“Food gives me ‘hugs,’ ” Ms. S* said as her eyes lit up. Finally, after weeks of working together, she could articulate her complex relationship with food. She had been struggling to explain why she continued to eat when she was full or consumed foods she knew wouldn’t help her health.

Like millions of people struggling with their weight or the disease of obesity, Ms. S had tried multiple diets and programs but continued to return to unhelpful eating patterns. Ms. S was an emotional eater, and the pandemic only worsened her emotional eating. As a single professional forced to work from home during the pandemic, she became lonely. She went from working in a busy downtown office, training for half-marathons, and teaching live workout sessions to being alone daily. Her only “real” human interaction was when she ordered daily delivery meals of her favorite comfort foods. As a person with type 2 diabetes, she knew that her delivery habit was wrecking her health, but willpower wasn’t enough to make her stop.

Her psychologist referred her to our virtual integrative obesity practice to help her lose weight and find long-term solutions. Ms. S admitted that she knew what she was doing as an emotional eater. But like many emotional eaters, she didn’t know why or how to switch from emotional eating to eating based on her biological hunger signals. As a trained obesity expert and recovering emotional eater of 8 years, personally and professionally I can appreciate the challenges of emotional eating and how it can sabotage even the best weight loss plan. In this article, I will share facts and feelings that drive emotional eating. I aim to empower clinicians seeking to help patients with emotional eating.
 

Fact: Emotional eating isn’t all emotional

It’s important not to dismiss emotional eating as all emotion driven. Recall that hunger is hormonally regulated. There are two main hunger pathways: the homeostatic pathway and the hedonic pathway. The homeostatic pathway is our biological hunger pathway and is driven by the need for energy in calories. Conversely, hedonic eating is pleasure-driven and uses emotional stimuli to “bypass” the physical hunger/satisfaction signals.

Emotional eating falls under the hedonic pathway. As clinicians, the first step in helping a patient struggling with emotional eating is empathetically listening, then assessing for any physiologic causes.

Several factors can disrupt physiologic appetite regulation, such as sleep disturbances; high stress levels; and many medical conditions, including but not limited to obesity, diabetes, and polycystic ovarian syndrome. Such factors as insulin resistance and inflammation are a common link in these conditions. Both contribute to the pathophysiology of the changes in appetite and can influence other hormones that lead to reduced satisfaction after eating. Furthermore, mental health conditions may disrupt levels of neurotransmitters such as serotonin and dopamine, which can also cause appetite changes.

These settings of physiologically disrupted appetite can trigger hedonic eating. But the relationship is complex. For example, one way to research hedonic eating is by using the Power of Food Scale. Functional MRI studies show that people with higher Power of Food Scale readings have more brain activity in the visual cortex when they see highly palatable foods. While more studies are needed to better understand the clinical implications of this finding, it’s yet another indicator that “emotional” eating isn’t all emotional. It’s also physiologic.
 

Feelings: Patterns, personality, places, psychological factors

Physiology only explains part of emotional eating. Like Ms. S, emotional eaters have strong emotional connections to food and behavior patterns. Often, physiologic cues have been coupled with psychological habits.

For example, menses is a common physiologic trigger for stress-eating for many of my patients. Studies have shown that in addition to iron levels changing during menses, calcium, magnesium, and phosphorous levels also change. Emotionally, the discomfort of “that time of the month” can lead to solace in comfort foods such as chocolate in different forms. But this isn’t surprising, as cacao and its derivative, chocolate, are rich in iron and other minerals. The chocolate is actually addressing a physical and emotional need. It can be helpful to point out this association to your patients. Suggest choosing a lower-sugar form of chocolate, such as dark chocolate, or even trying cacao nibs, while addressing any emotions.

But physiologic conditions and patterns aren’t the only emotional eating triggers. Places and psychological conditions can also trigger emotional eating.
 

Places and people 

Celebrations, vacations, proximity to certain restaurants, exposure to food marketing, and major life shifts can lead to increased hedonic eating. Helping patients recognize this connection opens the door to advance preparation for these situations.

Psychological conditions can be connected to emotional eating. It’s important to screen for mental health conditions and past traumas. For example, emotional eating could be a symptom of binge eating disorder, major depression, or generalized anxiety disorder. Childhood trauma is associated with disordered eating. The adverse childhood events quiz can be used clinically.

Emotional eating can lead to feelings of guilt, shame, and negative self-talk. It’s helpful to offer patients reassurance and encourage self-compassion. After all, it’s natural to eat. The goal isn’t to stop eating but to eat on the basis of physiologic needs.
 

Putting it together: Addressing the facts and feelings of emotional eating

1. Treat biological causes that impact physiologic hunger and trigger emotional eating.

2. Triggers: Address patterns, places/people, psychological events.

3. Transition to non-food rewards; the key to emotional eating is eating. While healthier substitutes can be a short-term solution for improving eating behaviors, ultimately, helping patients find non-food ways to address emotions is invaluable.

4. Stress management: Offer your patients ways to decrease stress levels through mindfulness and other techniques.

5. Professional support: Creating a multidisciplinary team is helpful, given the complexity of emotional eating. In addition to the primary care physician/clinician, other team members may include:

• Psychologist
• Psychiatrist
•  coach and/or certified wellness coaches
• Obesity specialist

Back to Ms. S

Ms. S is doing well. We started her on a GLP-1 agonist to address her underlying insulin resistance. Together we’ve found creative ways to satisfy her loneliness, such as volunteering and teaching virtual workout classes. Her emotional eating has decreased by over 60%, and we continue to discover new strategies to address her emotional eating triggers.

Conclusion

Despite being common, the impact of emotional eating is often minimized. With no DSM-5 criteria or ICD-11 code, it’s easy to dismiss emotional eating clinically. However, emotional eating is common and associated with weight gain.

In light of the obesity epidemic, this significance can’t be overlooked. Thankfully we have groundbreaking medications to address the homeostatic hunger pathway and physiologic drivers of emotional eating, but they’re not a substitute for addressing the psychosocial components of emotional eating.

As clinicians, we can have a meaningful impact on our patients’ lives beyond writing a prescription.

*Name/initial changed for privacy.

Sylvia Gonsahn-Bollie, MD, DipABOM, is an integrative obesity specialist focused on individualized solutions for emotional and biological overeating.

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

“Food gives me ‘hugs,’ ” Ms. S* said as her eyes lit up. Finally, after weeks of working together, she could articulate her complex relationship with food. She had been struggling to explain why she continued to eat when she was full or consumed foods she knew wouldn’t help her health.

Like millions of people struggling with their weight or the disease of obesity, Ms. S had tried multiple diets and programs but continued to return to unhelpful eating patterns. Ms. S was an emotional eater, and the pandemic only worsened her emotional eating. As a single professional forced to work from home during the pandemic, she became lonely. She went from working in a busy downtown office, training for half-marathons, and teaching live workout sessions to being alone daily. Her only “real” human interaction was when she ordered daily delivery meals of her favorite comfort foods. As a person with type 2 diabetes, she knew that her delivery habit was wrecking her health, but willpower wasn’t enough to make her stop.

Her psychologist referred her to our virtual integrative obesity practice to help her lose weight and find long-term solutions. Ms. S admitted that she knew what she was doing as an emotional eater. But like many emotional eaters, she didn’t know why or how to switch from emotional eating to eating based on her biological hunger signals. As a trained obesity expert and recovering emotional eater of 8 years, personally and professionally I can appreciate the challenges of emotional eating and how it can sabotage even the best weight loss plan. In this article, I will share facts and feelings that drive emotional eating. I aim to empower clinicians seeking to help patients with emotional eating.
 

Fact: Emotional eating isn’t all emotional

It’s important not to dismiss emotional eating as all emotion driven. Recall that hunger is hormonally regulated. There are two main hunger pathways: the homeostatic pathway and the hedonic pathway. The homeostatic pathway is our biological hunger pathway and is driven by the need for energy in calories. Conversely, hedonic eating is pleasure-driven and uses emotional stimuli to “bypass” the physical hunger/satisfaction signals.

