularly in individuals younger than 45 years — an age group not currently recommended for CRC screening.

Studies have shown that the risk for early-onset advanced neoplasia varies based on several factors, including sex, race, family history of CRC, smoking, alcohol consumption, diabetes, hyperlipidemia, obesity, and diet.

A score that incorporates some of these factors to identify which younger adults are at higher risk for advanced neoplasia, a precursor to CRC, could support earlier, more targeted screening interventions.

The simple clinical score can be easily calculated by primary care providers in the office, Carole Macaron, MD, lead author of the study and a gastroenterologist at Cleveland Clinic, told GI & Hepatology News. “Patients with a high-risk score would be referred for colorectal cancer screening.”

The study was published in Digestive Diseases and Sciences.

To develop and validate their risk score, Macaron and colleagues did a retrospective cross-sectional analysis of 9446 individuals aged 18-44 years (mean age, 36.8 years; 61% women) who underwent colonoscopy at their center.

Advanced neoplasia was defined as a tubular adenoma ≥ 10 mm or any adenoma with villous features or high-grade dysplasia, sessile serrated polyp ≥ 10 mm, sessile serrated polyp with dysplasia, traditional serrated adenoma, or invasive adenocarcinoma.

The 346 (3.7%) individuals found to have advanced neoplasia served as the case group, and the remainder with normal colonoscopy or non-advanced neoplasia served as controls.

A multivariate logistic regression model identified three independent risk factors significantly associated with advanced neoplasia: Higher body mass index (BMI; P = .0157), former and current tobacco use (P = .0009 and P = .0015, respectively), and having a first-degree relative with CRC < 60 years (P < .0001) or other family history of CRC (P = .0117).

The researchers used these risk factors to develop a risk prediction score to estimate the likelihood of detecting advanced neoplasia, which ranged from a risk of 1.8% for patients with a score of 1 to 22.2% for those with a score of 12. Individuals with a score of ≥ 9 had a 14% or higher risk for advanced neoplasia.

Based on the risk model, the likelihood of detecting advanced neoplasia in an asymptomatic 32-year-old overweight individual, with a history of previous tobacco use and a first-degree relative younger than age 60 with CRC would be 20.3%, Macaron and colleagues noted.

The model demonstrated “moderate” discriminatory power in the validation set (C-statistic: 0.645), indicating that it can effectively differentiate between individuals at a higher and lower risk for advanced neoplasia.

Additionally, the authors are exploring ways to improve the discriminatory power of the score, possibly by including additional risk factors.

Given the score is calculated using easily obtainable risk factors for individuals younger than 45 who are at risk for early-onset colorectal neoplasia, it could help guide individualized screening decisions for those in whom screening is not currently offered, Macaron said. It could also serve as a tool for risk communication and shared decision-making.

Integration into electronic health records or online calculators may enhance its accessibility and clinical utility.

The authors noted that this retrospective study was conducted at a single center caring mainly for White non-Hispanic adults, limiting generalizability to the general population and to other races and ethnicities.

 

Validation in Real-World Setting Needed

“There are no currently accepted advanced colorectal neoplasia risk scores that are used in general practice,” said Steven H. Itzkowitz, MD, AGAF, professor of medicine, oncological sciences, and medical education, Icahn School of Medicine at Mount Sinai in New York City. “If these lesions can be predicted, it would enable these young individuals to undergo screening colonoscopy, which could detect and remove these lesions, thereby preventing CRC.”

Many of the known risk factors (family history, high BMI, or smoking) for CRC development at any age are incorporated within this tool, so it should be feasible to collect these data,” said Itzkowitz, who was not involved with the study.

But he cautioned that accurate and adequate family histories are not always performed. Clinicians also may not have considered combining these factors into an actionable risk score.

“If this score can be externally validated in a real-world setting, it could be a useful addition in our efforts to lower CRC rates among young individuals,” Itzkowitz said.

The study did not receive any funding. Macaron and Itzkowitz reported no competing interests.

A version of this article first appeared on Medscape.com.

Researchers have developed and internally validated a simple score using clinical factors that can help estimate the likelihood of advanced colorectal neoplasia in adults younger than age 45 years.

While colorectal cancer (CRC) incidence has declined overall due to screening, early-onset CRC is on the rise, particularly in individuals younger than 45 years — an age group not currently recommended for CRC screening.

Studies have shown that the risk for early-onset advanced neoplasia varies based on several factors, including sex, race, family history of CRC, smoking, alcohol consumption, diabetes, hyperlipidemia, obesity, and diet.

A score that incorporates some of these factors to identify which younger adults are at higher risk for advanced neoplasia, a precursor to CRC, could support earlier, more targeted screening interventions.

