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More support for MDMA-assisted psychotherapy for PTSD
The MAPP2 study is the second randomized, double-blind, placebo-controlled study to demonstrate the safety and efficacy of MDMA-assisted therapy for PTSD.
The investigators confirm results of the MAPP1 study, which were published in Nature Medicine. Patients who received MDMA-assisted psychotherapy in MAPP1 demonstrated greater improvement in PTSD symptoms, mood, and empathy, compared with participants who received psychotherapy with placebo.
The design of the MAPP2 study was similar to that of MAPP1, and its results were similar, the nonprofit Multidisciplinary Association for Psychedelic Studies (MAPS), which sponsored MAPP1 and MAPP2, said in a news release.
No specific results from MAPP2 were provided at this time. The full data from MAPP2 are expected to be published in a peer-reviewed journal later this year, and a new drug application to the U.S. Food and Drug Administration will follow.
The FDA granted breakthrough therapy designation to MDMA as an adjunct to psychotherapy for adults with PTSD in 2017.
MAPS was founded in 1986 to fund and facilitate research into the potential of psychedelic-assisted therapies; to educate the public about psychedelics for medical, social, and spiritual use; and to advocate for drug policy reform.
“When I first articulated a plan to legitimize a psychedelic-assisted therapy through FDA approval, many people said it was impossible,” Rick Doblin, PhD, founder and executive director of MAPS, said in the news release.
“Thirty-seven years later, we are on the precipice of bringing a novel therapy to the millions of Americans living with PTSD who haven’t found relief through current treatments,” said Dr. Doblin.
“The impossible became possible through the bravery of clinical trial participants, the compassion of mental health practitioners, and the generosity of thousands of donors. Today, we can imagine that MDMA-assisted therapy for PTSD may soon be available and accessible to all who could benefit,” Dr. Doblin added.
According to MAPS, phase 2 trials are being planned or conducted regarding the efficacy of MDMA-assisted therapies for substance use disorder and eating disorders, as well as couples therapy and group therapy among veterans.
Currently, no psychedelic-assisted therapy has been approved by the FDA or other regulatory authorities.
A version of this article first appeared on Medscape.com.
The MAPP2 study is the second randomized, double-blind, placebo-controlled study to demonstrate the safety and efficacy of MDMA-assisted therapy for PTSD.
The investigators confirm results of the MAPP1 study, which were published in Nature Medicine. Patients who received MDMA-assisted psychotherapy in MAPP1 demonstrated greater improvement in PTSD symptoms, mood, and empathy, compared with participants who received psychotherapy with placebo.
The design of the MAPP2 study was similar to that of MAPP1, and its results were similar, the nonprofit Multidisciplinary Association for Psychedelic Studies (MAPS), which sponsored MAPP1 and MAPP2, said in a news release.
No specific results from MAPP2 were provided at this time. The full data from MAPP2 are expected to be published in a peer-reviewed journal later this year, and a new drug application to the U.S. Food and Drug Administration will follow.
The FDA granted breakthrough therapy designation to MDMA as an adjunct to psychotherapy for adults with PTSD in 2017.
MAPS was founded in 1986 to fund and facilitate research into the potential of psychedelic-assisted therapies; to educate the public about psychedelics for medical, social, and spiritual use; and to advocate for drug policy reform.
“When I first articulated a plan to legitimize a psychedelic-assisted therapy through FDA approval, many people said it was impossible,” Rick Doblin, PhD, founder and executive director of MAPS, said in the news release.
“Thirty-seven years later, we are on the precipice of bringing a novel therapy to the millions of Americans living with PTSD who haven’t found relief through current treatments,” said Dr. Doblin.
“The impossible became possible through the bravery of clinical trial participants, the compassion of mental health practitioners, and the generosity of thousands of donors. Today, we can imagine that MDMA-assisted therapy for PTSD may soon be available and accessible to all who could benefit,” Dr. Doblin added.
According to MAPS, phase 2 trials are being planned or conducted regarding the efficacy of MDMA-assisted therapies for substance use disorder and eating disorders, as well as couples therapy and group therapy among veterans.
Currently, no psychedelic-assisted therapy has been approved by the FDA or other regulatory authorities.
A version of this article first appeared on Medscape.com.
The MAPP2 study is the second randomized, double-blind, placebo-controlled study to demonstrate the safety and efficacy of MDMA-assisted therapy for PTSD.
The investigators confirm results of the MAPP1 study, which were published in Nature Medicine. Patients who received MDMA-assisted psychotherapy in MAPP1 demonstrated greater improvement in PTSD symptoms, mood, and empathy, compared with participants who received psychotherapy with placebo.
The design of the MAPP2 study was similar to that of MAPP1, and its results were similar, the nonprofit Multidisciplinary Association for Psychedelic Studies (MAPS), which sponsored MAPP1 and MAPP2, said in a news release.
No specific results from MAPP2 were provided at this time. The full data from MAPP2 are expected to be published in a peer-reviewed journal later this year, and a new drug application to the U.S. Food and Drug Administration will follow.
The FDA granted breakthrough therapy designation to MDMA as an adjunct to psychotherapy for adults with PTSD in 2017.
MAPS was founded in 1986 to fund and facilitate research into the potential of psychedelic-assisted therapies; to educate the public about psychedelics for medical, social, and spiritual use; and to advocate for drug policy reform.
“When I first articulated a plan to legitimize a psychedelic-assisted therapy through FDA approval, many people said it was impossible,” Rick Doblin, PhD, founder and executive director of MAPS, said in the news release.
“Thirty-seven years later, we are on the precipice of bringing a novel therapy to the millions of Americans living with PTSD who haven’t found relief through current treatments,” said Dr. Doblin.
“The impossible became possible through the bravery of clinical trial participants, the compassion of mental health practitioners, and the generosity of thousands of donors. Today, we can imagine that MDMA-assisted therapy for PTSD may soon be available and accessible to all who could benefit,” Dr. Doblin added.
According to MAPS, phase 2 trials are being planned or conducted regarding the efficacy of MDMA-assisted therapies for substance use disorder and eating disorders, as well as couples therapy and group therapy among veterans.
Currently, no psychedelic-assisted therapy has been approved by the FDA or other regulatory authorities.
A version of this article first appeared on Medscape.com.
Novel antipsychotic ‘encouraging’ for resistant schizophrenia
The topline results from an exploratory study, which were released by the developer Newron Pharmaceuticals, are “very encouraging,” Stephen R. Marder, MD, professor of psychiatry and biobehavioral sciences at the University of California, Los Angeles, said in a company news release.
“The magnitude of the improvements experienced by these TRS patients, not responding to their current antipsychotic, on evenamide was substantial, improved over time, and was likely to be clinically meaningful,” Dr. Marder said.
First 100 patients
The topline results are based on the first 100 patients enrolled in study 014 and randomly assigned to receive evenamide at 7.5 mg, 15 mg, or 30 mg twice daily, as well as patients in the extension arm (study 015) that have completed 30 weeks.
Key findings released by the company included statistically significant improvement over baseline at 30 weeks (P < .001) in Positive and Negative Syndrome Scale (PANSS) scores, with continued improvement over that seen at 6 weeks.
The proportion of patients with clinically meaningful PANSS improvement at 30 weeks more than doubled from 16.5% at 6 weeks.
In addition, results showed statistically significant improvement (P < .001) at week 30 compared with baseline in illness severity as measured by the Clinical Global Impression of Severity (CGI-S), with continued improvement over that seen at 6 weeks.
The proportion of patients whose illness improved by at least one level of severity was 60% at week 6 and increased approximately by an additional 20% at week 30.
The proportion of patients judged to have clinically meaningful improvement, defined as at least “much improved,” on the Clinical Global Impression of Change (CGI-C) was 27% at week 6 – and increased a further 10% at week 30.
Evenamide was also well tolerated, with few adverse effects reported, and 85 of 100 patients remained on treatment at 30 weeks.
New options ‘desperately needed’
Newron plans to present the full results from study 014 at the European Congress of Psychiatry, scheduled for March 25-28 in Paris.
The extension study 015 is ongoing and will provide results on evenamide treatment for up to 1 year by the second quarter of 2023.
The company reported it expects to launch a randomized, placebo-controlled study (study 003) of the drug in TRS this year.
If the current results are confirmed in the randomized controlled trial, “evenamide would be the first medication that could be added to an antipsychotic to improve symptoms in treatment-refractory schizophrenia,” Dr. Marder said.
New therapeutic options for TRS, which occurs in about one-third of patients, are “desperately needed,” Ravi Anand, MD, chief medical officer at Newron, said in the release.
The reported data, comparing the effect of evenamide at 6 weeks vs. 6 months, “suggest that not only was there sustained improvement in the key measures, but the proportion of patients achieving clinically meaningful improvement increased over time,” Dr. Anand added.
A version of this article first appeared on Medscape.com.
The topline results from an exploratory study, which were released by the developer Newron Pharmaceuticals, are “very encouraging,” Stephen R. Marder, MD, professor of psychiatry and biobehavioral sciences at the University of California, Los Angeles, said in a company news release.
“The magnitude of the improvements experienced by these TRS patients, not responding to their current antipsychotic, on evenamide was substantial, improved over time, and was likely to be clinically meaningful,” Dr. Marder said.
First 100 patients
The topline results are based on the first 100 patients enrolled in study 014 and randomly assigned to receive evenamide at 7.5 mg, 15 mg, or 30 mg twice daily, as well as patients in the extension arm (study 015) that have completed 30 weeks.
Key findings released by the company included statistically significant improvement over baseline at 30 weeks (P < .001) in Positive and Negative Syndrome Scale (PANSS) scores, with continued improvement over that seen at 6 weeks.
The proportion of patients with clinically meaningful PANSS improvement at 30 weeks more than doubled from 16.5% at 6 weeks.
In addition, results showed statistically significant improvement (P < .001) at week 30 compared with baseline in illness severity as measured by the Clinical Global Impression of Severity (CGI-S), with continued improvement over that seen at 6 weeks.
The proportion of patients whose illness improved by at least one level of severity was 60% at week 6 and increased approximately by an additional 20% at week 30.
The proportion of patients judged to have clinically meaningful improvement, defined as at least “much improved,” on the Clinical Global Impression of Change (CGI-C) was 27% at week 6 – and increased a further 10% at week 30.
Evenamide was also well tolerated, with few adverse effects reported, and 85 of 100 patients remained on treatment at 30 weeks.
New options ‘desperately needed’
Newron plans to present the full results from study 014 at the European Congress of Psychiatry, scheduled for March 25-28 in Paris.
The extension study 015 is ongoing and will provide results on evenamide treatment for up to 1 year by the second quarter of 2023.
The company reported it expects to launch a randomized, placebo-controlled study (study 003) of the drug in TRS this year.
If the current results are confirmed in the randomized controlled trial, “evenamide would be the first medication that could be added to an antipsychotic to improve symptoms in treatment-refractory schizophrenia,” Dr. Marder said.
New therapeutic options for TRS, which occurs in about one-third of patients, are “desperately needed,” Ravi Anand, MD, chief medical officer at Newron, said in the release.
The reported data, comparing the effect of evenamide at 6 weeks vs. 6 months, “suggest that not only was there sustained improvement in the key measures, but the proportion of patients achieving clinically meaningful improvement increased over time,” Dr. Anand added.
A version of this article first appeared on Medscape.com.
The topline results from an exploratory study, which were released by the developer Newron Pharmaceuticals, are “very encouraging,” Stephen R. Marder, MD, professor of psychiatry and biobehavioral sciences at the University of California, Los Angeles, said in a company news release.
“The magnitude of the improvements experienced by these TRS patients, not responding to their current antipsychotic, on evenamide was substantial, improved over time, and was likely to be clinically meaningful,” Dr. Marder said.
First 100 patients
The topline results are based on the first 100 patients enrolled in study 014 and randomly assigned to receive evenamide at 7.5 mg, 15 mg, or 30 mg twice daily, as well as patients in the extension arm (study 015) that have completed 30 weeks.
