Genetic effects on abdominal obesity may be more pronounced than those on general obesity during weight regain, a new study suggests.

People with a genetic predisposition for abdominal adiposity regained more weight around their waist after weight loss than other people.

However, people with a genetic predisposition for a higher body mass index did not regain more weight after weight loss than others.

These findings are from a secondary analysis of data from participants in the Look AHEAD trial who had type 2 diabetes and overweight/obesity and had lost at least 3% of their initial weight after 1 year of intensive lifestyle intervention or control, who were followed for another 3 years.

The study showed that change in waist circumference (aka abdominal obesity) is regulated by a separate pathway from overall obesity during weight regain, the researchers report in their paper, published in Diabetes.

“These findings are the first of their kind and provide new insights into the mechanisms of weight regain,” they conclude.

“It was already known in the scientific literature that genes that are associated with abdominal fat deposition are different from the ones associated with overall obesity,” Malene Revsbech Christiansen, a PhD student, and Tuomas O. Kilpeläinen, PhD, associate professor, Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, said in a joint email to this news organization.

Genetic variants associated with obesity are expressed in the central nervous system. However, genetic variants associated with waist circumference are expressed in the adipose tissues and might be involved in insulin sensitivity, or fat cell shape and differentiation, influencing how much adipose cells can expand in size or in number.

If those genes can function as targets for therapeutic agents, this might benefit patients who possess the genetic variants that predispose them to a higher waist-to-hip ratio adjusted for BMI (WHR-adjBMI), they said.

“However, this is a preliminary study that discovered an association between genetic variants and abdominal fat changes during weight loss,” they cautioned.

Further study is needed, they said, to test the associations in people without obesity and type 2 diabetes and to investigate this research question in people who underwent bariatric surgery or took weight-loss medications, “especially now that Wegovy has increased in popularity.”

“Genetic profiling,” they noted, “is becoming more popular as the prices go down, and future treatments are moving towards precision medicine, where treatments are tailored towards individuals rather than ‘one size fits all.’ ”

In the future, genetic tests might identify people who are more predisposed to abdominal fat deposition, hence needing more follow-up and help with lifestyle changes.

“For now, it does not seem realistic to test individuals for all these 481 [genetic] variants [predisposing to abdominal adiposity]. Each of these genetic variants predisposes, but is not deterministic, for the outcome, because of their individual small effects on waist circumference.”

“It should be stated,” they added, “that changing the diet, physical activity pattern, and behavior are still the main factors when losing weight and maintaining a healthy body.”    
 

Maintaining weight loss is the big challenge

“Lifestyle interventions typically result in an average weight loss of 7%-10 % within 6 months; however, maintaining the weight loss is a significant challenge, as participants often regain an average one-third of the lost weight within 1 year and 50%-100% within 5 years,” the researchers write.

They aimed to study whether genetic predisposition to general or abdominal obesity predicts weight gain after weight loss, based on data from 822 women and 593 men in the Look AHEAD trial.

On average, at 1 year after the intervention, the participants in the intensive lifestyle group lost 24 lbs (10.9 kg) and 3.55 inches (9 cm) around the waist, and participants in the control group lost 15 lbs (6.8 kg) pounds and 1.98 inches (5 cm) around the waist.

From year 1 to year 2, participants in the intensive lifestyle group regained 6.09 lbs and 0.98 inches around the waist, and participants in the control group lost 1.41 lbs and 0.17 inches around the waist.

From year 1 to year 4, participants in the intensive lifestyle group regained 11.05 lbs and 1.92 inches around the waist, and participants in the control group lost 2.24 lbs and 0.76 inches around the waist.

From genome-wide association studies (GWAS) in about 700,000 mainly White individuals of European origin, the researchers constructed a genetic risk score based on 894 independent single nucleotide polymorphisms (SNPs) associated with high BMI and another genetic risk score based on 481 SNPs associated with high WHR-adjBMI.

Having a genetic predisposition to higher WHR-adjBMI predicted an increase in abdominal obesity after weight loss, whereas having a genetic predisposition to higher BMI did not predict weight regain.

“These results suggest that genetic effects on abdominal obesity may be more pronounced than those on general obesity during weight regain,” the researchers conclude.

The researchers were supported by grants from the Novo Nordisk Foundation and the Danish Diabetes Academy (funded by the Novo Nordisk Foundation). The authors report no relevant financial relationships.

A version of this article appeared on Medscape.com.

Genetic effects on abdominal obesity may be more pronounced than those on general obesity during weight regain, a new study suggests.

People with a genetic predisposition for abdominal adiposity regained more weight around their waist after weight loss than other people.

However, people with a genetic predisposition for a higher body mass index did not regain more weight after weight loss than others.

These findings are from a secondary analysis of data from participants in the Look AHEAD trial who had type 2 diabetes and overweight/obesity and had lost at least 3% of their initial weight after 1 year of intensive lifestyle intervention or control, who were followed for another 3 years.

The study showed that change in waist circumference (aka abdominal obesity) is regulated by a separate pathway from overall obesity during weight regain, the researchers report in their paper, published in Diabetes.

“These findings are the first of their kind and provide new insights into the mechanisms of weight regain,” they conclude.

“It was already known in the scientific literature that genes that are associated with abdominal fat deposition are different from the ones associated with overall obesity,” Malene Revsbech Christiansen, a PhD student, and Tuomas O. Kilpeläinen, PhD, associate professor, Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, said in a joint email to this news organization.

Genetic variants associated with obesity are expressed in the central nervous system. However, genetic variants associated with waist circumference are expressed in the adipose tissues and might be involved in insulin sensitivity, or fat cell shape and differentiation, influencing how much adipose cells can expand in size or in number.

If those genes can function as targets for therapeutic agents, this might benefit patients who possess the genetic variants that predispose them to a higher waist-to-hip ratio adjusted for BMI (WHR-adjBMI), they said.

“However, this is a preliminary study that discovered an association between genetic variants and abdominal fat changes during weight loss,” they cautioned.

Further study is needed, they said, to test the associations in people without obesity and type 2 diabetes and to investigate this research question in people who underwent bariatric surgery or took weight-loss medications, “especially now that Wegovy has increased in popularity.”

“Genetic profiling,” they noted, “is becoming more popular as the prices go down, and future treatments are moving towards precision medicine, where treatments are tailored towards individuals rather than ‘one size fits all.’ ”

In the future, genetic tests might identify people who are more predisposed to abdominal fat deposition, hence needing more follow-up and help with lifestyle changes.

“For now, it does not seem realistic to test individuals for all these 481 [genetic] variants [predisposing to abdominal adiposity]. Each of these genetic variants predisposes, but is not deterministic, for the outcome, because of their individual small effects on waist circumference.”

“It should be stated,” they added, “that changing the diet, physical activity pattern, and behavior are still the main factors when losing weight and maintaining a healthy body.”    
 

Maintaining weight loss is the big challenge

“Lifestyle interventions typically result in an average weight loss of 7%-10 % within 6 months; however, maintaining the weight loss is a significant challenge, as participants often regain an average one-third of the lost weight within 1 year and 50%-100% within 5 years,” the researchers write.

They aimed to study whether genetic predisposition to general or abdominal obesity predicts weight gain after weight loss, based on data from 822 women and 593 men in the Look AHEAD trial.

On average, at 1 year after the intervention, the participants in the intensive lifestyle group lost 24 lbs (10.9 kg) and 3.55 inches (9 cm) around the waist, and participants in the control group lost 15 lbs (6.8 kg) pounds and 1.98 inches (5 cm) around the waist.

From year 1 to year 2, participants in the intensive lifestyle group regained 6.09 lbs and 0.98 inches around the waist, and participants in the control group lost 1.41 lbs and 0.17 inches around the waist.

From year 1 to year 4, participants in the intensive lifestyle group regained 11.05 lbs and 1.92 inches around the waist, and participants in the control group lost 2.24 lbs and 0.76 inches around the waist.

From genome-wide association studies (GWAS) in about 700,000 mainly White individuals of European origin, the researchers constructed a genetic risk score based on 894 independent single nucleotide polymorphisms (SNPs) associated with high BMI and another genetic risk score based on 481 SNPs associated with high WHR-adjBMI.

Having a genetic predisposition to higher WHR-adjBMI predicted an increase in abdominal obesity after weight loss, whereas having a genetic predisposition to higher BMI did not predict weight regain.

“These results suggest that genetic effects on abdominal obesity may be more pronounced than those on general obesity during weight regain,” the researchers conclude.

The researchers were supported by grants from the Novo Nordisk Foundation and the Danish Diabetes Academy (funded by the Novo Nordisk Foundation). The authors report no relevant financial relationships.

A version of this article appeared on Medscape.com.

Genetic effects on abdominal obesity may be more pronounced than those on general obesity during weight regain, a new study suggests.

People with a genetic predisposition for abdominal adiposity regained more weight around their waist after weight loss than other people.

However, people with a genetic predisposition for a higher body mass index did not regain more weight after weight loss than others.

These findings are from a secondary analysis of data from participants in the Look AHEAD trial who had type 2 diabetes and overweight/obesity and had lost at least 3% of their initial weight after 1 year of intensive lifestyle intervention or control, who were followed for another 3 years.

The study showed that change in waist circumference (aka abdominal obesity) is regulated by a separate pathway from overall obesity during weight regain, the researchers report in their paper, published in Diabetes.

“These findings are the first of their kind and provide new insights into the mechanisms of weight regain,” they conclude.

“It was already known in the scientific literature that genes that are associated with abdominal fat deposition are different from the ones associated with overall obesity,” Malene Revsbech Christiansen, a PhD student, and Tuomas O. Kilpeläinen, PhD, associate professor, Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, said in a joint email to this news organization.

Genetic variants associated with obesity are expressed in the central nervous system. However, genetic variants associated with waist circumference are expressed in the adipose tissues and might be involved in insulin sensitivity, or fat cell shape and differentiation, influencing how much adipose cells can expand in size or in number.

If those genes can function as targets for therapeutic agents, this might benefit patients who possess the genetic variants that predispose them to a higher waist-to-hip ratio adjusted for BMI (WHR-adjBMI), they said.

“However, this is a preliminary study that discovered an association between genetic variants and abdominal fat changes during weight loss,” they cautioned.

Further study is needed, they said, to test the associations in people without obesity and type 2 diabetes and to investigate this research question in people who underwent bariatric surgery or took weight-loss medications, “especially now that Wegovy has increased in popularity.”

“Genetic profiling,” they noted, “is becoming more popular as the prices go down, and future treatments are moving towards precision medicine, where treatments are tailored towards individuals rather than ‘one size fits all.’ ”

In the future, genetic tests might identify people who are more predisposed to abdominal fat deposition, hence needing more follow-up and help with lifestyle changes.