The simple clinical score can be easily calculated by primary care providers in the office, Carole Macaron, MD, lead author of the study and a gastroenterologist at Cleveland Clinic, told GI & Hepatology News. “Patients with a high-risk score would be referred for colorectal cancer screening.”

The study was published in Digestive Diseases and Sciences.

To develop and validate their risk score, Macaron and colleagues did a retrospective cross-sectional analysis of 9446 individuals aged 18-44 years (mean age, 36.8 years; 61% women) who underwent colonoscopy at their center.

Advanced neoplasia was defined as a tubular adenoma ≥ 10 mm or any adenoma with villous features or high-grade dysplasia, sessile serrated polyp ≥ 10 mm, sessile serrated polyp with dysplasia, traditional serrated adenoma, or invasive adenocarcinoma.

The 346 (3.7%) individuals found to have advanced neoplasia served as the case group, and the remainder with normal colonoscopy or non-advanced neoplasia served as controls.

A multivariate logistic regression model identified three independent risk factors significantly associated with advanced neoplasia: Higher body mass index (BMI; P = .0157), former and current tobacco use (P = .0009 and P = .0015, respectively), and having a first-degree relative with CRC < 60 years (P < .0001) or other family history of CRC (P = .0117).

The researchers used these risk factors to develop a risk prediction score to estimate the likelihood of detecting advanced neoplasia, which ranged from a risk of 1.8% for patients with a score of 1 to 22.2% for those with a score of 12. Individuals with a score of ≥ 9 had a 14% or higher risk for advanced neoplasia.

Based on the risk model, the likelihood of detecting advanced neoplasia in an asymptomatic 32-year-old overweight individual, with a history of previous tobacco use and a first-degree relative younger than age 60 with CRC would be 20.3%, Macaron and colleagues noted.

The model demonstrated “moderate” discriminatory power in the validation set (C-statistic: 0.645), indicating that it can effectively differentiate between individuals at a higher and lower risk for advanced neoplasia.

Additionally, the authors are exploring ways to improve the discriminatory power of the score, possibly by including additional risk factors.

Given the score is calculated using easily obtainable risk factors for individuals younger than 45 who are at risk for early-onset colorectal neoplasia, it could help guide individualized screening decisions for those in whom screening is not currently offered, Macaron said. It could also serve as a tool for risk communication and shared decision-making.

Integration into electronic health records or online calculators may enhance its accessibility and clinical utility.

The authors noted that this retrospective study was conducted at a single center caring mainly for White non-Hispanic adults, limiting generalizability to the general population and to other races and ethnicities.

 

Validation in Real-World Setting Needed

“There are no currently accepted advanced colorectal neoplasia risk scores that are used in general practice,” said Steven H. Itzkowitz, MD, AGAF, professor of medicine, oncological sciences, and medical education, Icahn School of Medicine at Mount Sinai in New York City. “If these lesions can be predicted, it would enable these young individuals to undergo screening colonoscopy, which could detect and remove these lesions, thereby preventing CRC.”

Many of the known risk factors (family history, high BMI, or smoking) for CRC development at any age are incorporated within this tool, so it should be feasible to collect these data,” said Itzkowitz, who was not involved with the study.

But he cautioned that accurate and adequate family histories are not always performed. Clinicians also may not have considered combining these factors into an actionable risk score.

“If this score can be externally validated in a real-world setting, it could be a useful addition in our efforts to lower CRC rates among young individuals,” Itzkowitz said.

The study did not receive any funding. Macaron and Itzkowitz reported no competing interests.

A version of this article first appeared on Medscape.com.

Researchers have developed and internally validated a simple score using clinical factors that can help estimate the likelihood of advanced colorectal neoplasia in adults younger than age 45 years.

While colorectal cancer (CRC) incidence has declined overall due to screening, early-onset CRC is on the rise, particularly in individuals younger than 45 years — an age group not currently recommended for CRC screening.

Studies have shown that the risk for early-onset advanced neoplasia varies based on several factors, including sex, race, family history of CRC, smoking, alcohol consumption, diabetes, hyperlipidemia, obesity, and diet.

A score that incorporates some of these factors to identify which younger adults are at higher risk for advanced neoplasia, a precursor to CRC, could support earlier, more targeted screening interventions.

The simple clinical score can be easily calculated by primary care providers in the office, Carole Macaron, MD, lead author of the study and a gastroenterologist at Cleveland Clinic, told GI & Hepatology News. “Patients with a high-risk score would be referred for colorectal cancer screening.”

The study was published in Digestive Diseases and Sciences.

To develop and validate their risk score, Macaron and colleagues did a retrospective cross-sectional analysis of 9446 individuals aged 18-44 years (mean age, 36.8 years; 61% women) who underwent colonoscopy at their center.