Key findings released by the company included statistically significant improvement over baseline at 30 weeks (P < .001) in Positive and Negative Syndrome Scale (PANSS) scores, with continued improvement over that seen at 6 weeks.
The proportion of patients with clinically meaningful PANSS improvement at 30 weeks more than doubled from 16.5% at 6 weeks.
In addition, results showed statistically significant improvement (P < .001) at week 30 compared with baseline in illness severity as measured by the Clinical Global Impression of Severity (CGI-S), with continued improvement over that seen at 6 weeks.
The proportion of patients whose illness improved by at least one level of severity was 60% at week 6 and increased approximately by an additional 20% at week 30.
The proportion of patients judged to have clinically meaningful improvement, defined as at least “much improved,” on the Clinical Global Impression of Change (CGI-C) was 27% at week 6 – and increased a further 10% at week 30.
Evenamide was also well tolerated, with few adverse effects reported, and 85 of 100 patients remained on treatment at 30 weeks.
New options ‘desperately needed’
Newron plans to present the full results from study 014 at the European Congress of Psychiatry, scheduled for March 25-28 in Paris.
The extension study 015 is ongoing and will provide results on evenamide treatment for up to 1 year by the second quarter of 2023.
The company reported it expects to launch a randomized, placebo-controlled study (study 003) of the drug in TRS this year.
If the current results are confirmed in the randomized controlled trial, “evenamide would be the first medication that could be added to an antipsychotic to improve symptoms in treatment-refractory schizophrenia,” Dr. Marder said.
New therapeutic options for TRS, which occurs in about one-third of patients, are “desperately needed,” Ravi Anand, MD, chief medical officer at Newron, said in the release.
The reported data, comparing the effect of evenamide at 6 weeks vs. 6 months, “suggest that not only was there sustained improvement in the key measures, but the proportion of patients achieving clinically meaningful improvement increased over time,” Dr. Anand added.
A version of this article first appeared on Medscape.com.
Renowned stroke expert Ralph L. Sacco, MD, dies
Ralph L. Sacco, MD, the first neurologist to serve as president of the American Heart Association and the only physician to serve as president of both the AHA and the American Academy of Neurology, died Jan. 17 at the age of 65.
He died of a brain tumor at his home in Amagansett, N.Y., according to an obituary published in Neurology, Circulation, and Stroke.
“Ralph was one of a kind,” Nancy Brown, chief executive officer for the AHA and American Stroke Association, said in a statement. “His leadership was unparalleled, and his warm, generous heart and care transcended his research and clinic to every person fortunate to meet him and likely become a friend,” Ms. Brown said.
In a tweet, Natalia S. Rost, MD, professor of neurology at Harvard Medical School, Boston, called him, “a dear friend, an inspiring colleague, a generous mentor, an astute scientist, a consummate advocate for brain health worldwide.”
Dedicated to improving stroke care
Dr. Sacco was chair of the University of Miami Miller School of Medicine in the department of neurology; the Olemberg Family Chair in Neurological Disorders; professor of neurology, public health sciences, human genetics, and neurosurgery; executive director of the Evelyn F. McKnight Brain Institute; director and multi-principal investigator of the Miami Clinical and Translational Science Institute; and senior associate dean for clinical and translational science.
Dr. Sacco was a population-based researcher in the field of cerebrovascular diseases.
As founder of the Northern Manhattan Study, he paved the way for examining the differences in stroke risk related to race, ethnicity, sex, and neighborhood, and realizing the impact of modifiable lifestyle behaviors, such as alcohol consumption and physical activity, on stroke risk.
Dr. Sacco’s work led to more targeted stroke prevention programs and his “drive and dedication fueled changes that improved stroke research and fostered the development of targeted stroke care delivery, ultimately improving stroke recovery and post-stroke quality of life for many,” the AHA statement said.
Dr. Sacco was also founder and executive director of the Florida Stroke Registry, which consists of 167 Florida stroke centers. He was a member of the National Academy of Medicine.
In an obituary written by Orly Avitzur, MD, current president of the AAN, she notes that he “was the only physician to have become both the president of the AHA (2010-2011) and the AAN (2017-2019), positions that reflected the respect and admiration of professional colleagues earned over the years.”
During his tenure as AAN president, Dr. Sacco led an initiative to ensure that academic neurology, from department chairs to professors to students, knew about the abundance of academy resources available to them, the AAN noted in a statement.
Dr. Sacco was a “strong proponent of enlarging the neurology workforce through the academic pipeline and promoted the concept of the ‘newrologist’ to get people excited in careers in neurology, moving beyond just diagnosis and treatments to include interventions, preventative care, and the future of regenerative care,” the AAN said.
Dr. Sacco received numerous awards throughout his career, most recently the AHA 2022 Distinguished Scientist award. He also received the 2015 Gold Heart Award, the 2011 Distinguished National Leadership Award, and the 2006 William Feinberg Award.
In addition to his husband, Scott Dutcher, Dr. Sacco is survived by his father, Anthony P. Sacco, and his father’s wife, Rosemary; and his four siblings and their families, along with many nieces and nephews.
A version of this article first appeared on Medscape.com.
Ralph L. Sacco, MD, the first neurologist to serve as president of the American Heart Association and the only physician to serve as president of both the AHA and the American Academy of Neurology, died Jan. 17 at the age of 65.
He died of a brain tumor at his home in Amagansett, N.Y., according to an obituary published in Neurology, Circulation, and Stroke.
“Ralph was one of a kind,” Nancy Brown, chief executive officer for the AHA and American Stroke Association, said in a statement. “His leadership was unparalleled, and his warm, generous heart and care transcended his research and clinic to every person fortunate to meet him and likely become a friend,” Ms. Brown said.
In a tweet, Natalia S. Rost, MD, professor of neurology at Harvard Medical School, Boston, called him, “a dear friend, an inspiring colleague, a generous mentor, an astute scientist, a consummate advocate for brain health worldwide.”
Dedicated to improving stroke care
Dr. Sacco was chair of the University of Miami Miller School of Medicine in the department of neurology; the Olemberg Family Chair in Neurological Disorders; professor of neurology, public health sciences, human genetics, and neurosurgery; executive director of the Evelyn F. McKnight Brain Institute; director and multi-principal investigator of the Miami Clinical and Translational Science Institute; and senior associate dean for clinical and translational science.
Dr. Sacco was a population-based researcher in the field of cerebrovascular diseases.
As founder of the Northern Manhattan Study, he paved the way for examining the differences in stroke risk related to race, ethnicity, sex, and neighborhood, and realizing the impact of modifiable lifestyle behaviors, such as alcohol consumption and physical activity, on stroke risk.
Dr. Sacco’s work led to more targeted stroke prevention programs and his “drive and dedication fueled changes that improved stroke research and fostered the development of targeted stroke care delivery, ultimately improving stroke recovery and post-stroke quality of life for many,” the AHA statement said.
Dr. Sacco was also founder and executive director of the Florida Stroke Registry, which consists of 167 Florida stroke centers. He was a member of the National Academy of Medicine.
In an obituary written by Orly Avitzur, MD, current president of the AAN, she notes that he “was the only physician to have become both the president of the AHA (2010-2011) and the AAN (2017-2019), positions that reflected the respect and admiration of professional colleagues earned over the years.”
During his tenure as AAN president, Dr. Sacco led an initiative to ensure that academic neurology, from department chairs to professors to students, knew about the abundance of academy resources available to them, the AAN noted in a statement.
Dr. Sacco was a “strong proponent of enlarging the neurology workforce through the academic pipeline and promoted the concept of the ‘newrologist’ to get people excited in careers in neurology, moving beyond just diagnosis and treatments to include interventions, preventative care, and the future of regenerative care,” the AAN said.
Dr. Sacco received numerous awards throughout his career, most recently the AHA 2022 Distinguished Scientist award. He also received the 2015 Gold Heart Award, the 2011 Distinguished National Leadership Award, and the 2006 William Feinberg Award.
In addition to his husband, Scott Dutcher, Dr. Sacco is survived by his father, Anthony P. Sacco, and his father’s wife, Rosemary; and his four siblings and their families, along with many nieces and nephews.
A version of this article first appeared on Medscape.com.
Ralph L. Sacco, MD, the first neurologist to serve as president of the American Heart Association and the only physician to serve as president of both the AHA and the American Academy of Neurology, died Jan. 17 at the age of 65.
He died of a brain tumor at his home in Amagansett, N.Y., according to an obituary published in Neurology, Circulation, and Stroke.
“Ralph was one of a kind,” Nancy Brown, chief executive officer for the AHA and American Stroke Association, said in a statement. “His leadership was unparalleled, and his warm, generous heart and care transcended his research and clinic to every person fortunate to meet him and likely become a friend,” Ms. Brown said.
In a tweet, Natalia S. Rost, MD, professor of neurology at Harvard Medical School, Boston, called him, “a dear friend, an inspiring colleague, a generous mentor, an astute scientist, a consummate advocate for brain health worldwide.”
Dedicated to improving stroke care
Dr. Sacco was chair of the University of Miami Miller School of Medicine in the department of neurology; the Olemberg Family Chair in Neurological Disorders; professor of neurology, public health sciences, human genetics, and neurosurgery; executive director of the Evelyn F. McKnight Brain Institute; director and multi-principal investigator of the Miami Clinical and Translational Science Institute; and senior associate dean for clinical and translational science.
Dr. Sacco was a population-based researcher in the field of cerebrovascular diseases.
As founder of the Northern Manhattan Study, he paved the way for examining the differences in stroke risk related to race, ethnicity, sex, and neighborhood, and realizing the impact of modifiable lifestyle behaviors, such as alcohol consumption and physical activity, on stroke risk.
Dr. Sacco’s work led to more targeted stroke prevention programs and his “drive and dedication fueled changes that improved stroke research and fostered the development of targeted stroke care delivery, ultimately improving stroke recovery and post-stroke quality of life for many,” the AHA statement said.
Dr. Sacco was also founder and executive director of the Florida Stroke Registry, which consists of 167 Florida stroke centers. He was a member of the National Academy of Medicine.
In an obituary written by Orly Avitzur, MD, current president of the AAN, she notes that he “was the only physician to have become both the president of the AHA (2010-2011) and the AAN (2017-2019), positions that reflected the respect and admiration of professional colleagues earned over the years.”
During his tenure as AAN president, Dr. Sacco led an initiative to ensure that academic neurology, from department chairs to professors to students, knew about the abundance of academy resources available to them, the AAN noted in a statement.
Dr. Sacco was a “strong proponent of enlarging the neurology workforce through the academic pipeline and promoted the concept of the ‘newrologist’ to get people excited in careers in neurology, moving beyond just diagnosis and treatments to include interventions, preventative care, and the future of regenerative care,” the AAN said.
Dr. Sacco received numerous awards throughout his career, most recently the AHA 2022 Distinguished Scientist award. He also received the 2015 Gold Heart Award, the 2011 Distinguished National Leadership Award, and the 2006 William Feinberg Award.
In addition to his husband, Scott Dutcher, Dr. Sacco is survived by his father, Anthony P. Sacco, and his father’s wife, Rosemary; and his four siblings and their families, along with many nieces and nephews.
A version of this article first appeared on Medscape.com.
Diet packed with fast food found hard on the liver
The study finds that getting one-fifth or more of total daily calories from fast food can increase the risk of nonalcoholic fatty liver disease, which can lead to cirrhosis and its complications, including liver failure and liver cancer.
Although the magnitude of association was modest among the general population, “striking” elevations in steatosis were evident among persons with obesity and diabetes who consumed fast food, in comparison with their counterparts who did not have obesity and diabetes, the researchers reported.
“My hope is that this study encourages people to seek out more nutritious, healthy food options and provides information that clinicians can use to counsel their patients, particularly those with underlying metabolic risk factors, of the importance of avoiding foods that are high in fat, carbohydrates, and processed sugars,” lead investigator Ani Kardashian, MD, hepatologist with the University of Southern California, Los Angeles, said in an interview.
