User login
Cardiologist sues hospital, claims he was fired in retaliation
alleging that he was fired and maligned after raising concerns about poorly performed surgeries and poor ethical practices at the hospital.
Dr. Zelman, from Barnstable, Mass., has been affiliated with Cape Cod Hospital in Hyannis, Mass., for more than 30 years. He helped found the hospital’s Heart and Vascular Institute and has served as its medical director since 2018.
In his lawsuit filed Dec. 6, Dr. Zelman alleges that the defendants, under Mr. Lauf’s leadership, “placed profit above all else, including by prioritizing revenue generation over patient safety and public health.”
Dr. Zelman says the defendants supported him “to the extent his actions were profitable.”
Yet, when he raised patient safety concerns that harmed that bottom line, Dr. Zelman says the defendants retaliated against him, including by threatening his career and reputation and unlawfully terminating his employment with the hospital.
The complaint notes Dr. Zelman is bringing this action “to recover damages for violations of the Massachusetts Healthcare Provider Whistleblower Statute ... as well as for breach of contract and common law claims.”
Dr. Zelman’s complaint alleges the defendants refused to adequately address the “dangerous care and violations of the professional standards of practice” that he reported, “resulting in harmful and tragic consequences.”
It also alleges Mr. Lauf restricted the use of a cerebral protection device used in patients undergoing transcatheter aortic-valve replacement (TAVR) deemed to be at high risk for periprocedural stroke to only those patients whose insurance reimbursed at higher rates.
Dr. Zelman says he objected to this prohibition “in accordance with his contractual and ethical obligations to ensure treatment of patients without regard to their ability to pay.”
Dr. Zelman’s lawsuit further alleges that Mr. Lauf launched a “trumped-up” and “baseless, biased, and retaliatory sham” investigation against him.
In a statement sent to the Boston Globe, Cape Cod Hospital denied Dr. Zelman’s claims that the cardiologist was retaliated against for raising patient safety issues, or that the hospital didn’t take action to improve cardiac care at the facility.
Voiced concerns
In a statement sent to this news organization, Dr. Zelman, now in private practice, said, “Over the past 25 years, I have been instrumental in bringing advanced cardiac care to Cape Cod. My commitment has always been to delivering the same quality outcomes and safety as the academic centers in Boston.
“Unfortunately, over the past 5 years, there has been inadequate oversight by the hospital administration and problems have occurred that in my opinion have led to serious patient consequences,” Dr. Zelman stated.
He said he has “voiced concerns over several years and they have been ignored.”
He added that Cape Cod Hospital offered him a million-dollar contract as long as he agreed to immediately issue a written statement endorsing the quality and safety of the cardiac surgical program that no longer exists.
“No amount of money was going to buy my silence,” Dr. Zelman told this news organization.
In his lawsuit, Dr. Zelman is seeking an undisclosed amount in damages, including back and front pay, lost benefits, physical and emotional distress, and attorneys’ fees.
This news organization reached out to Cape Cod Hospital for comment but has not yet received a response.
A version of this article first appeared on Medscape.com.
alleging that he was fired and maligned after raising concerns about poorly performed surgeries and poor ethical practices at the hospital.
Dr. Zelman, from Barnstable, Mass., has been affiliated with Cape Cod Hospital in Hyannis, Mass., for more than 30 years. He helped found the hospital’s Heart and Vascular Institute and has served as its medical director since 2018.
In his lawsuit filed Dec. 6, Dr. Zelman alleges that the defendants, under Mr. Lauf’s leadership, “placed profit above all else, including by prioritizing revenue generation over patient safety and public health.”
Dr. Zelman says the defendants supported him “to the extent his actions were profitable.”
Yet, when he raised patient safety concerns that harmed that bottom line, Dr. Zelman says the defendants retaliated against him, including by threatening his career and reputation and unlawfully terminating his employment with the hospital.
The complaint notes Dr. Zelman is bringing this action “to recover damages for violations of the Massachusetts Healthcare Provider Whistleblower Statute ... as well as for breach of contract and common law claims.”
Dr. Zelman’s complaint alleges the defendants refused to adequately address the “dangerous care and violations of the professional standards of practice” that he reported, “resulting in harmful and tragic consequences.”
It also alleges Mr. Lauf restricted the use of a cerebral protection device used in patients undergoing transcatheter aortic-valve replacement (TAVR) deemed to be at high risk for periprocedural stroke to only those patients whose insurance reimbursed at higher rates.
Dr. Zelman says he objected to this prohibition “in accordance with his contractual and ethical obligations to ensure treatment of patients without regard to their ability to pay.”
Dr. Zelman’s lawsuit further alleges that Mr. Lauf launched a “trumped-up” and “baseless, biased, and retaliatory sham” investigation against him.
In a statement sent to the Boston Globe, Cape Cod Hospital denied Dr. Zelman’s claims that the cardiologist was retaliated against for raising patient safety issues, or that the hospital didn’t take action to improve cardiac care at the facility.
Voiced concerns
In a statement sent to this news organization, Dr. Zelman, now in private practice, said, “Over the past 25 years, I have been instrumental in bringing advanced cardiac care to Cape Cod. My commitment has always been to delivering the same quality outcomes and safety as the academic centers in Boston.
“Unfortunately, over the past 5 years, there has been inadequate oversight by the hospital administration and problems have occurred that in my opinion have led to serious patient consequences,” Dr. Zelman stated.
He said he has “voiced concerns over several years and they have been ignored.”
He added that Cape Cod Hospital offered him a million-dollar contract as long as he agreed to immediately issue a written statement endorsing the quality and safety of the cardiac surgical program that no longer exists.
“No amount of money was going to buy my silence,” Dr. Zelman told this news organization.
In his lawsuit, Dr. Zelman is seeking an undisclosed amount in damages, including back and front pay, lost benefits, physical and emotional distress, and attorneys’ fees.
This news organization reached out to Cape Cod Hospital for comment but has not yet received a response.
A version of this article first appeared on Medscape.com.
alleging that he was fired and maligned after raising concerns about poorly performed surgeries and poor ethical practices at the hospital.
Dr. Zelman, from Barnstable, Mass., has been affiliated with Cape Cod Hospital in Hyannis, Mass., for more than 30 years. He helped found the hospital’s Heart and Vascular Institute and has served as its medical director since 2018.
In his lawsuit filed Dec. 6, Dr. Zelman alleges that the defendants, under Mr. Lauf’s leadership, “placed profit above all else, including by prioritizing revenue generation over patient safety and public health.”
Dr. Zelman says the defendants supported him “to the extent his actions were profitable.”
Yet, when he raised patient safety concerns that harmed that bottom line, Dr. Zelman says the defendants retaliated against him, including by threatening his career and reputation and unlawfully terminating his employment with the hospital.
The complaint notes Dr. Zelman is bringing this action “to recover damages for violations of the Massachusetts Healthcare Provider Whistleblower Statute ... as well as for breach of contract and common law claims.”
Dr. Zelman’s complaint alleges the defendants refused to adequately address the “dangerous care and violations of the professional standards of practice” that he reported, “resulting in harmful and tragic consequences.”
It also alleges Mr. Lauf restricted the use of a cerebral protection device used in patients undergoing transcatheter aortic-valve replacement (TAVR) deemed to be at high risk for periprocedural stroke to only those patients whose insurance reimbursed at higher rates.
Dr. Zelman says he objected to this prohibition “in accordance with his contractual and ethical obligations to ensure treatment of patients without regard to their ability to pay.”
Dr. Zelman’s lawsuit further alleges that Mr. Lauf launched a “trumped-up” and “baseless, biased, and retaliatory sham” investigation against him.
In a statement sent to the Boston Globe, Cape Cod Hospital denied Dr. Zelman’s claims that the cardiologist was retaliated against for raising patient safety issues, or that the hospital didn’t take action to improve cardiac care at the facility.
Voiced concerns
In a statement sent to this news organization, Dr. Zelman, now in private practice, said, “Over the past 25 years, I have been instrumental in bringing advanced cardiac care to Cape Cod. My commitment has always been to delivering the same quality outcomes and safety as the academic centers in Boston.
“Unfortunately, over the past 5 years, there has been inadequate oversight by the hospital administration and problems have occurred that in my opinion have led to serious patient consequences,” Dr. Zelman stated.
He said he has “voiced concerns over several years and they have been ignored.”
He added that Cape Cod Hospital offered him a million-dollar contract as long as he agreed to immediately issue a written statement endorsing the quality and safety of the cardiac surgical program that no longer exists.
“No amount of money was going to buy my silence,” Dr. Zelman told this news organization.
In his lawsuit, Dr. Zelman is seeking an undisclosed amount in damages, including back and front pay, lost benefits, physical and emotional distress, and attorneys’ fees.
This news organization reached out to Cape Cod Hospital for comment but has not yet received a response.
A version of this article first appeared on Medscape.com.
New AHA statement on complementary medicine in heart failure
There are some benefits and potentially serious risks associated with complementary and alternative medicines (CAM) patients with heart failure (HF) may use to manage symptoms, the American Heart Association noted in a new scientific statement on the topic.
For example, yoga and tai chi can be helpful for people with HF, and omega-3 polyunsaturated fatty acids may also have benefits. However, there are safety concerns with other commonly used over-the-counter CAM therapies, including vitamin D, blue cohosh, and Lily of the Valley, the writing group said.
It’s estimated that roughly one in three patients with HF use CAM. But often patients don’t report their CAM use to their clinicians and clinicians may not routinely ask about CAM use or have the resources to evaluate CAM therapies, writing group chair Sheryl L. Chow, PharmD, told this news organization.
“This represents a major public health problem given that consumers are frequently purchasing these potentially dangerous and minimally regulated products without the knowledge or advice from a health care professional,” said Dr. Chow, of Western University of Health Sciences, Pomona, Calif., and University of California, Irvine.
The 27-page statement was published online in Circulation.
CAM use common in HF
The statement defines CAM as medical practices, supplements, and approaches that do not conform to the standards of conventional, evidence-based practice guidelines. CAM products are available without prescriptions or medical guidance at pharmacies, health food stores, and online retailers.
“These agents are largely unregulated by the [Food and Drug Administration] and manufacturers do not need to demonstrate efficacy or safety. It is important that both health care professionals and consumers improve communication with respect to OTC therapies and are educated about potential efficacy and risk of harm so that shared and informed decision-making can occur,” Dr. Chow said.
The writing group reviewed research published before November 2021 on CAM among people with HF.
Omega-3 polyunsaturated fatty acids (PUFAs), such as fish oil, have the strongest evidence among CAM agents for clinical benefit in HF and may be used safely by patients in moderation and in consultation with their health care team, the writing group said.
Research has shown that omega-3 PUFAs are associated with a lower risk of developing HF as well as improvements in left ventricular systolic function in those with existing HF, they pointed out.
However, two clinical trials found a higher incidence of atrial fibrillation with high-dose omega-3 PUFA administration. “This risk appears to be dose-related and increased when exceeding 2 g/d of fish oil,” the writing group said.
Research suggests that yoga and tai chi, when added to standard HF treatment, may help improve exercise tolerance and quality of life and decrease blood pressure.
Inconclusive or potentially harmful CAM therapies
Other CAM therapies for HF have been shown as ineffective based on current data, have mixed findings, or appear to be harmful. The writers highlighted the following examples:
- Overall evidence regarding the value of vitamin D supplementation in patients with HF remains “inconclusive” and may be harmful when taken with HF medications such as digoxin, calcium channel blockers, and diuretics.
- Routine thiamine supplementation in patients with HF and without clinically significant thiamine deficiency may not be efficacious and should be avoided.
- Research on alcohol varies, with some data showing that drinking low-to-moderate amounts (one to two drinks per day) may help prevent HF, while habitual drinking or consuming higher amounts is known to contribute to HF.
- The literature is mixed on vitamin E. It may have some benefit in reducing the risk of HF with preserved ejection fraction but has also been associated with an increased risk of HF hospitalization.
- Coenzyme Q10 (Co-Q10), commonly taken as a dietary supplement, may help improve HF class, symptoms, and quality of life, but it also may interact with antihypertensive and anticoagulant medication. Co-Q10 remains of “uncertain” value in HF at this time. Large-scale randomized controlled trials are needed before any definitive conclusion can be reached.
- Hawthorn, a flowering shrub, has been shown in some studies to increase exercise tolerance and improve HF symptoms such as fatigue. Yet it also has the potential to worsen HF, and there is conflicting research about whether it interacts with digoxin.
- The herbal supplement blue cohosh, from the root of a flowering plant found in hardwood forests, could cause tachycardia, high blood pressure, chest pain, and increased blood glucose. It may also decrease the effect of medications taken to treat high blood pressure and type 2 diabetes, they noted.
- Lily of the Valley, the root, stems, and flower of which are used in supplements, has long been used in mild HF because it contains active chemicals similar to digoxin. But when taken with digoxin, it could lead to hypokalemia.
In an AHA news release, Dr. Chow said, “Overall, more quality research and well-powered randomized controlled trials are needed to better understand the risks and benefits” of CAM therapies for HF.
“This scientific statement provides critical information to health care professionals who treat people with heart failure and may be used as a resource for consumers about the potential benefit and harm associated with complementary and alternative medicine products,” Dr. Chow added.
The writing group encourages health care professionals to routinely ask their HF patients about their use of CAM therapies. They also say pharmacists should be included in the multidisciplinary health care team to provide consultations about the use of CAM therapies for HF patients.
The scientific statement does not include cannabis or traditional Chinese medicine, which have also been used in HF.
In 2020, the AHA published a separate scientific statement on the use of medical marijuana and recreational cannabis on cardiovascular health, as reported previously by this news organization.
The scientific statement on CAM for HF was prepared by the volunteer writing group on behalf of the AHA Clinical Pharmacology Committee and Heart Failure and Transplantation Committee of the Council on Clinical Cardiology; the Council on Epidemiology and Prevention; and the Council on Cardiovascular and Stroke Nursing.
A version of this article first appeared on Medscape.com.
There are some benefits and potentially serious risks associated with complementary and alternative medicines (CAM) patients with heart failure (HF) may use to manage symptoms, the American Heart Association noted in a new scientific statement on the topic.
For example, yoga and tai chi can be helpful for people with HF, and omega-3 polyunsaturated fatty acids may also have benefits. However, there are safety concerns with other commonly used over-the-counter CAM therapies, including vitamin D, blue cohosh, and Lily of the Valley, the writing group said.
It’s estimated that roughly one in three patients with HF use CAM. But often patients don’t report their CAM use to their clinicians and clinicians may not routinely ask about CAM use or have the resources to evaluate CAM therapies, writing group chair Sheryl L. Chow, PharmD, told this news organization.
“This represents a major public health problem given that consumers are frequently purchasing these potentially dangerous and minimally regulated products without the knowledge or advice from a health care professional,” said Dr. Chow, of Western University of Health Sciences, Pomona, Calif., and University of California, Irvine.
The 27-page statement was published online in Circulation.
CAM use common in HF
The statement defines CAM as medical practices, supplements, and approaches that do not conform to the standards of conventional, evidence-based practice guidelines. CAM products are available without prescriptions or medical guidance at pharmacies, health food stores, and online retailers.
“These agents are largely unregulated by the [Food and Drug Administration] and manufacturers do not need to demonstrate efficacy or safety. It is important that both health care professionals and consumers improve communication with respect to OTC therapies and are educated about potential efficacy and risk of harm so that shared and informed decision-making can occur,” Dr. Chow said.
The writing group reviewed research published before November 2021 on CAM among people with HF.