Emotional eating falls under the hedonic pathway. As clinicians, the first step in helping a patient struggling with emotional eating is empathetically listening, then assessing for any physiologic causes.

Several factors can disrupt physiologic appetite regulation, such as sleep disturbances; high stress levels; and many medical conditions, including but not limited to obesity, diabetes, and polycystic ovarian syndrome. Such factors as insulin resistance and inflammation are a common link in these conditions. Both contribute to the pathophysiology of the changes in appetite and can influence other hormones that lead to reduced satisfaction after eating. Furthermore, mental health conditions may disrupt levels of neurotransmitters such as serotonin and dopamine, which can also cause appetite changes.

These settings of physiologically disrupted appetite can trigger hedonic eating. But the relationship is complex. For example, one way to research hedonic eating is by using the Power of Food Scale. Functional MRI studies show that people with higher Power of Food Scale readings have more brain activity in the visual cortex when they see highly palatable foods. While more studies are needed to better understand the clinical implications of this finding, it’s yet another indicator that “emotional” eating isn’t all emotional. It’s also physiologic.
 

Feelings: Patterns, personality, places, psychological factors

Physiology only explains part of emotional eating. Like Ms. S, emotional eaters have strong emotional connections to food and behavior patterns. Often, physiologic cues have been coupled with psychological habits.

For example, menses is a common physiologic trigger for stress-eating for many of my patients. Studies have shown that in addition to iron levels changing during menses, calcium, magnesium, and phosphorous levels also change. Emotionally, the discomfort of “that time of the month” can lead to solace in comfort foods such as chocolate in different forms. But this isn’t surprising, as cacao and its derivative, chocolate, are rich in iron and other minerals. The chocolate is actually addressing a physical and emotional need. It can be helpful to point out this association to your patients. Suggest choosing a lower-sugar form of chocolate, such as dark chocolate, or even trying cacao nibs, while addressing any emotions.

But physiologic conditions and patterns aren’t the only emotional eating triggers. Places and psychological conditions can also trigger emotional eating.
 

Places and people 

Celebrations, vacations, proximity to certain restaurants, exposure to food marketing, and major life shifts can lead to increased hedonic eating. Helping patients recognize this connection opens the door to advance preparation for these situations.

Psychological conditions can be connected to emotional eating. It’s important to screen for mental health conditions and past traumas. For example, emotional eating could be a symptom of binge eating disorder, major depression, or generalized anxiety disorder. Childhood trauma is associated with disordered eating. The adverse childhood events quiz can be used clinically.

Emotional eating can lead to feelings of guilt, shame, and negative self-talk. It’s helpful to offer patients reassurance and encourage self-compassion. After all, it’s natural to eat. The goal isn’t to stop eating but to eat on the basis of physiologic needs.
 

Putting it together: Addressing the facts and feelings of emotional eating

1. Treat biological causes that impact physiologic hunger and trigger emotional eating.

2. Triggers: Address patterns, places/people, psychological events.

3. Transition to non-food rewards; the key to emotional eating is eating. While healthier substitutes can be a short-term solution for improving eating behaviors, ultimately, helping patients find non-food ways to address emotions is invaluable.

4. Stress management: Offer your patients ways to decrease stress levels through mindfulness and other techniques.

5. Professional support: Creating a multidisciplinary team is helpful, given the complexity of emotional eating. In addition to the primary care physician/clinician, other team members may include:

• Psychologist
• Psychiatrist
•  coach and/or certified wellness coaches
• Obesity specialist

Back to Ms. S

Ms. S is doing well. We started her on a GLP-1 agonist to address her underlying insulin resistance. Together we’ve found creative ways to satisfy her loneliness, such as volunteering and teaching virtual workout classes. Her emotional eating has decreased by over 60%, and we continue to discover new strategies to address her emotional eating triggers.

Conclusion

Despite being common, the impact of emotional eating is often minimized. With no DSM-5 criteria or ICD-11 code, it’s easy to dismiss emotional eating clinically. However, emotional eating is common and associated with weight gain.

In light of the obesity epidemic, this significance can’t be overlooked. Thankfully we have groundbreaking medications to address the homeostatic hunger pathway and physiologic drivers of emotional eating, but they’re not a substitute for addressing the psychosocial components of emotional eating.

As clinicians, we can have a meaningful impact on our patients’ lives beyond writing a prescription.

*Name/initial changed for privacy.

Sylvia Gonsahn-Bollie, MD, DipABOM, is an integrative obesity specialist focused on individualized solutions for emotional and biological overeating.

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

“Food gives me ‘hugs,’ ” Ms. S* said as her eyes lit up. Finally, after weeks of working together, she could articulate her complex relationship with food. She had been struggling to explain why she continued to eat when she was full or consumed foods she knew wouldn’t help her health.

Like millions of people struggling with their weight or the disease of obesity, Ms. S had tried multiple diets and programs but continued to return to unhelpful eating patterns. Ms. S was an emotional eater, and the pandemic only worsened her emotional eating. As a single professional forced to work from home during the pandemic, she became lonely. She went from working in a busy downtown office, training for half-marathons, and teaching live workout sessions to being alone daily. Her only “real” human interaction was when she ordered daily delivery meals of her favorite comfort foods. As a person with type 2 diabetes, she knew that her delivery habit was wrecking her health, but willpower wasn’t enough to make her stop.

Her psychologist referred her to our virtual integrative obesity practice to help her lose weight and find long-term solutions. Ms. S admitted that she knew what she was doing as an emotional eater. But like many emotional eaters, she didn’t know why or how to switch from emotional eating to eating based on her biological hunger signals. As a trained obesity expert and recovering emotional eater of 8 years, personally and professionally I can appreciate the challenges of emotional eating and how it can sabotage even the best weight loss plan. In this article, I will share facts and feelings that drive emotional eating. I aim to empower clinicians seeking to help patients with emotional eating.
 

Fact: Emotional eating isn’t all emotional

It’s important not to dismiss emotional eating as all emotion driven. Recall that hunger is hormonally regulated. There are two main hunger pathways: the homeostatic pathway and the hedonic pathway. The homeostatic pathway is our biological hunger pathway and is driven by the need for energy in calories. Conversely, hedonic eating is pleasure-driven and uses emotional stimuli to “bypass” the physical hunger/satisfaction signals.

Emotional eating falls under the hedonic pathway. As clinicians, the first step in helping a patient struggling with emotional eating is empathetically listening, then assessing for any physiologic causes.

Several factors can disrupt physiologic appetite regulation, such as sleep disturbances; high stress levels; and many medical conditions, including but not limited to obesity, diabetes, and polycystic ovarian syndrome. Such factors as insulin resistance and inflammation are a common link in these conditions. Both contribute to the pathophysiology of the changes in appetite and can influence other hormones that lead to reduced satisfaction after eating. Furthermore, mental health conditions may disrupt levels of neurotransmitters such as serotonin and dopamine, which can also cause appetite changes.

These settings of physiologically disrupted appetite can trigger hedonic eating. But the relationship is complex. For example, one way to research hedonic eating is by using the Power of Food Scale. Functional MRI studies show that people with higher Power of Food Scale readings have more brain activity in the visual cortex when they see highly palatable foods. While more studies are needed to better understand the clinical implications of this finding, it’s yet another indicator that “emotional” eating isn’t all emotional. It’s also physiologic.
 

Feelings: Patterns, personality, places, psychological factors

Physiology only explains part of emotional eating. Like Ms. S, emotional eaters have strong emotional connections to food and behavior patterns. Often, physiologic cues have been coupled with psychological habits.

For example, menses is a common physiologic trigger for stress-eating for many of my patients. Studies have shown that in addition to iron levels changing during menses, calcium, magnesium, and phosphorous levels also change. Emotionally, the discomfort of “that time of the month” can lead to solace in comfort foods such as chocolate in different forms. But this isn’t surprising, as cacao and its derivative, chocolate, are rich in iron and other minerals. The chocolate is actually addressing a physical and emotional need. It can be helpful to point out this association to your patients. Suggest choosing a lower-sugar form of chocolate, such as dark chocolate, or even trying cacao nibs, while addressing any emotions.