“For now, it does not seem realistic to test individuals for all these 481 [genetic] variants [predisposing to abdominal adiposity]. Each of these genetic variants predisposes, but is not deterministic, for the outcome, because of their individual small effects on waist circumference.”

“It should be stated,” they added, “that changing the diet, physical activity pattern, and behavior are still the main factors when losing weight and maintaining a healthy body.”    
 

Maintaining weight loss is the big challenge

“Lifestyle interventions typically result in an average weight loss of 7%-10 % within 6 months; however, maintaining the weight loss is a significant challenge, as participants often regain an average one-third of the lost weight within 1 year and 50%-100% within 5 years,” the researchers write.

They aimed to study whether genetic predisposition to general or abdominal obesity predicts weight gain after weight loss, based on data from 822 women and 593 men in the Look AHEAD trial.

On average, at 1 year after the intervention, the participants in the intensive lifestyle group lost 24 lbs (10.9 kg) and 3.55 inches (9 cm) around the waist, and participants in the control group lost 15 lbs (6.8 kg) pounds and 1.98 inches (5 cm) around the waist.

From year 1 to year 2, participants in the intensive lifestyle group regained 6.09 lbs and 0.98 inches around the waist, and participants in the control group lost 1.41 lbs and 0.17 inches around the waist.

From year 1 to year 4, participants in the intensive lifestyle group regained 11.05 lbs and 1.92 inches around the waist, and participants in the control group lost 2.24 lbs and 0.76 inches around the waist.

From genome-wide association studies (GWAS) in about 700,000 mainly White individuals of European origin, the researchers constructed a genetic risk score based on 894 independent single nucleotide polymorphisms (SNPs) associated with high BMI and another genetic risk score based on 481 SNPs associated with high WHR-adjBMI.

Having a genetic predisposition to higher WHR-adjBMI predicted an increase in abdominal obesity after weight loss, whereas having a genetic predisposition to higher BMI did not predict weight regain.

“These results suggest that genetic effects on abdominal obesity may be more pronounced than those on general obesity during weight regain,” the researchers conclude.

The researchers were supported by grants from the Novo Nordisk Foundation and the Danish Diabetes Academy (funded by the Novo Nordisk Foundation). The authors report no relevant financial relationships.

A version of this article appeared on Medscape.com.

In July, the Centers for Medicare and Medicaid Services released the 2024 Physician Fee Schedule (PFS) proposed rule on proposed policy changes for Medicare payments. The proposed rule contains 2,883 pages of proposals for physician, hospital outpatient department, and ambulatory surgery center (ASC) payments for calendar year 2024. For gastroenterologists, there was good news and bad news.

CMS proposed to decrease the RVU conversion factor from $33.8872 in 2023 to $32.7476 in 2024, which would result in a 3.36% cut to physician payment. Medicare physician payments have been cut each year for the better part of a decade, with additional cuts proposed for 2024.

According to the American Medical Assocition, Medicare physician payment has already declined 26% in the last 22 years when adjusting for inflation, and that’s before factoring in the proposed cuts for 2024. Physicians are one of the only health care providers without an automatic inflationary increase, the AMA reports.

AGA opposes additional cuts to physician payments and will continue to advocate to stop them. AGA and many other specialty societies support H.R. 2474, the Strengthening Medicare for Patients and Providers Act. This bill would provide a permanent, annual update equal to the increase in the Medicare Economic Index, which is how the government measures inflation in medical practice. We will continue to advocate for permanent positive annual inflation updates, which would allow physicians to invest in their practices and implement new strategies to provide high-value care.

But in some positive news from the 2024 Medicare PFS, the Hospital Outpatient Prospective Payment System (OPPS) and the ASC proposed rules include increased hospital outpatient departments and ASC payments, continued telemedicine reimbursement and coverage through 2024, and a second one-year delay in changes to rules governing split/shared visits. Specifically:

OPPS Conversion Factor: The proposed CY 2024 Medicare conversion factor for outpatient hospital departments is $87.488, an increase of 2.8%, for hospitals that meet applicable quality reporting requirements.

ASC Conversion Factor: The proposed CY 2024 Ambulatory Surgical Center conversion factor is $53.397, an increase of 2.8%, for ASCs that meet applicable quality reporting requirements. The AGA and our sister societies continue to urge CMS to reduce this gap in the ASC facility fees, when compared to the outpatient hospital facility rates, which are estimated to be a roughly 48% differential in CY 2024.

Telehealth: CMS proposes to continue reimbursing telehealth services at current levels through 2024. Payment for audio-only evaluation and management (E/M) codes will continue at parity with follow-up in-person visits as it has throughout the pandemic. Additionally, CMS is implementing telehealth flexibilities that were included in the Consolidated Appropriations Act 2023 by allowing telehealth visits to originate at any site in the United States. This will allow patients throughout the country to maintain access to needed telehealth services without facing the logistical and safety challenges that can surround in-person visits. CMS is proposing to pay telehealth services at the nonfacility payment rate, which is the same rate as in-person office visits, lift the frequency limits on telehealth visits for subsequent hospital and skilled nursing facility visits, and allow direct supervision to be provided virtually.

Split (or shared) visits: CMS has proposed a second one-year delay to its proposed split/shared visits policy. The original proposal required that the billing provider in split/shared visits be whoever spent more than half of the total time with the patient (making time the only way to define substantive portion). CMS plans to delay that through at least Dec. 31, 2024. In the interim, practices can continue to use one of the three key components (history, exam, or medical decision-making) or more than half of the total time spent to determine who can bill for the visit. The GI societies will continue to advocate for appropriate reimbursement to align with new team-based models of care delivery.

Notably, the split (or shared) visits policy was also delayed in 2023 because of widespread concerns and feedback that the policy would disrupt team-based care and care delivery in the hospital setting. The American Medical Association CPT editorial panel, the body responsible for creating and maintaining CPT codes, has approved revisions to E/M guidelines that may help address some of CMS’s concerns.

For more information on issues affecting gastroenterologists in the 2024 Medicare PFS and OPPS/ASC proposed rules, visit the AGA news website.

Dr. Garcia serves as an advisor to the AGA AMA Relative-value Update Committee. She is clinical associate professor of medicine at Stanford (Calif.) University, where she is director of the neurogastroenterology and motility laboratory in the division of gastroenterology and hepatology, and associate chief medical information officer in ambulatory care at Stanford Health Care.

Dr. Mehta serves as an alternate advisor to the AGA AMA Relative-value Update Committee. She is associate chief innovation officer, Penn Medicine, and associate professor of medicine and health policy, University of Pennsylvania, Philadelphia.

Neither author has relevant conflicts of interest.

In July, the Centers for Medicare and Medicaid Services released the 2024 Physician Fee Schedule (PFS) proposed rule on proposed policy changes for Medicare payments. The proposed rule contains 2,883 pages of proposals for physician, hospital outpatient department, and ambulatory surgery center (ASC) payments for calendar year 2024. For gastroenterologists, there was good news and bad news.

CMS proposed to decrease the RVU conversion factor from $33.8872 in 2023 to $32.7476 in 2024, which would result in a 3.36% cut to physician payment. Medicare physician payments have been cut each year for the better part of a decade, with additional cuts proposed for 2024.

According to the American Medical Assocition, Medicare physician payment has already declined 26% in the last 22 years when adjusting for inflation, and that’s before factoring in the proposed cuts for 2024. Physicians are one of the only health care providers without an automatic inflationary increase, the AMA reports.

AGA opposes additional cuts to physician payments and will continue to advocate to stop them. AGA and many other specialty societies support H.R. 2474, the Strengthening Medicare for Patients and Providers Act. This bill would provide a permanent, annual update equal to the increase in the Medicare Economic Index, which is how the government measures inflation in medical practice. We will continue to advocate for permanent positive annual inflation updates, which would allow physicians to invest in their practices and implement new strategies to provide high-value care.

But in some positive news from the 2024 Medicare PFS, the Hospital Outpatient Prospective Payment System (OPPS) and the ASC proposed rules include increased hospital outpatient departments and ASC payments, continued telemedicine reimbursement and coverage through 2024, and a second one-year delay in changes to rules governing split/shared visits. Specifically:

OPPS Conversion Factor: The proposed CY 2024 Medicare conversion factor for outpatient hospital departments is $87.488, an increase of 2.8%, for hospitals that meet applicable quality reporting requirements.

ASC Conversion Factor: The proposed CY 2024 Ambulatory Surgical Center conversion factor is $53.397, an increase of 2.8%, for ASCs that meet applicable quality reporting requirements. The AGA and our sister societies continue to urge CMS to reduce this gap in the ASC facility fees, when compared to the outpatient hospital facility rates, which are estimated to be a roughly 48% differential in CY 2024.

Telehealth: CMS proposes to continue reimbursing telehealth services at current levels through 2024. Payment for audio-only evaluation and management (E/M) codes will continue at parity with follow-up in-person visits as it has throughout the pandemic. Additionally, CMS is implementing telehealth flexibilities that were included in the Consolidated Appropriations Act 2023 by allowing telehealth visits to originate at any site in the United States. This will allow patients throughout the country to maintain access to needed telehealth services without facing the logistical and safety challenges that can surround in-person visits. CMS is proposing to pay telehealth services at the nonfacility payment rate, which is the same rate as in-person office visits, lift the frequency limits on telehealth visits for subsequent hospital and skilled nursing facility visits, and allow direct supervision to be provided virtually.

Split (or shared) visits: CMS has proposed a second one-year delay to its proposed split/shared visits policy. The original proposal required that the billing provider in split/shared visits be whoever spent more than half of the total time with the patient (making time the only way to define substantive portion). CMS plans to delay that through at least Dec. 31, 2024. In the interim, practices can continue to use one of the three key components (history, exam, or medical decision-making) or more than half of the total time spent to determine who can bill for the visit. The GI societies will continue to advocate for appropriate reimbursement to align with new team-based models of care delivery.

Notably, the split (or shared) visits policy was also delayed in 2023 because of widespread concerns and feedback that the policy would disrupt team-based care and care delivery in the hospital setting. The American Medical Association CPT editorial panel, the body responsible for creating and maintaining CPT codes, has approved revisions to E/M guidelines that may help address some of CMS’s concerns.

For more information on issues affecting gastroenterologists in the 2024 Medicare PFS and OPPS/ASC proposed rules, visit the AGA news website.

Dr. Garcia serves as an advisor to the AGA AMA Relative-value Update Committee. She is clinical associate professor of medicine at Stanford (Calif.) University, where she is director of the neurogastroenterology and motility laboratory in the division of gastroenterology and hepatology, and associate chief medical information officer in ambulatory care at Stanford Health Care.

Dr. Mehta serves as an alternate advisor to the AGA AMA Relative-value Update Committee. She is associate chief innovation officer, Penn Medicine, and associate professor of medicine and health policy, University of Pennsylvania, Philadelphia.

Neither author has relevant conflicts of interest.