Omega-3 polyunsaturated fatty acids (PUFAs), such as fish oil, have the strongest evidence among CAM agents for clinical benefit in HF and may be used safely by patients in moderation and in consultation with their health care team, the writing group said.
Research has shown that omega-3 PUFAs are associated with a lower risk of developing HF as well as improvements in left ventricular systolic function in those with existing HF, they pointed out.
However, two clinical trials found a higher incidence of atrial fibrillation with high-dose omega-3 PUFA administration. “This risk appears to be dose-related and increased when exceeding 2 g/d of fish oil,” the writing group said.
Research suggests that yoga and tai chi, when added to standard HF treatment, may help improve exercise tolerance and quality of life and decrease blood pressure.
Inconclusive or potentially harmful CAM therapies
Other CAM therapies for HF have been shown as ineffective based on current data, have mixed findings, or appear to be harmful. The writers highlighted the following examples:
- Overall evidence regarding the value of vitamin D supplementation in patients with HF remains “inconclusive” and may be harmful when taken with HF medications such as digoxin, calcium channel blockers, and diuretics.
- Routine thiamine supplementation in patients with HF and without clinically significant thiamine deficiency may not be efficacious and should be avoided.
- Research on alcohol varies, with some data showing that drinking low-to-moderate amounts (one to two drinks per day) may help prevent HF, while habitual drinking or consuming higher amounts is known to contribute to HF.
- The literature is mixed on vitamin E. It may have some benefit in reducing the risk of HF with preserved ejection fraction but has also been associated with an increased risk of HF hospitalization.
- Coenzyme Q10 (Co-Q10), commonly taken as a dietary supplement, may help improve HF class, symptoms, and quality of life, but it also may interact with antihypertensive and anticoagulant medication. Co-Q10 remains of “uncertain” value in HF at this time. Large-scale randomized controlled trials are needed before any definitive conclusion can be reached.
- Hawthorn, a flowering shrub, has been shown in some studies to increase exercise tolerance and improve HF symptoms such as fatigue. Yet it also has the potential to worsen HF, and there is conflicting research about whether it interacts with digoxin.
- The herbal supplement blue cohosh, from the root of a flowering plant found in hardwood forests, could cause tachycardia, high blood pressure, chest pain, and increased blood glucose. It may also decrease the effect of medications taken to treat high blood pressure and type 2 diabetes, they noted.
- Lily of the Valley, the root, stems, and flower of which are used in supplements, has long been used in mild HF because it contains active chemicals similar to digoxin. But when taken with digoxin, it could lead to hypokalemia.
In an AHA news release, Dr. Chow said, “Overall, more quality research and well-powered randomized controlled trials are needed to better understand the risks and benefits” of CAM therapies for HF.
“This scientific statement provides critical information to health care professionals who treat people with heart failure and may be used as a resource for consumers about the potential benefit and harm associated with complementary and alternative medicine products,” Dr. Chow added.
The writing group encourages health care professionals to routinely ask their HF patients about their use of CAM therapies. They also say pharmacists should be included in the multidisciplinary health care team to provide consultations about the use of CAM therapies for HF patients.
The scientific statement does not include cannabis or traditional Chinese medicine, which have also been used in HF.
In 2020, the AHA published a separate scientific statement on the use of medical marijuana and recreational cannabis on cardiovascular health, as reported previously by this news organization.
The scientific statement on CAM for HF was prepared by the volunteer writing group on behalf of the AHA Clinical Pharmacology Committee and Heart Failure and Transplantation Committee of the Council on Clinical Cardiology; the Council on Epidemiology and Prevention; and the Council on Cardiovascular and Stroke Nursing.
A version of this article first appeared on Medscape.com.
There are some benefits and potentially serious risks associated with complementary and alternative medicines (CAM) patients with heart failure (HF) may use to manage symptoms, the American Heart Association noted in a new scientific statement on the topic.
For example, yoga and tai chi can be helpful for people with HF, and omega-3 polyunsaturated fatty acids may also have benefits. However, there are safety concerns with other commonly used over-the-counter CAM therapies, including vitamin D, blue cohosh, and Lily of the Valley, the writing group said.
It’s estimated that roughly one in three patients with HF use CAM. But often patients don’t report their CAM use to their clinicians and clinicians may not routinely ask about CAM use or have the resources to evaluate CAM therapies, writing group chair Sheryl L. Chow, PharmD, told this news organization.
“This represents a major public health problem given that consumers are frequently purchasing these potentially dangerous and minimally regulated products without the knowledge or advice from a health care professional,” said Dr. Chow, of Western University of Health Sciences, Pomona, Calif., and University of California, Irvine.
The 27-page statement was published online in Circulation.
CAM use common in HF
The statement defines CAM as medical practices, supplements, and approaches that do not conform to the standards of conventional, evidence-based practice guidelines. CAM products are available without prescriptions or medical guidance at pharmacies, health food stores, and online retailers.
“These agents are largely unregulated by the [Food and Drug Administration] and manufacturers do not need to demonstrate efficacy or safety. It is important that both health care professionals and consumers improve communication with respect to OTC therapies and are educated about potential efficacy and risk of harm so that shared and informed decision-making can occur,” Dr. Chow said.
The writing group reviewed research published before November 2021 on CAM among people with HF.
Omega-3 polyunsaturated fatty acids (PUFAs), such as fish oil, have the strongest evidence among CAM agents for clinical benefit in HF and may be used safely by patients in moderation and in consultation with their health care team, the writing group said.
Research has shown that omega-3 PUFAs are associated with a lower risk of developing HF as well as improvements in left ventricular systolic function in those with existing HF, they pointed out.
However, two clinical trials found a higher incidence of atrial fibrillation with high-dose omega-3 PUFA administration. “This risk appears to be dose-related and increased when exceeding 2 g/d of fish oil,” the writing group said.
Research suggests that yoga and tai chi, when added to standard HF treatment, may help improve exercise tolerance and quality of life and decrease blood pressure.
Inconclusive or potentially harmful CAM therapies
Other CAM therapies for HF have been shown as ineffective based on current data, have mixed findings, or appear to be harmful. The writers highlighted the following examples:
- Overall evidence regarding the value of vitamin D supplementation in patients with HF remains “inconclusive” and may be harmful when taken with HF medications such as digoxin, calcium channel blockers, and diuretics.
- Routine thiamine supplementation in patients with HF and without clinically significant thiamine deficiency may not be efficacious and should be avoided.
- Research on alcohol varies, with some data showing that drinking low-to-moderate amounts (one to two drinks per day) may help prevent HF, while habitual drinking or consuming higher amounts is known to contribute to HF.
- The literature is mixed on vitamin E. It may have some benefit in reducing the risk of HF with preserved ejection fraction but has also been associated with an increased risk of HF hospitalization.
- Coenzyme Q10 (Co-Q10), commonly taken as a dietary supplement, may help improve HF class, symptoms, and quality of life, but it also may interact with antihypertensive and anticoagulant medication. Co-Q10 remains of “uncertain” value in HF at this time. Large-scale randomized controlled trials are needed before any definitive conclusion can be reached.
- Hawthorn, a flowering shrub, has been shown in some studies to increase exercise tolerance and improve HF symptoms such as fatigue. Yet it also has the potential to worsen HF, and there is conflicting research about whether it interacts with digoxin.
- The herbal supplement blue cohosh, from the root of a flowering plant found in hardwood forests, could cause tachycardia, high blood pressure, chest pain, and increased blood glucose. It may also decrease the effect of medications taken to treat high blood pressure and type 2 diabetes, they noted.
- Lily of the Valley, the root, stems, and flower of which are used in supplements, has long been used in mild HF because it contains active chemicals similar to digoxin. But when taken with digoxin, it could lead to hypokalemia.
In an AHA news release, Dr. Chow said, “Overall, more quality research and well-powered randomized controlled trials are needed to better understand the risks and benefits” of CAM therapies for HF.
“This scientific statement provides critical information to health care professionals who treat people with heart failure and may be used as a resource for consumers about the potential benefit and harm associated with complementary and alternative medicine products,” Dr. Chow added.
The writing group encourages health care professionals to routinely ask their HF patients about their use of CAM therapies. They also say pharmacists should be included in the multidisciplinary health care team to provide consultations about the use of CAM therapies for HF patients.
The scientific statement does not include cannabis or traditional Chinese medicine, which have also been used in HF.
In 2020, the AHA published a separate scientific statement on the use of medical marijuana and recreational cannabis on cardiovascular health, as reported previously by this news organization.
The scientific statement on CAM for HF was prepared by the volunteer writing group on behalf of the AHA Clinical Pharmacology Committee and Heart Failure and Transplantation Committee of the Council on Clinical Cardiology; the Council on Epidemiology and Prevention; and the Council on Cardiovascular and Stroke Nursing.
A version of this article first appeared on Medscape.com.
FROM CIRCULATION
Blame IBS on gravity intolerance?
The precise cause of irritable bowel syndrome (IBS) remains a mystery. A novel new hypothesis suggests that IBS could result from the body’s inability to manage gravity.
Gravity may be the “unifying factor in multiple seemingly disparate and mutually incompatible theories of IBS,” Brennan Spiegel, MD, director of Health Services Research at Cedars-Sinai Medical Center, Los Angeles, told this news organization. Dr. Spiegel’s gravity hypothesis of IBS is described in an article published in the December issue of American Journal of Gastroenterology.
A human being’s relationship to gravity is not unlike the relationship of a fish to water, he explained.
“We live our entire life in it, are shaped by it, yet hardly notice its ever-present influence on our body. Every fiber of our body is affected by gravity every day, including our gastrointestinal tract,” said Dr. Spiegel.
The abdominal contents are like a sack of heavy potatoes that we’re destined to carry around for our entire lives. To meet this demand, our body evolved to support the abdominal load with a set of mechanisms that hoist the viscera against gravity in an upright posture, Dr. Spiegel explained.
A failure of these mechanisms could lead to a host of problems, including motility problems or bacterial overgrowth in the gut and symptoms of IBS.
Dr. Spiegel’s gravity hypothesis, however, goes beyond the gastrointestinal tract.
“Our nervous system has evolved its own ways of managing gravity and how gut feelings arise when our nervous system detects gravity challenges, like getting ‘butterflies’ when falling on a roller coaster or in a turbulent airplane,” Dr. Spiegel said.
“Even our neuropsychological orientation to gravity is found in our language, like when people talk about feeling down in the dumps, feeling low, [or say they] can’t get out of bed. These are directional metaphors that we use that refer to the fact that there is something about getting pulled down that’s obviously negative,” he noted.
‘A big ask’
Dr. Spiegel said his gravity theory of IBS draws from “extensive literature to build a hypothesis that IBS may result from ineffective anatomical, physiological, and neuropsychological gravity-management systems designed to optimize GI form and function, protect body integrity, and maximize survival in a gravity-bound world.”
He acknowledged that it’s “a big ask” to get people to consider a unifying theory of anything. “But when we dig down deep, it’s not terribly controversial to me to suggest that our health has something to do with gravity. How could it not?” he said.
Dr. Spiegel also thinks this line of thinking has clinical implications.
“While we can’t change gravity, we can change our relationship to gravity in different ways,” he said.
“For starters, we can bolster our body to manage gravity better, through losing weight, exercise, and strengthening the anti-gravity extensor muscles along the back, which supports the spine, which is the chassis that holds up the whole body and includes maintaining the shape of the abdominal cavity,” Dr. Spiegel said.
The reason physical therapy and exercise are effective for IBS could be because these interventions strengthen the GI support systems, he said.
Testable theory
Before Dr. Spiegel “got up the courage” to submit his paper, he sent it to leading IBS researchers in the United States to get their honest opinion, he said.
“To my surprise, they wrote back and said this makes sense. And a few said this could have implications for other diseases,” he said in an interview.
Some of his patients with IBS have told him how the paper resonates and the specific ways they have noticed the impact of gravity and related air pressure on their IBS symptoms.
Some have reported that their symptoms get better when they scuba dive but worsen when they get out of the ocean; others said they feel much better up in the mountains versus at sea level; another said doing a headstand during yoga eases their GI symptoms.
“These may just be anecdotes, but they’re really striking,” Dr. Spiegel said.
His theory is not meant to replace any of the many existing theories of IBS, Dr. Spiegel emphasized. Rather, it’s an attempt to pull together the different theories under a single, potentially unifying explanation.
His paper includes a list of research projects that might help explore the gravity theory of IBS.
“It may be that none of this ends up being true, or bits and pieces of it are kind of true,” Dr. Spiegel said.
A research challenge
Dr. Spiegel has given researchers an “intriguing and interesting thought experiment and kind of a challenge to go out there and determine whether or not this hypothesis may actually be true,” Millie Long, MD, co–editor-in-chief of the American Journal of Gastroenterology, said in a podcast.
Dr. Long, a gastroenterologist and professor at the University of North Carolina at Chapel Hill School of Medicine, encouraged listeners to “dig deep into this hypothesis.”
The gravity hypothesis is provocative, “but the best thing about it is that it is testable,” Shelly Lu, MD, director of the Division of Digestive and Liver Diseases at Cedars-Sinai, Los Angeles, said in a news release issued by the medical center.
“If proved correct, it is a major paradigm shift in the way we think about IBS and possibly treatment as well,” said Dr. Lu.
Also weighing in, Brian Lacy, MD, PhD, a gastroenterologist with the Mayo Clinic, Jacksonville, Fla., noted that “our understanding of the etiopathophysiology of IBS has evolved over the past 50 years.”
“Once thought to be a psychiatric disorder (‘nervous colitis’) or a disorder simply of gut spasms (‘spastic colitis’), we now understand that symptoms of IBS develop for a multitude of reasons, including alterations in the gut microbiome, changes in gut sensation and motility, and modulation of the brain-gut axis, to name just a few,” Dr. Lacy said in an interview.
“Dr. Spiegel’s intriguing manuscript opens the door for us to think about IBS in a completely different way,” said Dr. Lacy.
“His novel hypothesis is a superb challenge to researchers and clinicians who can directly test his theory with a number of intriguing experiments. The results of these experiments may completely change the treatment paradigm for IBS patients,” Dr. Lacy added.
This research had no financial support. Dr. Spiegel and Dr. Lacy report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The precise cause of irritable bowel syndrome (IBS) remains a mystery. A novel new hypothesis suggests that IBS could result from the body’s inability to manage gravity.
Gravity may be the “unifying factor in multiple seemingly disparate and mutually incompatible theories of IBS,” Brennan Spiegel, MD, director of Health Services Research at Cedars-Sinai Medical Center, Los Angeles, told this news organization. Dr. Spiegel’s gravity hypothesis of IBS is described in an article published in the December issue of American Journal of Gastroenterology.
A human being’s relationship to gravity is not unlike the relationship of a fish to water, he explained.
“We live our entire life in it, are shaped by it, yet hardly notice its ever-present influence on our body. Every fiber of our body is affected by gravity every day, including our gastrointestinal tract,” said Dr. Spiegel.
The abdominal contents are like a sack of heavy potatoes that we’re destined to carry around for our entire lives. To meet this demand, our body evolved to support the abdominal load with a set of mechanisms that hoist the viscera against gravity in an upright posture, Dr. Spiegel explained.
A failure of these mechanisms could lead to a host of problems, including motility problems or bacterial overgrowth in the gut and symptoms of IBS.
Dr. Spiegel’s gravity hypothesis, however, goes beyond the gastrointestinal tract.
“Our nervous system has evolved its own ways of managing gravity and how gut feelings arise when our nervous system detects gravity challenges, like getting ‘butterflies’ when falling on a roller coaster or in a turbulent airplane,” Dr. Spiegel said.