“At a policy level, public health efforts are needed to improve access to affordable, healthy, and nutritious food options across the U.S. This is especially important as more people have turned to fast foods during the pandemic and as the price of food as risen dramatically over the past year due to food inflation,” Dr. Kardashian added.
The study was published online in Clinical Gastroenterology and Hepatology.
More fast food, greater steatosis
The findings are based on data from 3,954 adults who participated in the National Health and Nutrition Examination Survey (NHANES) of 2017-2018 and who underwent vibration-controlled transient elastography. Of these participants, data regarding 1- or 2-day dietary recall were available.
Steatosis, the primary outcome, was measured via controlled attenuation parameter (CAP). Two validated cutoffs were utilized (CAP ≥ 263 dB/m and CAP ≥ 285 dB/m).
Of those surveyed, 52% consumed any fast food, and 29% derived 20% or more of their daily calories from fast food.
Fast-food intake of 20% or more of daily calories was significantly associated with greater steatosis after multivariable adjustment, both as a continuous measure (4.6 dB/m higher CAP score) and with respect to the CAP ≥ 263 dB/m cutoff (odds ratio [OR], 1.45).
“The negative effects are particularly severe in people who already have diabetes and obesity,” Dr. Kardashian told this news organization.
For example, with diabetes and fast-food intake of 20% or more of daily calories, the ORs of meeting the CAP ≥ 263 dB/m cutoff and the CAP ≥ 285 dB/m cutoff were 2.3 and 2.48, respectively.
The researchers said their findings are particularly “alarming,” given the overall increase in fast-food consumption over the past 50 years in the United States, regardless of socioeconomic status.
Diet coaching
The finding that fast food has more deleterious impact on those with obesity and diabetes “emphasizes that it is not just one insult but multiple factors that contribute to overall health,” said Nancy Reau, MD, section chief of hepatology at Rush University Medical Center in Chicago.
“This is actually great news, because diet is modifiable, vs. your genetics, which you currently can’t change. This doesn’t mean if you’re lean you can eat whatever you want, but if you are overweight, being careful with your diet does have impact, even if it doesn’t lead to substantial weight changes,” said Dr. Reau, who is not affiliated with the study.
For people who have limited options and need to eat fast food, “there are healthy choices at most restaurants; you just need to be smart about reading labels, watching calories, and ordering the healthier options,” Dr. Reau said in an interview.
Fast food and fatty liver go “hand in hand,” Lisa Ganjhu, DO, gastroenterologist and hepatologist at NYU Langone Health in New York, told this news organization.
“I counsel and coach my patients on healthy diet and exercise, and I’ve been pretty successful,” said Dr. Ganjhu, who was not involved with the study.
“If my patient is eating at McDonald’s a lot, I basically walk through the menu with them and help them find something healthy. When patients see the benefits of cutting out fat and reducing carbohydrates, they are more apt to continue,” Dr. Ganjhu said.
The study was funded by the University of Southern California. Dr. Kardashian, Dr. Reau, and Dr. Ganjhu have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The study finds that getting one-fifth or more of total daily calories from fast food can increase the risk of nonalcoholic fatty liver disease, which can lead to cirrhosis and its complications, including liver failure and liver cancer.
Although the magnitude of association was modest among the general population, “striking” elevations in steatosis were evident among persons with obesity and diabetes who consumed fast food, in comparison with their counterparts who did not have obesity and diabetes, the researchers reported.
“My hope is that this study encourages people to seek out more nutritious, healthy food options and provides information that clinicians can use to counsel their patients, particularly those with underlying metabolic risk factors, of the importance of avoiding foods that are high in fat, carbohydrates, and processed sugars,” lead investigator Ani Kardashian, MD, hepatologist with the University of Southern California, Los Angeles, said in an interview.
“At a policy level, public health efforts are needed to improve access to affordable, healthy, and nutritious food options across the U.S. This is especially important as more people have turned to fast foods during the pandemic and as the price of food as risen dramatically over the past year due to food inflation,” Dr. Kardashian added.
The study was published online in Clinical Gastroenterology and Hepatology.
More fast food, greater steatosis
The findings are based on data from 3,954 adults who participated in the National Health and Nutrition Examination Survey (NHANES) of 2017-2018 and who underwent vibration-controlled transient elastography. Of these participants, data regarding 1- or 2-day dietary recall were available.
Steatosis, the primary outcome, was measured via controlled attenuation parameter (CAP). Two validated cutoffs were utilized (CAP ≥ 263 dB/m and CAP ≥ 285 dB/m).
Of those surveyed, 52% consumed any fast food, and 29% derived 20% or more of their daily calories from fast food.
Fast-food intake of 20% or more of daily calories was significantly associated with greater steatosis after multivariable adjustment, both as a continuous measure (4.6 dB/m higher CAP score) and with respect to the CAP ≥ 263 dB/m cutoff (odds ratio [OR], 1.45).
“The negative effects are particularly severe in people who already have diabetes and obesity,” Dr. Kardashian told this news organization.
For example, with diabetes and fast-food intake of 20% or more of daily calories, the ORs of meeting the CAP ≥ 263 dB/m cutoff and the CAP ≥ 285 dB/m cutoff were 2.3 and 2.48, respectively.
The researchers said their findings are particularly “alarming,” given the overall increase in fast-food consumption over the past 50 years in the United States, regardless of socioeconomic status.
Diet coaching
The finding that fast food has more deleterious impact on those with obesity and diabetes “emphasizes that it is not just one insult but multiple factors that contribute to overall health,” said Nancy Reau, MD, section chief of hepatology at Rush University Medical Center in Chicago.
“This is actually great news, because diet is modifiable, vs. your genetics, which you currently can’t change. This doesn’t mean if you’re lean you can eat whatever you want, but if you are overweight, being careful with your diet does have impact, even if it doesn’t lead to substantial weight changes,” said Dr. Reau, who is not affiliated with the study.
For people who have limited options and need to eat fast food, “there are healthy choices at most restaurants; you just need to be smart about reading labels, watching calories, and ordering the healthier options,” Dr. Reau said in an interview.
Fast food and fatty liver go “hand in hand,” Lisa Ganjhu, DO, gastroenterologist and hepatologist at NYU Langone Health in New York, told this news organization.
“I counsel and coach my patients on healthy diet and exercise, and I’ve been pretty successful,” said Dr. Ganjhu, who was not involved with the study.
“If my patient is eating at McDonald’s a lot, I basically walk through the menu with them and help them find something healthy. When patients see the benefits of cutting out fat and reducing carbohydrates, they are more apt to continue,” Dr. Ganjhu said.
The study was funded by the University of Southern California. Dr. Kardashian, Dr. Reau, and Dr. Ganjhu have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The study finds that getting one-fifth or more of total daily calories from fast food can increase the risk of nonalcoholic fatty liver disease, which can lead to cirrhosis and its complications, including liver failure and liver cancer.
Although the magnitude of association was modest among the general population, “striking” elevations in steatosis were evident among persons with obesity and diabetes who consumed fast food, in comparison with their counterparts who did not have obesity and diabetes, the researchers reported.
“My hope is that this study encourages people to seek out more nutritious, healthy food options and provides information that clinicians can use to counsel their patients, particularly those with underlying metabolic risk factors, of the importance of avoiding foods that are high in fat, carbohydrates, and processed sugars,” lead investigator Ani Kardashian, MD, hepatologist with the University of Southern California, Los Angeles, said in an interview.
“At a policy level, public health efforts are needed to improve access to affordable, healthy, and nutritious food options across the U.S. This is especially important as more people have turned to fast foods during the pandemic and as the price of food as risen dramatically over the past year due to food inflation,” Dr. Kardashian added.
The study was published online in Clinical Gastroenterology and Hepatology.
More fast food, greater steatosis
The findings are based on data from 3,954 adults who participated in the National Health and Nutrition Examination Survey (NHANES) of 2017-2018 and who underwent vibration-controlled transient elastography. Of these participants, data regarding 1- or 2-day dietary recall were available.
Steatosis, the primary outcome, was measured via controlled attenuation parameter (CAP). Two validated cutoffs were utilized (CAP ≥ 263 dB/m and CAP ≥ 285 dB/m).
Of those surveyed, 52% consumed any fast food, and 29% derived 20% or more of their daily calories from fast food.
Fast-food intake of 20% or more of daily calories was significantly associated with greater steatosis after multivariable adjustment, both as a continuous measure (4.6 dB/m higher CAP score) and with respect to the CAP ≥ 263 dB/m cutoff (odds ratio [OR], 1.45).
“The negative effects are particularly severe in people who already have diabetes and obesity,” Dr. Kardashian told this news organization.
For example, with diabetes and fast-food intake of 20% or more of daily calories, the ORs of meeting the CAP ≥ 263 dB/m cutoff and the CAP ≥ 285 dB/m cutoff were 2.3 and 2.48, respectively.
The researchers said their findings are particularly “alarming,” given the overall increase in fast-food consumption over the past 50 years in the United States, regardless of socioeconomic status.
Diet coaching
The finding that fast food has more deleterious impact on those with obesity and diabetes “emphasizes that it is not just one insult but multiple factors that contribute to overall health,” said Nancy Reau, MD, section chief of hepatology at Rush University Medical Center in Chicago.
“This is actually great news, because diet is modifiable, vs. your genetics, which you currently can’t change. This doesn’t mean if you’re lean you can eat whatever you want, but if you are overweight, being careful with your diet does have impact, even if it doesn’t lead to substantial weight changes,” said Dr. Reau, who is not affiliated with the study.
For people who have limited options and need to eat fast food, “there are healthy choices at most restaurants; you just need to be smart about reading labels, watching calories, and ordering the healthier options,” Dr. Reau said in an interview.
Fast food and fatty liver go “hand in hand,” Lisa Ganjhu, DO, gastroenterologist and hepatologist at NYU Langone Health in New York, told this news organization.
“I counsel and coach my patients on healthy diet and exercise, and I’ve been pretty successful,” said Dr. Ganjhu, who was not involved with the study.
“If my patient is eating at McDonald’s a lot, I basically walk through the menu with them and help them find something healthy. When patients see the benefits of cutting out fat and reducing carbohydrates, they are more apt to continue,” Dr. Ganjhu said.
The study was funded by the University of Southern California. Dr. Kardashian, Dr. Reau, and Dr. Ganjhu have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
Can 6 minutes of intense cycling put the brakes on Alzheimer’s?
new research suggests.
In a small study of healthy adults, 6 minutes of high-intensity cycling increased circulating levels of brain-derived neurotrophic factor (BDNF) to a significantly greater extent than prolonged light cycling or fasting.
However, the data do not suggest that 6 minutes of high-intensity exercise “wards off dementia,” cautioned lead investigator Travis Gibbons, MSc, PhD candidate in environmental physiology at the University of Otago (New Zealand), Dunedin, and now postdoctoral fellow at the University of British Columbia – Okanagan, Kelowna.
“Like all science, this is just a small piece that supports a potential mechanistic role for how exercise might improve brain health,” Dr. Gibbons told this news organization.
The findings were published online in the Journal of Physiology.
Targeting BDNF
Both intermittent fasting and exercise have previously been shown to have potent neuroprotective effects; and an acute upregulation of BDNF appears to be a common mechanistic link.
To tease apart the influence of fasting and exercise on BDNF production, Dr. Gibbons and colleagues studied 12 aerobically fit, healthy men (n = 6) and women (n = 6) aged 20-40 years.
In a study that employed a repeated-measures crossover design, they assessed circulating BDNF levels after a 20-hour fast, prolonged (90-min) light cycling, short (6-min) high-intensity cycling, and combined fasting and exercise.
Six minutes of high-intensity exercise appeared to be the most efficient way to increase BDNF.
Fasting for 20 hours led to a ninefold increase in ketone body delivery to the brain but had no effect on any metric of BDNF in peripheral circulation at rest or during exercise.
Six minutes of high-intensity exercise increased every metric of circulating BDNF four to five times more than prolonged low-intensity exercise.