In July, the Centers for Medicare and Medicaid Services released the 2024 Physician Fee Schedule (PFS) proposed rule on proposed policy changes for Medicare payments. The proposed rule contains 2,883 pages of proposals for physician, hospital outpatient department, and ambulatory surgery center (ASC) payments for calendar year 2024. For gastroenterologists, there was good news and bad news.

CMS proposed to decrease the RVU conversion factor from $33.8872 in 2023 to $32.7476 in 2024, which would result in a 3.36% cut to physician payment. Medicare physician payments have been cut each year for the better part of a decade, with additional cuts proposed for 2024.

According to the American Medical Assocition, Medicare physician payment has already declined 26% in the last 22 years when adjusting for inflation, and that’s before factoring in the proposed cuts for 2024. Physicians are one of the only health care providers without an automatic inflationary increase, the AMA reports.

AGA opposes additional cuts to physician payments and will continue to advocate to stop them. AGA and many other specialty societies support H.R. 2474, the Strengthening Medicare for Patients and Providers Act. This bill would provide a permanent, annual update equal to the increase in the Medicare Economic Index, which is how the government measures inflation in medical practice. We will continue to advocate for permanent positive annual inflation updates, which would allow physicians to invest in their practices and implement new strategies to provide high-value care.

But in some positive news from the 2024 Medicare PFS, the Hospital Outpatient Prospective Payment System (OPPS) and the ASC proposed rules include increased hospital outpatient departments and ASC payments, continued telemedicine reimbursement and coverage through 2024, and a second one-year delay in changes to rules governing split/shared visits. Specifically:

OPPS Conversion Factor: The proposed CY 2024 Medicare conversion factor for outpatient hospital departments is $87.488, an increase of 2.8%, for hospitals that meet applicable quality reporting requirements.

ASC Conversion Factor: The proposed CY 2024 Ambulatory Surgical Center conversion factor is $53.397, an increase of 2.8%, for ASCs that meet applicable quality reporting requirements. The AGA and our sister societies continue to urge CMS to reduce this gap in the ASC facility fees, when compared to the outpatient hospital facility rates, which are estimated to be a roughly 48% differential in CY 2024.

Telehealth: CMS proposes to continue reimbursing telehealth services at current levels through 2024. Payment for audio-only evaluation and management (E/M) codes will continue at parity with follow-up in-person visits as it has throughout the pandemic. Additionally, CMS is implementing telehealth flexibilities that were included in the Consolidated Appropriations Act 2023 by allowing telehealth visits to originate at any site in the United States. This will allow patients throughout the country to maintain access to needed telehealth services without facing the logistical and safety challenges that can surround in-person visits. CMS is proposing to pay telehealth services at the nonfacility payment rate, which is the same rate as in-person office visits, lift the frequency limits on telehealth visits for subsequent hospital and skilled nursing facility visits, and allow direct supervision to be provided virtually.

Split (or shared) visits: CMS has proposed a second one-year delay to its proposed split/shared visits policy. The original proposal required that the billing provider in split/shared visits be whoever spent more than half of the total time with the patient (making time the only way to define substantive portion). CMS plans to delay that through at least Dec. 31, 2024. In the interim, practices can continue to use one of the three key components (history, exam, or medical decision-making) or more than half of the total time spent to determine who can bill for the visit. The GI societies will continue to advocate for appropriate reimbursement to align with new team-based models of care delivery.

Notably, the split (or shared) visits policy was also delayed in 2023 because of widespread concerns and feedback that the policy would disrupt team-based care and care delivery in the hospital setting. The American Medical Association CPT editorial panel, the body responsible for creating and maintaining CPT codes, has approved revisions to E/M guidelines that may help address some of CMS’s concerns.

For more information on issues affecting gastroenterologists in the 2024 Medicare PFS and OPPS/ASC proposed rules, visit the AGA news website.

Dr. Garcia serves as an advisor to the AGA AMA Relative-value Update Committee. She is clinical associate professor of medicine at Stanford (Calif.) University, where she is director of the neurogastroenterology and motility laboratory in the division of gastroenterology and hepatology, and associate chief medical information officer in ambulatory care at Stanford Health Care.

Dr. Mehta serves as an alternate advisor to the AGA AMA Relative-value Update Committee. She is associate chief innovation officer, Penn Medicine, and associate professor of medicine and health policy, University of Pennsylvania, Philadelphia.

Neither author has relevant conflicts of interest.

Even at an advanced age, superagers have the memory of someone 20 or 30 years their junior. But why is that? A new study shows that, in superagers, age-related atrophy of the gray matter, especially in the areas responsible for memory, develops much more slowly than in normal older adults. However, the study also emphasizes the importance of physical and mental fitness for a healthy aging process.

“One of the most important unanswered questions with regard to superagers is: ‘Are they resistant to age-related memory loss, or do they have coping mechanisms that allow them to better offset this memory loss?’ ” wrote Marta Garo-Pascual, a PhD candidate at the Autonomous University of Madrid, Spain, and colleagues in the Lancet Healthy Longevity. “Our results indicate that superagers are resistant to these processes.”
 

Six years’ monitoring

From a cohort of older adults who had participated in a study aiming to identify early indicators of Alzheimer’s disease, the research group chose 64 superagers and 55 normal senior citizens. The latter served as the control group. While the superagers performed just as well in a memory test as people 30 years their junior, the control group’s performance was in line with their age and level of education.

All study participants were over age 79 years. Both the group of superagers and the control group included more females than males. On average, they were monitored for 6 years. During this period, a checkup was scheduled annually with an MRI examination, clinical tests, blood tests, and documentation of lifestyle factors.

For Alessandro Cellerino, PhD, of the Leibniz Institute on Aging–Fritz Lipmann Institute in Jena, Germany, this is the most crucial aspect of the study. “Even before this study, we knew that superagers demonstrated less atrophy in certain areas of the brain, but this was always only ever based on a single measurement.”
 

Memory centers protected

The MRI examinations confirmed that in superagers, gray matter atrophy in the regions responsible for memory (such as the medial temporal lobe and cholinergic forebrain), as well in regions important for movement (such as the motor thalamus), was less pronounced. In addition, the volume of gray matter in these regions, especially in the medial temporal lobe, decreased much more slowly in the superagers than in the control subjects over the study period.

Ms. Garo-Pascual and associates used a machine-learning algorithm to differentiate between superagers and normal older adults. From the 89 demographic, lifestyle, and clinical factors entered into the algorithm, two were the most important for the classification: the ability to move and mental health.
 

Mobility and mental health

Clinical tests such as the Timed Up-and-Go Test and the Finger Tapping Test revealed that superagers can be distinguished from the normally aging control subjects with regard to their mobility and fine motor skills. Their physical condition was better, although they, by their own admission, did not move any more than the control subjects in day-to-day life. According to Dr. Cellerino, this finding confirms that physical activity is paramount for cognitive function. “These people were over 80 years old – the fact that there was not much difference between their levels of activity is not surprising. Much more relevant is the question of how you get there – i.e., how active you are at the ages of 40, 50 or even 60 years old.”

Remaining active is important

As a matter of fact, the superagers indicated that generally they had been more active than the control subjects during their middle years. “Attempting to stay physically fit is essential; even if it just means going for a walk or taking the stairs,” said Dr. Cellerino.

On average, the superagers also fared much better in tests on physical health than the control subjects. They suffered significantly less from depression or anxiety disorders. “Earlier studies suggest that depression and anxiety disorders may influence performance in memory tests across all ages and that they are risk factors for developing dementia,” said Dr. Cellerino.

To avoid mental health issues in later life, gerontologist Dr. Cellerino recommended remaining socially engaged and involved. “Depression and anxiety are commonly also a consequence of social isolation,” he said.
 

Potential genetic differences

Blood sample analyses demonstrated that the superagers exhibited lower concentrations of biomarkers for neurodegenerative diseases than the control group did. In contrast, there was no difference between the two groups in the prevalence of the apo e4 allele, one of the most important genetic risk factors for Alzheimer’s disease. Nevertheless, Ms. Garo-Pascual and associates assume that genetics also play a role. They found that, despite 89 variables employed, the algorithm used could only distinguish superagers from normal older adults 66% of the time. This suggests that additional factors must be in play, such as genetic differences.

Body and mind

Since this is an observational study, whether the determined factors have a direct effect on superaging cannot be ascertained, the authors wrote. However, the results are consistent with earlier findings.

“Regarding the management of old age, we actually haven’t learned anything more than what we already knew. But it does confirm that physical and mental function are closely entwined and that we must maintain both to age healthily,” Dr. Cellerino concluded.

This article was translated from the Medscape German Edition. A version appeared on Medscape.com.

Even at an advanced age, superagers have the memory of someone 20 or 30 years their junior. But why is that? A new study shows that, in superagers, age-related atrophy of the gray matter, especially in the areas responsible for memory, develops much more slowly than in normal older adults. However, the study also emphasizes the importance of physical and mental fitness for a healthy aging process.

“One of the most important unanswered questions with regard to superagers is: ‘Are they resistant to age-related memory loss, or do they have coping mechanisms that allow them to better offset this memory loss?’ ” wrote Marta Garo-Pascual, a PhD candidate at the Autonomous University of Madrid, Spain, and colleagues in the Lancet Healthy Longevity. “Our results indicate that superagers are resistant to these processes.”
 

Six years’ monitoring

From a cohort of older adults who had participated in a study aiming to identify early indicators of Alzheimer’s disease, the research group chose 64 superagers and 55 normal senior citizens. The latter served as the control group. While the superagers performed just as well in a memory test as people 30 years their junior, the control group’s performance was in line with their age and level of education.

All study participants were over age 79 years. Both the group of superagers and the control group included more females than males. On average, they were monitored for 6 years. During this period, a checkup was scheduled annually with an MRI examination, clinical tests, blood tests, and documentation of lifestyle factors.

For Alessandro Cellerino, PhD, of the Leibniz Institute on Aging–Fritz Lipmann Institute in Jena, Germany, this is the most crucial aspect of the study. “Even before this study, we knew that superagers demonstrated less atrophy in certain areas of the brain, but this was always only ever based on a single measurement.”
 

Memory centers protected

The MRI examinations confirmed that in superagers, gray matter atrophy in the regions responsible for memory (such as the medial temporal lobe and cholinergic forebrain), as well in regions important for movement (such as the motor thalamus), was less pronounced. In addition, the volume of gray matter in these regions, especially in the medial temporal lobe, decreased much more slowly in the superagers than in the control subjects over the study period.

Ms. Garo-Pascual and associates used a machine-learning algorithm to differentiate between superagers and normal older adults. From the 89 demographic, lifestyle, and clinical factors entered into the algorithm, two were the most important for the classification: the ability to move and mental health.
 