Advanced neoplasia was defined as a tubular adenoma ≥ 10 mm or any adenoma with villous features or high-grade dysplasia, sessile serrated polyp ≥ 10 mm, sessile serrated polyp with dysplasia, traditional serrated adenoma, or invasive adenocarcinoma.

The 346 (3.7%) individuals found to have advanced neoplasia served as the case group, and the remainder with normal colonoscopy or non-advanced neoplasia served as controls.

A multivariate logistic regression model identified three independent risk factors significantly associated with advanced neoplasia: Higher body mass index (BMI; P = .0157), former and current tobacco use (P = .0009 and P = .0015, respectively), and having a first-degree relative with CRC < 60 years (P < .0001) or other family history of CRC (P = .0117).

The researchers used these risk factors to develop a risk prediction score to estimate the likelihood of detecting advanced neoplasia, which ranged from a risk of 1.8% for patients with a score of 1 to 22.2% for those with a score of 12. Individuals with a score of ≥ 9 had a 14% or higher risk for advanced neoplasia.

Based on the risk model, the likelihood of detecting advanced neoplasia in an asymptomatic 32-year-old overweight individual, with a history of previous tobacco use and a first-degree relative younger than age 60 with CRC would be 20.3%, Macaron and colleagues noted.

The model demonstrated “moderate” discriminatory power in the validation set (C-statistic: 0.645), indicating that it can effectively differentiate between individuals at a higher and lower risk for advanced neoplasia.

Additionally, the authors are exploring ways to improve the discriminatory power of the score, possibly by including additional risk factors.

Given the score is calculated using easily obtainable risk factors for individuals younger than 45 who are at risk for early-onset colorectal neoplasia, it could help guide individualized screening decisions for those in whom screening is not currently offered, Macaron said. It could also serve as a tool for risk communication and shared decision-making.

Integration into electronic health records or online calculators may enhance its accessibility and clinical utility.

The authors noted that this retrospective study was conducted at a single center caring mainly for White non-Hispanic adults, limiting generalizability to the general population and to other races and ethnicities.

 

Validation in Real-World Setting Needed

“There are no currently accepted advanced colorectal neoplasia risk scores that are used in general practice,” said Steven H. Itzkowitz, MD, AGAF, professor of medicine, oncological sciences, and medical education, Icahn School of Medicine at Mount Sinai in New York City. “If these lesions can be predicted, it would enable these young individuals to undergo screening colonoscopy, which could detect and remove these lesions, thereby preventing CRC.”

Many of the known risk factors (family history, high BMI, or smoking) for CRC development at any age are incorporated within this tool, so it should be feasible to collect these data,” said Itzkowitz, who was not involved with the study.

But he cautioned that accurate and adequate family histories are not always performed. Clinicians also may not have considered combining these factors into an actionable risk score.

“If this score can be externally validated in a real-world setting, it could be a useful addition in our efforts to lower CRC rates among young individuals,” Itzkowitz said.

The study did not receive any funding. Macaron and Itzkowitz reported no competing interests.

A version of this article first appeared on Medscape.com.

The United States Food and Drug Administration (FDA) approved guselkumab (Tremfya, Johnson & Johnson) for the treatment of adults with moderately to severely active Crohn’s disease (CD).

The approval marks the fourth indication for guselkumab, which was approved for moderate to severe plaque psoriasis in 2017, active psoriatic arthritis in 2020, and moderately to severely active ulcerative colitis in 2024. 

Guselkumab is the first and only interleukin-23 (IL-23) inhibitor that offers both subcutaneous (SC) and intravenous (IV) induction options for CD, the company said in a news release. 

“Despite the progress in the management of Crohn’s disease, many patients experience debilitating symptoms and are in need of new treatment options,” Remo Panaccione, MD, director of the Inflammatory Bowel Disease Unit at the University of Calgary, Calgary, Alberta, Canada, said in the release. 

“The approval of Tremfya offers an IL-23 inhibitor that has shown robust rates of endoscopic remission with both subcutaneous and intravenous induction regimens. Importantly, the fully subcutaneous regimen offers choice and flexibility for patients and providers not available before,” said Panaccione.

The FDA nod in CD was based on positive results from three phase 3 trials evaluating guselkumab in more than 1300 patients with moderately to severely active CD who failed or were intolerant to corticosteroids, immunomodulators, or biologics. 

The GRAVITI trial showed that guselkumab as SC induction and maintenance therapy was superior to placebo in clinical remission as well as endoscopic response and remission and deep remission. 

Results from GALAXI 2 and GALAXI 3 showed that guselkumab was superior to ustekinumab (Stelara) on all pooled endoscopic endpoints. 

Guselkumab is the only IL-23 inhibitor to demonstrate “clinical remission and endoscopic response, both at 1 year, with a fully subcutaneous induction regimen,” the company said. 