In addition, the increase in plasma-derived BDNF correlated with a sixfold increase in circulating lactate irrespective of feeding or fasting state.
Lactate delivery?
“My leading theory is that, during and following intense exercise, lactate produced by muscles is delivered and consumed by the brain,” Dr. Gibbons noted.
“It takes high-intensity exercise to provoke this ‘cerebral substrate switch’ from glucose to lactate. Critically, this cerebral substrate switch has been shown to contribute to the early processes that upregulate BDNF production in the brain,” he said.
However, “Whether this translates to ‘warding off dementia’ is not clear,” Dr. Gibbons added.
The study also suggests that increases in plasma volume and platelet concentration appear to play a role in concentrating BDNF in the circulation during exercise.
The investigators note that BDNF and other neurotrophic-based pharmaceutical therapies have shown “great promise” in slowing and even arresting neurodegenerative processes in animals, but attempts to harness the protective power of BDNF in human neurodegeneration have thus far failed.
“Whether episodically upregulating BDNF production with intense exercise is an effective strategy to curb age-related cognitive decline in humans is unknown, but animal models indicate that it is and that BDNF plays a primary role,” the researchers write.
Funding for the study was provided by the Healthcare Otago Charitable Trust. The investigators have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
new research suggests.
In a small study of healthy adults, 6 minutes of high-intensity cycling increased circulating levels of brain-derived neurotrophic factor (BDNF) to a significantly greater extent than prolonged light cycling or fasting.
However, the data do not suggest that 6 minutes of high-intensity exercise “wards off dementia,” cautioned lead investigator Travis Gibbons, MSc, PhD candidate in environmental physiology at the University of Otago (New Zealand), Dunedin, and now postdoctoral fellow at the University of British Columbia – Okanagan, Kelowna.
“Like all science, this is just a small piece that supports a potential mechanistic role for how exercise might improve brain health,” Dr. Gibbons told this news organization.
The findings were published online in the Journal of Physiology.
Targeting BDNF
Both intermittent fasting and exercise have previously been shown to have potent neuroprotective effects; and an acute upregulation of BDNF appears to be a common mechanistic link.
To tease apart the influence of fasting and exercise on BDNF production, Dr. Gibbons and colleagues studied 12 aerobically fit, healthy men (n = 6) and women (n = 6) aged 20-40 years.
In a study that employed a repeated-measures crossover design, they assessed circulating BDNF levels after a 20-hour fast, prolonged (90-min) light cycling, short (6-min) high-intensity cycling, and combined fasting and exercise.
Six minutes of high-intensity exercise appeared to be the most efficient way to increase BDNF.
Fasting for 20 hours led to a ninefold increase in ketone body delivery to the brain but had no effect on any metric of BDNF in peripheral circulation at rest or during exercise.
Six minutes of high-intensity exercise increased every metric of circulating BDNF four to five times more than prolonged low-intensity exercise.
In addition, the increase in plasma-derived BDNF correlated with a sixfold increase in circulating lactate irrespective of feeding or fasting state.
Lactate delivery?
“My leading theory is that, during and following intense exercise, lactate produced by muscles is delivered and consumed by the brain,” Dr. Gibbons noted.
“It takes high-intensity exercise to provoke this ‘cerebral substrate switch’ from glucose to lactate. Critically, this cerebral substrate switch has been shown to contribute to the early processes that upregulate BDNF production in the brain,” he said.
However, “Whether this translates to ‘warding off dementia’ is not clear,” Dr. Gibbons added.
The study also suggests that increases in plasma volume and platelet concentration appear to play a role in concentrating BDNF in the circulation during exercise.
The investigators note that BDNF and other neurotrophic-based pharmaceutical therapies have shown “great promise” in slowing and even arresting neurodegenerative processes in animals, but attempts to harness the protective power of BDNF in human neurodegeneration have thus far failed.
“Whether episodically upregulating BDNF production with intense exercise is an effective strategy to curb age-related cognitive decline in humans is unknown, but animal models indicate that it is and that BDNF plays a primary role,” the researchers write.
Funding for the study was provided by the Healthcare Otago Charitable Trust. The investigators have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
new research suggests.
In a small study of healthy adults, 6 minutes of high-intensity cycling increased circulating levels of brain-derived neurotrophic factor (BDNF) to a significantly greater extent than prolonged light cycling or fasting.
However, the data do not suggest that 6 minutes of high-intensity exercise “wards off dementia,” cautioned lead investigator Travis Gibbons, MSc, PhD candidate in environmental physiology at the University of Otago (New Zealand), Dunedin, and now postdoctoral fellow at the University of British Columbia – Okanagan, Kelowna.
“Like all science, this is just a small piece that supports a potential mechanistic role for how exercise might improve brain health,” Dr. Gibbons told this news organization.
The findings were published online in the Journal of Physiology.
Targeting BDNF
Both intermittent fasting and exercise have previously been shown to have potent neuroprotective effects; and an acute upregulation of BDNF appears to be a common mechanistic link.
To tease apart the influence of fasting and exercise on BDNF production, Dr. Gibbons and colleagues studied 12 aerobically fit, healthy men (n = 6) and women (n = 6) aged 20-40 years.
In a study that employed a repeated-measures crossover design, they assessed circulating BDNF levels after a 20-hour fast, prolonged (90-min) light cycling, short (6-min) high-intensity cycling, and combined fasting and exercise.
Six minutes of high-intensity exercise appeared to be the most efficient way to increase BDNF.
Fasting for 20 hours led to a ninefold increase in ketone body delivery to the brain but had no effect on any metric of BDNF in peripheral circulation at rest or during exercise.
Six minutes of high-intensity exercise increased every metric of circulating BDNF four to five times more than prolonged low-intensity exercise.
In addition, the increase in plasma-derived BDNF correlated with a sixfold increase in circulating lactate irrespective of feeding or fasting state.
Lactate delivery?
“My leading theory is that, during and following intense exercise, lactate produced by muscles is delivered and consumed by the brain,” Dr. Gibbons noted.
“It takes high-intensity exercise to provoke this ‘cerebral substrate switch’ from glucose to lactate. Critically, this cerebral substrate switch has been shown to contribute to the early processes that upregulate BDNF production in the brain,” he said.
However, “Whether this translates to ‘warding off dementia’ is not clear,” Dr. Gibbons added.
The study also suggests that increases in plasma volume and platelet concentration appear to play a role in concentrating BDNF in the circulation during exercise.
The investigators note that BDNF and other neurotrophic-based pharmaceutical therapies have shown “great promise” in slowing and even arresting neurodegenerative processes in animals, but attempts to harness the protective power of BDNF in human neurodegeneration have thus far failed.
“Whether episodically upregulating BDNF production with intense exercise is an effective strategy to curb age-related cognitive decline in humans is unknown, but animal models indicate that it is and that BDNF plays a primary role,” the researchers write.
Funding for the study was provided by the Healthcare Otago Charitable Trust. The investigators have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF PHYSIOLOGY
‘Clinical paradox’? Bariatric surgery may protect from GI cancers
In fact, an analysis of close to 1 million French adults suggests that the weight-loss surgery may offer some protection against these cancers.
The study results present a “clinical paradox,” according to authors of a commentary published this week along with the study in JAMA Surgery. A procedure known to increase the risk of gastroesophageal reflux disease (GERD), and potentially adenocarcinoma of the distal esophagus and gastroesophageal junction, may help shield patients from esophagogastric cancer.
The study marks “an important step toward improving the understanding of potential lifetime risks of bariatric surgery and overall major health benefits of surgically induced weight loss,” commentary authors Piotr Gorecki, MD, and Michael Zenilman, MD, with Weill Cornell Medicine in New York, write.
Recent data indicate that excess body weight is associated with nearly 8% of cancer cases and 6.5% of cancer deaths. Studies also show that bariatric surgery can reduce the risk of some cancers, but whether this extends to esophageal and gastric cancer remains unclear.
To investigate, the researchers used French national data to compare the incidence of esophageal and gastric cancer in 303,709 mostly female patients with obesity who underwent bariatric surgery and a matched group of 605,140 patients with obesity who did not undergo the surgery.
The mean age of the cohort was about 40 years. The mean period of follow-up was 6 years for the surgery group and 5.6 years for the control arm. A total of 337 patients underwent esophagogastric cancer – 83 in the surgical group and 254 in the control group. Gastric cancer was about two times more common than esophageal cancer (225 vs. 112 patients).
The incidence rate of esophagogastric cancer was higher in the control group than in the surgery group – 6.9 vs. 4.9 cases per 100,000 population per year, for an incidence rate ratio of 1.42 (P = .005).
Bariatric surgery was associated with a significant 24% lower risk of esophagogastric cancer (hazard ratio, 0.76; P = .03) and a 40% lower risk of overall in-hospital mortality, defined as “any death occurring during a hospital stay regardless of the cause” (HR, 0.60; P < .001).
The authors also found no significant difference in cancer outcomes and type of bariatric procedure, which included sleeve gastrectomy, gastric bypass, and adjustable gastric banding.
They note that key study limitations include the retrospective design, limited follow-up period, and lack of histologic data on the specific cancers. In addition, the study population was relatively young, whereas esophageal cancer is more common in older people.
But overall, the findings suggest that bariatric surgery can be performed to treat severe obesity without increasing the risk of esophageal and gastric cancer, the authors conclude.
“It seems that the balance between protective factors (weight loss, metabolic effects, and eradication of H. pylori infection) and risk factors (GERD and bile reflux) for cancer after bariatric surgery is in favor of protective factors,” the authors, led by Andrea Lazzati, MD, PhD, of Centre Hospitalier Intercommunal de Créteil, France, explain.
Although the potential protective mechanisms remain unclear, in their commentary, Dr. Gorecki and Dr. Zenilman suggest that a reduction in chronic inflammation and immunosuppression following bariatric surgery could help explain the results.
Although the study provides “reassurance of the protective clinical benefits of weight loss surgery,” more large-scale studies are needed to “better identify, elucidate, and address the pathophysiological processes of bariatric procedure,” Dr. Gorecki and Dr. Zenilman conclude.
No specific funding for the study was reported. Dr. Lazzati has received personal fees from Johnson & Johnson, Medtronic, and Gore. Dr. Zenilman has received personal fees from Academic Medical Professionals Insurance and Mohamed & Obaid Almulla Group.
A version of this article first appeared on Medscape.com.
In fact, an analysis of close to 1 million French adults suggests that the weight-loss surgery may offer some protection against these cancers.
The study results present a “clinical paradox,” according to authors of a commentary published this week along with the study in JAMA Surgery. A procedure known to increase the risk of gastroesophageal reflux disease (GERD), and potentially adenocarcinoma of the distal esophagus and gastroesophageal junction, may help shield patients from esophagogastric cancer.
The study marks “an important step toward improving the understanding of potential lifetime risks of bariatric surgery and overall major health benefits of surgically induced weight loss,” commentary authors Piotr Gorecki, MD, and Michael Zenilman, MD, with Weill Cornell Medicine in New York, write.
Recent data indicate that excess body weight is associated with nearly 8% of cancer cases and 6.5% of cancer deaths. Studies also show that bariatric surgery can reduce the risk of some cancers, but whether this extends to esophageal and gastric cancer remains unclear.
To investigate, the researchers used French national data to compare the incidence of esophageal and gastric cancer in 303,709 mostly female patients with obesity who underwent bariatric surgery and a matched group of 605,140 patients with obesity who did not undergo the surgery.
The mean age of the cohort was about 40 years. The mean period of follow-up was 6 years for the surgery group and 5.6 years for the control arm. A total of 337 patients underwent esophagogastric cancer – 83 in the surgical group and 254 in the control group. Gastric cancer was about two times more common than esophageal cancer (225 vs. 112 patients).
The incidence rate of esophagogastric cancer was higher in the control group than in the surgery group – 6.9 vs. 4.9 cases per 100,000 population per year, for an incidence rate ratio of 1.42 (P = .005).