Mobility and mental health

Clinical tests such as the Timed Up-and-Go Test and the Finger Tapping Test revealed that superagers can be distinguished from the normally aging control subjects with regard to their mobility and fine motor skills. Their physical condition was better, although they, by their own admission, did not move any more than the control subjects in day-to-day life. According to Dr. Cellerino, this finding confirms that physical activity is paramount for cognitive function. “These people were over 80 years old – the fact that there was not much difference between their levels of activity is not surprising. Much more relevant is the question of how you get there – i.e., how active you are at the ages of 40, 50 or even 60 years old.”

Remaining active is important

As a matter of fact, the superagers indicated that generally they had been more active than the control subjects during their middle years. “Attempting to stay physically fit is essential; even if it just means going for a walk or taking the stairs,” said Dr. Cellerino.

On average, the superagers also fared much better in tests on physical health than the control subjects. They suffered significantly less from depression or anxiety disorders. “Earlier studies suggest that depression and anxiety disorders may influence performance in memory tests across all ages and that they are risk factors for developing dementia,” said Dr. Cellerino.

To avoid mental health issues in later life, gerontologist Dr. Cellerino recommended remaining socially engaged and involved. “Depression and anxiety are commonly also a consequence of social isolation,” he said.
 

Potential genetic differences

Blood sample analyses demonstrated that the superagers exhibited lower concentrations of biomarkers for neurodegenerative diseases than the control group did. In contrast, there was no difference between the two groups in the prevalence of the apo e4 allele, one of the most important genetic risk factors for Alzheimer’s disease. Nevertheless, Ms. Garo-Pascual and associates assume that genetics also play a role. They found that, despite 89 variables employed, the algorithm used could only distinguish superagers from normal older adults 66% of the time. This suggests that additional factors must be in play, such as genetic differences.

Body and mind

Since this is an observational study, whether the determined factors have a direct effect on superaging cannot be ascertained, the authors wrote. However, the results are consistent with earlier findings.

“Regarding the management of old age, we actually haven’t learned anything more than what we already knew. But it does confirm that physical and mental function are closely entwined and that we must maintain both to age healthily,” Dr. Cellerino concluded.

This article was translated from the Medscape German Edition. A version appeared on Medscape.com.

Even at an advanced age, superagers have the memory of someone 20 or 30 years their junior. But why is that? A new study shows that, in superagers, age-related atrophy of the gray matter, especially in the areas responsible for memory, develops much more slowly than in normal older adults. However, the study also emphasizes the importance of physical and mental fitness for a healthy aging process.

“One of the most important unanswered questions with regard to superagers is: ‘Are they resistant to age-related memory loss, or do they have coping mechanisms that allow them to better offset this memory loss?’ ” wrote Marta Garo-Pascual, a PhD candidate at the Autonomous University of Madrid, Spain, and colleagues in the Lancet Healthy Longevity. “Our results indicate that superagers are resistant to these processes.”
 

Six years’ monitoring

From a cohort of older adults who had participated in a study aiming to identify early indicators of Alzheimer’s disease, the research group chose 64 superagers and 55 normal senior citizens. The latter served as the control group. While the superagers performed just as well in a memory test as people 30 years their junior, the control group’s performance was in line with their age and level of education.

All study participants were over age 79 years. Both the group of superagers and the control group included more females than males. On average, they were monitored for 6 years. During this period, a checkup was scheduled annually with an MRI examination, clinical tests, blood tests, and documentation of lifestyle factors.

For Alessandro Cellerino, PhD, of the Leibniz Institute on Aging–Fritz Lipmann Institute in Jena, Germany, this is the most crucial aspect of the study. “Even before this study, we knew that superagers demonstrated less atrophy in certain areas of the brain, but this was always only ever based on a single measurement.”
 

Memory centers protected

The MRI examinations confirmed that in superagers, gray matter atrophy in the regions responsible for memory (such as the medial temporal lobe and cholinergic forebrain), as well in regions important for movement (such as the motor thalamus), was less pronounced. In addition, the volume of gray matter in these regions, especially in the medial temporal lobe, decreased much more slowly in the superagers than in the control subjects over the study period.

Ms. Garo-Pascual and associates used a machine-learning algorithm to differentiate between superagers and normal older adults. From the 89 demographic, lifestyle, and clinical factors entered into the algorithm, two were the most important for the classification: the ability to move and mental health.
 

Mobility and mental health

Clinical tests such as the Timed Up-and-Go Test and the Finger Tapping Test revealed that superagers can be distinguished from the normally aging control subjects with regard to their mobility and fine motor skills. Their physical condition was better, although they, by their own admission, did not move any more than the control subjects in day-to-day life. According to Dr. Cellerino, this finding confirms that physical activity is paramount for cognitive function. “These people were over 80 years old – the fact that there was not much difference between their levels of activity is not surprising. Much more relevant is the question of how you get there – i.e., how active you are at the ages of 40, 50 or even 60 years old.”

Remaining active is important

As a matter of fact, the superagers indicated that generally they had been more active than the control subjects during their middle years. “Attempting to stay physically fit is essential; even if it just means going for a walk or taking the stairs,” said Dr. Cellerino.

On average, the superagers also fared much better in tests on physical health than the control subjects. They suffered significantly less from depression or anxiety disorders. “Earlier studies suggest that depression and anxiety disorders may influence performance in memory tests across all ages and that they are risk factors for developing dementia,” said Dr. Cellerino.

To avoid mental health issues in later life, gerontologist Dr. Cellerino recommended remaining socially engaged and involved. “Depression and anxiety are commonly also a consequence of social isolation,” he said.
 

Potential genetic differences

Blood sample analyses demonstrated that the superagers exhibited lower concentrations of biomarkers for neurodegenerative diseases than the control group did. In contrast, there was no difference between the two groups in the prevalence of the apo e4 allele, one of the most important genetic risk factors for Alzheimer’s disease. Nevertheless, Ms. Garo-Pascual and associates assume that genetics also play a role. They found that, despite 89 variables employed, the algorithm used could only distinguish superagers from normal older adults 66% of the time. This suggests that additional factors must be in play, such as genetic differences.

Body and mind

Since this is an observational study, whether the determined factors have a direct effect on superaging cannot be ascertained, the authors wrote. However, the results are consistent with earlier findings.

“Regarding the management of old age, we actually haven’t learned anything more than what we already knew. But it does confirm that physical and mental function are closely entwined and that we must maintain both to age healthily,” Dr. Cellerino concluded.

This article was translated from the Medscape German Edition. A version appeared on Medscape.com.

In a case series of 17 men with central centrifugal cicatricial alopecia (CCCA), almost half had a family history of alopecia, most were Black, and the most common symptom was scalp pruritus.

Researchers retrospectively reviewed the medical records of 17 male patients with a clinical diagnosis of CCCA who were seen at University of Pennsylvania outpatient clinics between 2012 and 2022. They excluded patients who had no scalp biopsy or if the scalp biopsy features limited characterization. Temitayo Ogunleye, MD, of the department of dermatology, University of Pennsylvania, Philadelphia, led the study, published in the Journal of the American Academy of Dermatology.

CCCA, a type of scarring alopecia, most often affects women of African descent, and published data on the demographics, clinical findings, and medical histories of CCCA in men are limited, according to the authors.

The average age of the men was 43 years and 88.2% were Black, similar to women with CCCA, who tend to be middle-aged and Black. The four most common symptoms were scalp pruritus (58.8%), lesions (29.4%), pain or tenderness (23.5%), and hair thinning (23.5%). None of the men had type 2 diabetes (considered a possible CCCA risk factor), but 47.1% had a family history of alopecia. The four most common CCCA distributions were classic (47.1%), occipital (17.6%), patchy (11.8%), and posterior vertex (11.8%).

“Larger studies are needed to fully elucidate these relationships and explore etiology in males with CCCA,” the researchers wrote. “Nonetheless, we hope the data will prompt clinicians to assess for CCCA and risk factors in adult males with scarring alopecia.”

Limitations of the study included the retrospective, single-center design, and small sample size.

The researchers reported having no relevant financial relationships.

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

In a case series of 17 men with central centrifugal cicatricial alopecia (CCCA), almost half had a family history of alopecia, most were Black, and the most common symptom was scalp pruritus.

Researchers retrospectively reviewed the medical records of 17 male patients with a clinical diagnosis of CCCA who were seen at University of Pennsylvania outpatient clinics between 2012 and 2022. They excluded patients who had no scalp biopsy or if the scalp biopsy features limited characterization. Temitayo Ogunleye, MD, of the department of dermatology, University of Pennsylvania, Philadelphia, led the study, published in the Journal of the American Academy of Dermatology.

CCCA, a type of scarring alopecia, most often affects women of African descent, and published data on the demographics, clinical findings, and medical histories of CCCA in men are limited, according to the authors.

The average age of the men was 43 years and 88.2% were Black, similar to women with CCCA, who tend to be middle-aged and Black. The four most common symptoms were scalp pruritus (58.8%), lesions (29.4%), pain or tenderness (23.5%), and hair thinning (23.5%). None of the men had type 2 diabetes (considered a possible CCCA risk factor), but 47.1% had a family history of alopecia. The four most common CCCA distributions were classic (47.1%), occipital (17.6%), patchy (11.8%), and posterior vertex (11.8%).

“Larger studies are needed to fully elucidate these relationships and explore etiology in males with CCCA,” the researchers wrote. “Nonetheless, we hope the data will prompt clinicians to assess for CCCA and risk factors in adult males with scarring alopecia.”

Limitations of the study included the retrospective, single-center design, and small sample size.

The researchers reported having no relevant financial relationships.

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

In a case series of 17 men with central centrifugal cicatricial alopecia (CCCA), almost half had a family history of alopecia, most were Black, and the most common symptom was scalp pruritus.

Researchers retrospectively reviewed the medical records of 17 male patients with a clinical diagnosis of CCCA who were seen at University of Pennsylvania outpatient clinics between 2012 and 2022. They excluded patients who had no scalp biopsy or if the scalp biopsy features limited characterization. Temitayo Ogunleye, MD, of the department of dermatology, University of Pennsylvania, Philadelphia, led the study, published in the Journal of the American Academy of Dermatology.

CCCA, a type of scarring alopecia, most often affects women of African descent, and published data on the demographics, clinical findings, and medical histories of CCCA in men are limited, according to the authors.

The average age of the men was 43 years and 88.2% were Black, similar to women with CCCA, who tend to be middle-aged and Black. The four most common symptoms were scalp pruritus (58.8%), lesions (29.4%), pain or tenderness (23.5%), and hair thinning (23.5%). None of the men had type 2 diabetes (considered a possible CCCA risk factor), but 47.1% had a family history of alopecia. The four most common CCCA distributions were classic (47.1%), occipital (17.6%), patchy (11.8%), and posterior vertex (11.8%).

“Larger studies are needed to fully elucidate these relationships and explore etiology in males with CCCA,” the researchers wrote. “Nonetheless, we hope the data will prompt clinicians to assess for CCCA and risk factors in adult males with scarring alopecia.”