But physiologic conditions and patterns aren’t the only emotional eating triggers. Places and psychological conditions can also trigger emotional eating.
 

Places and people 

Celebrations, vacations, proximity to certain restaurants, exposure to food marketing, and major life shifts can lead to increased hedonic eating. Helping patients recognize this connection opens the door to advance preparation for these situations.

Psychological conditions can be connected to emotional eating. It’s important to screen for mental health conditions and past traumas. For example, emotional eating could be a symptom of binge eating disorder, major depression, or generalized anxiety disorder. Childhood trauma is associated with disordered eating. The adverse childhood events quiz can be used clinically.

Emotional eating can lead to feelings of guilt, shame, and negative self-talk. It’s helpful to offer patients reassurance and encourage self-compassion. After all, it’s natural to eat. The goal isn’t to stop eating but to eat on the basis of physiologic needs.
 

Putting it together: Addressing the facts and feelings of emotional eating

1. Treat biological causes that impact physiologic hunger and trigger emotional eating.

2. Triggers: Address patterns, places/people, psychological events.

3. Transition to non-food rewards; the key to emotional eating is eating. While healthier substitutes can be a short-term solution for improving eating behaviors, ultimately, helping patients find non-food ways to address emotions is invaluable.

4. Stress management: Offer your patients ways to decrease stress levels through mindfulness and other techniques.

5. Professional support: Creating a multidisciplinary team is helpful, given the complexity of emotional eating. In addition to the primary care physician/clinician, other team members may include:

• Psychologist
• Psychiatrist
•  coach and/or certified wellness coaches
• Obesity specialist

Back to Ms. S

Ms. S is doing well. We started her on a GLP-1 agonist to address her underlying insulin resistance. Together we’ve found creative ways to satisfy her loneliness, such as volunteering and teaching virtual workout classes. Her emotional eating has decreased by over 60%, and we continue to discover new strategies to address her emotional eating triggers.

Conclusion

Despite being common, the impact of emotional eating is often minimized. With no DSM-5 criteria or ICD-11 code, it’s easy to dismiss emotional eating clinically. However, emotional eating is common and associated with weight gain.

In light of the obesity epidemic, this significance can’t be overlooked. Thankfully we have groundbreaking medications to address the homeostatic hunger pathway and physiologic drivers of emotional eating, but they’re not a substitute for addressing the psychosocial components of emotional eating.

As clinicians, we can have a meaningful impact on our patients’ lives beyond writing a prescription.

*Name/initial changed for privacy.

Sylvia Gonsahn-Bollie, MD, DipABOM, is an integrative obesity specialist focused on individualized solutions for emotional and biological overeating.

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

CHICAGO – New data from an ongoing study shows that regular meat consumption is associated with inflammatory bowel disease (IBD) flares, specifically for patients with ulcerative colitis.

The data, which was presented on May 7 in Chicago at the annual Digestive Disease Week® meeting, is based on an analysis of data from the PREdiCCt study (Prognostic Effect of Environmental Factors in Crohn’s and Colitis) in which diets of patients with IBD were tracked over 2-3 months with 2-year follow-ups. While the study itself includes nearly 3,000 patients from the United Kingdom who are in clinical remission, this analysis included 497 patients with Crohn’s disease and 520 with ulcerative colitis.

The highest level of patient-reported meat consumption was associated with doubled risk for hard flares – defined as an increase in symptoms plus elevation in c-reactive protein (CRP) and fecal calprotection (FCAL) plus a change in IBD therapy – in patients with ulcerative colitis, said study author Charlie W Lees, PhD, FRCP(Ed), Western General Hospital and University of Edinburgh.

Investigators also evaluated the occurrence of soft flares, which was defined as a negative response to the question, “Do you think your disease has been well controlled in the past month or since you last logged on to the portal?”

After a median follow-up of 1,481.5 days, hard flares occurred at a rate of 5.6% per year, but it did not differ by IBD subtype. However, soft flares accumulated rapidly. Hard flares with baseline FCAL levels in the 50-250 mcg/g range, as well as FCAL levels above 250 mcg, were associated with flares.

The mean baseline total protein intake was 91.9 g per day of which 35.8 g came from animal sources. The hazard ratio for the highest vs. lowest quartile of meat intake in the ulcerative colitis group was 2.08. They found no associations between hard flares with intake of total dietary fiber, N-6 polyunsaturated acids, or ultraprocessed foods, which Dr. Lees found surprising.

“Perhaps most intriguingly, when we look at ultraprocessed food intake, no difference in Crohn’s disease, and no difference in ulcerative colitis,” Dr. Lees said.

The finding is in contradiction to a study reported at the Crohn’s & Colitis Congress this year that found additives in ultraprocessed foods appear to have deleterious effects on intestinal microbiota, while others may exert their influence through mechanisms, such as endoplasmic stress.

However, the new data are consistent with a previously reported association between meat consumption and ulcerative colitis development, and suggests that reducing meat consumption could help to reduce the risk of flare in patients with ulcerative colitis.

PREdiCCt is designed to examine dietary, environmental, genetic, and microbiotic factors that are associated with disease flares in patients with Crohn’s disease and ulcerative colitis. Investigators are evaluating potential contributions to disease flares from total animal protein intake, dietary fiber, N-6 polyunsaturated fatty acids, dietary emulsifiers, and ultraprocessed foods, and total bacterial gene count in stool samples. They aim to examine data from 2,500 microbiome samples currently being sequenced at the Wellcome Sanger Institute in Hinxton, England, to determine whether the association between meat and ulcerative colitis flares could be related, as they hypothesize, to diet-induced alterations in the gut microbiome.

The research is preliminary with many unanswered questions, said Russell D. Cohen, MD, director of the inflammatory bowel disease center at the University of Chicago.

“I think he still has to evaluate a lot of the data that he has already collected because, are you talking about meat? Are you talking about poultry? Are you talking about fish? It is interesting, but it still needs to be evaluated further before we make any conclusive decisions,” he said. Dr. Cohen was not involved in the research.

He said the presumed effect of meat consumption on disease exacerbation appeared to take years, “which is a little surprising. If you really thought that IBD was due to something in diet, you would see the response right away, so it doesn’t follow timewise. Why does it takes 5 years? It should be within 5 weeks or 5 days.”

Dr. Lees disclosed relationships with Abbvie, Takeda, Pfizer, Galapagos, and BDD Pharma, among others.

DDW is sponsored by the American Gastroenterological Association, the American Association for the Study of Liver Diseases, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.

CHICAGO – New data from an ongoing study shows that regular meat consumption is associated with inflammatory bowel disease (IBD) flares, specifically for patients with ulcerative colitis.

The data, which was presented on May 7 in Chicago at the annual Digestive Disease Week® meeting, is based on an analysis of data from the PREdiCCt study (Prognostic Effect of Environmental Factors in Crohn’s and Colitis) in which diets of patients with IBD were tracked over 2-3 months with 2-year follow-ups. While the study itself includes nearly 3,000 patients from the United Kingdom who are in clinical remission, this analysis included 497 patients with Crohn’s disease and 520 with ulcerative colitis.

The highest level of patient-reported meat consumption was associated with doubled risk for hard flares – defined as an increase in symptoms plus elevation in c-reactive protein (CRP) and fecal calprotection (FCAL) plus a change in IBD therapy – in patients with ulcerative colitis, said study author Charlie W Lees, PhD, FRCP(Ed), Western General Hospital and University of Edinburgh.

Investigators also evaluated the occurrence of soft flares, which was defined as a negative response to the question, “Do you think your disease has been well controlled in the past month or since you last logged on to the portal?”

After a median follow-up of 1,481.5 days, hard flares occurred at a rate of 5.6% per year, but it did not differ by IBD subtype. However, soft flares accumulated rapidly. Hard flares with baseline FCAL levels in the 50-250 mcg/g range, as well as FCAL levels above 250 mcg, were associated with flares.