The recommended SC induction dose of guselkumab is 400 mg (given as two consecutive injections of 200 mg each, dispensed in one induction pack) at weeks 0, 4 and 8. The drug is also available in a 200 mg prefilled syringe. For the IV induction option, 200 mg IV infusions are administered at weeks 0, 4, and 8.

The recommended maintenance dosage is 100 mg administered by SC injection at week 16, and every 8 weeks thereafter, or 200 mg administered by SC injection at week 12, and every 4 weeks thereafter. 

Use of the lowest effective recommended dosage to maintain therapeutic response is recommended. 

Full prescribing information and medication guide are available online.

A version of this article first appeared on Medscape.com.

The United States Food and Drug Administration (FDA) approved guselkumab (Tremfya, Johnson & Johnson) for the treatment of adults with moderately to severely active Crohn’s disease (CD).

The approval marks the fourth indication for guselkumab, which was approved for moderate to severe plaque psoriasis in 2017, active psoriatic arthritis in 2020, and moderately to severely active ulcerative colitis in 2024. 

Guselkumab is the first and only interleukin-23 (IL-23) inhibitor that offers both subcutaneous (SC) and intravenous (IV) induction options for CD, the company said in a news release. 

“Despite the progress in the management of Crohn’s disease, many patients experience debilitating symptoms and are in need of new treatment options,” Remo Panaccione, MD, director of the Inflammatory Bowel Disease Unit at the University of Calgary, Calgary, Alberta, Canada, said in the release. 

“The approval of Tremfya offers an IL-23 inhibitor that has shown robust rates of endoscopic remission with both subcutaneous and intravenous induction regimens. Importantly, the fully subcutaneous regimen offers choice and flexibility for patients and providers not available before,” said Panaccione.

The FDA nod in CD was based on positive results from three phase 3 trials evaluating guselkumab in more than 1300 patients with moderately to severely active CD who failed or were intolerant to corticosteroids, immunomodulators, or biologics. 

The GRAVITI trial showed that guselkumab as SC induction and maintenance therapy was superior to placebo in clinical remission as well as endoscopic response and remission and deep remission. 

Results from GALAXI 2 and GALAXI 3 showed that guselkumab was superior to ustekinumab (Stelara) on all pooled endoscopic endpoints. 

Guselkumab is the only IL-23 inhibitor to demonstrate “clinical remission and endoscopic response, both at 1 year, with a fully subcutaneous induction regimen,” the company said. 

The recommended SC induction dose of guselkumab is 400 mg (given as two consecutive injections of 200 mg each, dispensed in one induction pack) at weeks 0, 4 and 8. The drug is also available in a 200 mg prefilled syringe. For the IV induction option, 200 mg IV infusions are administered at weeks 0, 4, and 8.

The recommended maintenance dosage is 100 mg administered by SC injection at week 16, and every 8 weeks thereafter, or 200 mg administered by SC injection at week 12, and every 4 weeks thereafter. 

Use of the lowest effective recommended dosage to maintain therapeutic response is recommended. 

Full prescribing information and medication guide are available online.

A version of this article first appeared on Medscape.com.

The United States Food and Drug Administration (FDA) approved guselkumab (Tremfya, Johnson & Johnson) for the treatment of adults with moderately to severely active Crohn’s disease (CD).

The approval marks the fourth indication for guselkumab, which was approved for moderate to severe plaque psoriasis in 2017, active psoriatic arthritis in 2020, and moderately to severely active ulcerative colitis in 2024. 

Guselkumab is the first and only interleukin-23 (IL-23) inhibitor that offers both subcutaneous (SC) and intravenous (IV) induction options for CD, the company said in a news release. 

“Despite the progress in the management of Crohn’s disease, many patients experience debilitating symptoms and are in need of new treatment options,” Remo Panaccione, MD, director of the Inflammatory Bowel Disease Unit at the University of Calgary, Calgary, Alberta, Canada, said in the release. 

“The approval of Tremfya offers an IL-23 inhibitor that has shown robust rates of endoscopic remission with both subcutaneous and intravenous induction regimens. Importantly, the fully subcutaneous regimen offers choice and flexibility for patients and providers not available before,” said Panaccione.

The FDA nod in CD was based on positive results from three phase 3 trials evaluating guselkumab in more than 1300 patients with moderately to severely active CD who failed or were intolerant to corticosteroids, immunomodulators, or biologics. 

The GRAVITI trial showed that guselkumab as SC induction and maintenance therapy was superior to placebo in clinical remission as well as endoscopic response and remission and deep remission. 

Results from GALAXI 2 and GALAXI 3 showed that guselkumab was superior to ustekinumab (Stelara) on all pooled endoscopic endpoints. 