“Even our neuropsychological orientation to gravity is found in our language, like when people talk about feeling down in the dumps, feeling low, [or say they] can’t get out of bed. These are directional metaphors that we use that refer to the fact that there is something about getting pulled down that’s obviously negative,” he noted.
‘A big ask’
Dr. Spiegel said his gravity theory of IBS draws from “extensive literature to build a hypothesis that IBS may result from ineffective anatomical, physiological, and neuropsychological gravity-management systems designed to optimize GI form and function, protect body integrity, and maximize survival in a gravity-bound world.”
He acknowledged that it’s “a big ask” to get people to consider a unifying theory of anything. “But when we dig down deep, it’s not terribly controversial to me to suggest that our health has something to do with gravity. How could it not?” he said.
Dr. Spiegel also thinks this line of thinking has clinical implications.
“While we can’t change gravity, we can change our relationship to gravity in different ways,” he said.
“For starters, we can bolster our body to manage gravity better, through losing weight, exercise, and strengthening the anti-gravity extensor muscles along the back, which supports the spine, which is the chassis that holds up the whole body and includes maintaining the shape of the abdominal cavity,” Dr. Spiegel said.
The reason physical therapy and exercise are effective for IBS could be because these interventions strengthen the GI support systems, he said.
Testable theory
Before Dr. Spiegel “got up the courage” to submit his paper, he sent it to leading IBS researchers in the United States to get their honest opinion, he said.
“To my surprise, they wrote back and said this makes sense. And a few said this could have implications for other diseases,” he said in an interview.
Some of his patients with IBS have told him how the paper resonates and the specific ways they have noticed the impact of gravity and related air pressure on their IBS symptoms.
Some have reported that their symptoms get better when they scuba dive but worsen when they get out of the ocean; others said they feel much better up in the mountains versus at sea level; another said doing a headstand during yoga eases their GI symptoms.
“These may just be anecdotes, but they’re really striking,” Dr. Spiegel said.
His theory is not meant to replace any of the many existing theories of IBS, Dr. Spiegel emphasized. Rather, it’s an attempt to pull together the different theories under a single, potentially unifying explanation.
His paper includes a list of research projects that might help explore the gravity theory of IBS.
“It may be that none of this ends up being true, or bits and pieces of it are kind of true,” Dr. Spiegel said.
A research challenge
Dr. Spiegel has given researchers an “intriguing and interesting thought experiment and kind of a challenge to go out there and determine whether or not this hypothesis may actually be true,” Millie Long, MD, co–editor-in-chief of the American Journal of Gastroenterology, said in a podcast.
Dr. Long, a gastroenterologist and professor at the University of North Carolina at Chapel Hill School of Medicine, encouraged listeners to “dig deep into this hypothesis.”
The gravity hypothesis is provocative, “but the best thing about it is that it is testable,” Shelly Lu, MD, director of the Division of Digestive and Liver Diseases at Cedars-Sinai, Los Angeles, said in a news release issued by the medical center.
“If proved correct, it is a major paradigm shift in the way we think about IBS and possibly treatment as well,” said Dr. Lu.
Also weighing in, Brian Lacy, MD, PhD, a gastroenterologist with the Mayo Clinic, Jacksonville, Fla., noted that “our understanding of the etiopathophysiology of IBS has evolved over the past 50 years.”
“Once thought to be a psychiatric disorder (‘nervous colitis’) or a disorder simply of gut spasms (‘spastic colitis’), we now understand that symptoms of IBS develop for a multitude of reasons, including alterations in the gut microbiome, changes in gut sensation and motility, and modulation of the brain-gut axis, to name just a few,” Dr. Lacy said in an interview.
“Dr. Spiegel’s intriguing manuscript opens the door for us to think about IBS in a completely different way,” said Dr. Lacy.
“His novel hypothesis is a superb challenge to researchers and clinicians who can directly test his theory with a number of intriguing experiments. The results of these experiments may completely change the treatment paradigm for IBS patients,” Dr. Lacy added.
This research had no financial support. Dr. Spiegel and Dr. Lacy report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The precise cause of irritable bowel syndrome (IBS) remains a mystery. A novel new hypothesis suggests that IBS could result from the body’s inability to manage gravity.
Gravity may be the “unifying factor in multiple seemingly disparate and mutually incompatible theories of IBS,” Brennan Spiegel, MD, director of Health Services Research at Cedars-Sinai Medical Center, Los Angeles, told this news organization. Dr. Spiegel’s gravity hypothesis of IBS is described in an article published in the December issue of American Journal of Gastroenterology.
A human being’s relationship to gravity is not unlike the relationship of a fish to water, he explained.
“We live our entire life in it, are shaped by it, yet hardly notice its ever-present influence on our body. Every fiber of our body is affected by gravity every day, including our gastrointestinal tract,” said Dr. Spiegel.
The abdominal contents are like a sack of heavy potatoes that we’re destined to carry around for our entire lives. To meet this demand, our body evolved to support the abdominal load with a set of mechanisms that hoist the viscera against gravity in an upright posture, Dr. Spiegel explained.
A failure of these mechanisms could lead to a host of problems, including motility problems or bacterial overgrowth in the gut and symptoms of IBS.
Dr. Spiegel’s gravity hypothesis, however, goes beyond the gastrointestinal tract.
“Our nervous system has evolved its own ways of managing gravity and how gut feelings arise when our nervous system detects gravity challenges, like getting ‘butterflies’ when falling on a roller coaster or in a turbulent airplane,” Dr. Spiegel said.
“Even our neuropsychological orientation to gravity is found in our language, like when people talk about feeling down in the dumps, feeling low, [or say they] can’t get out of bed. These are directional metaphors that we use that refer to the fact that there is something about getting pulled down that’s obviously negative,” he noted.
‘A big ask’
Dr. Spiegel said his gravity theory of IBS draws from “extensive literature to build a hypothesis that IBS may result from ineffective anatomical, physiological, and neuropsychological gravity-management systems designed to optimize GI form and function, protect body integrity, and maximize survival in a gravity-bound world.”
He acknowledged that it’s “a big ask” to get people to consider a unifying theory of anything. “But when we dig down deep, it’s not terribly controversial to me to suggest that our health has something to do with gravity. How could it not?” he said.
Dr. Spiegel also thinks this line of thinking has clinical implications.
“While we can’t change gravity, we can change our relationship to gravity in different ways,” he said.
“For starters, we can bolster our body to manage gravity better, through losing weight, exercise, and strengthening the anti-gravity extensor muscles along the back, which supports the spine, which is the chassis that holds up the whole body and includes maintaining the shape of the abdominal cavity,” Dr. Spiegel said.
The reason physical therapy and exercise are effective for IBS could be because these interventions strengthen the GI support systems, he said.
Testable theory
Before Dr. Spiegel “got up the courage” to submit his paper, he sent it to leading IBS researchers in the United States to get their honest opinion, he said.
“To my surprise, they wrote back and said this makes sense. And a few said this could have implications for other diseases,” he said in an interview.
Some of his patients with IBS have told him how the paper resonates and the specific ways they have noticed the impact of gravity and related air pressure on their IBS symptoms.
Some have reported that their symptoms get better when they scuba dive but worsen when they get out of the ocean; others said they feel much better up in the mountains versus at sea level; another said doing a headstand during yoga eases their GI symptoms.
“These may just be anecdotes, but they’re really striking,” Dr. Spiegel said.
His theory is not meant to replace any of the many existing theories of IBS, Dr. Spiegel emphasized. Rather, it’s an attempt to pull together the different theories under a single, potentially unifying explanation.
His paper includes a list of research projects that might help explore the gravity theory of IBS.
“It may be that none of this ends up being true, or bits and pieces of it are kind of true,” Dr. Spiegel said.
A research challenge
Dr. Spiegel has given researchers an “intriguing and interesting thought experiment and kind of a challenge to go out there and determine whether or not this hypothesis may actually be true,” Millie Long, MD, co–editor-in-chief of the American Journal of Gastroenterology, said in a podcast.
Dr. Long, a gastroenterologist and professor at the University of North Carolina at Chapel Hill School of Medicine, encouraged listeners to “dig deep into this hypothesis.”
The gravity hypothesis is provocative, “but the best thing about it is that it is testable,” Shelly Lu, MD, director of the Division of Digestive and Liver Diseases at Cedars-Sinai, Los Angeles, said in a news release issued by the medical center.
“If proved correct, it is a major paradigm shift in the way we think about IBS and possibly treatment as well,” said Dr. Lu.
Also weighing in, Brian Lacy, MD, PhD, a gastroenterologist with the Mayo Clinic, Jacksonville, Fla., noted that “our understanding of the etiopathophysiology of IBS has evolved over the past 50 years.”
“Once thought to be a psychiatric disorder (‘nervous colitis’) or a disorder simply of gut spasms (‘spastic colitis’), we now understand that symptoms of IBS develop for a multitude of reasons, including alterations in the gut microbiome, changes in gut sensation and motility, and modulation of the brain-gut axis, to name just a few,” Dr. Lacy said in an interview.
“Dr. Spiegel’s intriguing manuscript opens the door for us to think about IBS in a completely different way,” said Dr. Lacy.
“His novel hypothesis is a superb challenge to researchers and clinicians who can directly test his theory with a number of intriguing experiments. The results of these experiments may completely change the treatment paradigm for IBS patients,” Dr. Lacy added.
This research had no financial support. Dr. Spiegel and Dr. Lacy report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM THE AMERICAN JOURNAL OF GASTROENTEROLOGY
Ultraprocessed foods tied to faster rate of cognitive decline
Results from the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil), which included more than 10,000 people aged 35 and older, showed that higher intake of UPF was significantly associated with a faster rate of decline in executive and global cognitive function.
“These findings show that lifestyle choices, particularly high intake of ultraprocessed foods, can influence our cognitive health many years later,” coinvestigator Natalia Goncalves, PhD, University of São Paulo, Brazil, said in an interview.
The study was published online in JAMA Neurology.
The study’s findings were presented in August at the Alzheimer’s Association International Conference (AAIC) 2022 and were reported by this news organization at that time.
High sugar, salt, fat
The new results align with another recent study linking a diet high in UPFs to an increased risk for dementia.
UPFs are highly manipulated, are packed with added ingredients, including sugar, fat, and salt, and are low in protein and fiber. Examples of UPFs are soft drinks, chips, chocolate, candy, ice cream, sweetened breakfast cereals, packaged soups, chicken nuggets, hot dogs, and fries.
The ELSA-Brasil study comprised 10,775 adults (mean age, 50.6 years at baseline; 55% women; 53% White) who were evaluated in three waves approximately 4 years apart from 2008 to 2017.
Information on diet was obtained via food frequency questionnaires and included details regarding consumption of unprocessed foods, minimally processed foods, and UPFs.
Participants were grouped according to UPF consumption quartiles (lowest to highest). Cognitive performance was evaluated by use of a standardized battery of tests.
During median follow-up of 8 years, people who consumed more than 20% of daily calories from UPFs (quartiles 2-4) experienced a 28% faster rate of decline in global cognition (beta = –0.004; 95% confidence interval [CI], –0.006 to –0.001; P = .003) and a 25% faster rate of decline in executive function (beta = –0.003, 95% CI, –0.005 to 0.000; P = .01) compared to peers in quartile 1 who consumed less than 20% of daily calories from UPFs.
The researchers did not investigate individual groups of UPFs.
However, Dr. Goncalves noted that some studies have linked the consumption of sugar-sweetened beverages with lower cognitive performance, lower brain volume, and poorer memory performance. Another group of ultraprocessed foods, processed meats, has been associated with increased all-cause dementia and Alzheimer’s disease.
Other limitations include the fact that self-reported diet habits were assessed only at baseline using a food frequency questionnaire that was not designed to assess the degree of processing.
While analyses were adjusted for several sociodemographic and clinical confounders, the researchers said they could not exclude the possibility of residual confounding.
Also, since neuroimaging is not available in the ELSA-Brasil study, they were not able to investigate potential mechanisms that could explain the association between higher UPF consumption and cognitive decline.
Despite these limitations, the researchers said their findings suggest that “limiting UPF consumption, particularly in middle-aged adults, may be an efficient form to prevent cognitive decline.”
Weighing the evidence
Several experts weighed in on the results in a statement from the UK nonprofit organization, Science Media Centre.
Kevin McConway, PhD, with Open University, Milton Keynes, England, said it’s important to note that the study suggests “an association, a correlation, and that doesn’t necessarily mean that the cognitive decline was caused by eating more ultra-processed foods.”
He also noted that some types of cognitive decline that are associated with aging occurred in participants in all four quartiles, which were defined by the percentage of their daily energy that came from consuming UPFs.
“That’s hardly surprising – it’s a sad fact of life that pretty well all of us gradually lose some of our cognitive functions as we go through middle and older age,” Dr. McConway said.
“The study doesn’t establish that differences in speed of cognitive decline are caused by ultra-processed food consumption anyway. That’s because it’s an observational study. If the consumption of ultra-processed food causes the differences in rate of cognitive decline, then eating less of it might slow cognitive decline, but if the cause is something else, then that won’t happen,” Dr. McConway added.
Gunter Kuhnle, PhD, professor of nutrition and food science, University of Reading, England, noted that UPFs have become a “fashionable term to explain associations between diet and ill health, and many studies have attempted to show associations.
“Most studies have been observational and had a key limitation: It is very difficult to determine ultra-processed food intake using methods that are not designed to do so, and so authors need to make a lot of assumptions. Bread and meat products are often classed as ‘ultra-processed,’ even though this is often wrong,” Dr. Kuhnle noted.
“The same applies to this study – the method used to measure ultra-processed food intake was not designed for that task and relied on assumptions. This makes it virtually impossible to draw any conclusions,” Dr. Kuhnle said.
Duane Mellor, PhD, RD, RNutr, registered dietitian and senior teaching fellow, Aston University, Birmingham, England, said the study does not change how we should try to eat to maintain good brain function and cognition.
“We should try to eat less foods which are high in added sugar, salt, and fat, which would include many of the foods classified as being ultra-processed, while eating more in terms of both quantity and variety of vegetables, fruit, nuts, seeds, and pulses, which are known to be beneficial for both our cognitive and overall health,” Dr. Mellor said.
The ELSA-Brasil study was supported by the Brazilian Ministry of Health, the Ministry of Science, Technology and Innovation, and the National Council for Scientific and Technological Development. The authors as well as Dr. McConway, Dr. Mellor, and Dr. Kuhnle have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Results from the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil), which included more than 10,000 people aged 35 and older, showed that higher intake of UPF was significantly associated with a faster rate of decline in executive and global cognitive function.
“These findings show that lifestyle choices, particularly high intake of ultraprocessed foods, can influence our cognitive health many years later,” coinvestigator Natalia Goncalves, PhD, University of São Paulo, Brazil, said in an interview.
The study was published online in JAMA Neurology.
The study’s findings were presented in August at the Alzheimer’s Association International Conference (AAIC) 2022 and were reported by this news organization at that time.
High sugar, salt, fat
The new results align with another recent study linking a diet high in UPFs to an increased risk for dementia.
UPFs are highly manipulated, are packed with added ingredients, including sugar, fat, and salt, and are low in protein and fiber. Examples of UPFs are soft drinks, chips, chocolate, candy, ice cream, sweetened breakfast cereals, packaged soups, chicken nuggets, hot dogs, and fries.