The mean baseline total protein intake was 91.9 g per day of which 35.8 g came from animal sources. The hazard ratio for the highest vs. lowest quartile of meat intake in the ulcerative colitis group was 2.08. They found no associations between hard flares with intake of total dietary fiber, N-6 polyunsaturated acids, or ultraprocessed foods, which Dr. Lees found surprising.

“Perhaps most intriguingly, when we look at ultraprocessed food intake, no difference in Crohn’s disease, and no difference in ulcerative colitis,” Dr. Lees said.

The finding is in contradiction to a study reported at the Crohn’s & Colitis Congress this year that found additives in ultraprocessed foods appear to have deleterious effects on intestinal microbiota, while others may exert their influence through mechanisms, such as endoplasmic stress.

However, the new data are consistent with a previously reported association between meat consumption and ulcerative colitis development, and suggests that reducing meat consumption could help to reduce the risk of flare in patients with ulcerative colitis.

PREdiCCt is designed to examine dietary, environmental, genetic, and microbiotic factors that are associated with disease flares in patients with Crohn’s disease and ulcerative colitis. Investigators are evaluating potential contributions to disease flares from total animal protein intake, dietary fiber, N-6 polyunsaturated fatty acids, dietary emulsifiers, and ultraprocessed foods, and total bacterial gene count in stool samples. They aim to examine data from 2,500 microbiome samples currently being sequenced at the Wellcome Sanger Institute in Hinxton, England, to determine whether the association between meat and ulcerative colitis flares could be related, as they hypothesize, to diet-induced alterations in the gut microbiome.

The research is preliminary with many unanswered questions, said Russell D. Cohen, MD, director of the inflammatory bowel disease center at the University of Chicago.

“I think he still has to evaluate a lot of the data that he has already collected because, are you talking about meat? Are you talking about poultry? Are you talking about fish? It is interesting, but it still needs to be evaluated further before we make any conclusive decisions,” he said. Dr. Cohen was not involved in the research.

He said the presumed effect of meat consumption on disease exacerbation appeared to take years, “which is a little surprising. If you really thought that IBD was due to something in diet, you would see the response right away, so it doesn’t follow timewise. Why does it takes 5 years? It should be within 5 weeks or 5 days.”

Dr. Lees disclosed relationships with Abbvie, Takeda, Pfizer, Galapagos, and BDD Pharma, among others.

DDW is sponsored by the American Gastroenterological Association, the American Association for the Study of Liver Diseases, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.

CHICAGO – New data from an ongoing study shows that regular meat consumption is associated with inflammatory bowel disease (IBD) flares, specifically for patients with ulcerative colitis.

The data, which was presented on May 7 in Chicago at the annual Digestive Disease Week® meeting, is based on an analysis of data from the PREdiCCt study (Prognostic Effect of Environmental Factors in Crohn’s and Colitis) in which diets of patients with IBD were tracked over 2-3 months with 2-year follow-ups. While the study itself includes nearly 3,000 patients from the United Kingdom who are in clinical remission, this analysis included 497 patients with Crohn’s disease and 520 with ulcerative colitis.

The highest level of patient-reported meat consumption was associated with doubled risk for hard flares – defined as an increase in symptoms plus elevation in c-reactive protein (CRP) and fecal calprotection (FCAL) plus a change in IBD therapy – in patients with ulcerative colitis, said study author Charlie W Lees, PhD, FRCP(Ed), Western General Hospital and University of Edinburgh.

Investigators also evaluated the occurrence of soft flares, which was defined as a negative response to the question, “Do you think your disease has been well controlled in the past month or since you last logged on to the portal?”

After a median follow-up of 1,481.5 days, hard flares occurred at a rate of 5.6% per year, but it did not differ by IBD subtype. However, soft flares accumulated rapidly. Hard flares with baseline FCAL levels in the 50-250 mcg/g range, as well as FCAL levels above 250 mcg, were associated with flares.

The mean baseline total protein intake was 91.9 g per day of which 35.8 g came from animal sources. The hazard ratio for the highest vs. lowest quartile of meat intake in the ulcerative colitis group was 2.08. They found no associations between hard flares with intake of total dietary fiber, N-6 polyunsaturated acids, or ultraprocessed foods, which Dr. Lees found surprising.

“Perhaps most intriguingly, when we look at ultraprocessed food intake, no difference in Crohn’s disease, and no difference in ulcerative colitis,” Dr. Lees said.

The finding is in contradiction to a study reported at the Crohn’s & Colitis Congress this year that found additives in ultraprocessed foods appear to have deleterious effects on intestinal microbiota, while others may exert their influence through mechanisms, such as endoplasmic stress.

However, the new data are consistent with a previously reported association between meat consumption and ulcerative colitis development, and suggests that reducing meat consumption could help to reduce the risk of flare in patients with ulcerative colitis.

PREdiCCt is designed to examine dietary, environmental, genetic, and microbiotic factors that are associated with disease flares in patients with Crohn’s disease and ulcerative colitis. Investigators are evaluating potential contributions to disease flares from total animal protein intake, dietary fiber, N-6 polyunsaturated fatty acids, dietary emulsifiers, and ultraprocessed foods, and total bacterial gene count in stool samples. They aim to examine data from 2,500 microbiome samples currently being sequenced at the Wellcome Sanger Institute in Hinxton, England, to determine whether the association between meat and ulcerative colitis flares could be related, as they hypothesize, to diet-induced alterations in the gut microbiome.

The research is preliminary with many unanswered questions, said Russell D. Cohen, MD, director of the inflammatory bowel disease center at the University of Chicago.

“I think he still has to evaluate a lot of the data that he has already collected because, are you talking about meat? Are you talking about poultry? Are you talking about fish? It is interesting, but it still needs to be evaluated further before we make any conclusive decisions,” he said. Dr. Cohen was not involved in the research.

He said the presumed effect of meat consumption on disease exacerbation appeared to take years, “which is a little surprising. If you really thought that IBD was due to something in diet, you would see the response right away, so it doesn’t follow timewise. Why does it takes 5 years? It should be within 5 weeks or 5 days.”

Dr. Lees disclosed relationships with Abbvie, Takeda, Pfizer, Galapagos, and BDD Pharma, among others.

DDW is sponsored by the American Gastroenterological Association, the American Association for the Study of Liver Diseases, the American Society for Gastrointestinal Endoscopy, and the Society for Surgery of the Alimentary Tract.

The Food and Drug Administration has expanded the indication for Abbott Laboratories’ spinal cord stimulation (SCS) devices to include treatment of chronic back pain in patients who have not had, or are not eligible for, back surgery, the company has announced.
 

The new indication spans all of Abbott’s SCS devices in the United States, which include the recharge-free Proclaim SCS family and the rechargeable Eterna SCS platform.

The devices feature the company’s proprietary, low-energy BurstDR stimulation waveform, a form of stimulation therapy that uses bursts of mild electrical energy without causing an abnormal tingling sensation to help disrupt pain signals before they can reach the brain, the company explained.

The expanded indication was supported by results from the DISTINCT study, which enrolled 270 adults suffering from severe, disabling chronic back pain for an average of more than 12 years and who were not eligible for surgery.

The study showed that significantly more patients who were treated with SCS achieved significant improvements in back pain, function, quality of life, and psychological status than peers treated with conservative medical management.

“To date, we have struggled with how to treat people who weren’t considered a good surgical candidate because we didn’t have clear, data-driven treatment options for non-surgical back pain,” Timothy Deer, MD, president and CEO of the Spine and Nerve Centers of the Virginias in Charleston, W.Va., said in a news release.

“This new indication for Abbott’s SCS devices, together with BurstDR stimulation, allows physicians the ability to identify and treat a new group of people, providing them with relief from chronic back pain,” Dr. Deer said.