Guselkumab is the only IL-23 inhibitor to demonstrate “clinical remission and endoscopic response, both at 1 year, with a fully subcutaneous induction regimen,” the company said. 

The recommended SC induction dose of guselkumab is 400 mg (given as two consecutive injections of 200 mg each, dispensed in one induction pack) at weeks 0, 4 and 8. The drug is also available in a 200 mg prefilled syringe. For the IV induction option, 200 mg IV infusions are administered at weeks 0, 4, and 8.

The recommended maintenance dosage is 100 mg administered by SC injection at week 16, and every 8 weeks thereafter, or 200 mg administered by SC injection at week 12, and every 4 weeks thereafter. 

Use of the lowest effective recommended dosage to maintain therapeutic response is recommended. 

Full prescribing information and medication guide are available online.

A version of this article first appeared on Medscape.com.

In patients with gastroesophageal reflux (GERD) symptoms undergoing screening upper endoscopy, adjunctive use of wide-area transepithelial sampling with 3D computer-assisted analysis (WATS-3D) increases detection of Barrett’s esophagus (BE) and dysplasia, new research showed. 

Compared with forceps biopsies (FB) alone, the addition of WATS-3D led to confirmation of BE in an additional one fifth of patients, roughly doubled dysplasia diagnoses, and influenced clinical management in the majority of patients. 

“The big take-home point here is that the use of WATS-3D brushing along with conventional biopsies increases the likelihood that intestinal metaplasia will be identified,” first author Nicholas Shaheen, MD, MPH, AGAF, with the Center for Esophageal Diseases and Swallowing, University of North Carolina School of Medicine at Chapel Hill, North Carolina, told GI & Hepatology News. 

“Almost 20% of patients who harbor BE were only identified by WATS-3D and might have otherwise gone undiagnosed had only forceps biopsies been performed,” Shaheen said. 

The study was published in The American Journal of Gastroenterology.

 

Beyond Traditional Biopsies

BE develops as a complication of chronic GERD and is the chief precursor to esophageal adenocarcinoma. Early detection of BE and dysplasia is crucial to enable timely intervention. 

The current gold standard for BE screening involves upper endoscopy with FB following the Seattle protocol, which consists of four-quadrant biopsies from every 1-2 cm of areas of columnar-lined epithelium (CLE) to confirm the presence of intestinal metaplasia. However, this protocol is prone to sampling errors and high false-negative rates, leading to repeat endoscopy, the study team pointed out. 

WATS-3D (CDx Diagnostics) is a complementary technique designed to improve diagnostic yield by using brush biopsy to sample more tissue than routine biopsies.

WATS-3D has been shown to increase detection of dysplasia in patients with BE undergoing surveillance for BE, but less is known about the value of WATS-3D for BE screening in a community-based cohort of patients with GERD. 

To investigate, Shaheen and colleagues studied 23,933 consecutive patients enrolled in a prospective observational registry assessing the utility of WATS-3D in the screening of symptomatic GERD patients for BE. 

Patients had both WATS-3D and FB in the same endoscopic session. No patient had a history of BE, intestinal metaplasia or dysplasia in esophageal mucosa, or esophageal surgery, endoscopic ablation or endoscopic mucosal resection prior to enrollment. 

Overall, 6829 patients (29%) met endoscopic criteria for BE (≥ 1 cm esophageal CLE with accompanying biopsies showing intestinal metaplasia). 

Of these, 2878 (42%) had intestinal metaplasia identified by either FB or WATS-3D, but 19.3% had their BE diagnosis confirmed solely on the basis of WATS-3D findings. 

Among patients who fulfilled the endoscopic criteria for BE, the adjunctive yield of WATS-3D was 76.5% and the absolute yield was 18.1%.

Of the 240 (1.0%) patients with dysplasia, 107 (45%) were found solely by WATS-3D.

 

‘Clinically Valuable Adjunct’

Among patients with positive WATS-3D but negative FB results, clinical management changed in 90.7% of cases, mostly involving initiation or modification of surveillance and proton pump inhibitor therapy. 

These results suggest that WATS-3D is a “clinically valuable adjunct” to FB for the diagnosis of BE when used as a screening tool in symptomatic GERD patients and particularly in patients with endoscopic evidence of > 1 cm esophageal columnar-lined epithelium, the study team wrote. 

Adjunctive use of WATS-3D when BE is suspected “may save endoscopies and lead to quicker, more accurate diagnoses,” they added. 

The investigators said a limitation of the study is the lack of central pathology review, potentially leading to diagnostic variability. They also noted that over half of the detected dysplasia cases were crypt dysplasia or indefinite for dysplasia, raising concerns about clinical significance. 