The ELSA-Brasil study comprised 10,775 adults (mean age, 50.6 years at baseline; 55% women; 53% White) who were evaluated in three waves approximately 4 years apart from 2008 to 2017.
Information on diet was obtained via food frequency questionnaires and included details regarding consumption of unprocessed foods, minimally processed foods, and UPFs.
Participants were grouped according to UPF consumption quartiles (lowest to highest). Cognitive performance was evaluated by use of a standardized battery of tests.
During median follow-up of 8 years, people who consumed more than 20% of daily calories from UPFs (quartiles 2-4) experienced a 28% faster rate of decline in global cognition (beta = –0.004; 95% confidence interval [CI], –0.006 to –0.001; P = .003) and a 25% faster rate of decline in executive function (beta = –0.003, 95% CI, –0.005 to 0.000; P = .01) compared to peers in quartile 1 who consumed less than 20% of daily calories from UPFs.
The researchers did not investigate individual groups of UPFs.
However, Dr. Goncalves noted that some studies have linked the consumption of sugar-sweetened beverages with lower cognitive performance, lower brain volume, and poorer memory performance. Another group of ultraprocessed foods, processed meats, has been associated with increased all-cause dementia and Alzheimer’s disease.
Other limitations include the fact that self-reported diet habits were assessed only at baseline using a food frequency questionnaire that was not designed to assess the degree of processing.
While analyses were adjusted for several sociodemographic and clinical confounders, the researchers said they could not exclude the possibility of residual confounding.
Also, since neuroimaging is not available in the ELSA-Brasil study, they were not able to investigate potential mechanisms that could explain the association between higher UPF consumption and cognitive decline.
Despite these limitations, the researchers said their findings suggest that “limiting UPF consumption, particularly in middle-aged adults, may be an efficient form to prevent cognitive decline.”
Weighing the evidence
Several experts weighed in on the results in a statement from the UK nonprofit organization, Science Media Centre.
Kevin McConway, PhD, with Open University, Milton Keynes, England, said it’s important to note that the study suggests “an association, a correlation, and that doesn’t necessarily mean that the cognitive decline was caused by eating more ultra-processed foods.”
He also noted that some types of cognitive decline that are associated with aging occurred in participants in all four quartiles, which were defined by the percentage of their daily energy that came from consuming UPFs.
“That’s hardly surprising – it’s a sad fact of life that pretty well all of us gradually lose some of our cognitive functions as we go through middle and older age,” Dr. McConway said.
“The study doesn’t establish that differences in speed of cognitive decline are caused by ultra-processed food consumption anyway. That’s because it’s an observational study. If the consumption of ultra-processed food causes the differences in rate of cognitive decline, then eating less of it might slow cognitive decline, but if the cause is something else, then that won’t happen,” Dr. McConway added.
Gunter Kuhnle, PhD, professor of nutrition and food science, University of Reading, England, noted that UPFs have become a “fashionable term to explain associations between diet and ill health, and many studies have attempted to show associations.
“Most studies have been observational and had a key limitation: It is very difficult to determine ultra-processed food intake using methods that are not designed to do so, and so authors need to make a lot of assumptions. Bread and meat products are often classed as ‘ultra-processed,’ even though this is often wrong,” Dr. Kuhnle noted.
“The same applies to this study – the method used to measure ultra-processed food intake was not designed for that task and relied on assumptions. This makes it virtually impossible to draw any conclusions,” Dr. Kuhnle said.
Duane Mellor, PhD, RD, RNutr, registered dietitian and senior teaching fellow, Aston University, Birmingham, England, said the study does not change how we should try to eat to maintain good brain function and cognition.
“We should try to eat less foods which are high in added sugar, salt, and fat, which would include many of the foods classified as being ultra-processed, while eating more in terms of both quantity and variety of vegetables, fruit, nuts, seeds, and pulses, which are known to be beneficial for both our cognitive and overall health,” Dr. Mellor said.
The ELSA-Brasil study was supported by the Brazilian Ministry of Health, the Ministry of Science, Technology and Innovation, and the National Council for Scientific and Technological Development. The authors as well as Dr. McConway, Dr. Mellor, and Dr. Kuhnle have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Results from the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil), which included more than 10,000 people aged 35 and older, showed that higher intake of UPF was significantly associated with a faster rate of decline in executive and global cognitive function.
“These findings show that lifestyle choices, particularly high intake of ultraprocessed foods, can influence our cognitive health many years later,” coinvestigator Natalia Goncalves, PhD, University of São Paulo, Brazil, said in an interview.
The study was published online in JAMA Neurology.
The study’s findings were presented in August at the Alzheimer’s Association International Conference (AAIC) 2022 and were reported by this news organization at that time.
High sugar, salt, fat
The new results align with another recent study linking a diet high in UPFs to an increased risk for dementia.
UPFs are highly manipulated, are packed with added ingredients, including sugar, fat, and salt, and are low in protein and fiber. Examples of UPFs are soft drinks, chips, chocolate, candy, ice cream, sweetened breakfast cereals, packaged soups, chicken nuggets, hot dogs, and fries.
The ELSA-Brasil study comprised 10,775 adults (mean age, 50.6 years at baseline; 55% women; 53% White) who were evaluated in three waves approximately 4 years apart from 2008 to 2017.
Information on diet was obtained via food frequency questionnaires and included details regarding consumption of unprocessed foods, minimally processed foods, and UPFs.
Participants were grouped according to UPF consumption quartiles (lowest to highest). Cognitive performance was evaluated by use of a standardized battery of tests.
During median follow-up of 8 years, people who consumed more than 20% of daily calories from UPFs (quartiles 2-4) experienced a 28% faster rate of decline in global cognition (beta = –0.004; 95% confidence interval [CI], –0.006 to –0.001; P = .003) and a 25% faster rate of decline in executive function (beta = –0.003, 95% CI, –0.005 to 0.000; P = .01) compared to peers in quartile 1 who consumed less than 20% of daily calories from UPFs.
The researchers did not investigate individual groups of UPFs.
However, Dr. Goncalves noted that some studies have linked the consumption of sugar-sweetened beverages with lower cognitive performance, lower brain volume, and poorer memory performance. Another group of ultraprocessed foods, processed meats, has been associated with increased all-cause dementia and Alzheimer’s disease.
Other limitations include the fact that self-reported diet habits were assessed only at baseline using a food frequency questionnaire that was not designed to assess the degree of processing.
While analyses were adjusted for several sociodemographic and clinical confounders, the researchers said they could not exclude the possibility of residual confounding.
Also, since neuroimaging is not available in the ELSA-Brasil study, they were not able to investigate potential mechanisms that could explain the association between higher UPF consumption and cognitive decline.
Despite these limitations, the researchers said their findings suggest that “limiting UPF consumption, particularly in middle-aged adults, may be an efficient form to prevent cognitive decline.”
Weighing the evidence
Several experts weighed in on the results in a statement from the UK nonprofit organization, Science Media Centre.
Kevin McConway, PhD, with Open University, Milton Keynes, England, said it’s important to note that the study suggests “an association, a correlation, and that doesn’t necessarily mean that the cognitive decline was caused by eating more ultra-processed foods.”
He also noted that some types of cognitive decline that are associated with aging occurred in participants in all four quartiles, which were defined by the percentage of their daily energy that came from consuming UPFs.
“That’s hardly surprising – it’s a sad fact of life that pretty well all of us gradually lose some of our cognitive functions as we go through middle and older age,” Dr. McConway said.
“The study doesn’t establish that differences in speed of cognitive decline are caused by ultra-processed food consumption anyway. That’s because it’s an observational study. If the consumption of ultra-processed food causes the differences in rate of cognitive decline, then eating less of it might slow cognitive decline, but if the cause is something else, then that won’t happen,” Dr. McConway added.
Gunter Kuhnle, PhD, professor of nutrition and food science, University of Reading, England, noted that UPFs have become a “fashionable term to explain associations between diet and ill health, and many studies have attempted to show associations.
“Most studies have been observational and had a key limitation: It is very difficult to determine ultra-processed food intake using methods that are not designed to do so, and so authors need to make a lot of assumptions. Bread and meat products are often classed as ‘ultra-processed,’ even though this is often wrong,” Dr. Kuhnle noted.
“The same applies to this study – the method used to measure ultra-processed food intake was not designed for that task and relied on assumptions. This makes it virtually impossible to draw any conclusions,” Dr. Kuhnle said.
Duane Mellor, PhD, RD, RNutr, registered dietitian and senior teaching fellow, Aston University, Birmingham, England, said the study does not change how we should try to eat to maintain good brain function and cognition.
“We should try to eat less foods which are high in added sugar, salt, and fat, which would include many of the foods classified as being ultra-processed, while eating more in terms of both quantity and variety of vegetables, fruit, nuts, seeds, and pulses, which are known to be beneficial for both our cognitive and overall health,” Dr. Mellor said.
The ELSA-Brasil study was supported by the Brazilian Ministry of Health, the Ministry of Science, Technology and Innovation, and the National Council for Scientific and Technological Development. The authors as well as Dr. McConway, Dr. Mellor, and Dr. Kuhnle have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM JAMA NEUROLOGY
‘Meth’ heart failure on the rise, often more severe
a literature review indicates.
MethHF is associated with increased severity for HF, longer inpatient stay, and more readmissions, compared with non-MethHF, the data show.
Clinicians “need to consider methamphetamine as a potential etiology for heart failure and include a substance use history when evaluating patients. Treating methamphetamine use disorder improves heart failure outcomes,” first author Veena Manja, MD, PhD, with Stanford (Calif.) University, said in an interview.
The study was published online in the journal Heart.
Poor outcomes, ‘staggering’ costs
This “thoughtful” review is “important and necessary,” Jonathan Davis, MD, director of the heart failure program, Zuckerberg San Francisco General Hospital, wrote in an editorial in the journal.
Dr. Davis noted that patients with Meth HF are at increased risk for poor outcomes and death and the health care costs related to MethHF are “staggering.”
As an example, inpatient data for California show annual charges related to MethHF rose by 840% from 2008 to 2018, from $41.5 million to $390.2 million, compared with 82% for all HF, which rose from $3.5 billion to $6.8 billion.
Illicit use of methamphetamine – also known as “crystal meth,” “ice,” and “speed” – has been linked to hypertension, MI, stroke, aortic dissection, and sudden death. But until now, there was no comprehensive systematic review of published studies on MethHF.
“Our goal was to compile current knowledge on the topic, increase awareness of this condition and identify areas for future research,” Dr. Manja said.
The researchers reviewed 21 observational studies, mostly from the United States (14 from California), between 1997 and 2020. The mean age of adults with MethHF ranged in age from 35 to 60 and more than half were male (57%).
Illicit methamphetamine was inhaled, injected, swallowed, smoked, and snorted. The reported frequency ranged from daily to every other week, and the total monthly dose ranged from 0.35 g to 24.5 g.
The average duration of meth use before HF diagnosis was 5 years. However, 18% of users developed HF within 1 year of starting to use illicit methamphetamine. In some cases, HF was diagnosed after a single use.
The researchers also note that MethHF with preserved left ventricular ejection fraction, seen in up to 44% of cases, is a distinct entity that may progress to reduced LVEF with continued use.
MethHF is also associated with a greater likelihood of other substance abuse, PTSD, depression, and other heart and kidney disease.
Factors associated with improved MethHF outcomes include female sex, meth abstinence, and adherence to guideline-directed HF therapy.
Improvement in MethHF outcomes is possible even if abstinence is not consistent, a finding that lends support to harm reduction principles of “meeting patients where they are instead of insisting on complete abstinence,” the researchers said.
Large gaps in knowledge
They were unable to combine the results into a meta-analysis because of heterogeneity in study design, population, comparator, and outcome assessment. Also, the overall risk of bias is moderate because of the presence of confounders, selection bias and poor matching, and the overall certainty in the evidence is very low,.
No study evaluated the incidence or prevalence of HF among methamphetamine users and inconsistent history taking and testing in patients with HF impeded accurate MethHF prevalence assessment.
Several studies, however, document an increasing incidence of MethHF, particularly over the past decade.
One study from California reported a 585% increase in MethHF hospital admissions between 2008 and 2018. An analysis of the National Inpatient Survey found a 12-fold increase in annual MethHF hospitalizations between 2002 and 2014.
“The results of this systematic review highlight large gaps in our knowledge” of MethHF, Dr. Manja said in an interview.
“We need to understand the epidemiology, prevalence, factors that confer susceptibility to cardiovascular outcomes, and need research into treatment targeted toward this disease,” Dr. Manja added. “We should consider options to integrate substance use treatment in HF/cardiology/primary care clinics and design a multidisciplinary patient-centered approach.”
Dr. Davis agreed. This work “highlights that the standard of care academically and clinically must be a broad team across the care spectrum to simultaneously address methamphetamine use, heart failure, and social determinants of health.”
This research had no specific funding. Dr. Manja and Dr. Davis reported no relevant disclosures.
A version of this article first appeared on Medscape.com.
a literature review indicates.
MethHF is associated with increased severity for HF, longer inpatient stay, and more readmissions, compared with non-MethHF, the data show.
Clinicians “need to consider methamphetamine as a potential etiology for heart failure and include a substance use history when evaluating patients. Treating methamphetamine use disorder improves heart failure outcomes,” first author Veena Manja, MD, PhD, with Stanford (Calif.) University, said in an interview.
The study was published online in the journal Heart.
Poor outcomes, ‘staggering’ costs
This “thoughtful” review is “important and necessary,” Jonathan Davis, MD, director of the heart failure program, Zuckerberg San Francisco General Hospital, wrote in an editorial in the journal.
Dr. Davis noted that patients with Meth HF are at increased risk for poor outcomes and death and the health care costs related to MethHF are “staggering.”
As an example, inpatient data for California show annual charges related to MethHF rose by 840% from 2008 to 2018, from $41.5 million to $390.2 million, compared with 82% for all HF, which rose from $3.5 billion to $6.8 billion.
Illicit use of methamphetamine – also known as “crystal meth,” “ice,” and “speed” – has been linked to hypertension, MI, stroke, aortic dissection, and sudden death. But until now, there was no comprehensive systematic review of published studies on MethHF.
“Our goal was to compile current knowledge on the topic, increase awareness of this condition and identify areas for future research,” Dr. Manja said.
The researchers reviewed 21 observational studies, mostly from the United States (14 from California), between 1997 and 2020. The mean age of adults with MethHF ranged in age from 35 to 60 and more than half were male (57%).
Illicit methamphetamine was inhaled, injected, swallowed, smoked, and snorted. The reported frequency ranged from daily to every other week, and the total monthly dose ranged from 0.35 g to 24.5 g.
The average duration of meth use before HF diagnosis was 5 years. However, 18% of users developed HF within 1 year of starting to use illicit methamphetamine. In some cases, HF was diagnosed after a single use.
The researchers also note that MethHF with preserved left ventricular ejection fraction, seen in up to 44% of cases, is a distinct entity that may progress to reduced LVEF with continued use.
MethHF is also associated with a greater likelihood of other substance abuse, PTSD, depression, and other heart and kidney disease.
Factors associated with improved MethHF outcomes include female sex, meth abstinence, and adherence to guideline-directed HF therapy.
Improvement in MethHF outcomes is possible even if abstinence is not consistent, a finding that lends support to harm reduction principles of “meeting patients where they are instead of insisting on complete abstinence,” the researchers said.
Large gaps in knowledge
They were unable to combine the results into a meta-analysis because of heterogeneity in study design, population, comparator, and outcome assessment. Also, the overall risk of bias is moderate because of the presence of confounders, selection bias and poor matching, and the overall certainty in the evidence is very low,.