Bariatric surgery was associated with a significant 24% lower risk of esophagogastric cancer (hazard ratio, 0.76; P = .03) and a 40% lower risk of overall in-hospital mortality, defined as “any death occurring during a hospital stay regardless of the cause” (HR, 0.60; P < .001).
The authors also found no significant difference in cancer outcomes and type of bariatric procedure, which included sleeve gastrectomy, gastric bypass, and adjustable gastric banding.
They note that key study limitations include the retrospective design, limited follow-up period, and lack of histologic data on the specific cancers. In addition, the study population was relatively young, whereas esophageal cancer is more common in older people.
But overall, the findings suggest that bariatric surgery can be performed to treat severe obesity without increasing the risk of esophageal and gastric cancer, the authors conclude.
“It seems that the balance between protective factors (weight loss, metabolic effects, and eradication of H. pylori infection) and risk factors (GERD and bile reflux) for cancer after bariatric surgery is in favor of protective factors,” the authors, led by Andrea Lazzati, MD, PhD, of Centre Hospitalier Intercommunal de Créteil, France, explain.
Although the potential protective mechanisms remain unclear, in their commentary, Dr. Gorecki and Dr. Zenilman suggest that a reduction in chronic inflammation and immunosuppression following bariatric surgery could help explain the results.
Although the study provides “reassurance of the protective clinical benefits of weight loss surgery,” more large-scale studies are needed to “better identify, elucidate, and address the pathophysiological processes of bariatric procedure,” Dr. Gorecki and Dr. Zenilman conclude.
No specific funding for the study was reported. Dr. Lazzati has received personal fees from Johnson & Johnson, Medtronic, and Gore. Dr. Zenilman has received personal fees from Academic Medical Professionals Insurance and Mohamed & Obaid Almulla Group.
A version of this article first appeared on Medscape.com.
In fact, an analysis of close to 1 million French adults suggests that the weight-loss surgery may offer some protection against these cancers.
The study results present a “clinical paradox,” according to authors of a commentary published this week along with the study in JAMA Surgery. A procedure known to increase the risk of gastroesophageal reflux disease (GERD), and potentially adenocarcinoma of the distal esophagus and gastroesophageal junction, may help shield patients from esophagogastric cancer.
The study marks “an important step toward improving the understanding of potential lifetime risks of bariatric surgery and overall major health benefits of surgically induced weight loss,” commentary authors Piotr Gorecki, MD, and Michael Zenilman, MD, with Weill Cornell Medicine in New York, write.
Recent data indicate that excess body weight is associated with nearly 8% of cancer cases and 6.5% of cancer deaths. Studies also show that bariatric surgery can reduce the risk of some cancers, but whether this extends to esophageal and gastric cancer remains unclear.
To investigate, the researchers used French national data to compare the incidence of esophageal and gastric cancer in 303,709 mostly female patients with obesity who underwent bariatric surgery and a matched group of 605,140 patients with obesity who did not undergo the surgery.
The mean age of the cohort was about 40 years. The mean period of follow-up was 6 years for the surgery group and 5.6 years for the control arm. A total of 337 patients underwent esophagogastric cancer – 83 in the surgical group and 254 in the control group. Gastric cancer was about two times more common than esophageal cancer (225 vs. 112 patients).
The incidence rate of esophagogastric cancer was higher in the control group than in the surgery group – 6.9 vs. 4.9 cases per 100,000 population per year, for an incidence rate ratio of 1.42 (P = .005).
Bariatric surgery was associated with a significant 24% lower risk of esophagogastric cancer (hazard ratio, 0.76; P = .03) and a 40% lower risk of overall in-hospital mortality, defined as “any death occurring during a hospital stay regardless of the cause” (HR, 0.60; P < .001).
The authors also found no significant difference in cancer outcomes and type of bariatric procedure, which included sleeve gastrectomy, gastric bypass, and adjustable gastric banding.
They note that key study limitations include the retrospective design, limited follow-up period, and lack of histologic data on the specific cancers. In addition, the study population was relatively young, whereas esophageal cancer is more common in older people.
But overall, the findings suggest that bariatric surgery can be performed to treat severe obesity without increasing the risk of esophageal and gastric cancer, the authors conclude.
“It seems that the balance between protective factors (weight loss, metabolic effects, and eradication of H. pylori infection) and risk factors (GERD and bile reflux) for cancer after bariatric surgery is in favor of protective factors,” the authors, led by Andrea Lazzati, MD, PhD, of Centre Hospitalier Intercommunal de Créteil, France, explain.
Although the potential protective mechanisms remain unclear, in their commentary, Dr. Gorecki and Dr. Zenilman suggest that a reduction in chronic inflammation and immunosuppression following bariatric surgery could help explain the results.
Although the study provides “reassurance of the protective clinical benefits of weight loss surgery,” more large-scale studies are needed to “better identify, elucidate, and address the pathophysiological processes of bariatric procedure,” Dr. Gorecki and Dr. Zenilman conclude.
No specific funding for the study was reported. Dr. Lazzati has received personal fees from Johnson & Johnson, Medtronic, and Gore. Dr. Zenilman has received personal fees from Academic Medical Professionals Insurance and Mohamed & Obaid Almulla Group.
A version of this article first appeared on Medscape.com.
FROM JAMA SURGERY
Two novel JAK inhibitors show promise in ulcerative colitis
of the two investigational agents.
The study by William J. Sandborn, MD, division of gastroenterology, University of California, San Diego, and colleagues was published online in Clinical Gastroenterology and Hepatology.
Ritlecitinib is a dual inhibitor that selectively inhibits Janus kinase 3 (JAK3) and the TEC family of tyrosine kinases, while brepocitinib is a dual tyrosine kinase 2 (TYK2) and JAK1 inhibitor.
Both agents have demonstrated efficacy and acceptable safety in the treatment of alopecia areata and rheumatoid arthritis and are being evaluated for treating vitiligo, Crohn’s disease, and UC.
The different JAK selectivity profiles of ritlecitinib (JAK3/TEC) and brepocitinib (TYK2/JAK1), compared with other JAK inhibitors, could further the understanding of the role these pathways play in UC, the investigators note.
The VIBRATO study
As part of the phase 2b VIBRATO study, 317 patients with moderate to severe active UC (total Mayo Score ≥ 6) were randomly assigned to an 8-week induction course of once-daily oral ritlecitinib (20, 70, or 200 mg), brepocitinib (10, 30, or 60 mg), or matching placebo.
At week 8, compared with placebo, treatment with ritlecitinib or brepocitinib was associated with significantly lower mean total Mayo Scores (the primary endpoint) and higher rates of clinical remission, endoscopic and histologic improvement, and mucosal healing.
For both drugs, improvement on most metrics was dose dependent, with greater benefit at the highest dose.
For example, the placebo-adjusted mean total Mayo Score at week 8 was −4.6 for ritlecitinib 200 mg (P < .001) and −3.2 for brepocitinib 60 mg (P < .001). Both agents showed a “rapid” onset of action, with significant effects on the partial Mayo Score seen after just 2 weeks of treatment, the authors report.
Modified clinical remission at week 8 (a key secondary endpoint) was achieved in 36% of patients taking ritlecitinib 200 mg and 25.5% of those taking brepocitinib 60 mg (vs. 0% for patients taking placebo).
Endoscopic and histologic improvement, clinical response, mucosal healing, and the patient-reported outcome on the Inflammatory Bowel Disease Questionnaire followed a similar pattern, with a dose-dependent increase in treatment effect observed in most parameters at week 8, compared with placebo.
Longer-term data needed
Both agents were well tolerated with “acceptable short-term safety profiles,” the authors say.
There were no clinically significant findings for any laboratory parameters evaluated. Adverse events were mostly mild.
Infections were observed in 8.7% of patients taking ritlecitinib and 16.9% of those taking brepocitinib, compared with 4% of patients taking placebo. No serious cases of herpes zoster occurred.
One patient taking ritlecitinib suffered myocardial infarction and died, and one patient taking brepocitinib had peripheral artery thrombosis (left tibial artery). Both cases were considered unrelated to the study drug.
“As JAK inhibitors are associated with increased risk of major cardiovascular events and venous thromboembolisms, larger studies are needed for ritlecitinib and brepocitinib to fully understand their safety profiles,” the investigators say.
Limitations of the study include the small sample size and short 8-week treatment period. Longer-term safety and efficacy of both agents are being investigated.
The study was sponsored by Pfizer, which is developing both drugs. Dr. Sandborn and several coauthors have disclosed financial relationships with the company.
A version of this article first appeared on Medscape.com.
of the two investigational agents.
The study by William J. Sandborn, MD, division of gastroenterology, University of California, San Diego, and colleagues was published online in Clinical Gastroenterology and Hepatology.
Ritlecitinib is a dual inhibitor that selectively inhibits Janus kinase 3 (JAK3) and the TEC family of tyrosine kinases, while brepocitinib is a dual tyrosine kinase 2 (TYK2) and JAK1 inhibitor.
Both agents have demonstrated efficacy and acceptable safety in the treatment of alopecia areata and rheumatoid arthritis and are being evaluated for treating vitiligo, Crohn’s disease, and UC.
The different JAK selectivity profiles of ritlecitinib (JAK3/TEC) and brepocitinib (TYK2/JAK1), compared with other JAK inhibitors, could further the understanding of the role these pathways play in UC, the investigators note.
The VIBRATO study
As part of the phase 2b VIBRATO study, 317 patients with moderate to severe active UC (total Mayo Score ≥ 6) were randomly assigned to an 8-week induction course of once-daily oral ritlecitinib (20, 70, or 200 mg), brepocitinib (10, 30, or 60 mg), or matching placebo.
At week 8, compared with placebo, treatment with ritlecitinib or brepocitinib was associated with significantly lower mean total Mayo Scores (the primary endpoint) and higher rates of clinical remission, endoscopic and histologic improvement, and mucosal healing.
For both drugs, improvement on most metrics was dose dependent, with greater benefit at the highest dose.
For example, the placebo-adjusted mean total Mayo Score at week 8 was −4.6 for ritlecitinib 200 mg (P < .001) and −3.2 for brepocitinib 60 mg (P < .001). Both agents showed a “rapid” onset of action, with significant effects on the partial Mayo Score seen after just 2 weeks of treatment, the authors report.
Modified clinical remission at week 8 (a key secondary endpoint) was achieved in 36% of patients taking ritlecitinib 200 mg and 25.5% of those taking brepocitinib 60 mg (vs. 0% for patients taking placebo).
Endoscopic and histologic improvement, clinical response, mucosal healing, and the patient-reported outcome on the Inflammatory Bowel Disease Questionnaire followed a similar pattern, with a dose-dependent increase in treatment effect observed in most parameters at week 8, compared with placebo.
Longer-term data needed
Both agents were well tolerated with “acceptable short-term safety profiles,” the authors say.
There were no clinically significant findings for any laboratory parameters evaluated. Adverse events were mostly mild.
Infections were observed in 8.7% of patients taking ritlecitinib and 16.9% of those taking brepocitinib, compared with 4% of patients taking placebo. No serious cases of herpes zoster occurred.
One patient taking ritlecitinib suffered myocardial infarction and died, and one patient taking brepocitinib had peripheral artery thrombosis (left tibial artery). Both cases were considered unrelated to the study drug.
“As JAK inhibitors are associated with increased risk of major cardiovascular events and venous thromboembolisms, larger studies are needed for ritlecitinib and brepocitinib to fully understand their safety profiles,” the investigators say.
Limitations of the study include the small sample size and short 8-week treatment period. Longer-term safety and efficacy of both agents are being investigated.
The study was sponsored by Pfizer, which is developing both drugs. Dr. Sandborn and several coauthors have disclosed financial relationships with the company.
A version of this article first appeared on Medscape.com.
of the two investigational agents.
The study by William J. Sandborn, MD, division of gastroenterology, University of California, San Diego, and colleagues was published online in Clinical Gastroenterology and Hepatology.