Limitations of the study included the retrospective, single-center design, and small sample size.

The researchers reported having no relevant financial relationships.

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

Sudden cardiac arrest is the term given to death that results from a cardiac cause and occurs within an hour of symptoms being observed. If no witnesses are present, sudden cardiac arrest is present if the person had been in apparently good health 24 hours before cardiac death. Fatality is usually a result of sustained ventricular fibrillation or sustained ventricular tachycardia that leads to cardiac arrest.

What should primary care practitioners consider in order to detect at-risk patients in time?
 

Recognizing warning signs

Warning signs that should prompt physicians to consider an increased risk of sudden cardiac arrest include the following:

• Unexplained, brief fainting episodes that above all occur with stress, physical activity, or loud noises (for example, alarm ringing)
• Seizures without a clear pathologic EEG result (for example, epilepsy)
• Unexplained accidents or car crashes
• Heart failure or pacemaker dependency before age 50 years

“These are all indications that could point to an underlying heart disease that should be investigated by a medical professional,” explained Silke Kauferstein, PhD, head of the Center for Sudden Cardiac Arrest and Familial Arrhythmia Syndrome at the Institute of Forensic Medicine of the University Frankfurt am Main (Germany), in a podcast by the German Heart Foundation.
 

Sports rarely responsible

Sudden cardiac arrest has numerous causes. Sudden cardiac arrests in a professional sports environment always attract attention. Yet sports play a less important role in sudden cardiac arrest than is often assumed, even in young individuals.

“The incidence of sudden cardiac arrest is on average 0.7-3 per 100,000 sports players from all age groups,” said Thomas Voigtländer, MD, chair of the German Heart Foundation, in an interview. Men make up 95% of those affected, and 90% of these events occur during recreational sports.
 

Inherited disorders

The most significant risk factor for sudden cardiac arrest is age; it is often associated with coronary heart disease. This factor can be significant from as early as age 35 years. Among young individuals, sudden cardiac arrest is often a result of congenital heart diseases, such as hypertrophic cardiomyopathy or arrhythmogenic right ventricular cardiomyopathy. Diseases such as long QT syndrome and Brugada syndrome can also lead to sudden cardiac arrest.

Among young sports players who experience sudden cardiac arrest, the cause is often an overlooked hereditary factor. “Cardiac screening is recommended in particular for young, high-performance athletes from around 14 years old,” said Dr. Voigtländer, who is also a cardiologist and medical director of the Agaplesion Bethanien Hospital in Frankfurt.
 

Testing of family

“If sudden cardiac arrest or an unexplained sudden death occurs at a young age in the family, the primary care practitioner must be aware that this could be due to heart diseases that could affect the rest of the family,” said Dr. Voigtländer.

In these cases, primary care practitioners must connect the other family members to specialist outpatient departments that can test for genetic factors, he added. “Many of these genetic diseases can be treated successfully if they are diagnosed promptly.”
 

Lack of knowledge

Dr. Kauferstein, who runs such a specialist outpatient department, said, “unfortunately, many affected families do not know that they should be tested as well. This lack of knowledge can also lead to fatal consequences for relatives.”

For this reason, she believes that it is crucial to provide more information to the general population. Sudden cardiac arrest is often the first sign of an underlying heart disease in young, healthy individuals. “We do see warning signals in our in-depth testing of sudden cardiac arrest cases that have often been overlooked,” said Dr. Kauferstein.

This article was translated from the Medscape German Edition. A version appeared on Medscape.com.

Sudden cardiac arrest is the term given to death that results from a cardiac cause and occurs within an hour of symptoms being observed. If no witnesses are present, sudden cardiac arrest is present if the person had been in apparently good health 24 hours before cardiac death. Fatality is usually a result of sustained ventricular fibrillation or sustained ventricular tachycardia that leads to cardiac arrest.

What should primary care practitioners consider in order to detect at-risk patients in time?
 

Recognizing warning signs

Warning signs that should prompt physicians to consider an increased risk of sudden cardiac arrest include the following:

• Unexplained, brief fainting episodes that above all occur with stress, physical activity, or loud noises (for example, alarm ringing)
• Seizures without a clear pathologic EEG result (for example, epilepsy)
• Unexplained accidents or car crashes
• Heart failure or pacemaker dependency before age 50 years

“These are all indications that could point to an underlying heart disease that should be investigated by a medical professional,” explained Silke Kauferstein, PhD, head of the Center for Sudden Cardiac Arrest and Familial Arrhythmia Syndrome at the Institute of Forensic Medicine of the University Frankfurt am Main (Germany), in a podcast by the German Heart Foundation.
 

Sports rarely responsible

Sudden cardiac arrest has numerous causes. Sudden cardiac arrests in a professional sports environment always attract attention. Yet sports play a less important role in sudden cardiac arrest than is often assumed, even in young individuals.

“The incidence of sudden cardiac arrest is on average 0.7-3 per 100,000 sports players from all age groups,” said Thomas Voigtländer, MD, chair of the German Heart Foundation, in an interview. Men make up 95% of those affected, and 90% of these events occur during recreational sports.
 

Inherited disorders

The most significant risk factor for sudden cardiac arrest is age; it is often associated with coronary heart disease. This factor can be significant from as early as age 35 years. Among young individuals, sudden cardiac arrest is often a result of congenital heart diseases, such as hypertrophic cardiomyopathy or arrhythmogenic right ventricular cardiomyopathy. Diseases such as long QT syndrome and Brugada syndrome can also lead to sudden cardiac arrest.

Among young sports players who experience sudden cardiac arrest, the cause is often an overlooked hereditary factor. “Cardiac screening is recommended in particular for young, high-performance athletes from around 14 years old,” said Dr. Voigtländer, who is also a cardiologist and medical director of the Agaplesion Bethanien Hospital in Frankfurt.
 

Testing of family

“If sudden cardiac arrest or an unexplained sudden death occurs at a young age in the family, the primary care practitioner must be aware that this could be due to heart diseases that could affect the rest of the family,” said Dr. Voigtländer.

In these cases, primary care practitioners must connect the other family members to specialist outpatient departments that can test for genetic factors, he added. “Many of these genetic diseases can be treated successfully if they are diagnosed promptly.”
 

Lack of knowledge

Dr. Kauferstein, who runs such a specialist outpatient department, said, “unfortunately, many affected families do not know that they should be tested as well. This lack of knowledge can also lead to fatal consequences for relatives.”

For this reason, she believes that it is crucial to provide more information to the general population. Sudden cardiac arrest is often the first sign of an underlying heart disease in young, healthy individuals. “We do see warning signals in our in-depth testing of sudden cardiac arrest cases that have often been overlooked,” said Dr. Kauferstein.

This article was translated from the Medscape German Edition. A version appeared on Medscape.com.

Sudden cardiac arrest is the term given to death that results from a cardiac cause and occurs within an hour of symptoms being observed. If no witnesses are present, sudden cardiac arrest is present if the person had been in apparently good health 24 hours before cardiac death. Fatality is usually a result of sustained ventricular fibrillation or sustained ventricular tachycardia that leads to cardiac arrest.

What should primary care practitioners consider in order to detect at-risk patients in time?
 

Recognizing warning signs

Warning signs that should prompt physicians to consider an increased risk of sudden cardiac arrest include the following:

• Unexplained, brief fainting episodes that above all occur with stress, physical activity, or loud noises (for example, alarm ringing)
• Seizures without a clear pathologic EEG result (for example, epilepsy)
• Unexplained accidents or car crashes
• Heart failure or pacemaker dependency before age 50 years

“These are all indications that could point to an underlying heart disease that should be investigated by a medical professional,” explained Silke Kauferstein, PhD, head of the Center for Sudden Cardiac Arrest and Familial Arrhythmia Syndrome at the Institute of Forensic Medicine of the University Frankfurt am Main (Germany), in a podcast by the German Heart Foundation.
 

Sports rarely responsible

Sudden cardiac arrest has numerous causes. Sudden cardiac arrests in a professional sports environment always attract attention. Yet sports play a less important role in sudden cardiac arrest than is often assumed, even in young individuals.

“The incidence of sudden cardiac arrest is on average 0.7-3 per 100,000 sports players from all age groups,” said Thomas Voigtländer, MD, chair of the German Heart Foundation, in an interview. Men make up 95% of those affected, and 90% of these events occur during recreational sports.
 

Inherited disorders

The most significant risk factor for sudden cardiac arrest is age; it is often associated with coronary heart disease. This factor can be significant from as early as age 35 years. Among young individuals, sudden cardiac arrest is often a result of congenital heart diseases, such as hypertrophic cardiomyopathy or arrhythmogenic right ventricular cardiomyopathy. Diseases such as long QT syndrome and Brugada syndrome can also lead to sudden cardiac arrest.

Among young sports players who experience sudden cardiac arrest, the cause is often an overlooked hereditary factor. “Cardiac screening is recommended in particular for young, high-performance athletes from around 14 years old,” said Dr. Voigtländer, who is also a cardiologist and medical director of the Agaplesion Bethanien Hospital in Frankfurt.
 

Testing of family

“If sudden cardiac arrest or an unexplained sudden death occurs at a young age in the family, the primary care practitioner must be aware that this could be due to heart diseases that could affect the rest of the family,” said Dr. Voigtländer.

In these cases, primary care practitioners must connect the other family members to specialist outpatient departments that can test for genetic factors, he added. “Many of these genetic diseases can be treated successfully if they are diagnosed promptly.”
 

Lack of knowledge

Dr. Kauferstein, who runs such a specialist outpatient department, said, “unfortunately, many affected families do not know that they should be tested as well. This lack of knowledge can also lead to fatal consequences for relatives.”

For this reason, she believes that it is crucial to provide more information to the general population. Sudden cardiac arrest is often the first sign of an underlying heart disease in young, healthy individuals. “We do see warning signals in our in-depth testing of sudden cardiac arrest cases that have often been overlooked,” said Dr. Kauferstein.

This article was translated from the Medscape German Edition. A version appeared on Medscape.com.

The Diagnosis: Pretibial Myxedema

Histopathology showed superficial and deep mucin deposition with proliferation of fibroblasts and thin wiry collagen bundles that were consistent with a diagnosis of pretibial myxedema. The patient was treated with clobetasol ointment 0.05% twice daily for 3 months, followed by a trial of pentoxifylline 400 mg 3 times daily for 3 months. After this treatment failed, she was started on rituximab infusions of 1 g biweekly for 1 month, followed by 500 mg at 6 months, with marked improvement after the first 2 doses of 1 g.