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

The Food and Drug Administration has expanded the indication for Abbott Laboratories’ spinal cord stimulation (SCS) devices to include treatment of chronic back pain in patients who have not had, or are not eligible for, back surgery, the company has announced.
 

The new indication spans all of Abbott’s SCS devices in the United States, which include the recharge-free Proclaim SCS family and the rechargeable Eterna SCS platform.

The devices feature the company’s proprietary, low-energy BurstDR stimulation waveform, a form of stimulation therapy that uses bursts of mild electrical energy without causing an abnormal tingling sensation to help disrupt pain signals before they can reach the brain, the company explained.

The expanded indication was supported by results from the DISTINCT study, which enrolled 270 adults suffering from severe, disabling chronic back pain for an average of more than 12 years and who were not eligible for surgery.

The study showed that significantly more patients who were treated with SCS achieved significant improvements in back pain, function, quality of life, and psychological status than peers treated with conservative medical management.

“To date, we have struggled with how to treat people who weren’t considered a good surgical candidate because we didn’t have clear, data-driven treatment options for non-surgical back pain,” Timothy Deer, MD, president and CEO of the Spine and Nerve Centers of the Virginias in Charleston, W.Va., said in a news release.

“This new indication for Abbott’s SCS devices, together with BurstDR stimulation, allows physicians the ability to identify and treat a new group of people, providing them with relief from chronic back pain,” Dr. Deer said.

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

The Food and Drug Administration has expanded the indication for Abbott Laboratories’ spinal cord stimulation (SCS) devices to include treatment of chronic back pain in patients who have not had, or are not eligible for, back surgery, the company has announced.
 

The new indication spans all of Abbott’s SCS devices in the United States, which include the recharge-free Proclaim SCS family and the rechargeable Eterna SCS platform.

The devices feature the company’s proprietary, low-energy BurstDR stimulation waveform, a form of stimulation therapy that uses bursts of mild electrical energy without causing an abnormal tingling sensation to help disrupt pain signals before they can reach the brain, the company explained.

The expanded indication was supported by results from the DISTINCT study, which enrolled 270 adults suffering from severe, disabling chronic back pain for an average of more than 12 years and who were not eligible for surgery.

The study showed that significantly more patients who were treated with SCS achieved significant improvements in back pain, function, quality of life, and psychological status than peers treated with conservative medical management.

“To date, we have struggled with how to treat people who weren’t considered a good surgical candidate because we didn’t have clear, data-driven treatment options for non-surgical back pain,” Timothy Deer, MD, president and CEO of the Spine and Nerve Centers of the Virginias in Charleston, W.Va., said in a news release.

“This new indication for Abbott’s SCS devices, together with BurstDR stimulation, allows physicians the ability to identify and treat a new group of people, providing them with relief from chronic back pain,” Dr. Deer said.

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

SEATTLE – Palopegteriparatide (TransCon PTH, Ascendis Pharma) is a potential long-term therapy for adults with hypoparathyroidism, new findings suggest.

Findings from 110-week phase 2 data for the once-daily investigational parathyroid hormone (PTH) replacement drug were recently presented at the annual scientific & clinical congress of the American Association of Clinical Endocrinology.

Overall, the drug was associated with independence from conventional calcium and active vitamin D therapy in most patients at 110 weeks, with no discontinuations due to adverse effects.  

“Patients with hypoparathyroidism have low serum calcium levels and struggle with quality of life and biochemical abnormalities. The data from the TransCon PTH studies seem to show that a lot of these abnormalities can be reversed,” presenter Mishaela R. Rubin, MD, said in an interview.  

Other PTH replacement therapies such as Nupara (now discontinued) and teriparatide (off-label) have been used in some patients with hypoparathyroidism.

However, “[TransCon PTH] is delivered in such a way as to have a prolonged half-life, so that’s kind of a special benefit that it has,” added Dr. Rubin of the division of endocrinology and metabolic bone disease, department of medicine, Columbia University, New York.

Asked to comment, session moderator Thanh Hoang, DO, of Walter Reed National Military Medical Center, Silver Spring, Md., said: “I think it’s a very promising medication because right now we don’t have a lot of options ... I think it would help a lot of patients.”
 

Approval denied, company addressing concerns

On May 1, the Food and Drug Administration issued a complete response letter, signaling denial of approval for the TransCon PTH, citing concerns related to manufacturing control of the product’s drug/device combination product, but not about the product’s safety and efficacy, according to an Ascendis statement.

The company is now working with the FDA to address these issues and is awaiting a European Union decision later this year.

The FDA did not request that the company conduct further clinical trials of TransCon PTH, which now include published 26-week phase 2 and phase 3 data along with the current longer-term phase 2 data presented at AACE.

“The company has said that they’re hopeful the issues will be addressable and that the FDA did not have any concerns about safety,” Dr. Rubin said in an interview.
 

Calcium normalized, bone turnover improved

Dr. Rubin presented long-term efficacy and safety data from the Phase 2 PaTH Forward trial, which involved 57 of the initial 59 participants who completed week 110 of an open-label extension of the trial.

During the first 4 weeks, patients had been randomized to TransCon PTH at fixed doses of 15 µg/day, 18 µg/day, 21 µg/day, or placebo. After week 4, all patients switched to TransCon PTH titrated to doses of 6-60 µg/day along with conventional therapy, with the goal of maintaining normocalcemia.

Participants were a mean age of 50 years, 81% were women, and 92% were White. Causes of hypoparathyroidism were neck surgery in 80%, autoimmune disease in 2%, and idiopathic disease in 19%. Disease duration was 12 years (range 1-39), and all were taking conventional therapy including calcium and active vitamin D (calcitriol or alfacaldiol).

At 110 weeks, all 57 patients were able to stop taking active vitamin D, and 53 of the 57 (93%) patients achieved independence from conventional therapy, defined as taking 0 µg/day of active vitamin D and no more than 600 mg/day of calcium (the dietary supplement dose). A total of 44 (77%) patients were not taking any calcium or active vitamin D.

“This really establishes the durability up to 2 years of keeping people off conventional therapy,” Dr. Rubin said during her presentation.

There was an initial uptick to 9.4 mg/dL in mean serum calcium, as some participants were still taking active vitamin D, but that dropped to 8.9 mg/dL by week 26. Mean 24-hour urine calcium dropped from 428 mg/day at baseline to 173 mg/day by week 26. Both serum calcium and urine calcium remained in the normal range through week 110 in all patients, at 8.6 mg/dL and 167 mg/day, respectively.

“This is a really important outcome because we know that high urine calcium in these patients sets them at risk for going on to develop nephrocalcinosis, nephrolithiasis, and ultimately, chronic kidney disease,” Dr. Rubin said.

Serum levels of two bone formation markers peaked at 12 weeks after initiation of TransCon PTH. Both trended downward thereafter through week 110 to levels approximating those of age- and sex-matched controls.  

“Both markers started off low, consistent with hypoparathyroidism, but with initiation of TransCon PTH we see a robust increase in bone turnover markers, almost as if the bone is ‘waking up,’ if you will. And this is consistent with calcium being mobilized from the skeleton and going into the circulation,” Dr. Rubin explained.

Bone mineral density assessed by dual-energy x-ray absorptiometry normalized, primarily in the first 26 weeks. For lumbar spine L1-L4, mean Z-scores dropped from 1.6 to 1.0 at 26 weeks and down to 0.7 by week 100. For total hip, those values were 1.0, 0.6, and 0.4, respectively. The values approached age- and sex-matched norms, Dr. Rubin noted, to “perhaps where their skeleton would be if they hadn’t had hypoparathyroidism.”

Overall 56 of the 57 (94.9%) patients reported treatment-emergent adverse events, of which 25 (42.4%) were treatment related and none were deemed serious. There were no treatment-emergent adverse events related to hypercalcemia or hypocalcemia leading to health care visits or hospitalization, none leading to discontinuation of study drug, and none to death.

“So overall, a reassuring safety profile,” Dr. Rubin said. “We look forward to presenting the next 2 years’ worth of data to the end of the open-label extension study.”