Ritlecitinib is a dual inhibitor that selectively inhibits Janus kinase 3 (JAK3) and the TEC family of tyrosine kinases, while brepocitinib is a dual tyrosine kinase 2 (TYK2) and JAK1 inhibitor.
Both agents have demonstrated efficacy and acceptable safety in the treatment of alopecia areata and rheumatoid arthritis and are being evaluated for treating vitiligo, Crohn’s disease, and UC.
The different JAK selectivity profiles of ritlecitinib (JAK3/TEC) and brepocitinib (TYK2/JAK1), compared with other JAK inhibitors, could further the understanding of the role these pathways play in UC, the investigators note.
The VIBRATO study
As part of the phase 2b VIBRATO study, 317 patients with moderate to severe active UC (total Mayo Score ≥ 6) were randomly assigned to an 8-week induction course of once-daily oral ritlecitinib (20, 70, or 200 mg), brepocitinib (10, 30, or 60 mg), or matching placebo.
At week 8, compared with placebo, treatment with ritlecitinib or brepocitinib was associated with significantly lower mean total Mayo Scores (the primary endpoint) and higher rates of clinical remission, endoscopic and histologic improvement, and mucosal healing.
For both drugs, improvement on most metrics was dose dependent, with greater benefit at the highest dose.
For example, the placebo-adjusted mean total Mayo Score at week 8 was −4.6 for ritlecitinib 200 mg (P < .001) and −3.2 for brepocitinib 60 mg (P < .001). Both agents showed a “rapid” onset of action, with significant effects on the partial Mayo Score seen after just 2 weeks of treatment, the authors report.
Modified clinical remission at week 8 (a key secondary endpoint) was achieved in 36% of patients taking ritlecitinib 200 mg and 25.5% of those taking brepocitinib 60 mg (vs. 0% for patients taking placebo).
Endoscopic and histologic improvement, clinical response, mucosal healing, and the patient-reported outcome on the Inflammatory Bowel Disease Questionnaire followed a similar pattern, with a dose-dependent increase in treatment effect observed in most parameters at week 8, compared with placebo.
Longer-term data needed
Both agents were well tolerated with “acceptable short-term safety profiles,” the authors say.
There were no clinically significant findings for any laboratory parameters evaluated. Adverse events were mostly mild.
Infections were observed in 8.7% of patients taking ritlecitinib and 16.9% of those taking brepocitinib, compared with 4% of patients taking placebo. No serious cases of herpes zoster occurred.
One patient taking ritlecitinib suffered myocardial infarction and died, and one patient taking brepocitinib had peripheral artery thrombosis (left tibial artery). Both cases were considered unrelated to the study drug.
“As JAK inhibitors are associated with increased risk of major cardiovascular events and venous thromboembolisms, larger studies are needed for ritlecitinib and brepocitinib to fully understand their safety profiles,” the investigators say.
Limitations of the study include the small sample size and short 8-week treatment period. Longer-term safety and efficacy of both agents are being investigated.
The study was sponsored by Pfizer, which is developing both drugs. Dr. Sandborn and several coauthors have disclosed financial relationships with the company.
A version of this article first appeared on Medscape.com.
FROM CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
Arkansas cardiologist pays $900K to settle false claims allegations
in violation of the False Claims Act.
As part of the settlement, Dr. Tauth will enter into an integrity agreement with the U.S. Department of Health & Human Services, according to a news release from Henry Leventis, U.S. attorney for the Middle District of Tennessee.
“Health care fraud is a top priority of this office. We will aggressively pursue all those who are involved in fraud against government programs,” Mr. Leventis said.
Dr. Tauth formerly treated patients at National Park Medical Center (NPMC) in Hot Springs. The alleged false claims were submitted from September 2013 through August 2019.
The settlement with Dr. Tauth, aged 60, follows a November 2019 voluntary disclosure of the alleged false claims by Brentwood, Tenn.–based Lifepoint Health, which acquired NPMC and Hot Springs Cardiology Associates in November 2018.
NPMC and Hot Springs Cardiology entered into a settlement in October 2020 for the alleged violations and agreed to pay roughly $14.6 million, which includes over $9 million in restitution, according to the news release.
NPMC CEO Scott Smith said NPMC is “committed to maintaining high standards of integrity, legal compliance, and quality care for our patients. We regularly monitor our processes, procedures, and reporting and actively self-report concerns to regulators to ensure we are upholding these standards across our organization.”
“We are proud that our hospital took the appropriate steps to promptly self-report and finalize a settlement with the government for a swift resolution more than 2 years ago,” Mr. Smith said.
Dr. Tauth, however, maintains that the allegations made by NPMC are false.
“I am pleased to have reached a settlement agreement with the Department of Justice regarding allegations brought to them by my former employer, National Park Medical Center,” he said in a statement.
“The settlement agreement specifically states that it is not ‘an admission of liability’ by me, and I remain steadfast in my position that the allegations made by my former employer are false and without merit,” Dr. Tauth added.
He further stated that he has “chosen to enter into the settlement agreement because the legal process initiated by National Park’s allegations has been emotionally and financially damaging to me and my family in the extreme, and a settlement puts an end to the delays, uncertainties, inconveniences, and expenses of protracted litigation. Settlement is in the best interests of my family, my patients, and my medical practice.”
Dr. Tauth said he is “extremely grateful for the support I have received from my patients, medical staff, colleagues, friends, and family during this difficult time, and I look forward to providing high-quality cardiac care in the greater Hot Springs community for many years to come.”
A version of this article first appeared on Medscape.com.
in violation of the False Claims Act.
As part of the settlement, Dr. Tauth will enter into an integrity agreement with the U.S. Department of Health & Human Services, according to a news release from Henry Leventis, U.S. attorney for the Middle District of Tennessee.
“Health care fraud is a top priority of this office. We will aggressively pursue all those who are involved in fraud against government programs,” Mr. Leventis said.
Dr. Tauth formerly treated patients at National Park Medical Center (NPMC) in Hot Springs. The alleged false claims were submitted from September 2013 through August 2019.
The settlement with Dr. Tauth, aged 60, follows a November 2019 voluntary disclosure of the alleged false claims by Brentwood, Tenn.–based Lifepoint Health, which acquired NPMC and Hot Springs Cardiology Associates in November 2018.
NPMC and Hot Springs Cardiology entered into a settlement in October 2020 for the alleged violations and agreed to pay roughly $14.6 million, which includes over $9 million in restitution, according to the news release.
NPMC CEO Scott Smith said NPMC is “committed to maintaining high standards of integrity, legal compliance, and quality care for our patients. We regularly monitor our processes, procedures, and reporting and actively self-report concerns to regulators to ensure we are upholding these standards across our organization.”
“We are proud that our hospital took the appropriate steps to promptly self-report and finalize a settlement with the government for a swift resolution more than 2 years ago,” Mr. Smith said.
Dr. Tauth, however, maintains that the allegations made by NPMC are false.
“I am pleased to have reached a settlement agreement with the Department of Justice regarding allegations brought to them by my former employer, National Park Medical Center,” he said in a statement.
“The settlement agreement specifically states that it is not ‘an admission of liability’ by me, and I remain steadfast in my position that the allegations made by my former employer are false and without merit,” Dr. Tauth added.
He further stated that he has “chosen to enter into the settlement agreement because the legal process initiated by National Park’s allegations has been emotionally and financially damaging to me and my family in the extreme, and a settlement puts an end to the delays, uncertainties, inconveniences, and expenses of protracted litigation. Settlement is in the best interests of my family, my patients, and my medical practice.”
Dr. Tauth said he is “extremely grateful for the support I have received from my patients, medical staff, colleagues, friends, and family during this difficult time, and I look forward to providing high-quality cardiac care in the greater Hot Springs community for many years to come.”
A version of this article first appeared on Medscape.com.
in violation of the False Claims Act.
As part of the settlement, Dr. Tauth will enter into an integrity agreement with the U.S. Department of Health & Human Services, according to a news release from Henry Leventis, U.S. attorney for the Middle District of Tennessee.
“Health care fraud is a top priority of this office. We will aggressively pursue all those who are involved in fraud against government programs,” Mr. Leventis said.
Dr. Tauth formerly treated patients at National Park Medical Center (NPMC) in Hot Springs. The alleged false claims were submitted from September 2013 through August 2019.
The settlement with Dr. Tauth, aged 60, follows a November 2019 voluntary disclosure of the alleged false claims by Brentwood, Tenn.–based Lifepoint Health, which acquired NPMC and Hot Springs Cardiology Associates in November 2018.
NPMC and Hot Springs Cardiology entered into a settlement in October 2020 for the alleged violations and agreed to pay roughly $14.6 million, which includes over $9 million in restitution, according to the news release.
NPMC CEO Scott Smith said NPMC is “committed to maintaining high standards of integrity, legal compliance, and quality care for our patients. We regularly monitor our processes, procedures, and reporting and actively self-report concerns to regulators to ensure we are upholding these standards across our organization.”
“We are proud that our hospital took the appropriate steps to promptly self-report and finalize a settlement with the government for a swift resolution more than 2 years ago,” Mr. Smith said.
Dr. Tauth, however, maintains that the allegations made by NPMC are false.
“I am pleased to have reached a settlement agreement with the Department of Justice regarding allegations brought to them by my former employer, National Park Medical Center,” he said in a statement.
“The settlement agreement specifically states that it is not ‘an admission of liability’ by me, and I remain steadfast in my position that the allegations made by my former employer are false and without merit,” Dr. Tauth added.
He further stated that he has “chosen to enter into the settlement agreement because the legal process initiated by National Park’s allegations has been emotionally and financially damaging to me and my family in the extreme, and a settlement puts an end to the delays, uncertainties, inconveniences, and expenses of protracted litigation. Settlement is in the best interests of my family, my patients, and my medical practice.”
Dr. Tauth said he is “extremely grateful for the support I have received from my patients, medical staff, colleagues, friends, and family during this difficult time, and I look forward to providing high-quality cardiac care in the greater Hot Springs community for many years to come.”
A version of this article first appeared on Medscape.com.
Strong support to provide DAA therapy to all patients with HCV
, a large, real-world analysis finds.
Improved outcomes were seen among patients without cirrhosis, those with compensated cirrhosis, and those with existing liver decompensation, the authors noted.
The findings highlight a “substantial need to provide DAA therapy to all patients with HCV, regardless of disease stage or financial status,” wrote Mindie Nguyen, MD, of Stanford University Medical Center, Palo Alto, Calif., and coinvestigators.
“Additional national efforts are needed to reach and treat U.S. population groups that are underinsured or not insured, incarcerated and otherwise marginalized, such as users of illicit drugs, who are also at higher risk of disease complication and reinfection,” they said.
The study was published online in JAMA Internal Medicine.
CHC and its complications are associated with high rates of illness and death. However, large-scale data on long-term liver and nonliver effects of DAA treatment are limited.
For their study, Dr. Nguyen and colleagues analyzed administrative claims data from 2010 to 2021 for 245,596 adults with CHC, of whom 40,654 had received one or more DAA therapies (without interferon) and 204,942 had not received treatment.
DAA-treated patients were slightly older than their untreated peers (mean age, 59.9 years, vs. 58.5 years) and were more likely to be male (62% vs. 58%) and White (59% vs. 57%), and to have diabetes (26% vs. 25%) and cirrhosis (44% vs. 29%).
For liver outcomes, DAA therapy was associated with a lower incidence of decompensation (28.2 vs. 40.8 per 1,000 person-years; P < .001) and hepatocellular carcinoma (HCC) in compensated cirrhosis (20.1 vs. 41.8; P < .001).
For nonliver outcomes, DAA treatment was associated with a lower incidence of diabetes (30.2 vs. 37.2 per 1,000 person-years; P < .001) and chronic kidney disease (31.1 vs. 34.1; P < .001).
The all-cause mortality rate per 1,000 person-years was 36.5 in the DAA-treated group, vs. 64.7 in the untreated group (P < .001).