Pretibial myxedema is an uncommon cutaneous manifestation of autoimmune thyroid disease, occurring in 1% to 5% of patients with Graves disease. It usually occurs in older adult women on the pretibial regions and less commonly on the upper extremities, face, and areas of prior trauma.^1-3 Although typically asymptomatic, it can be painful and ulcerate.³ The clinical presentation consists of bilateral nonpitting edema with overlying indurated skin as well as flesh-colored, yellow-brown, violaceous, or peau d’orange papules and plaques.^2,3 Lesions develop over months and often have been associated with hyperhidrosis and hypertrichosis.² Many variants have been identified including nodular, plaquelike, diffuse swelling (ie, nonpitting edema), tumor, mixture, polypoid, and elephantiasis; severe cases with acral involvement are termed thyroid acropachy.^1-3 Pathogenesis likely involves the activation of thyrotropin receptors on fibroblasts by the circulating thyrotropin autoantibodies found in Graves disease. Activated fibroblasts upregulate glycosaminoglycan production, which osmotically drives the accumulation of dermal and subdermal fluid.^1,3

This diagnosis should be considered in any patient with pretibial edema or edema in areas of trauma. Graves disease most commonly is diagnosed 1 to 2 years prior to the development of pretibial myxedema; other extrathyroidal manifestations, most commonly ophthalmopathies, almost always are found in patients with pretibial myxedema. If a diagnosis of Graves disease has not been established, thyroid studies, including thyrotropin receptor antibody serum levels, should be obtained. Histopathology showing increased mucin in the dermis and increased fibroblasts can aid in diagnosis.^2,3

The differential diagnosis includes inflammatory dermatoses, such as stasis dermatitis and lipodermatosclerosis. Stasis dermatitis is characterized by lichenified yellowbrown plaques that present on the lower extremities; lipodermatosclerosis then can develop and present as atrophic sclerotic plaques with a champagne bottle–like appearance. Necrobiosis lipoidica demonstrates atrophic, shiny, yellow plaques with telangiectases and ulcerations. Hypertrophic lichen planus presents with hyperkeratotic hyperpigmented plaques on the shins.^1,2 Other diseases of cutaneous mucin deposition, namely scleromyxedema, demonstrate similar physical findings but more commonly are located on the trunk, face, and dorsal hands rather than the lower extremities.^1-3

Treatment of pretibial myxedema is difficult; normalization of thyroid function, weight reduction, and compression stockings can help reduce edema. Medical therapies aim to decrease glycosaminoglycan production by fibroblasts. First-line treatment includes topical steroids under occlusion, and second-line therapies include intralesional steroids, systemic corticosteroids, pentoxifylline, and octreotide.^2,3 Therapies for refractory disease include plasmapheresis, surgical excision, radiotherapy, and intravenous immunoglobulin; more recent studies also endorse the use of isotretinoin, intralesional hyaluronidase, and rituximab.^2,4 Success also has been observed with the insulin growth factor 1 receptor inhibitor teprotumumab in active thyroid eye disease, in which insulin growth factor 1 receptor is overexpressed by fibroblasts. Given the similar pathogenesis of thyroid ophthalmopathy with other extrathyroidal manifestations, teprotumumab is a promising option for refractory cases of pretibial myxedema and has led to disease resolution in several patients.⁴

The Diagnosis: Pretibial Myxedema

Histopathology showed superficial and deep mucin deposition with proliferation of fibroblasts and thin wiry collagen bundles that were consistent with a diagnosis of pretibial myxedema. The patient was treated with clobetasol ointment 0.05% twice daily for 3 months, followed by a trial of pentoxifylline 400 mg 3 times daily for 3 months. After this treatment failed, she was started on rituximab infusions of 1 g biweekly for 1 month, followed by 500 mg at 6 months, with marked improvement after the first 2 doses of 1 g.

Pretibial myxedema is an uncommon cutaneous manifestation of autoimmune thyroid disease, occurring in 1% to 5% of patients with Graves disease. It usually occurs in older adult women on the pretibial regions and less commonly on the upper extremities, face, and areas of prior trauma.^1-3 Although typically asymptomatic, it can be painful and ulcerate.³ The clinical presentation consists of bilateral nonpitting edema with overlying indurated skin as well as flesh-colored, yellow-brown, violaceous, or peau d’orange papules and plaques.^2,3 Lesions develop over months and often have been associated with hyperhidrosis and hypertrichosis.² Many variants have been identified including nodular, plaquelike, diffuse swelling (ie, nonpitting edema), tumor, mixture, polypoid, and elephantiasis; severe cases with acral involvement are termed thyroid acropachy.^1-3 Pathogenesis likely involves the activation of thyrotropin receptors on fibroblasts by the circulating thyrotropin autoantibodies found in Graves disease. Activated fibroblasts upregulate glycosaminoglycan production, which osmotically drives the accumulation of dermal and subdermal fluid.^1,3

This diagnosis should be considered in any patient with pretibial edema or edema in areas of trauma. Graves disease most commonly is diagnosed 1 to 2 years prior to the development of pretibial myxedema; other extrathyroidal manifestations, most commonly ophthalmopathies, almost always are found in patients with pretibial myxedema. If a diagnosis of Graves disease has not been established, thyroid studies, including thyrotropin receptor antibody serum levels, should be obtained. Histopathology showing increased mucin in the dermis and increased fibroblasts can aid in diagnosis.^2,3

The differential diagnosis includes inflammatory dermatoses, such as stasis dermatitis and lipodermatosclerosis. Stasis dermatitis is characterized by lichenified yellowbrown plaques that present on the lower extremities; lipodermatosclerosis then can develop and present as atrophic sclerotic plaques with a champagne bottle–like appearance. Necrobiosis lipoidica demonstrates atrophic, shiny, yellow plaques with telangiectases and ulcerations. Hypertrophic lichen planus presents with hyperkeratotic hyperpigmented plaques on the shins.^1,2 Other diseases of cutaneous mucin deposition, namely scleromyxedema, demonstrate similar physical findings but more commonly are located on the trunk, face, and dorsal hands rather than the lower extremities.^1-3

Treatment of pretibial myxedema is difficult; normalization of thyroid function, weight reduction, and compression stockings can help reduce edema. Medical therapies aim to decrease glycosaminoglycan production by fibroblasts. First-line treatment includes topical steroids under occlusion, and second-line therapies include intralesional steroids, systemic corticosteroids, pentoxifylline, and octreotide.^2,3 Therapies for refractory disease include plasmapheresis, surgical excision, radiotherapy, and intravenous immunoglobulin; more recent studies also endorse the use of isotretinoin, intralesional hyaluronidase, and rituximab.^2,4 Success also has been observed with the insulin growth factor 1 receptor inhibitor teprotumumab in active thyroid eye disease, in which insulin growth factor 1 receptor is overexpressed by fibroblasts. Given the similar pathogenesis of thyroid ophthalmopathy with other extrathyroidal manifestations, teprotumumab is a promising option for refractory cases of pretibial myxedema and has led to disease resolution in several patients.⁴

The Diagnosis: Pretibial Myxedema

Histopathology showed superficial and deep mucin deposition with proliferation of fibroblasts and thin wiry collagen bundles that were consistent with a diagnosis of pretibial myxedema. The patient was treated with clobetasol ointment 0.05% twice daily for 3 months, followed by a trial of pentoxifylline 400 mg 3 times daily for 3 months. After this treatment failed, she was started on rituximab infusions of 1 g biweekly for 1 month, followed by 500 mg at 6 months, with marked improvement after the first 2 doses of 1 g.

Pretibial myxedema is an uncommon cutaneous manifestation of autoimmune thyroid disease, occurring in 1% to 5% of patients with Graves disease. It usually occurs in older adult women on the pretibial regions and less commonly on the upper extremities, face, and areas of prior trauma.^1-3 Although typically asymptomatic, it can be painful and ulcerate.³ The clinical presentation consists of bilateral nonpitting edema with overlying indurated skin as well as flesh-colored, yellow-brown, violaceous, or peau d’orange papules and plaques.^2,3 Lesions develop over months and often have been associated with hyperhidrosis and hypertrichosis.² Many variants have been identified including nodular, plaquelike, diffuse swelling (ie, nonpitting edema), tumor, mixture, polypoid, and elephantiasis; severe cases with acral involvement are termed thyroid acropachy.^1-3 Pathogenesis likely involves the activation of thyrotropin receptors on fibroblasts by the circulating thyrotropin autoantibodies found in Graves disease. Activated fibroblasts upregulate glycosaminoglycan production, which osmotically drives the accumulation of dermal and subdermal fluid.^1,3

This diagnosis should be considered in any patient with pretibial edema or edema in areas of trauma. Graves disease most commonly is diagnosed 1 to 2 years prior to the development of pretibial myxedema; other extrathyroidal manifestations, most commonly ophthalmopathies, almost always are found in patients with pretibial myxedema. If a diagnosis of Graves disease has not been established, thyroid studies, including thyrotropin receptor antibody serum levels, should be obtained. Histopathology showing increased mucin in the dermis and increased fibroblasts can aid in diagnosis.^2,3

The differential diagnosis includes inflammatory dermatoses, such as stasis dermatitis and lipodermatosclerosis. Stasis dermatitis is characterized by lichenified yellowbrown plaques that present on the lower extremities; lipodermatosclerosis then can develop and present as atrophic sclerotic plaques with a champagne bottle–like appearance. Necrobiosis lipoidica demonstrates atrophic, shiny, yellow plaques with telangiectases and ulcerations. Hypertrophic lichen planus presents with hyperkeratotic hyperpigmented plaques on the shins.^1,2 Other diseases of cutaneous mucin deposition, namely scleromyxedema, demonstrate similar physical findings but more commonly are located on the trunk, face, and dorsal hands rather than the lower extremities.^1-3

Treatment of pretibial myxedema is difficult; normalization of thyroid function, weight reduction, and compression stockings can help reduce edema. Medical therapies aim to decrease glycosaminoglycan production by fibroblasts. First-line treatment includes topical steroids under occlusion, and second-line therapies include intralesional steroids, systemic corticosteroids, pentoxifylline, and octreotide.^2,3 Therapies for refractory disease include plasmapheresis, surgical excision, radiotherapy, and intravenous immunoglobulin; more recent studies also endorse the use of isotretinoin, intralesional hyaluronidase, and rituximab.^2,4 Success also has been observed with the insulin growth factor 1 receptor inhibitor teprotumumab in active thyroid eye disease, in which insulin growth factor 1 receptor is overexpressed by fibroblasts. Given the similar pathogenesis of thyroid ophthalmopathy with other extrathyroidal manifestations, teprotumumab is a promising option for refractory cases of pretibial myxedema and has led to disease resolution in several patients.⁴

A new study published in Neurology found an association between long–term proton-pump inhibitors (PPI) use and dementia. This was an observational study and does not prove that acid reflux drugs cause dementia.