Reached for comment, Philip O. Katz, MD, AGAF, professor of medicine and director of the GI Function Laboratories, Weill Cornell Medicine in New York, said he’s been using WATS for more than a decade as an adjunct to standard biopsy in patients undergoing screening and surveillance for BE and finds it clinically helpful in managing his patients.

This new study provides “further information that WATS added to biopsy that has been traditionally done with the Seattle protocol increases the yield of intestinal metaplasia and likely dysplasia in patients being screened for Barrett’s,” Katz, who wasn’t involved in the study, told GI & Hepatology News.

Funding for the study was provided by CDx Diagnostics. Shaheen and several coauthors disclosed relationships with the company. Katz disclosed relationships (consultant/advisor) for Phathom Pharmaceuticals and Sebella.

A version of this article appeared on Medscape.com.

In patients with gastroesophageal reflux (GERD) symptoms undergoing screening upper endoscopy, adjunctive use of wide-area transepithelial sampling with 3D computer-assisted analysis (WATS-3D) increases detection of Barrett’s esophagus (BE) and dysplasia, new research showed. 

Compared with forceps biopsies (FB) alone, the addition of WATS-3D led to confirmation of BE in an additional one fifth of patients, roughly doubled dysplasia diagnoses, and influenced clinical management in the majority of patients. 

“The big take-home point here is that the use of WATS-3D brushing along with conventional biopsies increases the likelihood that intestinal metaplasia will be identified,” first author Nicholas Shaheen, MD, MPH, AGAF, with the Center for Esophageal Diseases and Swallowing, University of North Carolina School of Medicine at Chapel Hill, North Carolina, told GI & Hepatology News. 

“Almost 20% of patients who harbor BE were only identified by WATS-3D and might have otherwise gone undiagnosed had only forceps biopsies been performed,” Shaheen said. 

The study was published in The American Journal of Gastroenterology.

 

Beyond Traditional Biopsies

BE develops as a complication of chronic GERD and is the chief precursor to esophageal adenocarcinoma. Early detection of BE and dysplasia is crucial to enable timely intervention. 

The current gold standard for BE screening involves upper endoscopy with FB following the Seattle protocol, which consists of four-quadrant biopsies from every 1-2 cm of areas of columnar-lined epithelium (CLE) to confirm the presence of intestinal metaplasia. However, this protocol is prone to sampling errors and high false-negative rates, leading to repeat endoscopy, the study team pointed out. 

WATS-3D (CDx Diagnostics) is a complementary technique designed to improve diagnostic yield by using brush biopsy to sample more tissue than routine biopsies.

WATS-3D has been shown to increase detection of dysplasia in patients with BE undergoing surveillance for BE, but less is known about the value of WATS-3D for BE screening in a community-based cohort of patients with GERD. 

To investigate, Shaheen and colleagues studied 23,933 consecutive patients enrolled in a prospective observational registry assessing the utility of WATS-3D in the screening of symptomatic GERD patients for BE. 

Patients had both WATS-3D and FB in the same endoscopic session. No patient had a history of BE, intestinal metaplasia or dysplasia in esophageal mucosa, or esophageal surgery, endoscopic ablation or endoscopic mucosal resection prior to enrollment. 

Overall, 6829 patients (29%) met endoscopic criteria for BE (≥ 1 cm esophageal CLE with accompanying biopsies showing intestinal metaplasia). 

Of these, 2878 (42%) had intestinal metaplasia identified by either FB or WATS-3D, but 19.3% had their BE diagnosis confirmed solely on the basis of WATS-3D findings. 

Among patients who fulfilled the endoscopic criteria for BE, the adjunctive yield of WATS-3D was 76.5% and the absolute yield was 18.1%.

Of the 240 (1.0%) patients with dysplasia, 107 (45%) were found solely by WATS-3D.

 

‘Clinically Valuable Adjunct’

Among patients with positive WATS-3D but negative FB results, clinical management changed in 90.7% of cases, mostly involving initiation or modification of surveillance and proton pump inhibitor therapy. 

These results suggest that WATS-3D is a “clinically valuable adjunct” to FB for the diagnosis of BE when used as a screening tool in symptomatic GERD patients and particularly in patients with endoscopic evidence of > 1 cm esophageal columnar-lined epithelium, the study team wrote. 

Adjunctive use of WATS-3D when BE is suspected “may save endoscopies and lead to quicker, more accurate diagnoses,” they added. 

The investigators said a limitation of the study is the lack of central pathology review, potentially leading to diagnostic variability. They also noted that over half of the detected dysplasia cases were crypt dysplasia or indefinite for dysplasia, raising concerns about clinical significance. 

Reached for comment, Philip O. Katz, MD, AGAF, professor of medicine and director of the GI Function Laboratories, Weill Cornell Medicine in New York, said he’s been using WATS for more than a decade as an adjunct to standard biopsy in patients undergoing screening and surveillance for BE and finds it clinically helpful in managing his patients.