Dr. Rubin is a paid researcher for Ascendis, which funded the study. Dr. Hoang has reported no relevant financial relationships.
 

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

SEATTLE – Palopegteriparatide (TransCon PTH, Ascendis Pharma) is a potential long-term therapy for adults with hypoparathyroidism, new findings suggest.

Findings from 110-week phase 2 data for the once-daily investigational parathyroid hormone (PTH) replacement drug were recently presented at the annual scientific & clinical congress of the American Association of Clinical Endocrinology.

Overall, the drug was associated with independence from conventional calcium and active vitamin D therapy in most patients at 110 weeks, with no discontinuations due to adverse effects.  

“Patients with hypoparathyroidism have low serum calcium levels and struggle with quality of life and biochemical abnormalities. The data from the TransCon PTH studies seem to show that a lot of these abnormalities can be reversed,” presenter Mishaela R. Rubin, MD, said in an interview.  

Other PTH replacement therapies such as Nupara (now discontinued) and teriparatide (off-label) have been used in some patients with hypoparathyroidism.

However, “[TransCon PTH] is delivered in such a way as to have a prolonged half-life, so that’s kind of a special benefit that it has,” added Dr. Rubin of the division of endocrinology and metabolic bone disease, department of medicine, Columbia University, New York.

Asked to comment, session moderator Thanh Hoang, DO, of Walter Reed National Military Medical Center, Silver Spring, Md., said: “I think it’s a very promising medication because right now we don’t have a lot of options ... I think it would help a lot of patients.”
 

Approval denied, company addressing concerns

On May 1, the Food and Drug Administration issued a complete response letter, signaling denial of approval for the TransCon PTH, citing concerns related to manufacturing control of the product’s drug/device combination product, but not about the product’s safety and efficacy, according to an Ascendis statement.

The company is now working with the FDA to address these issues and is awaiting a European Union decision later this year.

The FDA did not request that the company conduct further clinical trials of TransCon PTH, which now include published 26-week phase 2 and phase 3 data along with the current longer-term phase 2 data presented at AACE.

“The company has said that they’re hopeful the issues will be addressable and that the FDA did not have any concerns about safety,” Dr. Rubin said in an interview.
 

Calcium normalized, bone turnover improved

Dr. Rubin presented long-term efficacy and safety data from the Phase 2 PaTH Forward trial, which involved 57 of the initial 59 participants who completed week 110 of an open-label extension of the trial.

During the first 4 weeks, patients had been randomized to TransCon PTH at fixed doses of 15 µg/day, 18 µg/day, 21 µg/day, or placebo. After week 4, all patients switched to TransCon PTH titrated to doses of 6-60 µg/day along with conventional therapy, with the goal of maintaining normocalcemia.

Participants were a mean age of 50 years, 81% were women, and 92% were White. Causes of hypoparathyroidism were neck surgery in 80%, autoimmune disease in 2%, and idiopathic disease in 19%. Disease duration was 12 years (range 1-39), and all were taking conventional therapy including calcium and active vitamin D (calcitriol or alfacaldiol).

At 110 weeks, all 57 patients were able to stop taking active vitamin D, and 53 of the 57 (93%) patients achieved independence from conventional therapy, defined as taking 0 µg/day of active vitamin D and no more than 600 mg/day of calcium (the dietary supplement dose). A total of 44 (77%) patients were not taking any calcium or active vitamin D.

“This really establishes the durability up to 2 years of keeping people off conventional therapy,” Dr. Rubin said during her presentation.

There was an initial uptick to 9.4 mg/dL in mean serum calcium, as some participants were still taking active vitamin D, but that dropped to 8.9 mg/dL by week 26. Mean 24-hour urine calcium dropped from 428 mg/day at baseline to 173 mg/day by week 26. Both serum calcium and urine calcium remained in the normal range through week 110 in all patients, at 8.6 mg/dL and 167 mg/day, respectively.

“This is a really important outcome because we know that high urine calcium in these patients sets them at risk for going on to develop nephrocalcinosis, nephrolithiasis, and ultimately, chronic kidney disease,” Dr. Rubin said.

Serum levels of two bone formation markers peaked at 12 weeks after initiation of TransCon PTH. Both trended downward thereafter through week 110 to levels approximating those of age- and sex-matched controls.  

“Both markers started off low, consistent with hypoparathyroidism, but with initiation of TransCon PTH we see a robust increase in bone turnover markers, almost as if the bone is ‘waking up,’ if you will. And this is consistent with calcium being mobilized from the skeleton and going into the circulation,” Dr. Rubin explained.

Bone mineral density assessed by dual-energy x-ray absorptiometry normalized, primarily in the first 26 weeks. For lumbar spine L1-L4, mean Z-scores dropped from 1.6 to 1.0 at 26 weeks and down to 0.7 by week 100. For total hip, those values were 1.0, 0.6, and 0.4, respectively. The values approached age- and sex-matched norms, Dr. Rubin noted, to “perhaps where their skeleton would be if they hadn’t had hypoparathyroidism.”

Overall 56 of the 57 (94.9%) patients reported treatment-emergent adverse events, of which 25 (42.4%) were treatment related and none were deemed serious. There were no treatment-emergent adverse events related to hypercalcemia or hypocalcemia leading to health care visits or hospitalization, none leading to discontinuation of study drug, and none to death.

“So overall, a reassuring safety profile,” Dr. Rubin said. “We look forward to presenting the next 2 years’ worth of data to the end of the open-label extension study.”

Dr. Rubin is a paid researcher for Ascendis, which funded the study. Dr. Hoang has reported no relevant financial relationships.
 

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

SEATTLE – Palopegteriparatide (TransCon PTH, Ascendis Pharma) is a potential long-term therapy for adults with hypoparathyroidism, new findings suggest.

Findings from 110-week phase 2 data for the once-daily investigational parathyroid hormone (PTH) replacement drug were recently presented at the annual scientific & clinical congress of the American Association of Clinical Endocrinology.

Overall, the drug was associated with independence from conventional calcium and active vitamin D therapy in most patients at 110 weeks, with no discontinuations due to adverse effects.  

“Patients with hypoparathyroidism have low serum calcium levels and struggle with quality of life and biochemical abnormalities. The data from the TransCon PTH studies seem to show that a lot of these abnormalities can be reversed,” presenter Mishaela R. Rubin, MD, said in an interview.  

Other PTH replacement therapies such as Nupara (now discontinued) and teriparatide (off-label) have been used in some patients with hypoparathyroidism.

However, “[TransCon PTH] is delivered in such a way as to have a prolonged half-life, so that’s kind of a special benefit that it has,” added Dr. Rubin of the division of endocrinology and metabolic bone disease, department of medicine, Columbia University, New York.

Asked to comment, session moderator Thanh Hoang, DO, of Walter Reed National Military Medical Center, Silver Spring, Md., said: “I think it’s a very promising medication because right now we don’t have a lot of options ... I think it would help a lot of patients.”
 

Approval denied, company addressing concerns

On May 1, the Food and Drug Administration issued a complete response letter, signaling denial of approval for the TransCon PTH, citing concerns related to manufacturing control of the product’s drug/device combination product, but not about the product’s safety and efficacy, according to an Ascendis statement.

The company is now working with the FDA to address these issues and is awaiting a European Union decision later this year.

The FDA did not request that the company conduct further clinical trials of TransCon PTH, which now include published 26-week phase 2 and phase 3 data along with the current longer-term phase 2 data presented at AACE.

“The company has said that they’re hopeful the issues will be addressable and that the FDA did not have any concerns about safety,” Dr. Rubin said in an interview.
 

Calcium normalized, bone turnover improved

Dr. Rubin presented long-term efficacy and safety data from the Phase 2 PaTH Forward trial, which involved 57 of the initial 59 participants who completed week 110 of an open-label extension of the trial.

During the first 4 weeks, patients had been randomized to TransCon PTH at fixed doses of 15 µg/day, 18 µg/day, 21 µg/day, or placebo. After week 4, all patients switched to TransCon PTH titrated to doses of 6-60 µg/day along with conventional therapy, with the goal of maintaining normocalcemia.