No study evaluated the incidence or prevalence of HF among methamphetamine users and inconsistent history taking and testing in patients with HF impeded accurate MethHF prevalence assessment.
Several studies, however, document an increasing incidence of MethHF, particularly over the past decade.
One study from California reported a 585% increase in MethHF hospital admissions between 2008 and 2018. An analysis of the National Inpatient Survey found a 12-fold increase in annual MethHF hospitalizations between 2002 and 2014.
“The results of this systematic review highlight large gaps in our knowledge” of MethHF, Dr. Manja said in an interview.
“We need to understand the epidemiology, prevalence, factors that confer susceptibility to cardiovascular outcomes, and need research into treatment targeted toward this disease,” Dr. Manja added. “We should consider options to integrate substance use treatment in HF/cardiology/primary care clinics and design a multidisciplinary patient-centered approach.”
Dr. Davis agreed. This work “highlights that the standard of care academically and clinically must be a broad team across the care spectrum to simultaneously address methamphetamine use, heart failure, and social determinants of health.”
This research had no specific funding. Dr. Manja and Dr. Davis reported no relevant disclosures.
A version of this article first appeared on Medscape.com.
a literature review indicates.
MethHF is associated with increased severity for HF, longer inpatient stay, and more readmissions, compared with non-MethHF, the data show.
Clinicians “need to consider methamphetamine as a potential etiology for heart failure and include a substance use history when evaluating patients. Treating methamphetamine use disorder improves heart failure outcomes,” first author Veena Manja, MD, PhD, with Stanford (Calif.) University, said in an interview.
The study was published online in the journal Heart.
Poor outcomes, ‘staggering’ costs
This “thoughtful” review is “important and necessary,” Jonathan Davis, MD, director of the heart failure program, Zuckerberg San Francisco General Hospital, wrote in an editorial in the journal.
Dr. Davis noted that patients with Meth HF are at increased risk for poor outcomes and death and the health care costs related to MethHF are “staggering.”
As an example, inpatient data for California show annual charges related to MethHF rose by 840% from 2008 to 2018, from $41.5 million to $390.2 million, compared with 82% for all HF, which rose from $3.5 billion to $6.8 billion.
Illicit use of methamphetamine – also known as “crystal meth,” “ice,” and “speed” – has been linked to hypertension, MI, stroke, aortic dissection, and sudden death. But until now, there was no comprehensive systematic review of published studies on MethHF.
“Our goal was to compile current knowledge on the topic, increase awareness of this condition and identify areas for future research,” Dr. Manja said.
The researchers reviewed 21 observational studies, mostly from the United States (14 from California), between 1997 and 2020. The mean age of adults with MethHF ranged in age from 35 to 60 and more than half were male (57%).
Illicit methamphetamine was inhaled, injected, swallowed, smoked, and snorted. The reported frequency ranged from daily to every other week, and the total monthly dose ranged from 0.35 g to 24.5 g.
The average duration of meth use before HF diagnosis was 5 years. However, 18% of users developed HF within 1 year of starting to use illicit methamphetamine. In some cases, HF was diagnosed after a single use.
The researchers also note that MethHF with preserved left ventricular ejection fraction, seen in up to 44% of cases, is a distinct entity that may progress to reduced LVEF with continued use.
MethHF is also associated with a greater likelihood of other substance abuse, PTSD, depression, and other heart and kidney disease.
Factors associated with improved MethHF outcomes include female sex, meth abstinence, and adherence to guideline-directed HF therapy.
Improvement in MethHF outcomes is possible even if abstinence is not consistent, a finding that lends support to harm reduction principles of “meeting patients where they are instead of insisting on complete abstinence,” the researchers said.
Large gaps in knowledge
They were unable to combine the results into a meta-analysis because of heterogeneity in study design, population, comparator, and outcome assessment. Also, the overall risk of bias is moderate because of the presence of confounders, selection bias and poor matching, and the overall certainty in the evidence is very low,.
No study evaluated the incidence or prevalence of HF among methamphetamine users and inconsistent history taking and testing in patients with HF impeded accurate MethHF prevalence assessment.
Several studies, however, document an increasing incidence of MethHF, particularly over the past decade.
One study from California reported a 585% increase in MethHF hospital admissions between 2008 and 2018. An analysis of the National Inpatient Survey found a 12-fold increase in annual MethHF hospitalizations between 2002 and 2014.
“The results of this systematic review highlight large gaps in our knowledge” of MethHF, Dr. Manja said in an interview.
“We need to understand the epidemiology, prevalence, factors that confer susceptibility to cardiovascular outcomes, and need research into treatment targeted toward this disease,” Dr. Manja added. “We should consider options to integrate substance use treatment in HF/cardiology/primary care clinics and design a multidisciplinary patient-centered approach.”
Dr. Davis agreed. This work “highlights that the standard of care academically and clinically must be a broad team across the care spectrum to simultaneously address methamphetamine use, heart failure, and social determinants of health.”
This research had no specific funding. Dr. Manja and Dr. Davis reported no relevant disclosures.
A version of this article first appeared on Medscape.com.
FROM HEART
Not all plant-based diets equal for CRC risk reduction
although the strength of the association may vary by race and ethnicity and tumor site, new research shows.
The “take-home message is that improving the quality of plant foods and reducing animal food consumption can help prevent colorectal cancer in men,” Jihye Kim told this news organization.
The findings suggest that “not all plant-based diets are the same with regard to colorectal cancer protection/risk,” said Ms. Kim, a professor in the College of Life and Sciences at Kyung Hee University in South Korea.
The study was published online in BMC Medicine.
The researchers investigated the risk for CRC in association with three plant-based dietary patterns defined by a priori indices: an overall plant-based diet index (PDI), a healthful plant-based diet index (hPDI), and an unhealthful plant-based diet index (uPDI).
All three indices negatively weigh animal foods but weigh plant foods differently depending on their nutritional quality.
Examples of foods contained in the hPDI include whole grains, fruits, vegetables, vegetable oils, nuts, legumes, tea, and coffee. Foods in the uPDI include refined grains, fruit juices, potatoes, and added sugars.
They calculated the PDI, hPDI, and uPDI using data from quantitative food frequency questionnaires provided by 79,952 men (mean age, 60 years at baseline) and 93,475 women (mean age, 59 years at baseline) in the Multiethnic Cohort Study.
During a mean follow-up of about 19 years, 4,976 participants developed CRC.
The plant-based diet indices were significantly inversely associated with the risk for CRC in men.
Researchers found that men with the greatest adherence to PDI and hPDI had a 24% (hazard ratio, 0.76) and 21% (HR, 0.79) lower risk for CRC, respectively, compared with men with the lowest adherence. No significant association was found between the risk for CRC in men and uPDI.
None of the plant-based diet indices was significantly associated with the risk for CRC in women, which could be because of different dietary habits between men and women, the researchers say.
In general, women consume more plant foods and less animal foods than men do, they point out.
In addition, women in the Multiethnic Cohort Study consumed higher amounts of healthy plant foods and lower amounts of less healthy plant foods compared with men, so they may not have further benefits with high scores of plant-based diet indices. Also, men are at higher risk for CRC than women are in general.
These findings suggest that the benefits from plant-based diets may vary by sex, race, and ethnicity, and anatomic subsite of tumor.
In men, the inverse association of overall PDI was greater in Japanese American, Native Hawaiian, and White groups than in African American and Latino groups, and for left colon and rectum tumors than for right colon tumors. The decreased risk with the hPDI was suggested across racial and ethnic groups and was observed for all tumor subsites.
“It was interesting to see that the association of a plant-based diet with CRC varied by race and ethnicity. It is not clear why. It could be nondietary lifestyle factors or genetic factors,” Ms. Kim told this news organization.
“We should investigate that more in the future,” Ms. Kim added.
By way of limitations, it’s possible that residual or unmeasured confounding might exist despite adjustment for key CRC risk factors, the researchers say. However, the subgroup analyses suggest that the impact of residual confounding due to body mass index, smoking status, and alcohol consumption was “minimal,” they note.
Another limitation is that the analysis was based on diet measured only at baseline, but dietary habits might change over time.
Overall, the findings “support that improving the quality of plant foods and reducing animal food consumption can help prevent colorectal cancer,” Ms. Kim and colleagues say.
The study was supported by the National Research Foundation of Korea and the U.S. National Cancer Institute and National Institutes of Health. The authors have declared no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
although the strength of the association may vary by race and ethnicity and tumor site, new research shows.
The “take-home message is that improving the quality of plant foods and reducing animal food consumption can help prevent colorectal cancer in men,” Jihye Kim told this news organization.
The findings suggest that “not all plant-based diets are the same with regard to colorectal cancer protection/risk,” said Ms. Kim, a professor in the College of Life and Sciences at Kyung Hee University in South Korea.
The study was published online in BMC Medicine.
The researchers investigated the risk for CRC in association with three plant-based dietary patterns defined by a priori indices: an overall plant-based diet index (PDI), a healthful plant-based diet index (hPDI), and an unhealthful plant-based diet index (uPDI).
All three indices negatively weigh animal foods but weigh plant foods differently depending on their nutritional quality.
Examples of foods contained in the hPDI include whole grains, fruits, vegetables, vegetable oils, nuts, legumes, tea, and coffee. Foods in the uPDI include refined grains, fruit juices, potatoes, and added sugars.
They calculated the PDI, hPDI, and uPDI using data from quantitative food frequency questionnaires provided by 79,952 men (mean age, 60 years at baseline) and 93,475 women (mean age, 59 years at baseline) in the Multiethnic Cohort Study.
During a mean follow-up of about 19 years, 4,976 participants developed CRC.
The plant-based diet indices were significantly inversely associated with the risk for CRC in men.
Researchers found that men with the greatest adherence to PDI and hPDI had a 24% (hazard ratio, 0.76) and 21% (HR, 0.79) lower risk for CRC, respectively, compared with men with the lowest adherence. No significant association was found between the risk for CRC in men and uPDI.
None of the plant-based diet indices was significantly associated with the risk for CRC in women, which could be because of different dietary habits between men and women, the researchers say.
In general, women consume more plant foods and less animal foods than men do, they point out.
In addition, women in the Multiethnic Cohort Study consumed higher amounts of healthy plant foods and lower amounts of less healthy plant foods compared with men, so they may not have further benefits with high scores of plant-based diet indices. Also, men are at higher risk for CRC than women are in general.
These findings suggest that the benefits from plant-based diets may vary by sex, race, and ethnicity, and anatomic subsite of tumor.
In men, the inverse association of overall PDI was greater in Japanese American, Native Hawaiian, and White groups than in African American and Latino groups, and for left colon and rectum tumors than for right colon tumors. The decreased risk with the hPDI was suggested across racial and ethnic groups and was observed for all tumor subsites.
“It was interesting to see that the association of a plant-based diet with CRC varied by race and ethnicity. It is not clear why. It could be nondietary lifestyle factors or genetic factors,” Ms. Kim told this news organization.
“We should investigate that more in the future,” Ms. Kim added.
By way of limitations, it’s possible that residual or unmeasured confounding might exist despite adjustment for key CRC risk factors, the researchers say. However, the subgroup analyses suggest that the impact of residual confounding due to body mass index, smoking status, and alcohol consumption was “minimal,” they note.
Another limitation is that the analysis was based on diet measured only at baseline, but dietary habits might change over time.
Overall, the findings “support that improving the quality of plant foods and reducing animal food consumption can help prevent colorectal cancer,” Ms. Kim and colleagues say.
The study was supported by the National Research Foundation of Korea and the U.S. National Cancer Institute and National Institutes of Health. The authors have declared no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
although the strength of the association may vary by race and ethnicity and tumor site, new research shows.
The “take-home message is that improving the quality of plant foods and reducing animal food consumption can help prevent colorectal cancer in men,” Jihye Kim told this news organization.
The findings suggest that “not all plant-based diets are the same with regard to colorectal cancer protection/risk,” said Ms. Kim, a professor in the College of Life and Sciences at Kyung Hee University in South Korea.
The study was published online in BMC Medicine.
The researchers investigated the risk for CRC in association with three plant-based dietary patterns defined by a priori indices: an overall plant-based diet index (PDI), a healthful plant-based diet index (hPDI), and an unhealthful plant-based diet index (uPDI).
All three indices negatively weigh animal foods but weigh plant foods differently depending on their nutritional quality.
Examples of foods contained in the hPDI include whole grains, fruits, vegetables, vegetable oils, nuts, legumes, tea, and coffee. Foods in the uPDI include refined grains, fruit juices, potatoes, and added sugars.
They calculated the PDI, hPDI, and uPDI using data from quantitative food frequency questionnaires provided by 79,952 men (mean age, 60 years at baseline) and 93,475 women (mean age, 59 years at baseline) in the Multiethnic Cohort Study.
During a mean follow-up of about 19 years, 4,976 participants developed CRC.
The plant-based diet indices were significantly inversely associated with the risk for CRC in men.
Researchers found that men with the greatest adherence to PDI and hPDI had a 24% (hazard ratio, 0.76) and 21% (HR, 0.79) lower risk for CRC, respectively, compared with men with the lowest adherence. No significant association was found between the risk for CRC in men and uPDI.
None of the plant-based diet indices was significantly associated with the risk for CRC in women, which could be because of different dietary habits between men and women, the researchers say.
In general, women consume more plant foods and less animal foods than men do, they point out.
In addition, women in the Multiethnic Cohort Study consumed higher amounts of healthy plant foods and lower amounts of less healthy plant foods compared with men, so they may not have further benefits with high scores of plant-based diet indices. Also, men are at higher risk for CRC than women are in general.
These findings suggest that the benefits from plant-based diets may vary by sex, race, and ethnicity, and anatomic subsite of tumor.
In men, the inverse association of overall PDI was greater in Japanese American, Native Hawaiian, and White groups than in African American and Latino groups, and for left colon and rectum tumors than for right colon tumors. The decreased risk with the hPDI was suggested across racial and ethnic groups and was observed for all tumor subsites.
“It was interesting to see that the association of a plant-based diet with CRC varied by race and ethnicity. It is not clear why. It could be nondietary lifestyle factors or genetic factors,” Ms. Kim told this news organization.
“We should investigate that more in the future,” Ms. Kim added.
By way of limitations, it’s possible that residual or unmeasured confounding might exist despite adjustment for key CRC risk factors, the researchers say. However, the subgroup analyses suggest that the impact of residual confounding due to body mass index, smoking status, and alcohol consumption was “minimal,” they note.
Another limitation is that the analysis was based on diet measured only at baseline, but dietary habits might change over time.
Overall, the findings “support that improving the quality of plant foods and reducing animal food consumption can help prevent colorectal cancer,” Ms. Kim and colleagues say.
The study was supported by the National Research Foundation of Korea and the U.S. National Cancer Institute and National Institutes of Health. The authors have declared no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
FROM BMC MEDICINE
Strong two-way link between epilepsy and depression
, with implications for diagnosis and patient care. The findings “strongly support previous observations of a bidirectional association between these two brain disorders,” said Eva Bølling-Ladegaard, MD, a PhD student, department of clinical medicine (Neurology), Aarhus (Denmark) University.
“We add to the existing evidence in temporal range, showing that the increased risks of depression following epilepsy, and vice versa, are sustained over a much more extended time period than previously shown; that is, 20 years on both sides of receiving a diagnosis of the index disorder,” Ms. Bølling-Ladegaard said.
The study was published online in Neurology.