“In this study, the authors note that long-term PPI use, defined as more than 4.5 years of use, was associated with dementia. It is important to note, however, that this does not necessarily mean that PPIs cause dementia. With observational studies, there is an inherent risk of bias and confounding, as the authors report. Some of these confounders include Helicobacter pylori status, vitamin B₁₂ deficiency, depression, and socioeconomic status,” said Fouad J. Moawad, MD, graduate of the AGA FORWARD Program and gastroenterologist at Scripps Health in San Diego. A 2017 study led by Andrew T. Chan, MD, MPH, of Mass General Brigham, Boston, examined the association between proton pump inhibitor use and cognitive function in women. The investigators found no “convincing association between PPI use and cognitive function. Our data do not support the suggestion that PPI use increases dementia risk.”

A new article in press in Gastroenterology by Raaj S. Mehta and colleagues also studied this issue and concluded that in adults 65 years of age or older, PPIs were not associated with dementia or decline in cognition over time. These data provide reassurance about the safety of long-term use of PPIs among older adults.

The headlines may be confusing for patients. Here are AGA’s three talking points for communicating with patients about PPIs:

Talk to your doctor, before making any changes to your medication.

You have been prescribed PPIs for a reason, to treat a diagnosed medical condition. We can discuss the reason for your prescription, the dose and the timeframe for treatment.

Consider lifestyle modifications. 

These may reduce or eliminate the need for PPIs for long-term use. These may include weight loss, avoiding tobacco or a change in your eating patterns. We can work together to determine the changes that are right for you.

Keep in touch.

Research continues to be done on PPI use. Current research recommends that patients who have a diagnosed condition that is helped by PPIs should stay on them, as benefits can outweigh risks.

A new study published in Neurology found an association between long–term proton-pump inhibitors (PPI) use and dementia. This was an observational study and does not prove that acid reflux drugs cause dementia.

“In this study, the authors note that long-term PPI use, defined as more than 4.5 years of use, was associated with dementia. It is important to note, however, that this does not necessarily mean that PPIs cause dementia. With observational studies, there is an inherent risk of bias and confounding, as the authors report. Some of these confounders include Helicobacter pylori status, vitamin B₁₂ deficiency, depression, and socioeconomic status,” said Fouad J. Moawad, MD, graduate of the AGA FORWARD Program and gastroenterologist at Scripps Health in San Diego. A 2017 study led by Andrew T. Chan, MD, MPH, of Mass General Brigham, Boston, examined the association between proton pump inhibitor use and cognitive function in women. The investigators found no “convincing association between PPI use and cognitive function. Our data do not support the suggestion that PPI use increases dementia risk.”

A new article in press in Gastroenterology by Raaj S. Mehta and colleagues also studied this issue and concluded that in adults 65 years of age or older, PPIs were not associated with dementia or decline in cognition over time. These data provide reassurance about the safety of long-term use of PPIs among older adults.

The headlines may be confusing for patients. Here are AGA’s three talking points for communicating with patients about PPIs:

Talk to your doctor, before making any changes to your medication.

You have been prescribed PPIs for a reason, to treat a diagnosed medical condition. We can discuss the reason for your prescription, the dose and the timeframe for treatment.

Consider lifestyle modifications. 

These may reduce or eliminate the need for PPIs for long-term use. These may include weight loss, avoiding tobacco or a change in your eating patterns. We can work together to determine the changes that are right for you.

Keep in touch.

Research continues to be done on PPI use. Current research recommends that patients who have a diagnosed condition that is helped by PPIs should stay on them, as benefits can outweigh risks.

A new study published in Neurology found an association between long–term proton-pump inhibitors (PPI) use and dementia. This was an observational study and does not prove that acid reflux drugs cause dementia.

“In this study, the authors note that long-term PPI use, defined as more than 4.5 years of use, was associated with dementia. It is important to note, however, that this does not necessarily mean that PPIs cause dementia. With observational studies, there is an inherent risk of bias and confounding, as the authors report. Some of these confounders include Helicobacter pylori status, vitamin B₁₂ deficiency, depression, and socioeconomic status,” said Fouad J. Moawad, MD, graduate of the AGA FORWARD Program and gastroenterologist at Scripps Health in San Diego. A 2017 study led by Andrew T. Chan, MD, MPH, of Mass General Brigham, Boston, examined the association between proton pump inhibitor use and cognitive function in women. The investigators found no “convincing association between PPI use and cognitive function. Our data do not support the suggestion that PPI use increases dementia risk.”

A new article in press in Gastroenterology by Raaj S. Mehta and colleagues also studied this issue and concluded that in adults 65 years of age or older, PPIs were not associated with dementia or decline in cognition over time. These data provide reassurance about the safety of long-term use of PPIs among older adults.

The headlines may be confusing for patients. Here are AGA’s three talking points for communicating with patients about PPIs:

Talk to your doctor, before making any changes to your medication.

You have been prescribed PPIs for a reason, to treat a diagnosed medical condition. We can discuss the reason for your prescription, the dose and the timeframe for treatment.

Consider lifestyle modifications. 

These may reduce or eliminate the need for PPIs for long-term use. These may include weight loss, avoiding tobacco or a change in your eating patterns. We can work together to determine the changes that are right for you.

Keep in touch.

Research continues to be done on PPI use. Current research recommends that patients who have a diagnosed condition that is helped by PPIs should stay on them, as benefits can outweigh risks.

Ethylene oxide is a compound used to sterilize more than 20 billion devices sold in the U.S. every year. Although this sterilization process helps keep medical devices – and patients – safe, the odorless, flammable gas may also be harming people who live near sterilization plants and who may inhale the compound, which has been linked to an elevated risk of cancer.

Regulatory agencies are currently feuding over the best way to address the dilemma: preserving patient safety versus protecting public health. Lawmakers are weighing in on the matter, which has been the source of multiple civil lawsuits filed by individuals who say they have suffered health problems as a result of exposure to ethylene oxide.

The Environmental Protection Agency and the U.S. Food and Drug Administration agree that use of the compound should be limited, but they are at odds about how quickly limits should be put in place, according to Axios.

A new commercial standard for ethylene oxide proposed by the EPA in April would impose stricter emission restrictions for sterilization facilities and chemical plants – a move that would cut ethylene oxide emissions by 80%, the EPA estimates.

While the FDA says it “shares concerns about the release of ethylene oxide at unsafe levels into the environment,” the agency cautions that moving too fast to cut emissions would disrupt the medical supply chain, which is already experiencing turbulence. The U.S. has been facing the worst drug supply shortages in a decade in addition to severe medical device shortages.

Currently, other methods of sterilization cannot replace the use of ethylene oxide for many devices. Ethylene oxide is used to sterilize about half of all medical devices in the U.S., the FDA says. Given the country’s reliance on this compound for sterilization, the FDA says it is “equally concerned about the potential impact of shortages of sterilized medical devices that would result from disruptions in commercial sterilizer facility operations.”

In 2019, Illinois temporarily closed a sterilization facility over concern regarding ethylene oxide emissions. The closure caused a shortage of a pediatric breathing tube.

Some lawmakers agree that an Interior-Environment bill would require FDA certification that any action by the EPA would not cause a medical device shortage.

The FDA has been working to identify safe alternatives to ethylene oxide for sterilizing medical supplies as well as strategies to reduce emissions of ethylene oxide by capturing the gas or by turning it into a harmless byproduct. In 2019, the FDA launched a pilot program to incentivize companies to develop new sterilization technologies.

“The FDA remains focused in our commitment to encourage novel ways to sterilize medical devices while reducing adverse impacts on the environment and public health and developing solutions to avoid potential shortages of devices that the American public relies upon,” the agency said.

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

Ethylene oxide is a compound used to sterilize more than 20 billion devices sold in the U.S. every year. Although this sterilization process helps keep medical devices – and patients – safe, the odorless, flammable gas may also be harming people who live near sterilization plants and who may inhale the compound, which has been linked to an elevated risk of cancer.

Regulatory agencies are currently feuding over the best way to address the dilemma: preserving patient safety versus protecting public health. Lawmakers are weighing in on the matter, which has been the source of multiple civil lawsuits filed by individuals who say they have suffered health problems as a result of exposure to ethylene oxide.

The Environmental Protection Agency and the U.S. Food and Drug Administration agree that use of the compound should be limited, but they are at odds about how quickly limits should be put in place, according to Axios.

A new commercial standard for ethylene oxide proposed by the EPA in April would impose stricter emission restrictions for sterilization facilities and chemical plants – a move that would cut ethylene oxide emissions by 80%, the EPA estimates.

While the FDA says it “shares concerns about the release of ethylene oxide at unsafe levels into the environment,” the agency cautions that moving too fast to cut emissions would disrupt the medical supply chain, which is already experiencing turbulence. The U.S. has been facing the worst drug supply shortages in a decade in addition to severe medical device shortages.

Currently, other methods of sterilization cannot replace the use of ethylene oxide for many devices. Ethylene oxide is used to sterilize about half of all medical devices in the U.S., the FDA says. Given the country’s reliance on this compound for sterilization, the FDA says it is “equally concerned about the potential impact of shortages of sterilized medical devices that would result from disruptions in commercial sterilizer facility operations.”

In 2019, Illinois temporarily closed a sterilization facility over concern regarding ethylene oxide emissions. The closure caused a shortage of a pediatric breathing tube.

Some lawmakers agree that an Interior-Environment bill would require FDA certification that any action by the EPA would not cause a medical device shortage.

The FDA has been working to identify safe alternatives to ethylene oxide for sterilizing medical supplies as well as strategies to reduce emissions of ethylene oxide by capturing the gas or by turning it into a harmless byproduct. In 2019, the FDA launched a pilot program to incentivize companies to develop new sterilization technologies.

“The FDA remains focused in our commitment to encourage novel ways to sterilize medical devices while reducing adverse impacts on the environment and public health and developing solutions to avoid potential shortages of devices that the American public relies upon,” the agency said.

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

Ethylene oxide is a compound used to sterilize more than 20 billion devices sold in the U.S. every year. Although this sterilization process helps keep medical devices – and patients – safe, the odorless, flammable gas may also be harming people who live near sterilization plants and who may inhale the compound, which has been linked to an elevated risk of cancer.

Regulatory agencies are currently feuding over the best way to address the dilemma: preserving patient safety versus protecting public health. Lawmakers are weighing in on the matter, which has been the source of multiple civil lawsuits filed by individuals who say they have suffered health problems as a result of exposure to ethylene oxide.

The Environmental Protection Agency and the U.S. Food and Drug Administration agree that use of the compound should be limited, but they are at odds about how quickly limits should be put in place, according to Axios.

A new commercial standard for ethylene oxide proposed by the EPA in April would impose stricter emission restrictions for sterilization facilities and chemical plants – a move that would cut ethylene oxide emissions by 80%, the EPA estimates.

While the FDA says it “shares concerns about the release of ethylene oxide at unsafe levels into the environment,” the agency cautions that moving too fast to cut emissions would disrupt the medical supply chain, which is already experiencing turbulence. The U.S. has been facing the worst drug supply shortages in a decade in addition to severe medical device shortages.