In multivariable regression analysis, DAA treatment was independently associated with a significant decrease in the risk for HCC (adjusted hazard ratio [aHR], 0.73), decompensation (aHR, 0.36), diabetes (aHR, 0.74), chronic kidney disease (aHR, 0.81), cardiovascular disease (aHR, 0.90), nonliver cancer (aHR, 0.89), and mortality (aHR, 0.43).
The 57% lower mortality rate observed among DAA-treated vs. untreated patients aligns with a large French study of adults with CHC.
“Because HCV treatment with a DAA regimen is well tolerated for nearly all patients, we believe these findings provide further support for universal HCV treatment coverage for all patients affected by HCV,” Dr. Nguyen and colleagues wrote.
The strengths of this study are its large sample of DAA-treated and untreated patients from diverse racial and ethnic groups from across the United States and from diverse practice settings (not just tertiary centers).
One limitation is that the study cohort included only patients covered by private insurance; therefore, the findings may not be generalizable to individuals who are underinsured or not insured. Miscoding and misclassification are also possible with large claims databases.
Support for the study was provided by Stanford University and the Stanford Center for Population Health Sciences. Dr. Nguyen has received institutional grants and advisory board fees from Gilead Sciences outside the submitted work.
A version of this article first appeared on Medscape.com.
, a large, real-world analysis finds.
Improved outcomes were seen among patients without cirrhosis, those with compensated cirrhosis, and those with existing liver decompensation, the authors noted.
The findings highlight a “substantial need to provide DAA therapy to all patients with HCV, regardless of disease stage or financial status,” wrote Mindie Nguyen, MD, of Stanford University Medical Center, Palo Alto, Calif., and coinvestigators.
“Additional national efforts are needed to reach and treat U.S. population groups that are underinsured or not insured, incarcerated and otherwise marginalized, such as users of illicit drugs, who are also at higher risk of disease complication and reinfection,” they said.
The study was published online in JAMA Internal Medicine.
CHC and its complications are associated with high rates of illness and death. However, large-scale data on long-term liver and nonliver effects of DAA treatment are limited.
For their study, Dr. Nguyen and colleagues analyzed administrative claims data from 2010 to 2021 for 245,596 adults with CHC, of whom 40,654 had received one or more DAA therapies (without interferon) and 204,942 had not received treatment.
DAA-treated patients were slightly older than their untreated peers (mean age, 59.9 years, vs. 58.5 years) and were more likely to be male (62% vs. 58%) and White (59% vs. 57%), and to have diabetes (26% vs. 25%) and cirrhosis (44% vs. 29%).
For liver outcomes, DAA therapy was associated with a lower incidence of decompensation (28.2 vs. 40.8 per 1,000 person-years; P < .001) and hepatocellular carcinoma (HCC) in compensated cirrhosis (20.1 vs. 41.8; P < .001).
For nonliver outcomes, DAA treatment was associated with a lower incidence of diabetes (30.2 vs. 37.2 per 1,000 person-years; P < .001) and chronic kidney disease (31.1 vs. 34.1; P < .001).
The all-cause mortality rate per 1,000 person-years was 36.5 in the DAA-treated group, vs. 64.7 in the untreated group (P < .001).
In multivariable regression analysis, DAA treatment was independently associated with a significant decrease in the risk for HCC (adjusted hazard ratio [aHR], 0.73), decompensation (aHR, 0.36), diabetes (aHR, 0.74), chronic kidney disease (aHR, 0.81), cardiovascular disease (aHR, 0.90), nonliver cancer (aHR, 0.89), and mortality (aHR, 0.43).
The 57% lower mortality rate observed among DAA-treated vs. untreated patients aligns with a large French study of adults with CHC.
“Because HCV treatment with a DAA regimen is well tolerated for nearly all patients, we believe these findings provide further support for universal HCV treatment coverage for all patients affected by HCV,” Dr. Nguyen and colleagues wrote.
The strengths of this study are its large sample of DAA-treated and untreated patients from diverse racial and ethnic groups from across the United States and from diverse practice settings (not just tertiary centers).
One limitation is that the study cohort included only patients covered by private insurance; therefore, the findings may not be generalizable to individuals who are underinsured or not insured. Miscoding and misclassification are also possible with large claims databases.
Support for the study was provided by Stanford University and the Stanford Center for Population Health Sciences. Dr. Nguyen has received institutional grants and advisory board fees from Gilead Sciences outside the submitted work.
A version of this article first appeared on Medscape.com.
, a large, real-world analysis finds.
Improved outcomes were seen among patients without cirrhosis, those with compensated cirrhosis, and those with existing liver decompensation, the authors noted.
The findings highlight a “substantial need to provide DAA therapy to all patients with HCV, regardless of disease stage or financial status,” wrote Mindie Nguyen, MD, of Stanford University Medical Center, Palo Alto, Calif., and coinvestigators.
“Additional national efforts are needed to reach and treat U.S. population groups that are underinsured or not insured, incarcerated and otherwise marginalized, such as users of illicit drugs, who are also at higher risk of disease complication and reinfection,” they said.
The study was published online in JAMA Internal Medicine.
CHC and its complications are associated with high rates of illness and death. However, large-scale data on long-term liver and nonliver effects of DAA treatment are limited.
For their study, Dr. Nguyen and colleagues analyzed administrative claims data from 2010 to 2021 for 245,596 adults with CHC, of whom 40,654 had received one or more DAA therapies (without interferon) and 204,942 had not received treatment.
DAA-treated patients were slightly older than their untreated peers (mean age, 59.9 years, vs. 58.5 years) and were more likely to be male (62% vs. 58%) and White (59% vs. 57%), and to have diabetes (26% vs. 25%) and cirrhosis (44% vs. 29%).
For liver outcomes, DAA therapy was associated with a lower incidence of decompensation (28.2 vs. 40.8 per 1,000 person-years; P < .001) and hepatocellular carcinoma (HCC) in compensated cirrhosis (20.1 vs. 41.8; P < .001).
For nonliver outcomes, DAA treatment was associated with a lower incidence of diabetes (30.2 vs. 37.2 per 1,000 person-years; P < .001) and chronic kidney disease (31.1 vs. 34.1; P < .001).
The all-cause mortality rate per 1,000 person-years was 36.5 in the DAA-treated group, vs. 64.7 in the untreated group (P < .001).
In multivariable regression analysis, DAA treatment was independently associated with a significant decrease in the risk for HCC (adjusted hazard ratio [aHR], 0.73), decompensation (aHR, 0.36), diabetes (aHR, 0.74), chronic kidney disease (aHR, 0.81), cardiovascular disease (aHR, 0.90), nonliver cancer (aHR, 0.89), and mortality (aHR, 0.43).
The 57% lower mortality rate observed among DAA-treated vs. untreated patients aligns with a large French study of adults with CHC.
“Because HCV treatment with a DAA regimen is well tolerated for nearly all patients, we believe these findings provide further support for universal HCV treatment coverage for all patients affected by HCV,” Dr. Nguyen and colleagues wrote.
The strengths of this study are its large sample of DAA-treated and untreated patients from diverse racial and ethnic groups from across the United States and from diverse practice settings (not just tertiary centers).
One limitation is that the study cohort included only patients covered by private insurance; therefore, the findings may not be generalizable to individuals who are underinsured or not insured. Miscoding and misclassification are also possible with large claims databases.
Support for the study was provided by Stanford University and the Stanford Center for Population Health Sciences. Dr. Nguyen has received institutional grants and advisory board fees from Gilead Sciences outside the submitted work.
A version of this article first appeared on Medscape.com.
FROM JAMA INTERNAL MEDICINE
FDA approves second antiamyloid for Alzheimer’s disease
Like its controversial cousin aducanumab (Aduhelm, Biogen/Eisai), lecanemab was approved under the FDA’s accelerated approval pathway, which can be used to fast-track a drug that provides a meaningful therapeutic advantage over existing treatments for a serious or life-threatening illness.
Unlike aducanumab, however, there was no formal FDA advisory committee meeting on lecanemab prior to approval.
“Alzheimer’s disease immeasurably incapacitates the lives of those who suffer from it and has devastating effects on their loved ones,” Billy Dunn, MD, director of the Office of Neuroscience in the FDA’s Center for Drug Evaluation and Research, said in a press release.
“This treatment option is the latest therapy to target and affect the underlying disease process of Alzheimer’s, instead of only treating the symptoms of the disease,” Dr. Dunn added.
Eisai has reported that lecanemab will cost $26,500 a year.
Modest benefit, adverse events
The FDA noted, “The labeling states that treatment with Leqembi should be initiated in patients with mild cognitive impairment or mild dementia stage of disease, the population in which treatment was studied in clinical trials.”
The agency approved the treatment on the basis of findings from the CLARITY AD trial, which showed modest cognitive benefit for patients with early AD – but at a cost of increased risk for amyloid-related edema and effusions.
The trial enrolled 1,795 adults with mild cognitive impairment or early Alzheimer’s disease in whom amyloid pathology in the brain had been confirmed. Treatment consisted of lecanemab 10 mg/kg biweekly or matching placebo.
After 18 months of treatment, lecanemab slowed cognitive decline by 27%, compared with placebo, as measured by the Clinical Dementia Rating–Sum of Boxes (CDR-SB). This was an absolute difference of 0.45 points (change from baseline, 1.21 for lecanemab vs. 1.66 with placebo; P < .001).
While the results are “welcome news,” a 0.45-point difference on the CDR-SB might not be clinically meaningful, authors of a recent editorial in The Lancet cautioned.
Amyloid-related imaging abnormalities that manifest as edema or microhemorrhages also occurred in one in five patients taking lecanemab.
In addition, a newly published case report in The New England Journal of Medicine describes a patient with Alzheimer’s disease who was taking lecanemab and who died after experiencing numerous intracerebral hemorrhages during treatment with tissue plasminogen activator (tPA) for acute ischemic stroke.
“The findings raise the possibility of cerebral hemorrhages and necrotizing vasculopathy associated with tPA infusion in a patient with cerebrovascular amyloid who had received lecanemab,” the authors wrote.
Alzheimer’s Association reaction
Still, in anticipation of accelerated approval of lecanemab and the antiamyloid drug donanemab (Eli Lilly), which the FDA has also fast-tracked, the Alzheimer’s Association filed a formal request last month with the Centers for Medicare & Medicaid Services asking that it provide full and unrestricted coverage for FDA-approved Alzheimer’s disease treatments.
In a letter addressed to CMS administrator Chiquita Brooks-LaSure, the association asked the agency to remove the requirements for “coverage with evidence development” in its national coverage determination for FDA-approved antiamyloid monoclonal antibodies.
“Each day matters when it comes to slowing the progression of this disease,” Joanne Pike, DrPH, president and CEO for the Alzheimer’s Association, noted in a news release at the time.
“The current CMS policy to severely limit access to these treatments eliminates people’s options, is resulting in continued irreversible disease progression, and contributes to greater health inequities. That’s not acceptable,” Dr. Pike added.
After news of today’s approval was released, Dr. Pike noted in a new release, “The Alzheimer’s Association welcomes and celebrates this action by the FDA. We now have a second approved treatment that changes the course of Alzheimer’s disease in a meaningful way for people in the early stages of the disease.”
Maria C. Carrillo, PhD, chief science officer at the Alzheimer’s Association, called today’s approval “a milestone achievement.”
“The progress we’ve seen in not only this class of treatments but also in the diversification of treatment types and targets over the past few years is exciting and provides real hope to those impacted by this devastating disease,” Dr. Carrillo said.
Critical issues
Commenting on the approval, Alvaro Pascual-Leone, MD, PhD, professor of neurology at Harvard Medical School, Boston, and chief medical officer at Linus Health, said FDA approval of lecanemab and its adoption in the clinic represent a “very exciting development and prospect; but arguably some critical issues need to be considered.”
He noted that the health care system “is not currently prepared to cope with the challenges and demands of lecanemab,” as well as future pharmacologic agents.
“First, we need better workflows to identify suitable patients who can most benefit from this treatment,” said Dr. Pascual-Leone. He added that beyond identification of cognitive difficulties, amyloid status will need to be determined.