Epilepsy then depression
The researchers examined the magnitude and long-term temporal association between epilepsy and depression. They compared the risk of the two brain disorders following another chronic disorder (asthma) in a nationwide, register-based, matched cohort study.
In a population of more than 8.7 million people, they identified 139,014 persons with epilepsy (54% males; median age at diagnosis, 43 years), 219,990 with depression (37% males; median age at diagnosis, 43 years), and 358,821 with asthma (49% males; median age at diagnosis, 29 years).
The rate of developing depression was increased nearly twofold among people with epilepsy compared with the matched population who did not have epilepsy (adjusted hazard ratio, 1.88; 95% confidence interval, 1.82-1.95).
The rate of depression was highest during the first months and years after epilepsy diagnosis. It declined over time, yet remained significantly elevated throughout the 20+ years of observation.
The cumulative incidence of depression at 5 and 35 years’ follow-up in the epilepsy cohort was 1.37% and 6.05%, respectively, compared with 0.59% and 3.92% in the reference population.
The highest rate of depression after epilepsy was among individuals aged 40-59 years, and the lowest was among those aged 0-19 years at first epilepsy diagnosis.
Depression then epilepsy
The rate of developing epilepsy was increased more than twofold among patients with incident depression compared with the matched population who were without depression (aHR, 2.35; 95% CI, 2.25-2.44).
As in the opposite analysis, the rate of epilepsy was highest during the first months and years after depression diagnosis and declined over time.
The cumulative incidence of epilepsy at 5 and 35 years after depression diagnosis was 1.10% and 4.19%, respectively, compared with 0.32% and 2.06% in the reference population.
The rate of epilepsy was highest among those aged 0-19 years at time of first depression diagnosis and was lowest among those aged 80+ at first depression diagnosis.
For comparison, after asthma diagnosis, rates of depression and epilepsy were increased 1.63-fold (95% CI, 1.59-1.67) and 1.48-fold (95% CI, 1.44-1.53), respectively, compared with matched individuals without asthma.
Using admission with seizures as a proxy for treatment failure, the researchers observed an increased risk of treatment failure among people with epilepsy who were diagnosed with depression.
“Our results support previous findings indicating worse seizure outcomes in people with epilepsy and coexisting depression,” said Ms. Bølling-Ladegaard.
“Increased clinical awareness of the association between epilepsy and depression is therefore needed in order to increase the proportion of patients that receive appropriate treatment and improve outcomes for these patient groups,” she said.
Clinical implications
Reached for comment, Zulfi Haneef, MBBS, MD, associate professor of neurology, Baylor College of Medicine, Houston, noted that the link between epilepsy and depression is “well-known.”
“However, typically one thinks of epilepsy as leading to depression, not vice versa. Here they show the risk of epilepsy following depression to be high (highest of the risks given), which is thought provoking. However, association does not imply causation,” Dr. Haneef said.
“Prima facie, there is no biological rationale for depression to lead to epilepsy,” he said. He noted that some antidepressants can reduce the seizure threshold.
The findings do have implications for care, he said.
“For neurologists, this is another study that exhorts them to screen for depression and treat adequately in all patients with epilepsy,” Dr. Haneef said.
“For psychiatrists, this study may give guidance to watch more carefully for seizures in patients with depression, especially when using antidepressant medications that induce seizures.
“For the general public with either epilepsy or depression, it would help them be aware about this bidirectional association,” Dr. Haneef said.
The study was funded by the Lundbeck Foundation, the Danish Epilepsy Association, and the Novo Nordisk Foundation. Ms. Bølling-Ladegaard and Dr. Haneef have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, with implications for diagnosis and patient care. The findings “strongly support previous observations of a bidirectional association between these two brain disorders,” said Eva Bølling-Ladegaard, MD, a PhD student, department of clinical medicine (Neurology), Aarhus (Denmark) University.
“We add to the existing evidence in temporal range, showing that the increased risks of depression following epilepsy, and vice versa, are sustained over a much more extended time period than previously shown; that is, 20 years on both sides of receiving a diagnosis of the index disorder,” Ms. Bølling-Ladegaard said.
The study was published online in Neurology.
Epilepsy then depression
The researchers examined the magnitude and long-term temporal association between epilepsy and depression. They compared the risk of the two brain disorders following another chronic disorder (asthma) in a nationwide, register-based, matched cohort study.
In a population of more than 8.7 million people, they identified 139,014 persons with epilepsy (54% males; median age at diagnosis, 43 years), 219,990 with depression (37% males; median age at diagnosis, 43 years), and 358,821 with asthma (49% males; median age at diagnosis, 29 years).
The rate of developing depression was increased nearly twofold among people with epilepsy compared with the matched population who did not have epilepsy (adjusted hazard ratio, 1.88; 95% confidence interval, 1.82-1.95).
The rate of depression was highest during the first months and years after epilepsy diagnosis. It declined over time, yet remained significantly elevated throughout the 20+ years of observation.
The cumulative incidence of depression at 5 and 35 years’ follow-up in the epilepsy cohort was 1.37% and 6.05%, respectively, compared with 0.59% and 3.92% in the reference population.
The highest rate of depression after epilepsy was among individuals aged 40-59 years, and the lowest was among those aged 0-19 years at first epilepsy diagnosis.
Depression then epilepsy
The rate of developing epilepsy was increased more than twofold among patients with incident depression compared with the matched population who were without depression (aHR, 2.35; 95% CI, 2.25-2.44).
As in the opposite analysis, the rate of epilepsy was highest during the first months and years after depression diagnosis and declined over time.
The cumulative incidence of epilepsy at 5 and 35 years after depression diagnosis was 1.10% and 4.19%, respectively, compared with 0.32% and 2.06% in the reference population.
The rate of epilepsy was highest among those aged 0-19 years at time of first depression diagnosis and was lowest among those aged 80+ at first depression diagnosis.
For comparison, after asthma diagnosis, rates of depression and epilepsy were increased 1.63-fold (95% CI, 1.59-1.67) and 1.48-fold (95% CI, 1.44-1.53), respectively, compared with matched individuals without asthma.
Using admission with seizures as a proxy for treatment failure, the researchers observed an increased risk of treatment failure among people with epilepsy who were diagnosed with depression.
“Our results support previous findings indicating worse seizure outcomes in people with epilepsy and coexisting depression,” said Ms. Bølling-Ladegaard.
“Increased clinical awareness of the association between epilepsy and depression is therefore needed in order to increase the proportion of patients that receive appropriate treatment and improve outcomes for these patient groups,” she said.
Clinical implications
Reached for comment, Zulfi Haneef, MBBS, MD, associate professor of neurology, Baylor College of Medicine, Houston, noted that the link between epilepsy and depression is “well-known.”
“However, typically one thinks of epilepsy as leading to depression, not vice versa. Here they show the risk of epilepsy following depression to be high (highest of the risks given), which is thought provoking. However, association does not imply causation,” Dr. Haneef said.
“Prima facie, there is no biological rationale for depression to lead to epilepsy,” he said. He noted that some antidepressants can reduce the seizure threshold.
The findings do have implications for care, he said.
“For neurologists, this is another study that exhorts them to screen for depression and treat adequately in all patients with epilepsy,” Dr. Haneef said.
“For psychiatrists, this study may give guidance to watch more carefully for seizures in patients with depression, especially when using antidepressant medications that induce seizures.
“For the general public with either epilepsy or depression, it would help them be aware about this bidirectional association,” Dr. Haneef said.
The study was funded by the Lundbeck Foundation, the Danish Epilepsy Association, and the Novo Nordisk Foundation. Ms. Bølling-Ladegaard and Dr. Haneef have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, with implications for diagnosis and patient care. The findings “strongly support previous observations of a bidirectional association between these two brain disorders,” said Eva Bølling-Ladegaard, MD, a PhD student, department of clinical medicine (Neurology), Aarhus (Denmark) University.
“We add to the existing evidence in temporal range, showing that the increased risks of depression following epilepsy, and vice versa, are sustained over a much more extended time period than previously shown; that is, 20 years on both sides of receiving a diagnosis of the index disorder,” Ms. Bølling-Ladegaard said.
The study was published online in Neurology.
Epilepsy then depression
The researchers examined the magnitude and long-term temporal association between epilepsy and depression. They compared the risk of the two brain disorders following another chronic disorder (asthma) in a nationwide, register-based, matched cohort study.
In a population of more than 8.7 million people, they identified 139,014 persons with epilepsy (54% males; median age at diagnosis, 43 years), 219,990 with depression (37% males; median age at diagnosis, 43 years), and 358,821 with asthma (49% males; median age at diagnosis, 29 years).
The rate of developing depression was increased nearly twofold among people with epilepsy compared with the matched population who did not have epilepsy (adjusted hazard ratio, 1.88; 95% confidence interval, 1.82-1.95).
The rate of depression was highest during the first months and years after epilepsy diagnosis. It declined over time, yet remained significantly elevated throughout the 20+ years of observation.
The cumulative incidence of depression at 5 and 35 years’ follow-up in the epilepsy cohort was 1.37% and 6.05%, respectively, compared with 0.59% and 3.92% in the reference population.
The highest rate of depression after epilepsy was among individuals aged 40-59 years, and the lowest was among those aged 0-19 years at first epilepsy diagnosis.
Depression then epilepsy
The rate of developing epilepsy was increased more than twofold among patients with incident depression compared with the matched population who were without depression (aHR, 2.35; 95% CI, 2.25-2.44).
As in the opposite analysis, the rate of epilepsy was highest during the first months and years after depression diagnosis and declined over time.
The cumulative incidence of epilepsy at 5 and 35 years after depression diagnosis was 1.10% and 4.19%, respectively, compared with 0.32% and 2.06% in the reference population.
The rate of epilepsy was highest among those aged 0-19 years at time of first depression diagnosis and was lowest among those aged 80+ at first depression diagnosis.
For comparison, after asthma diagnosis, rates of depression and epilepsy were increased 1.63-fold (95% CI, 1.59-1.67) and 1.48-fold (95% CI, 1.44-1.53), respectively, compared with matched individuals without asthma.
Using admission with seizures as a proxy for treatment failure, the researchers observed an increased risk of treatment failure among people with epilepsy who were diagnosed with depression.
“Our results support previous findings indicating worse seizure outcomes in people with epilepsy and coexisting depression,” said Ms. Bølling-Ladegaard.
“Increased clinical awareness of the association between epilepsy and depression is therefore needed in order to increase the proportion of patients that receive appropriate treatment and improve outcomes for these patient groups,” she said.
Clinical implications
Reached for comment, Zulfi Haneef, MBBS, MD, associate professor of neurology, Baylor College of Medicine, Houston, noted that the link between epilepsy and depression is “well-known.”
“However, typically one thinks of epilepsy as leading to depression, not vice versa. Here they show the risk of epilepsy following depression to be high (highest of the risks given), which is thought provoking. However, association does not imply causation,” Dr. Haneef said.
“Prima facie, there is no biological rationale for depression to lead to epilepsy,” he said. He noted that some antidepressants can reduce the seizure threshold.
The findings do have implications for care, he said.
“For neurologists, this is another study that exhorts them to screen for depression and treat adequately in all patients with epilepsy,” Dr. Haneef said.
“For psychiatrists, this study may give guidance to watch more carefully for seizures in patients with depression, especially when using antidepressant medications that induce seizures.
“For the general public with either epilepsy or depression, it would help them be aware about this bidirectional association,” Dr. Haneef said.
The study was funded by the Lundbeck Foundation, the Danish Epilepsy Association, and the Novo Nordisk Foundation. Ms. Bølling-Ladegaard and Dr. Haneef have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM NEUROLOGY
Higher BMI may dampen steroid response in eosinophilic esophagitis
The higher the patient’s BMI level, the lower the individual’s response to tCS therapy from a symptomatic, endoscopic, and histologic perspective, researchers observed in a retrospective study.
Because there are few clinical predictors of response to topical steroids, clinicians may want to consider BMI in their treatment algorithm and when discussing therapeutic treatment options with patients with EoE, the investigators write in an article published online in Clinical Gastroenterology and Hepatology.
For EoE, current guidelines recommend the use of proton-pump inhibitor (PPI) therapy, topical steroids, and dietary elimination. In addition, the biologic dupilumab (Dupixent) was recently approved in the United States for EoE.
Determining what therapy patients with EoE will respond best to remains a challenge, and obesity’s role in treatment response has been unclear.
To investigate the effect patients’ weight might have on tCS therapy, Evan Dellon, MD, MPH, and colleagues at the University of North Carolina School of Medicine, Chapel Hill, reviewed cases involving 296 adults and adolescents aged 14 years and older who had received topical steroids for EoE.
Baseline characteristics were similar, although heartburn was more common among the 68 patients with obesity than among the non-obese patients (59% vs. 37%; P = .001), and the rate of hiatal hernias detected endoscopically was higher among the patients with obesity (22% vs. 11%; P = .02).
Following tCS treatment, peak eosinophil counts were higher for patients with obesity, compared with non-obese patients (36.1 vs. 21.5; P = .003).
Histologic response was significantly higher in non-obese patients, compared with patients with obesity, at less than 15 eosinophils per high-power field (eos/hpf: 61% vs. 47%; P = .049) and less than or equal to 6 eos/hpf (54% vs. 38%; P = .02).
Among the non-obese patients with EoE, global endoscopic response to tCS was significantly greater than among the patients with obesity (76% vs. 59%; P = .006).
In additon, among non-obese patients, the post-treatment EoE-Endoscopic Reference Score (2.4 vs. 3.2; P = .01) and the endoscopic severity score were significantly lower (2.0 vs. 2.4; P = .05).
Global symptomatic response to tCS was seen in 84% of non-obese patients, versus only 67% of those with obesity (P = .03).
On multivariate analysis, increasing BMI was independently associated with decreased histologic response after accounting for age, heartburn, dilation, and hiatal hernia.
This relationship persisted whether BMI was assessed as a continuous variable (adjusted odds ratio, 0.93 for each unit increase in BMI), as non-obese versus obese (aOR 0.38), as overweight versus normal weight (aOR 0.46), or obese versus normal weight (aOR 0.26).
Different treatment algorithm?
The results remained generally similar when patients were stratified by PPI response status and by continued use of PPIs.
The investigators note that in their cohort, only five patients responded to PPI therapy; all were non-obese. It’s possible, they note, that patients with a higher BMI may benefit from dual PPI/tCS treatment initially, but this strategy would require prospective assessment.
As for the mechanism behind obesity’s apparent negative impact on tCS therapy, the researchers say the low-grade systemic inflammatory state of obesity may make tCS therapy less effective, but they add that studies are needed to pinpoint the exact mechanism.
The study suggests that “a clinician can now add another epidemiologic risk factor for potential poor response to treatment for EoE, specifically steroids,” Philip Katz, MD, professor of medicine, division of gastroenterology and hepatology, Weill Cornell Medicine, New York, said in an interview when reached for comment.
However, it is “difficult, if not impossible, to discern from a retrospective study like this why higher BMI would be a risk factor for poor response,” said Dr. Katz, who was not affiliated with the study.
“The main potential clinical message here is that people who are overweight with EoE perhaps need to be looked at differently and might require a different treatment algorithm or treatment approach than a person who is ideal body weight,” Dr. Katz added.
Also commenting for this article, Shreya Chablaney, MD, a gastroenterologist at NYU Langone Health’s Center for Esophageal Health and clinical instructor at NYU Grossman School of Medicine, noted that predictors of patient response to various treatment options for EoE are not well understood and that more robust data are needed to guide appropriate patient selection when considering them.