This new study provides “further information that WATS added to biopsy that has been traditionally done with the Seattle protocol increases the yield of intestinal metaplasia and likely dysplasia in patients being screened for Barrett’s,” Katz, who wasn’t involved in the study, told GI & Hepatology News.

Funding for the study was provided by CDx Diagnostics. Shaheen and several coauthors disclosed relationships with the company. Katz disclosed relationships (consultant/advisor) for Phathom Pharmaceuticals and Sebella.

A version of this article appeared on Medscape.com.

In patients with gastroesophageal reflux (GERD) symptoms undergoing screening upper endoscopy, adjunctive use of wide-area transepithelial sampling with 3D computer-assisted analysis (WATS-3D) increases detection of Barrett’s esophagus (BE) and dysplasia, new research showed. 

Compared with forceps biopsies (FB) alone, the addition of WATS-3D led to confirmation of BE in an additional one fifth of patients, roughly doubled dysplasia diagnoses, and influenced clinical management in the majority of patients. 

“The big take-home point here is that the use of WATS-3D brushing along with conventional biopsies increases the likelihood that intestinal metaplasia will be identified,” first author Nicholas Shaheen, MD, MPH, AGAF, with the Center for Esophageal Diseases and Swallowing, University of North Carolina School of Medicine at Chapel Hill, North Carolina, told GI & Hepatology News. 

“Almost 20% of patients who harbor BE were only identified by WATS-3D and might have otherwise gone undiagnosed had only forceps biopsies been performed,” Shaheen said. 

The study was published in The American Journal of Gastroenterology.

 

Beyond Traditional Biopsies

BE develops as a complication of chronic GERD and is the chief precursor to esophageal adenocarcinoma. Early detection of BE and dysplasia is crucial to enable timely intervention. 

The current gold standard for BE screening involves upper endoscopy with FB following the Seattle protocol, which consists of four-quadrant biopsies from every 1-2 cm of areas of columnar-lined epithelium (CLE) to confirm the presence of intestinal metaplasia. However, this protocol is prone to sampling errors and high false-negative rates, leading to repeat endoscopy, the study team pointed out. 

WATS-3D (CDx Diagnostics) is a complementary technique designed to improve diagnostic yield by using brush biopsy to sample more tissue than routine biopsies.

WATS-3D has been shown to increase detection of dysplasia in patients with BE undergoing surveillance for BE, but less is known about the value of WATS-3D for BE screening in a community-based cohort of patients with GERD. 

To investigate, Shaheen and colleagues studied 23,933 consecutive patients enrolled in a prospective observational registry assessing the utility of WATS-3D in the screening of symptomatic GERD patients for BE. 

Patients had both WATS-3D and FB in the same endoscopic session. No patient had a history of BE, intestinal metaplasia or dysplasia in esophageal mucosa, or esophageal surgery, endoscopic ablation or endoscopic mucosal resection prior to enrollment. 

Overall, 6829 patients (29%) met endoscopic criteria for BE (≥ 1 cm esophageal CLE with accompanying biopsies showing intestinal metaplasia). 

Of these, 2878 (42%) had intestinal metaplasia identified by either FB or WATS-3D, but 19.3% had their BE diagnosis confirmed solely on the basis of WATS-3D findings. 

Among patients who fulfilled the endoscopic criteria for BE, the adjunctive yield of WATS-3D was 76.5% and the absolute yield was 18.1%.

Of the 240 (1.0%) patients with dysplasia, 107 (45%) were found solely by WATS-3D.

 

‘Clinically Valuable Adjunct’

Among patients with positive WATS-3D but negative FB results, clinical management changed in 90.7% of cases, mostly involving initiation or modification of surveillance and proton pump inhibitor therapy. 

These results suggest that WATS-3D is a “clinically valuable adjunct” to FB for the diagnosis of BE when used as a screening tool in symptomatic GERD patients and particularly in patients with endoscopic evidence of > 1 cm esophageal columnar-lined epithelium, the study team wrote. 

Adjunctive use of WATS-3D when BE is suspected “may save endoscopies and lead to quicker, more accurate diagnoses,” they added. 

The investigators said a limitation of the study is the lack of central pathology review, potentially leading to diagnostic variability. They also noted that over half of the detected dysplasia cases were crypt dysplasia or indefinite for dysplasia, raising concerns about clinical significance. 

Reached for comment, Philip O. Katz, MD, AGAF, professor of medicine and director of the GI Function Laboratories, Weill Cornell Medicine in New York, said he’s been using WATS for more than a decade as an adjunct to standard biopsy in patients undergoing screening and surveillance for BE and finds it clinically helpful in managing his patients.