“Presently, this requires expensive and invasive tests,” such as positron-emission tomography scans or lumbar punctures for cerebrospinal fluid analysis. However, these are not fully covered by insurance companies and would be challenging to fully scale, he noted.
“In addition to screening, health systems will need to resolve the logistics challenges around the administration of lecanemab with twice-monthly infusions and the need for careful longitudinal evaluations for potential side effects,” said Dr. Pascual-Leone.
“While lecanemab may represent the first disease-modifying therapy widely available for early Alzheimer’s disease, the likely more promising approach is the addition of other therapies to lecanemab as part of a multi-intervention strategy combining pharmacologic and nonpharmacologic interventions,” he added.
Dr. Pascual-Leone has served as a paid member on scientific advisory boards for Neuroelectrics, Magstim, TetraNeuron, Skin2Neuron, MedRhythms, and Hearts Radiant and is a cofounder of TI Solutions and Linus Health.
A version of this article first appeared on Medscape.com.
This article was updated 1/9/23.
Like its controversial cousin aducanumab (Aduhelm, Biogen/Eisai), lecanemab was approved under the FDA’s accelerated approval pathway, which can be used to fast-track a drug that provides a meaningful therapeutic advantage over existing treatments for a serious or life-threatening illness.
Unlike aducanumab, however, there was no formal FDA advisory committee meeting on lecanemab prior to approval.
“Alzheimer’s disease immeasurably incapacitates the lives of those who suffer from it and has devastating effects on their loved ones,” Billy Dunn, MD, director of the Office of Neuroscience in the FDA’s Center for Drug Evaluation and Research, said in a press release.
“This treatment option is the latest therapy to target and affect the underlying disease process of Alzheimer’s, instead of only treating the symptoms of the disease,” Dr. Dunn added.
Eisai has reported that lecanemab will cost $26,500 a year.
Modest benefit, adverse events
The FDA noted, “The labeling states that treatment with Leqembi should be initiated in patients with mild cognitive impairment or mild dementia stage of disease, the population in which treatment was studied in clinical trials.”
The agency approved the treatment on the basis of findings from the CLARITY AD trial, which showed modest cognitive benefit for patients with early AD – but at a cost of increased risk for amyloid-related edema and effusions.
The trial enrolled 1,795 adults with mild cognitive impairment or early Alzheimer’s disease in whom amyloid pathology in the brain had been confirmed. Treatment consisted of lecanemab 10 mg/kg biweekly or matching placebo.
After 18 months of treatment, lecanemab slowed cognitive decline by 27%, compared with placebo, as measured by the Clinical Dementia Rating–Sum of Boxes (CDR-SB). This was an absolute difference of 0.45 points (change from baseline, 1.21 for lecanemab vs. 1.66 with placebo; P < .001).
While the results are “welcome news,” a 0.45-point difference on the CDR-SB might not be clinically meaningful, authors of a recent editorial in The Lancet cautioned.
Amyloid-related imaging abnormalities that manifest as edema or microhemorrhages also occurred in one in five patients taking lecanemab.
In addition, a newly published case report in The New England Journal of Medicine describes a patient with Alzheimer’s disease who was taking lecanemab and who died after experiencing numerous intracerebral hemorrhages during treatment with tissue plasminogen activator (tPA) for acute ischemic stroke.
“The findings raise the possibility of cerebral hemorrhages and necrotizing vasculopathy associated with tPA infusion in a patient with cerebrovascular amyloid who had received lecanemab,” the authors wrote.
Alzheimer’s Association reaction
Still, in anticipation of accelerated approval of lecanemab and the antiamyloid drug donanemab (Eli Lilly), which the FDA has also fast-tracked, the Alzheimer’s Association filed a formal request last month with the Centers for Medicare & Medicaid Services asking that it provide full and unrestricted coverage for FDA-approved Alzheimer’s disease treatments.
In a letter addressed to CMS administrator Chiquita Brooks-LaSure, the association asked the agency to remove the requirements for “coverage with evidence development” in its national coverage determination for FDA-approved antiamyloid monoclonal antibodies.
“Each day matters when it comes to slowing the progression of this disease,” Joanne Pike, DrPH, president and CEO for the Alzheimer’s Association, noted in a news release at the time.
“The current CMS policy to severely limit access to these treatments eliminates people’s options, is resulting in continued irreversible disease progression, and contributes to greater health inequities. That’s not acceptable,” Dr. Pike added.
After news of today’s approval was released, Dr. Pike noted in a new release, “The Alzheimer’s Association welcomes and celebrates this action by the FDA. We now have a second approved treatment that changes the course of Alzheimer’s disease in a meaningful way for people in the early stages of the disease.”
Maria C. Carrillo, PhD, chief science officer at the Alzheimer’s Association, called today’s approval “a milestone achievement.”
“The progress we’ve seen in not only this class of treatments but also in the diversification of treatment types and targets over the past few years is exciting and provides real hope to those impacted by this devastating disease,” Dr. Carrillo said.
Critical issues
Commenting on the approval, Alvaro Pascual-Leone, MD, PhD, professor of neurology at Harvard Medical School, Boston, and chief medical officer at Linus Health, said FDA approval of lecanemab and its adoption in the clinic represent a “very exciting development and prospect; but arguably some critical issues need to be considered.”
He noted that the health care system “is not currently prepared to cope with the challenges and demands of lecanemab,” as well as future pharmacologic agents.
“First, we need better workflows to identify suitable patients who can most benefit from this treatment,” said Dr. Pascual-Leone. He added that beyond identification of cognitive difficulties, amyloid status will need to be determined.
“Presently, this requires expensive and invasive tests,” such as positron-emission tomography scans or lumbar punctures for cerebrospinal fluid analysis. However, these are not fully covered by insurance companies and would be challenging to fully scale, he noted.
“In addition to screening, health systems will need to resolve the logistics challenges around the administration of lecanemab with twice-monthly infusions and the need for careful longitudinal evaluations for potential side effects,” said Dr. Pascual-Leone.
“While lecanemab may represent the first disease-modifying therapy widely available for early Alzheimer’s disease, the likely more promising approach is the addition of other therapies to lecanemab as part of a multi-intervention strategy combining pharmacologic and nonpharmacologic interventions,” he added.
Dr. Pascual-Leone has served as a paid member on scientific advisory boards for Neuroelectrics, Magstim, TetraNeuron, Skin2Neuron, MedRhythms, and Hearts Radiant and is a cofounder of TI Solutions and Linus Health.
A version of this article first appeared on Medscape.com.
This article was updated 1/9/23.
Like its controversial cousin aducanumab (Aduhelm, Biogen/Eisai), lecanemab was approved under the FDA’s accelerated approval pathway, which can be used to fast-track a drug that provides a meaningful therapeutic advantage over existing treatments for a serious or life-threatening illness.
Unlike aducanumab, however, there was no formal FDA advisory committee meeting on lecanemab prior to approval.
“Alzheimer’s disease immeasurably incapacitates the lives of those who suffer from it and has devastating effects on their loved ones,” Billy Dunn, MD, director of the Office of Neuroscience in the FDA’s Center for Drug Evaluation and Research, said in a press release.
“This treatment option is the latest therapy to target and affect the underlying disease process of Alzheimer’s, instead of only treating the symptoms of the disease,” Dr. Dunn added.
Eisai has reported that lecanemab will cost $26,500 a year.
Modest benefit, adverse events
The FDA noted, “The labeling states that treatment with Leqembi should be initiated in patients with mild cognitive impairment or mild dementia stage of disease, the population in which treatment was studied in clinical trials.”
The agency approved the treatment on the basis of findings from the CLARITY AD trial, which showed modest cognitive benefit for patients with early AD – but at a cost of increased risk for amyloid-related edema and effusions.
The trial enrolled 1,795 adults with mild cognitive impairment or early Alzheimer’s disease in whom amyloid pathology in the brain had been confirmed. Treatment consisted of lecanemab 10 mg/kg biweekly or matching placebo.
After 18 months of treatment, lecanemab slowed cognitive decline by 27%, compared with placebo, as measured by the Clinical Dementia Rating–Sum of Boxes (CDR-SB). This was an absolute difference of 0.45 points (change from baseline, 1.21 for lecanemab vs. 1.66 with placebo; P < .001).
While the results are “welcome news,” a 0.45-point difference on the CDR-SB might not be clinically meaningful, authors of a recent editorial in The Lancet cautioned.
Amyloid-related imaging abnormalities that manifest as edema or microhemorrhages also occurred in one in five patients taking lecanemab.
In addition, a newly published case report in The New England Journal of Medicine describes a patient with Alzheimer’s disease who was taking lecanemab and who died after experiencing numerous intracerebral hemorrhages during treatment with tissue plasminogen activator (tPA) for acute ischemic stroke.
“The findings raise the possibility of cerebral hemorrhages and necrotizing vasculopathy associated with tPA infusion in a patient with cerebrovascular amyloid who had received lecanemab,” the authors wrote.
Alzheimer’s Association reaction
Still, in anticipation of accelerated approval of lecanemab and the antiamyloid drug donanemab (Eli Lilly), which the FDA has also fast-tracked, the Alzheimer’s Association filed a formal request last month with the Centers for Medicare & Medicaid Services asking that it provide full and unrestricted coverage for FDA-approved Alzheimer’s disease treatments.
In a letter addressed to CMS administrator Chiquita Brooks-LaSure, the association asked the agency to remove the requirements for “coverage with evidence development” in its national coverage determination for FDA-approved antiamyloid monoclonal antibodies.
“Each day matters when it comes to slowing the progression of this disease,” Joanne Pike, DrPH, president and CEO for the Alzheimer’s Association, noted in a news release at the time.
“The current CMS policy to severely limit access to these treatments eliminates people’s options, is resulting in continued irreversible disease progression, and contributes to greater health inequities. That’s not acceptable,” Dr. Pike added.
After news of today’s approval was released, Dr. Pike noted in a new release, “The Alzheimer’s Association welcomes and celebrates this action by the FDA. We now have a second approved treatment that changes the course of Alzheimer’s disease in a meaningful way for people in the early stages of the disease.”
Maria C. Carrillo, PhD, chief science officer at the Alzheimer’s Association, called today’s approval “a milestone achievement.”
“The progress we’ve seen in not only this class of treatments but also in the diversification of treatment types and targets over the past few years is exciting and provides real hope to those impacted by this devastating disease,” Dr. Carrillo said.
Critical issues
Commenting on the approval, Alvaro Pascual-Leone, MD, PhD, professor of neurology at Harvard Medical School, Boston, and chief medical officer at Linus Health, said FDA approval of lecanemab and its adoption in the clinic represent a “very exciting development and prospect; but arguably some critical issues need to be considered.”
He noted that the health care system “is not currently prepared to cope with the challenges and demands of lecanemab,” as well as future pharmacologic agents.
“First, we need better workflows to identify suitable patients who can most benefit from this treatment,” said Dr. Pascual-Leone. He added that beyond identification of cognitive difficulties, amyloid status will need to be determined.
“Presently, this requires expensive and invasive tests,” such as positron-emission tomography scans or lumbar punctures for cerebrospinal fluid analysis. However, these are not fully covered by insurance companies and would be challenging to fully scale, he noted.
“In addition to screening, health systems will need to resolve the logistics challenges around the administration of lecanemab with twice-monthly infusions and the need for careful longitudinal evaluations for potential side effects,” said Dr. Pascual-Leone.
“While lecanemab may represent the first disease-modifying therapy widely available for early Alzheimer’s disease, the likely more promising approach is the addition of other therapies to lecanemab as part of a multi-intervention strategy combining pharmacologic and nonpharmacologic interventions,” he added.
Dr. Pascual-Leone has served as a paid member on scientific advisory boards for Neuroelectrics, Magstim, TetraNeuron, Skin2Neuron, MedRhythms, and Hearts Radiant and is a cofounder of TI Solutions and Linus Health.
A version of this article first appeared on Medscape.com.
This article was updated 1/9/23.