“Though this is a relatively small, single-center, retrospective study, it shows an interesting finding, that high BMI is independently associated with a decrease in histologic, symptomatic, and endoscopic response to topical steroids, even when controlling for heartburn and the presence of a hiatal hernia,” she said.
“While these findings may not yet affect current management, it highlights the need for more prospective research to see if dosing adjustment, type of topical steroid, or alternative therapy altogether should be considered in patients who are obese,” Dr. Chablaney said.
Support for the study was provided by the National Institutes of Health. Dr. Dellon is a consultant for Abbott, AbbVie, Adare/ Ellodi, Aimmune, Akesobio, ALK, Allakos, Amgen, Arena, Aslan, AstraZeneca, Avir, Biorasi, Calypso, Celgene/Receptos/BMS, Celldex, Eli Lilly, EsoCap, Eurpaxia, Ferring, GSK, Gossamer Bio, Invea, Landos, LucidDx, Morphic, Nutricia, Parexel/Calyx, Phathom, Regeneron, Revolo, Robarts/Alimentiv, Salix, Sanofi, Shire/Takeda, and Target RWE. Dr. Katz is a consultant for Phathom Pharmaceuticals and Sebella Pharmaceuticals and serves on an advisory board for AstraZeneca. Dr. Chablaney reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The higher the patient’s BMI level, the lower the individual’s response to tCS therapy from a symptomatic, endoscopic, and histologic perspective, researchers observed in a retrospective study.
Because there are few clinical predictors of response to topical steroids, clinicians may want to consider BMI in their treatment algorithm and when discussing therapeutic treatment options with patients with EoE, the investigators write in an article published online in Clinical Gastroenterology and Hepatology.
For EoE, current guidelines recommend the use of proton-pump inhibitor (PPI) therapy, topical steroids, and dietary elimination. In addition, the biologic dupilumab (Dupixent) was recently approved in the United States for EoE.
Determining what therapy patients with EoE will respond best to remains a challenge, and obesity’s role in treatment response has been unclear.
To investigate the effect patients’ weight might have on tCS therapy, Evan Dellon, MD, MPH, and colleagues at the University of North Carolina School of Medicine, Chapel Hill, reviewed cases involving 296 adults and adolescents aged 14 years and older who had received topical steroids for EoE.
Baseline characteristics were similar, although heartburn was more common among the 68 patients with obesity than among the non-obese patients (59% vs. 37%; P = .001), and the rate of hiatal hernias detected endoscopically was higher among the patients with obesity (22% vs. 11%; P = .02).
Following tCS treatment, peak eosinophil counts were higher for patients with obesity, compared with non-obese patients (36.1 vs. 21.5; P = .003).
Histologic response was significantly higher in non-obese patients, compared with patients with obesity, at less than 15 eosinophils per high-power field (eos/hpf: 61% vs. 47%; P = .049) and less than or equal to 6 eos/hpf (54% vs. 38%; P = .02).
Among the non-obese patients with EoE, global endoscopic response to tCS was significantly greater than among the patients with obesity (76% vs. 59%; P = .006).
In additon, among non-obese patients, the post-treatment EoE-Endoscopic Reference Score (2.4 vs. 3.2; P = .01) and the endoscopic severity score were significantly lower (2.0 vs. 2.4; P = .05).
Global symptomatic response to tCS was seen in 84% of non-obese patients, versus only 67% of those with obesity (P = .03).
On multivariate analysis, increasing BMI was independently associated with decreased histologic response after accounting for age, heartburn, dilation, and hiatal hernia.
This relationship persisted whether BMI was assessed as a continuous variable (adjusted odds ratio, 0.93 for each unit increase in BMI), as non-obese versus obese (aOR 0.38), as overweight versus normal weight (aOR 0.46), or obese versus normal weight (aOR 0.26).
Different treatment algorithm?
The results remained generally similar when patients were stratified by PPI response status and by continued use of PPIs.
The investigators note that in their cohort, only five patients responded to PPI therapy; all were non-obese. It’s possible, they note, that patients with a higher BMI may benefit from dual PPI/tCS treatment initially, but this strategy would require prospective assessment.
As for the mechanism behind obesity’s apparent negative impact on tCS therapy, the researchers say the low-grade systemic inflammatory state of obesity may make tCS therapy less effective, but they add that studies are needed to pinpoint the exact mechanism.
The study suggests that “a clinician can now add another epidemiologic risk factor for potential poor response to treatment for EoE, specifically steroids,” Philip Katz, MD, professor of medicine, division of gastroenterology and hepatology, Weill Cornell Medicine, New York, said in an interview when reached for comment.
However, it is “difficult, if not impossible, to discern from a retrospective study like this why higher BMI would be a risk factor for poor response,” said Dr. Katz, who was not affiliated with the study.
“The main potential clinical message here is that people who are overweight with EoE perhaps need to be looked at differently and might require a different treatment algorithm or treatment approach than a person who is ideal body weight,” Dr. Katz added.
Also commenting for this article, Shreya Chablaney, MD, a gastroenterologist at NYU Langone Health’s Center for Esophageal Health and clinical instructor at NYU Grossman School of Medicine, noted that predictors of patient response to various treatment options for EoE are not well understood and that more robust data are needed to guide appropriate patient selection when considering them.
“Though this is a relatively small, single-center, retrospective study, it shows an interesting finding, that high BMI is independently associated with a decrease in histologic, symptomatic, and endoscopic response to topical steroids, even when controlling for heartburn and the presence of a hiatal hernia,” she said.
“While these findings may not yet affect current management, it highlights the need for more prospective research to see if dosing adjustment, type of topical steroid, or alternative therapy altogether should be considered in patients who are obese,” Dr. Chablaney said.
Support for the study was provided by the National Institutes of Health. Dr. Dellon is a consultant for Abbott, AbbVie, Adare/ Ellodi, Aimmune, Akesobio, ALK, Allakos, Amgen, Arena, Aslan, AstraZeneca, Avir, Biorasi, Calypso, Celgene/Receptos/BMS, Celldex, Eli Lilly, EsoCap, Eurpaxia, Ferring, GSK, Gossamer Bio, Invea, Landos, LucidDx, Morphic, Nutricia, Parexel/Calyx, Phathom, Regeneron, Revolo, Robarts/Alimentiv, Salix, Sanofi, Shire/Takeda, and Target RWE. Dr. Katz is a consultant for Phathom Pharmaceuticals and Sebella Pharmaceuticals and serves on an advisory board for AstraZeneca. Dr. Chablaney reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The higher the patient’s BMI level, the lower the individual’s response to tCS therapy from a symptomatic, endoscopic, and histologic perspective, researchers observed in a retrospective study.
Because there are few clinical predictors of response to topical steroids, clinicians may want to consider BMI in their treatment algorithm and when discussing therapeutic treatment options with patients with EoE, the investigators write in an article published online in Clinical Gastroenterology and Hepatology.
For EoE, current guidelines recommend the use of proton-pump inhibitor (PPI) therapy, topical steroids, and dietary elimination. In addition, the biologic dupilumab (Dupixent) was recently approved in the United States for EoE.
Determining what therapy patients with EoE will respond best to remains a challenge, and obesity’s role in treatment response has been unclear.
To investigate the effect patients’ weight might have on tCS therapy, Evan Dellon, MD, MPH, and colleagues at the University of North Carolina School of Medicine, Chapel Hill, reviewed cases involving 296 adults and adolescents aged 14 years and older who had received topical steroids for EoE.
Baseline characteristics were similar, although heartburn was more common among the 68 patients with obesity than among the non-obese patients (59% vs. 37%; P = .001), and the rate of hiatal hernias detected endoscopically was higher among the patients with obesity (22% vs. 11%; P = .02).
Following tCS treatment, peak eosinophil counts were higher for patients with obesity, compared with non-obese patients (36.1 vs. 21.5; P = .003).
Histologic response was significantly higher in non-obese patients, compared with patients with obesity, at less than 15 eosinophils per high-power field (eos/hpf: 61% vs. 47%; P = .049) and less than or equal to 6 eos/hpf (54% vs. 38%; P = .02).
Among the non-obese patients with EoE, global endoscopic response to tCS was significantly greater than among the patients with obesity (76% vs. 59%; P = .006).
In additon, among non-obese patients, the post-treatment EoE-Endoscopic Reference Score (2.4 vs. 3.2; P = .01) and the endoscopic severity score were significantly lower (2.0 vs. 2.4; P = .05).
Global symptomatic response to tCS was seen in 84% of non-obese patients, versus only 67% of those with obesity (P = .03).
On multivariate analysis, increasing BMI was independently associated with decreased histologic response after accounting for age, heartburn, dilation, and hiatal hernia.
This relationship persisted whether BMI was assessed as a continuous variable (adjusted odds ratio, 0.93 for each unit increase in BMI), as non-obese versus obese (aOR 0.38), as overweight versus normal weight (aOR 0.46), or obese versus normal weight (aOR 0.26).
Different treatment algorithm?
The results remained generally similar when patients were stratified by PPI response status and by continued use of PPIs.
The investigators note that in their cohort, only five patients responded to PPI therapy; all were non-obese. It’s possible, they note, that patients with a higher BMI may benefit from dual PPI/tCS treatment initially, but this strategy would require prospective assessment.
As for the mechanism behind obesity’s apparent negative impact on tCS therapy, the researchers say the low-grade systemic inflammatory state of obesity may make tCS therapy less effective, but they add that studies are needed to pinpoint the exact mechanism.
The study suggests that “a clinician can now add another epidemiologic risk factor for potential poor response to treatment for EoE, specifically steroids,” Philip Katz, MD, professor of medicine, division of gastroenterology and hepatology, Weill Cornell Medicine, New York, said in an interview when reached for comment.
However, it is “difficult, if not impossible, to discern from a retrospective study like this why higher BMI would be a risk factor for poor response,” said Dr. Katz, who was not affiliated with the study.
“The main potential clinical message here is that people who are overweight with EoE perhaps need to be looked at differently and might require a different treatment algorithm or treatment approach than a person who is ideal body weight,” Dr. Katz added.
Also commenting for this article, Shreya Chablaney, MD, a gastroenterologist at NYU Langone Health’s Center for Esophageal Health and clinical instructor at NYU Grossman School of Medicine, noted that predictors of patient response to various treatment options for EoE are not well understood and that more robust data are needed to guide appropriate patient selection when considering them.
“Though this is a relatively small, single-center, retrospective study, it shows an interesting finding, that high BMI is independently associated with a decrease in histologic, symptomatic, and endoscopic response to topical steroids, even when controlling for heartburn and the presence of a hiatal hernia,” she said.
“While these findings may not yet affect current management, it highlights the need for more prospective research to see if dosing adjustment, type of topical steroid, or alternative therapy altogether should be considered in patients who are obese,” Dr. Chablaney said.
Support for the study was provided by the National Institutes of Health. Dr. Dellon is a consultant for Abbott, AbbVie, Adare/ Ellodi, Aimmune, Akesobio, ALK, Allakos, Amgen, Arena, Aslan, AstraZeneca, Avir, Biorasi, Calypso, Celgene/Receptos/BMS, Celldex, Eli Lilly, EsoCap, Eurpaxia, Ferring, GSK, Gossamer Bio, Invea, Landos, LucidDx, Morphic, Nutricia, Parexel/Calyx, Phathom, Regeneron, Revolo, Robarts/Alimentiv, Salix, Sanofi, Shire/Takeda, and Target RWE. Dr. Katz is a consultant for Phathom Pharmaceuticals and Sebella Pharmaceuticals and serves on an advisory board for AstraZeneca. Dr. Chablaney reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
High drug costs exclude most neurology patients from cutting-edge treatment
, new research shows.
“Our study of people with neurologic conditions found that fewer than 20% were being treated with new medications,” study author Brian C. Callaghan, MD, with University of Michigan Health in Ann Arbor, said in a statement.
“For new, high-cost medications that have similar effectiveness to older drugs, limited use is likely appropriate. However, future studies are needed to look into whether the high costs are barriers to those new medications that can really make a difference for people living with neurologic disease,” Dr. Callaghan said.
The study was published online in Neurology.
Most expensive drugs
Using insurance claims data, the investigators compared the utilization and costs of new-to-market drugs from 2014 to 2018 with those for existing guideline-supported medications for treating 11 neurologic conditions.
The new drugs included:
- erenumab, fremanezumab, and galcanezumab for migraine.
- ocrelizumab and peginterferon beta-1a for multiple sclerosis (MS).
- pimavanserin and safinamide for Parkinson’s disease.
- droxidopa for orthostatic hypertension.
- eculizumab for myasthenia gravis (MG).
- edaravone for amyotrophic lateral sclerosis (ALS).
- deutetrabenazine and valbenazine for Huntington’s disease and tardive dyskinesia.
- patisiran and inotersen for transthyretin amyloidosis (ATTR).
- eteplirsen and deflazacort for Duchenne disease.
- nusinersen for spinal muscular atrophy (SMA).
Utilization of new drugs was modest – they accounted for one in five prescriptions for every condition except tardive dyskinesia (32% for valbenazine), the researchers noted.
Mean out-of-pocket costs were significantly higher for the new medications, although there was large variability among individual drugs.
The two most expensive drugs were edaravone, for ALS, with a mean out-of-pocket cost of $713 for a 30-day supply, and eculizumab, for MG, which costs $91 per month.
“For new-to-market medications, the distribution of out-of-pocket costs were highly variable and the trends over time were unpredictable compared with existing guideline-supported medications,” the authors reported.
They noted that potential reasons for low utilization of newer agents include delay in provider uptake and prescriber and/or patient avoidance because of high cost.
Given that most of the new neurologic agents offer little advantage compared with existing treatments – exceptions being new drugs for SMA and ATTR – drug costs should be a key consideration in prescribing decisions, Dr. Callaghan and colleagues concluded.
One limitation of the study is that follow-up time was short for some of the recently approved medications. Another limitation is that the number of people in the study who had rare diseases was small.
Revolution in neurotherapeutics
“We are living in a time when new treatments bring hope to people with neurologic diseases and disorders,” Orly Avitzur, MD, president of the American Academy of Neurology, said in a statement.
“However, even existing prescription medication can be expensive and drug prices continue to rise. In order for neurologists to provide people with the highest quality care, it is imperative that new drugs are accessible and affordable to the people who need them,” Dr. Avitzur added.
Writing in a linked editorial, A. Gordon Smith, MD, professor and chair, department of neurology, Virginia Commonwealth University, Richmond, said there is a revolution in neurotherapeutics, with particularly robust growth in new drug approvals for orphan diseases (those affecting < 200,000 Americans).
“This study adds to a growing literature indicating rising drug prices are a threat to the health care system. No matter how effective a disease-modifying therapy may be, if a patient cannot afford the cost, it doesn’t work,” Dr. Smith wrote.
He added that neurologists must be “diligent in assessing for financial toxicity and appropriately tailor individual treatment recommendations. We must insist on development of point-of-care tools to accurately estimate each patient’s potential financial toxicity including RTBT [real-time benefit tools].
“Neurologists’ primary obligation is to the individual patient, but we are also compelled to support access to high-quality care for all people, which requires advocacy for appropriate policy reforms to ensure value based and fair drug pricing and treatment success,” Dr. Smith added.
The study was funded by the American Academy of Neurology Health Services Research Subcommittee. Dr. Callaghan consults for a PCORI grant, DynaMed, receives research support from the American Academy of Neurology, and performs medical/legal consultations, including consultations for the Vaccine Injury Compensation Program. Dr. Smith has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, new research shows.