Currently, other methods of sterilization cannot replace the use of ethylene oxide for many devices. Ethylene oxide is used to sterilize about half of all medical devices in the U.S., the FDA says. Given the country’s reliance on this compound for sterilization, the FDA says it is “equally concerned about the potential impact of shortages of sterilized medical devices that would result from disruptions in commercial sterilizer facility operations.”

In 2019, Illinois temporarily closed a sterilization facility over concern regarding ethylene oxide emissions. The closure caused a shortage of a pediatric breathing tube.

Some lawmakers agree that an Interior-Environment bill would require FDA certification that any action by the EPA would not cause a medical device shortage.

The FDA has been working to identify safe alternatives to ethylene oxide for sterilizing medical supplies as well as strategies to reduce emissions of ethylene oxide by capturing the gas or by turning it into a harmless byproduct. In 2019, the FDA launched a pilot program to incentivize companies to develop new sterilization technologies.

“The FDA remains focused in our commitment to encourage novel ways to sterilize medical devices while reducing adverse impacts on the environment and public health and developing solutions to avoid potential shortages of devices that the American public relies upon,” the agency said.

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

Physicians tend to be compulsive multitaskers. We switch from one task to another all the time – even in front of patients. We think we are more efficient and productive, and that we are accomplishing more in less time. In fact, there is no credible evidence that this is true, and a mountain of evidence showing exactly the opposite.

According to this study and others, multitasking results in an average of 2 hours per day of lost productivity. It decreases the quality of work performed and increases cortisol levels, which impedes cognitive functioning, leading to a further decrease in productivity in a vicious cycle, making you increasingly ineffective and destroying your motivation and mood.

On the surface, the reasons for this are not intuitively obvious. After all, simple and routine tasks are easy to perform simultaneously; we can all walk and chew gum at the same time or eat a snack while watching TV. The problems arise when we try to multitask more complex tasks that require thought and decision-making.

It turns out that the pressures of our modern world have evolved faster than our brains. We are still hard-wired for monotasking. When we think we are completing two tasks simultaneously, we are actually performing individual actions in rapid succession. Each time you switch tasks, your brain must turn off the cognitive rules of the previous task and turn on new rules for the next one. When you switch back, the process repeats in reverse. Each of those mental gear shifts takes time and costs us productivity. According to one psychologist, even brief mental blocks created by shifting between tasks can cost as much as 40% of someone’s productive time. We are also far more likely to make mistakes while we are doing it.

Furthermore, you are stifling your creativity and innovation because you don’t focus on one task long enough to come up with original insights. Multitasking also slows down your general cognitive functions, in the same way that keeping many windows are open on your computer slows down the entire system. A study from my alma mater, the University of California, San Francisco, concluded that multitasking negativity affects memory in both younger and older adults (although the effects were greater in older adults) .

So, what to do? The fact remains that, all too often, there really are too many tasks and not enough hours in the day. How can you get through them without falling into the multitasking trap?

The first rule is to prioritize. In his book “The Seven Habits of Highly Effective People,” Stephen Covey makes an important distinction between tasks that are important and those that are merely urgent. Tasks that are important and urgent tend to make time for themselves, because they must be taken care of immediately.

Jobs that are important but not urgent are the ones we tend to try to multitask. Because there is no immediate deadline, we think we can do two or more of them simultaneously, or we fall into the other major productivity trap: procrastination. Neither of those strategies tends to end well. Identify those important but not urgent tasks and force yourself to go through them one by one.

Urgent but unimportant tasks are the productivity thieves. They demand your attention but are not worthy of it. Most tasks in this category can be delegated. I have written about physicians’ workaholic and perfectionist tendencies that drive our conviction that no one else can do anything as well as we can. Does that unimportant task, even if urgent, really demand your time, skills, education, and medical license? Is there someone in your office, or possibly an outside contractor, who could do it just as well, and maybe faster?

In fact, that is the question you should ask every time a project triggers your urge to multitask: “Who could be doing this job – or at least a major part of it – instead of me?”

If your multitasking urges are deeply ingrained – particularly those that involve phones, laptops, and the cloud – you might consider employing electronic aids. SelfControl, for example, is a free, open-sourced app that lets you block your own access to distracting websites, your email servers, social media, or anything else on the Internet. You list the sites you wish to block and set a period of time to block them. Until the set time expires, you will be unable to access those sites, even if you restart your computer or delete the application.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

Physicians tend to be compulsive multitaskers. We switch from one task to another all the time – even in front of patients. We think we are more efficient and productive, and that we are accomplishing more in less time. In fact, there is no credible evidence that this is true, and a mountain of evidence showing exactly the opposite.

According to this study and others, multitasking results in an average of 2 hours per day of lost productivity. It decreases the quality of work performed and increases cortisol levels, which impedes cognitive functioning, leading to a further decrease in productivity in a vicious cycle, making you increasingly ineffective and destroying your motivation and mood.

On the surface, the reasons for this are not intuitively obvious. After all, simple and routine tasks are easy to perform simultaneously; we can all walk and chew gum at the same time or eat a snack while watching TV. The problems arise when we try to multitask more complex tasks that require thought and decision-making.

It turns out that the pressures of our modern world have evolved faster than our brains. We are still hard-wired for monotasking. When we think we are completing two tasks simultaneously, we are actually performing individual actions in rapid succession. Each time you switch tasks, your brain must turn off the cognitive rules of the previous task and turn on new rules for the next one. When you switch back, the process repeats in reverse. Each of those mental gear shifts takes time and costs us productivity. According to one psychologist, even brief mental blocks created by shifting between tasks can cost as much as 40% of someone’s productive time. We are also far more likely to make mistakes while we are doing it.

Furthermore, you are stifling your creativity and innovation because you don’t focus on one task long enough to come up with original insights. Multitasking also slows down your general cognitive functions, in the same way that keeping many windows are open on your computer slows down the entire system. A study from my alma mater, the University of California, San Francisco, concluded that multitasking negativity affects memory in both younger and older adults (although the effects were greater in older adults) .

So, what to do? The fact remains that, all too often, there really are too many tasks and not enough hours in the day. How can you get through them without falling into the multitasking trap?

The first rule is to prioritize. In his book “The Seven Habits of Highly Effective People,” Stephen Covey makes an important distinction between tasks that are important and those that are merely urgent. Tasks that are important and urgent tend to make time for themselves, because they must be taken care of immediately.

Jobs that are important but not urgent are the ones we tend to try to multitask. Because there is no immediate deadline, we think we can do two or more of them simultaneously, or we fall into the other major productivity trap: procrastination. Neither of those strategies tends to end well. Identify those important but not urgent tasks and force yourself to go through them one by one.

Urgent but unimportant tasks are the productivity thieves. They demand your attention but are not worthy of it. Most tasks in this category can be delegated. I have written about physicians’ workaholic and perfectionist tendencies that drive our conviction that no one else can do anything as well as we can. Does that unimportant task, even if urgent, really demand your time, skills, education, and medical license? Is there someone in your office, or possibly an outside contractor, who could do it just as well, and maybe faster?

In fact, that is the question you should ask every time a project triggers your urge to multitask: “Who could be doing this job – or at least a major part of it – instead of me?”

If your multitasking urges are deeply ingrained – particularly those that involve phones, laptops, and the cloud – you might consider employing electronic aids. SelfControl, for example, is a free, open-sourced app that lets you block your own access to distracting websites, your email servers, social media, or anything else on the Internet. You list the sites you wish to block and set a period of time to block them. Until the set time expires, you will be unable to access those sites, even if you restart your computer or delete the application.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

Physicians tend to be compulsive multitaskers. We switch from one task to another all the time – even in front of patients. We think we are more efficient and productive, and that we are accomplishing more in less time. In fact, there is no credible evidence that this is true, and a mountain of evidence showing exactly the opposite.

According to this study and others, multitasking results in an average of 2 hours per day of lost productivity. It decreases the quality of work performed and increases cortisol levels, which impedes cognitive functioning, leading to a further decrease in productivity in a vicious cycle, making you increasingly ineffective and destroying your motivation and mood.

On the surface, the reasons for this are not intuitively obvious. After all, simple and routine tasks are easy to perform simultaneously; we can all walk and chew gum at the same time or eat a snack while watching TV. The problems arise when we try to multitask more complex tasks that require thought and decision-making.

It turns out that the pressures of our modern world have evolved faster than our brains. We are still hard-wired for monotasking. When we think we are completing two tasks simultaneously, we are actually performing individual actions in rapid succession. Each time you switch tasks, your brain must turn off the cognitive rules of the previous task and turn on new rules for the next one. When you switch back, the process repeats in reverse. Each of those mental gear shifts takes time and costs us productivity. According to one psychologist, even brief mental blocks created by shifting between tasks can cost as much as 40% of someone’s productive time. We are also far more likely to make mistakes while we are doing it.

Furthermore, you are stifling your creativity and innovation because you don’t focus on one task long enough to come up with original insights. Multitasking also slows down your general cognitive functions, in the same way that keeping many windows are open on your computer slows down the entire system. A study from my alma mater, the University of California, San Francisco, concluded that multitasking negativity affects memory in both younger and older adults (although the effects were greater in older adults) .

So, what to do? The fact remains that, all too often, there really are too many tasks and not enough hours in the day. How can you get through them without falling into the multitasking trap?

The first rule is to prioritize. In his book “The Seven Habits of Highly Effective People,” Stephen Covey makes an important distinction between tasks that are important and those that are merely urgent. Tasks that are important and urgent tend to make time for themselves, because they must be taken care of immediately.

Jobs that are important but not urgent are the ones we tend to try to multitask. Because there is no immediate deadline, we think we can do two or more of them simultaneously, or we fall into the other major productivity trap: procrastination. Neither of those strategies tends to end well. Identify those important but not urgent tasks and force yourself to go through them one by one.

Urgent but unimportant tasks are the productivity thieves. They demand your attention but are not worthy of it. Most tasks in this category can be delegated. I have written about physicians’ workaholic and perfectionist tendencies that drive our conviction that no one else can do anything as well as we can. Does that unimportant task, even if urgent, really demand your time, skills, education, and medical license? Is there someone in your office, or possibly an outside contractor, who could do it just as well, and maybe faster?

In fact, that is the question you should ask every time a project triggers your urge to multitask: “Who could be doing this job – or at least a major part of it – instead of me?”

If your multitasking urges are deeply ingrained – particularly those that involve phones, laptops, and the cloud – you might consider employing electronic aids. SelfControl, for example, is a free, open-sourced app that lets you block your own access to distracting websites, your email servers, social media, or anything else on the Internet. You list the sites you wish to block and set a period of time to block them. Until the set time expires, you will be unable to access those sites, even if you restart your computer or delete the application.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].