Participants were a mean age of 50 years, 81% were women, and 92% were White. Causes of hypoparathyroidism were neck surgery in 80%, autoimmune disease in 2%, and idiopathic disease in 19%. Disease duration was 12 years (range 1-39), and all were taking conventional therapy including calcium and active vitamin D (calcitriol or alfacaldiol).

At 110 weeks, all 57 patients were able to stop taking active vitamin D, and 53 of the 57 (93%) patients achieved independence from conventional therapy, defined as taking 0 µg/day of active vitamin D and no more than 600 mg/day of calcium (the dietary supplement dose). A total of 44 (77%) patients were not taking any calcium or active vitamin D.

“This really establishes the durability up to 2 years of keeping people off conventional therapy,” Dr. Rubin said during her presentation.

There was an initial uptick to 9.4 mg/dL in mean serum calcium, as some participants were still taking active vitamin D, but that dropped to 8.9 mg/dL by week 26. Mean 24-hour urine calcium dropped from 428 mg/day at baseline to 173 mg/day by week 26. Both serum calcium and urine calcium remained in the normal range through week 110 in all patients, at 8.6 mg/dL and 167 mg/day, respectively.

“This is a really important outcome because we know that high urine calcium in these patients sets them at risk for going on to develop nephrocalcinosis, nephrolithiasis, and ultimately, chronic kidney disease,” Dr. Rubin said.

Serum levels of two bone formation markers peaked at 12 weeks after initiation of TransCon PTH. Both trended downward thereafter through week 110 to levels approximating those of age- and sex-matched controls.  

“Both markers started off low, consistent with hypoparathyroidism, but with initiation of TransCon PTH we see a robust increase in bone turnover markers, almost as if the bone is ‘waking up,’ if you will. And this is consistent with calcium being mobilized from the skeleton and going into the circulation,” Dr. Rubin explained.

Bone mineral density assessed by dual-energy x-ray absorptiometry normalized, primarily in the first 26 weeks. For lumbar spine L1-L4, mean Z-scores dropped from 1.6 to 1.0 at 26 weeks and down to 0.7 by week 100. For total hip, those values were 1.0, 0.6, and 0.4, respectively. The values approached age- and sex-matched norms, Dr. Rubin noted, to “perhaps where their skeleton would be if they hadn’t had hypoparathyroidism.”

Overall 56 of the 57 (94.9%) patients reported treatment-emergent adverse events, of which 25 (42.4%) were treatment related and none were deemed serious. There were no treatment-emergent adverse events related to hypercalcemia or hypocalcemia leading to health care visits or hospitalization, none leading to discontinuation of study drug, and none to death.

“So overall, a reassuring safety profile,” Dr. Rubin said. “We look forward to presenting the next 2 years’ worth of data to the end of the open-label extension study.”

Dr. Rubin is a paid researcher for Ascendis, which funded the study. Dr. Hoang has reported no relevant financial relationships.
 

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

Even after 3 years of follow-up, redo transcatheter aortic valve replacement (TAVR) performs about as well as the first procedure, whether compared for hard endpoints, such as death and stroke, or for softer endpoints, such as function and quality of life, new registry data suggest.

The findings generally support redo-TAVR with balloon-expandable devices as “a reasonable treatment option for failed transcatheter heart valves,” reported Rajendra Makkar, MD, associate director, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles.

The results were presented at the annual meeting of the European Association of Percutaneous Cardiovascular Interventions.

Data for this analysis were drawn from 348,338 TAVR procedures with the Edwards balloon-expandable valves in the Society of Thoracic Surgeons/American College of Cardiology Transcatheter Valve Replacement Registry.

Of these, 1,216 were redo procedures. In 475 of the cases, the redo was performed in a patient whose first procedure was with an Edwards device. In the remaining 741 cases, the Edwards device replaced a different prosthetic heart valve. The median time to the redo from the first procedure was 26 months.

For the analysis, the redo-TAVRs were compared with native TAVR patients through 1:1 propensity matching employing 35 covariates, such as age, body mass index (BMI), baseline comorbidities, prior cardiovascular procedures, valve size, and Society of Thoracic Surgeons risk score.
 

Low death and stroke rates following TAVR redos

The rates of all-cause death or stroke within hospital (4.7% vs. 3.9%; P = .32) and at 30 days (6.1% vs. 5.9%; P = .77) were numerically but not statistically higher in the redo group.

At 1 year, the rates of death (17.3% vs. 17.7%; P = .961) and stroke (3.3% vs. 3.5%; P = .982) were numerically but not significantly lower among those who underwent a redo procedure.

The secondary endpoints told the same story. The one exception was the higher aortic valve reintervention rate (0.61% vs. 0.09%; P = .03) at 30 days in the redo group. This did reach statistical significance, but Dr. Makkar pointed out rates were very low regardless. The rates climbed in both groups by 1 year (1.09% vs. 0.21%; P = .01).

No other secondary endpoints differed significantly at 30 days or at 1 year. Even though some were numerically higher after redo at 1 year, such as major vascular complications (1.25 vs. 1.60; P = .51), others were lower, such as new-start dialysis (1.62 vs. 0.98; P = .26). All-cause readmission rates at 1 year were nearly identical (32.56% vs. 32.23%; P = .82).

Consistent with the comparable outcomes on the hard endpoints, major and similar improvements were seen in both the redo and the propensity-matched native TAVR patients on the Kansas City Cardiomyopathy Questionnaire Overall Summary. The slight advantage for the redo group was not significant at 30 days, but the degree of improvement was greater after the redo than after native TAVR at 1 year (15% vs. 10%; P = .03).

“You bring good news,” said Alain G. Cribier, MD, director of cardiology, Charles Nicolle Hospital, University of Rouen, France. Widely regarded as the father of TAVR for his first-in-human series in 2002, Dr. Cribier said that there are several reassuring take-home messages from this study.

“First, these data tell us that the redo rate is extremely low,” he said, noting that the registry data suggests a risk well below 1%. “Second, we are seeing from this data that there are no more complications [than TAVR in a native valve] if you need to do this.”
 

Redo patients are generally sicker

The propensity matching was designed to eliminate baseline differences for the outcome comparisons, but Dr. Makkar did point out that redo-TAVR patients were sicker than the native TAVR patients. For example, when compared prior to propensity matching, the STS score was higher (8.3 vs. 5.2; P < .01), more patients had atrial fibrillation (47.9% vs. 36.2%; P < .01), and more patients had a prior stroke (15.0% vs. 10.7%; P < .01).

The registry only has follow-up out to 1 year, but participating patients were matched to a claims database to capture outcomes out to 3 years. Mortality rates at long-term follow-up were not significantly different for redo vs. native TAVR (42.2% vs. 40.3% respectively; P = .98); for the entire dataset or when compared in subgroups defined by Edwards valve redo of an Edwards valve (P = .909) or an Edwards valve redo of a non-Edwards device (P = .871).

Whether an early redo, defined as 12 months after the index TAVR procedure, or a late redo, the rate of mortality ranged from approximately 16% to 18% with no significant difference between redo and native TAVR.

A moderator for the late-breaking trials session where these data were presented, Darren Mylotte, MD, a consultant in cardiology for the Galway University Hospitals, Ireland, challenged Dr. Makkar about the potential for selection bias. He said redo patients might be the ones that interventionalists feel confident about helping, making this comparison unrepresentative.

“I think that the selection bias is likely to cut both ways,” Dr. Makkar replied. For many patients with a failed TAVR, he explained that clinicians might think, “There is nothing to be done for this patient except to try a redo.”

Dr. Makkar reports financial relationships with Abbott, Cordis, Edwards Lifesciences, and Medtronic. Dr. Cribier reports a financial relationship with Edwards Lifesciences. Dr. Mylotte reports no potential conflicts of interest.