This new study provides “further information that WATS added to biopsy that has been traditionally done with the Seattle protocol increases the yield of intestinal metaplasia and likely dysplasia in patients being screened for Barrett’s,” Katz, who wasn’t involved in the study, told GI & Hepatology News.

Funding for the study was provided by CDx Diagnostics. Shaheen and several coauthors disclosed relationships with the company. Katz disclosed relationships (consultant/advisor) for Phathom Pharmaceuticals and Sebella.

A version of this article appeared on Medscape.com.

A recent study supports the importance of intensive nutrition therapy in managing patients with alcohol-related acute-on-chronic liver failure (ACLF).

In a randomized controlled trial, compared with standard care, dietitian-supported, intensive nutritional therapy improved survival, reduced frailty, and lowered hospitalization rates in men with alcohol-related ACLF.

The study, performed by a team from the Postgraduate Institute of Medical Education and Research, Chandigarh, India, was published in Clinical Gastroenterology and Hepatology.

ACLF related to alcohol use is associated with poor outcomes due to poor nutritional intake and frailty. Frail patients with ACLF face higher morbidity, mortality, and hospitalization rates than their nonfrail counterparts. However, research on the role of structured nutritional interventions in improving these outcomes is limited.

Patal Giri, MBBS, MD, and colleagues enrolled 70 men with alcohol-related ACLF and frailty (liver frailty index [LFI] > 4.5) in a single-center, open-label study. Half were randomly allocated to an intervention group receiving outpatient intensive nutrition therapy (OINT) plus standard medical treatment (SMT) and half to a control group receiving SMT alone for 3 months.

The intervention group received a monitored high-calorie, high-protein, and salt-restricted diet as prescribed by a dedicated senior liver dietitian. The control group received regular nutritional recommendations and were managed for the ACLF-associated complications, without intervention or guidance by the study team.

After 3 months follow-up, overall survival (the primary outcome) was significantly improved in the OINT group compared with the control group (91.4% vs 57.1%), “suggesting that the improvement in nutrition status is associated with better survival,” the study team noted. Three patients died in the OINT group vs 15 in the SMT group.

OINT also led to a significant improvement in frailty, with LFI scores decreasing by an average of 0.93 in the intervention group vs 0.33 in the control group; 97% of patients improved from frail to prefrail status in the OINT group, whereas only 20% of patients improved in the SMT group.

The mean change in LFI of 0.93 with OINT is “well above the substantially clinically important difference” (change of 0.8) established in a previous study, the authors noted.

Significant improvements in weight and body mass index were also observed in the OINT group relative to the control group.

Liver disease severity, including model for end-stage liver disease (MELD) scores, showed greater improvement in the OINT group than in the control group (−8.7 vs −6.3 points from baseline to 3 months).

During the follow-up period, fewer patients in the intervention group than in the control group required a hospital stay (17% vs 45.7%).

Limitations of the study include the single-center design and the short follow-up period of 3 months, which limits long-term outcome assessment. Further, the study only included patients meeting Asia Pacific Association for Study of Liver criteria for ACLF, which does not include the patients with organ failure as defined by European Association for the Study of the Liver-Chronic Liver Failure Consortium criteria. Patients with ACLF who had more severe disease (MELD score > 30 or AARC > 10) were also not included.

Despite these limitations, the authors said their study showed that “dietician-monitored goal-directed nutrition therapy is very important in the management of patients with alcohol-related ACLF along with SMT.”

 

Confirmatory Data 

Reached for comment, Katherine Patton, MEd, RD, a registered dietitian with the Center for Human Nutrition at Cleveland Clinic, Cleveland, Ohio, said it’s well known that the ACLF patient population has a “very high rate of morbidity and mortality and their quality of life tends to be poor due to their frailty. It is also fairly well-known that proper nutrition therapy can improve outcomes, however barriers to adequate nutrition include decreased appetite, nausea, pain, altered taste, and early satiety from ascites.”

“Hepatologists are likely stressing the importance of adequate protein energy intake and doctors may refer patients to an outpatient dietitian, but it is up to the patient to make that appointment and act on the recommendations,” Patton told GI & Hepatology News.

“If a dietitian works in the same clinic as the hepatologist and patients can be referred and seen the same day, this is ideal. During a hospital admission, protein/calorie intake can be more closely monitored and encouraged by a multi-disciplinary team,” Patton explained.

She cautioned that “the average patient is not familiar with how to apply general calorie and protein goals to their everyday eating habits. This study amplifies the role of a dietitian and what consistent education and resources can do to improve a patient’s quality of life and survival.”

This study had no specific funding. The authors have declared no relevant conflicts of interest. Patton had no relevant disclosures.

A version of this article appeared on Medscape.com.