“Our study of people with neurologic conditions found that fewer than 20% were being treated with new medications,” study author Brian C. Callaghan, MD, with University of Michigan Health in Ann Arbor, said in a statement.
“For new, high-cost medications that have similar effectiveness to older drugs, limited use is likely appropriate. However, future studies are needed to look into whether the high costs are barriers to those new medications that can really make a difference for people living with neurologic disease,” Dr. Callaghan said.
The study was published online in Neurology.
Most expensive drugs
Using insurance claims data, the investigators compared the utilization and costs of new-to-market drugs from 2014 to 2018 with those for existing guideline-supported medications for treating 11 neurologic conditions.
The new drugs included:
- erenumab, fremanezumab, and galcanezumab for migraine.
- ocrelizumab and peginterferon beta-1a for multiple sclerosis (MS).
- pimavanserin and safinamide for Parkinson’s disease.
- droxidopa for orthostatic hypertension.
- eculizumab for myasthenia gravis (MG).
- edaravone for amyotrophic lateral sclerosis (ALS).
- deutetrabenazine and valbenazine for Huntington’s disease and tardive dyskinesia.
- patisiran and inotersen for transthyretin amyloidosis (ATTR).
- eteplirsen and deflazacort for Duchenne disease.
- nusinersen for spinal muscular atrophy (SMA).
Utilization of new drugs was modest – they accounted for one in five prescriptions for every condition except tardive dyskinesia (32% for valbenazine), the researchers noted.
Mean out-of-pocket costs were significantly higher for the new medications, although there was large variability among individual drugs.
The two most expensive drugs were edaravone, for ALS, with a mean out-of-pocket cost of $713 for a 30-day supply, and eculizumab, for MG, which costs $91 per month.
“For new-to-market medications, the distribution of out-of-pocket costs were highly variable and the trends over time were unpredictable compared with existing guideline-supported medications,” the authors reported.
They noted that potential reasons for low utilization of newer agents include delay in provider uptake and prescriber and/or patient avoidance because of high cost.
Given that most of the new neurologic agents offer little advantage compared with existing treatments – exceptions being new drugs for SMA and ATTR – drug costs should be a key consideration in prescribing decisions, Dr. Callaghan and colleagues concluded.
One limitation of the study is that follow-up time was short for some of the recently approved medications. Another limitation is that the number of people in the study who had rare diseases was small.
Revolution in neurotherapeutics
“We are living in a time when new treatments bring hope to people with neurologic diseases and disorders,” Orly Avitzur, MD, president of the American Academy of Neurology, said in a statement.
“However, even existing prescription medication can be expensive and drug prices continue to rise. In order for neurologists to provide people with the highest quality care, it is imperative that new drugs are accessible and affordable to the people who need them,” Dr. Avitzur added.
Writing in a linked editorial, A. Gordon Smith, MD, professor and chair, department of neurology, Virginia Commonwealth University, Richmond, said there is a revolution in neurotherapeutics, with particularly robust growth in new drug approvals for orphan diseases (those affecting < 200,000 Americans).
“This study adds to a growing literature indicating rising drug prices are a threat to the health care system. No matter how effective a disease-modifying therapy may be, if a patient cannot afford the cost, it doesn’t work,” Dr. Smith wrote.
He added that neurologists must be “diligent in assessing for financial toxicity and appropriately tailor individual treatment recommendations. We must insist on development of point-of-care tools to accurately estimate each patient’s potential financial toxicity including RTBT [real-time benefit tools].
“Neurologists’ primary obligation is to the individual patient, but we are also compelled to support access to high-quality care for all people, which requires advocacy for appropriate policy reforms to ensure value based and fair drug pricing and treatment success,” Dr. Smith added.
The study was funded by the American Academy of Neurology Health Services Research Subcommittee. Dr. Callaghan consults for a PCORI grant, DynaMed, receives research support from the American Academy of Neurology, and performs medical/legal consultations, including consultations for the Vaccine Injury Compensation Program. Dr. Smith has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, new research shows.
“Our study of people with neurologic conditions found that fewer than 20% were being treated with new medications,” study author Brian C. Callaghan, MD, with University of Michigan Health in Ann Arbor, said in a statement.
“For new, high-cost medications that have similar effectiveness to older drugs, limited use is likely appropriate. However, future studies are needed to look into whether the high costs are barriers to those new medications that can really make a difference for people living with neurologic disease,” Dr. Callaghan said.
The study was published online in Neurology.
Most expensive drugs
Using insurance claims data, the investigators compared the utilization and costs of new-to-market drugs from 2014 to 2018 with those for existing guideline-supported medications for treating 11 neurologic conditions.
The new drugs included:
- erenumab, fremanezumab, and galcanezumab for migraine.
- ocrelizumab and peginterferon beta-1a for multiple sclerosis (MS).
- pimavanserin and safinamide for Parkinson’s disease.
- droxidopa for orthostatic hypertension.
- eculizumab for myasthenia gravis (MG).
- edaravone for amyotrophic lateral sclerosis (ALS).
- deutetrabenazine and valbenazine for Huntington’s disease and tardive dyskinesia.
- patisiran and inotersen for transthyretin amyloidosis (ATTR).
- eteplirsen and deflazacort for Duchenne disease.
- nusinersen for spinal muscular atrophy (SMA).
Utilization of new drugs was modest – they accounted for one in five prescriptions for every condition except tardive dyskinesia (32% for valbenazine), the researchers noted.
Mean out-of-pocket costs were significantly higher for the new medications, although there was large variability among individual drugs.
The two most expensive drugs were edaravone, for ALS, with a mean out-of-pocket cost of $713 for a 30-day supply, and eculizumab, for MG, which costs $91 per month.
“For new-to-market medications, the distribution of out-of-pocket costs were highly variable and the trends over time were unpredictable compared with existing guideline-supported medications,” the authors reported.
They noted that potential reasons for low utilization of newer agents include delay in provider uptake and prescriber and/or patient avoidance because of high cost.
Given that most of the new neurologic agents offer little advantage compared with existing treatments – exceptions being new drugs for SMA and ATTR – drug costs should be a key consideration in prescribing decisions, Dr. Callaghan and colleagues concluded.
One limitation of the study is that follow-up time was short for some of the recently approved medications. Another limitation is that the number of people in the study who had rare diseases was small.
Revolution in neurotherapeutics
“We are living in a time when new treatments bring hope to people with neurologic diseases and disorders,” Orly Avitzur, MD, president of the American Academy of Neurology, said in a statement.
“However, even existing prescription medication can be expensive and drug prices continue to rise. In order for neurologists to provide people with the highest quality care, it is imperative that new drugs are accessible and affordable to the people who need them,” Dr. Avitzur added.
Writing in a linked editorial, A. Gordon Smith, MD, professor and chair, department of neurology, Virginia Commonwealth University, Richmond, said there is a revolution in neurotherapeutics, with particularly robust growth in new drug approvals for orphan diseases (those affecting < 200,000 Americans).
“This study adds to a growing literature indicating rising drug prices are a threat to the health care system. No matter how effective a disease-modifying therapy may be, if a patient cannot afford the cost, it doesn’t work,” Dr. Smith wrote.
He added that neurologists must be “diligent in assessing for financial toxicity and appropriately tailor individual treatment recommendations. We must insist on development of point-of-care tools to accurately estimate each patient’s potential financial toxicity including RTBT [real-time benefit tools].
“Neurologists’ primary obligation is to the individual patient, but we are also compelled to support access to high-quality care for all people, which requires advocacy for appropriate policy reforms to ensure value based and fair drug pricing and treatment success,” Dr. Smith added.
The study was funded by the American Academy of Neurology Health Services Research Subcommittee. Dr. Callaghan consults for a PCORI grant, DynaMed, receives research support from the American Academy of Neurology, and performs medical/legal consultations, including consultations for the Vaccine Injury Compensation Program. Dr. Smith has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM NEUROLOGY
Confirmed: Amyloid, tau levels rise years before Alzheimer’s onset
“Our results confirm accelerated biomarker changes during preclinical AD and highlight the important role of amyloid levels in tau accelerations,” the investigators note.
“These data may suggest that there is a short therapeutic window for slowing AD pathogenesis prior to the emergence of clinical symptoms – and that this window may occur after amyloid accumulation begins but before amyloid has substantial impacts on tau accumulation,” study investigator Corinne Pettigrew, PhD, department of neurology, Johns Hopkins University School of Medicine, Baltimore, told this news organization.
The study was published online in Alzheimer’s and Dementia.
Novel long-term CSF data
The study builds on previous research by examining changes in cerebrospinal fluid (CSF) biomarkers over longer periods than had been done previously, particularly among largely middle-aged and cognitively normal at baseline individuals.
The researchers examined changes in amyloid beta (Aβ) 42/Aβ40, phosphorylated tau181 (p-tau181), and total tau (t-tau) in CSF over an average of 10.7 years (and up to 23 years) among 278 individuals who were largely middle-aged persons who were cognitively normal at baseline.
“To our knowledge, no prior study among initially cognitively normal, primarily middle-aged individuals has described CSF AD biomarker changes over this duration of follow-up,” the researchers write.
During follow-up, 94 individuals who initially had normal cognition developed mild cognitive impairment (MCI).
Lower baseline levels of amyloid were associated with greater increases in tau (more strongly in men than women), while accelerations in tau were more closely linked to onset of MCI, the researchers report.
Among individuals who developed MCI, biomarker levels were more abnormal and tau increased to a greater extent prior to the onset of MCI symptoms, they found.
Clear impact of APOE4
The findings also suggest that among APOE4 carriers, amyloid onset occurs at an earlier age and rates of amyloid positivity are higher, but there are no differences in rates of change in amyloid over time.
“APOE4 genetic status was not related to changes in CSF beta-amyloid after accounting for the fact that APOE4 carriers have higher rates of amyloid positivity,” said Dr. Pettigrew.
“These findings suggest that APOE4 genetic status shifts the age of onset of amyloid accumulation (with APOE4 carriers having an earlier age of onset compared to non-carriers), but that APOE4 is not related to rates of change in CSF beta-amyloid over time,” she added.
“Thus, cognitively normal APOE4 carriers may be in more advanced preclinical AD stages at younger ages than individuals who are not APOE4 carriers, which is likely relevant for optimizing clinical trial recruitment strategies,” she said.
Funding for the study was provided by the National Institutes of Health. Dr. Pettigrew has disclosed no relevant financial relationships. The original article contains a complete list of author disclosures.
A version of this article first appeared on Medscape.com.
“Our results confirm accelerated biomarker changes during preclinical AD and highlight the important role of amyloid levels in tau accelerations,” the investigators note.
“These data may suggest that there is a short therapeutic window for slowing AD pathogenesis prior to the emergence of clinical symptoms – and that this window may occur after amyloid accumulation begins but before amyloid has substantial impacts on tau accumulation,” study investigator Corinne Pettigrew, PhD, department of neurology, Johns Hopkins University School of Medicine, Baltimore, told this news organization.
The study was published online in Alzheimer’s and Dementia.
Novel long-term CSF data
The study builds on previous research by examining changes in cerebrospinal fluid (CSF) biomarkers over longer periods than had been done previously, particularly among largely middle-aged and cognitively normal at baseline individuals.
The researchers examined changes in amyloid beta (Aβ) 42/Aβ40, phosphorylated tau181 (p-tau181), and total tau (t-tau) in CSF over an average of 10.7 years (and up to 23 years) among 278 individuals who were largely middle-aged persons who were cognitively normal at baseline.
“To our knowledge, no prior study among initially cognitively normal, primarily middle-aged individuals has described CSF AD biomarker changes over this duration of follow-up,” the researchers write.
During follow-up, 94 individuals who initially had normal cognition developed mild cognitive impairment (MCI).
Lower baseline levels of amyloid were associated with greater increases in tau (more strongly in men than women), while accelerations in tau were more closely linked to onset of MCI, the researchers report.
Among individuals who developed MCI, biomarker levels were more abnormal and tau increased to a greater extent prior to the onset of MCI symptoms, they found.
Clear impact of APOE4
The findings also suggest that among APOE4 carriers, amyloid onset occurs at an earlier age and rates of amyloid positivity are higher, but there are no differences in rates of change in amyloid over time.
“APOE4 genetic status was not related to changes in CSF beta-amyloid after accounting for the fact that APOE4 carriers have higher rates of amyloid positivity,” said Dr. Pettigrew.
“These findings suggest that APOE4 genetic status shifts the age of onset of amyloid accumulation (with APOE4 carriers having an earlier age of onset compared to non-carriers), but that APOE4 is not related to rates of change in CSF beta-amyloid over time,” she added.
“Thus, cognitively normal APOE4 carriers may be in more advanced preclinical AD stages at younger ages than individuals who are not APOE4 carriers, which is likely relevant for optimizing clinical trial recruitment strategies,” she said.
Funding for the study was provided by the National Institutes of Health. Dr. Pettigrew has disclosed no relevant financial relationships. The original article contains a complete list of author disclosures.
A version of this article first appeared on Medscape.com.
“Our results confirm accelerated biomarker changes during preclinical AD and highlight the important role of amyloid levels in tau accelerations,” the investigators note.
“These data may suggest that there is a short therapeutic window for slowing AD pathogenesis prior to the emergence of clinical symptoms – and that this window may occur after amyloid accumulation begins but before amyloid has substantial impacts on tau accumulation,” study investigator Corinne Pettigrew, PhD, department of neurology, Johns Hopkins University School of Medicine, Baltimore, told this news organization.
The study was published online in Alzheimer’s and Dementia.
Novel long-term CSF data
The study builds on previous research by examining changes in cerebrospinal fluid (CSF) biomarkers over longer periods than had been done previously, particularly among largely middle-aged and cognitively normal at baseline individuals.
The researchers examined changes in amyloid beta (Aβ) 42/Aβ40, phosphorylated tau181 (p-tau181), and total tau (t-tau) in CSF over an average of 10.7 years (and up to 23 years) among 278 individuals who were largely middle-aged persons who were cognitively normal at baseline.
“To our knowledge, no prior study among initially cognitively normal, primarily middle-aged individuals has described CSF AD biomarker changes over this duration of follow-up,” the researchers write.
During follow-up, 94 individuals who initially had normal cognition developed mild cognitive impairment (MCI).
Lower baseline levels of amyloid were associated with greater increases in tau (more strongly in men than women), while accelerations in tau were more closely linked to onset of MCI, the researchers report.
Among individuals who developed MCI, biomarker levels were more abnormal and tau increased to a greater extent prior to the onset of MCI symptoms, they found.
Clear impact of APOE4
The findings also suggest that among APOE4 carriers, amyloid onset occurs at an earlier age and rates of amyloid positivity are higher, but there are no differences in rates of change in amyloid over time.
“APOE4 genetic status was not related to changes in CSF beta-amyloid after accounting for the fact that APOE4 carriers have higher rates of amyloid positivity,” said Dr. Pettigrew.
“These findings suggest that APOE4 genetic status shifts the age of onset of amyloid accumulation (with APOE4 carriers having an earlier age of onset compared to non-carriers), but that APOE4 is not related to rates of change in CSF beta-amyloid over time,” she added.
“Thus, cognitively normal APOE4 carriers may be in more advanced preclinical AD stages at younger ages than individuals who are not APOE4 carriers, which is likely relevant for optimizing clinical trial recruitment strategies,” she said.
Funding for the study was provided by the National Institutes of Health. Dr. Pettigrew has disclosed no relevant financial relationships. The original article contains a complete list of author disclosures.
A version of this article first appeared on Medscape.com.
FROM ALZHEIMER’S AND DEMENTIA