Even after 3 years of follow-up, redo transcatheter aortic valve replacement (TAVR) performs about as well as the first procedure, whether compared for hard endpoints, such as death and stroke, or for softer endpoints, such as function and quality of life, new registry data suggest.

The findings generally support redo-TAVR with balloon-expandable devices as “a reasonable treatment option for failed transcatheter heart valves,” reported Rajendra Makkar, MD, associate director, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles.

The results were presented at the annual meeting of the European Association of Percutaneous Cardiovascular Interventions.

Data for this analysis were drawn from 348,338 TAVR procedures with the Edwards balloon-expandable valves in the Society of Thoracic Surgeons/American College of Cardiology Transcatheter Valve Replacement Registry.

Of these, 1,216 were redo procedures. In 475 of the cases, the redo was performed in a patient whose first procedure was with an Edwards device. In the remaining 741 cases, the Edwards device replaced a different prosthetic heart valve. The median time to the redo from the first procedure was 26 months.

For the analysis, the redo-TAVRs were compared with native TAVR patients through 1:1 propensity matching employing 35 covariates, such as age, body mass index (BMI), baseline comorbidities, prior cardiovascular procedures, valve size, and Society of Thoracic Surgeons risk score.
 

Low death and stroke rates following TAVR redos

The rates of all-cause death or stroke within hospital (4.7% vs. 3.9%; P = .32) and at 30 days (6.1% vs. 5.9%; P = .77) were numerically but not statistically higher in the redo group.

At 1 year, the rates of death (17.3% vs. 17.7%; P = .961) and stroke (3.3% vs. 3.5%; P = .982) were numerically but not significantly lower among those who underwent a redo procedure.

The secondary endpoints told the same story. The one exception was the higher aortic valve reintervention rate (0.61% vs. 0.09%; P = .03) at 30 days in the redo group. This did reach statistical significance, but Dr. Makkar pointed out rates were very low regardless. The rates climbed in both groups by 1 year (1.09% vs. 0.21%; P = .01).

No other secondary endpoints differed significantly at 30 days or at 1 year. Even though some were numerically higher after redo at 1 year, such as major vascular complications (1.25 vs. 1.60; P = .51), others were lower, such as new-start dialysis (1.62 vs. 0.98; P = .26). All-cause readmission rates at 1 year were nearly identical (32.56% vs. 32.23%; P = .82).

Consistent with the comparable outcomes on the hard endpoints, major and similar improvements were seen in both the redo and the propensity-matched native TAVR patients on the Kansas City Cardiomyopathy Questionnaire Overall Summary. The slight advantage for the redo group was not significant at 30 days, but the degree of improvement was greater after the redo than after native TAVR at 1 year (15% vs. 10%; P = .03).

“You bring good news,” said Alain G. Cribier, MD, director of cardiology, Charles Nicolle Hospital, University of Rouen, France. Widely regarded as the father of TAVR for his first-in-human series in 2002, Dr. Cribier said that there are several reassuring take-home messages from this study.

“First, these data tell us that the redo rate is extremely low,” he said, noting that the registry data suggests a risk well below 1%. “Second, we are seeing from this data that there are no more complications [than TAVR in a native valve] if you need to do this.”
 

Redo patients are generally sicker

The propensity matching was designed to eliminate baseline differences for the outcome comparisons, but Dr. Makkar did point out that redo-TAVR patients were sicker than the native TAVR patients. For example, when compared prior to propensity matching, the STS score was higher (8.3 vs. 5.2; P < .01), more patients had atrial fibrillation (47.9% vs. 36.2%; P < .01), and more patients had a prior stroke (15.0% vs. 10.7%; P < .01).

The registry only has follow-up out to 1 year, but participating patients were matched to a claims database to capture outcomes out to 3 years. Mortality rates at long-term follow-up were not significantly different for redo vs. native TAVR (42.2% vs. 40.3% respectively; P = .98); for the entire dataset or when compared in subgroups defined by Edwards valve redo of an Edwards valve (P = .909) or an Edwards valve redo of a non-Edwards device (P = .871).

Whether an early redo, defined as 12 months after the index TAVR procedure, or a late redo, the rate of mortality ranged from approximately 16% to 18% with no significant difference between redo and native TAVR.

A moderator for the late-breaking trials session where these data were presented, Darren Mylotte, MD, a consultant in cardiology for the Galway University Hospitals, Ireland, challenged Dr. Makkar about the potential for selection bias. He said redo patients might be the ones that interventionalists feel confident about helping, making this comparison unrepresentative.

“I think that the selection bias is likely to cut both ways,” Dr. Makkar replied. For many patients with a failed TAVR, he explained that clinicians might think, “There is nothing to be done for this patient except to try a redo.”

Dr. Makkar reports financial relationships with Abbott, Cordis, Edwards Lifesciences, and Medtronic. Dr. Cribier reports a financial relationship with Edwards Lifesciences. Dr. Mylotte reports no potential conflicts of interest.

Even after 3 years of follow-up, redo transcatheter aortic valve replacement (TAVR) performs about as well as the first procedure, whether compared for hard endpoints, such as death and stroke, or for softer endpoints, such as function and quality of life, new registry data suggest.

The findings generally support redo-TAVR with balloon-expandable devices as “a reasonable treatment option for failed transcatheter heart valves,” reported Rajendra Makkar, MD, associate director, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles.

The results were presented at the annual meeting of the European Association of Percutaneous Cardiovascular Interventions.

Data for this analysis were drawn from 348,338 TAVR procedures with the Edwards balloon-expandable valves in the Society of Thoracic Surgeons/American College of Cardiology Transcatheter Valve Replacement Registry.

Of these, 1,216 were redo procedures. In 475 of the cases, the redo was performed in a patient whose first procedure was with an Edwards device. In the remaining 741 cases, the Edwards device replaced a different prosthetic heart valve. The median time to the redo from the first procedure was 26 months.

For the analysis, the redo-TAVRs were compared with native TAVR patients through 1:1 propensity matching employing 35 covariates, such as age, body mass index (BMI), baseline comorbidities, prior cardiovascular procedures, valve size, and Society of Thoracic Surgeons risk score.
 

Low death and stroke rates following TAVR redos

The rates of all-cause death or stroke within hospital (4.7% vs. 3.9%; P = .32) and at 30 days (6.1% vs. 5.9%; P = .77) were numerically but not statistically higher in the redo group.

At 1 year, the rates of death (17.3% vs. 17.7%; P = .961) and stroke (3.3% vs. 3.5%; P = .982) were numerically but not significantly lower among those who underwent a redo procedure.

The secondary endpoints told the same story. The one exception was the higher aortic valve reintervention rate (0.61% vs. 0.09%; P = .03) at 30 days in the redo group. This did reach statistical significance, but Dr. Makkar pointed out rates were very low regardless. The rates climbed in both groups by 1 year (1.09% vs. 0.21%; P = .01).

No other secondary endpoints differed significantly at 30 days or at 1 year. Even though some were numerically higher after redo at 1 year, such as major vascular complications (1.25 vs. 1.60; P = .51), others were lower, such as new-start dialysis (1.62 vs. 0.98; P = .26). All-cause readmission rates at 1 year were nearly identical (32.56% vs. 32.23%; P = .82).

Consistent with the comparable outcomes on the hard endpoints, major and similar improvements were seen in both the redo and the propensity-matched native TAVR patients on the Kansas City Cardiomyopathy Questionnaire Overall Summary. The slight advantage for the redo group was not significant at 30 days, but the degree of improvement was greater after the redo than after native TAVR at 1 year (15% vs. 10%; P = .03).

“You bring good news,” said Alain G. Cribier, MD, director of cardiology, Charles Nicolle Hospital, University of Rouen, France. Widely regarded as the father of TAVR for his first-in-human series in 2002, Dr. Cribier said that there are several reassuring take-home messages from this study.

“First, these data tell us that the redo rate is extremely low,” he said, noting that the registry data suggests a risk well below 1%. “Second, we are seeing from this data that there are no more complications [than TAVR in a native valve] if you need to do this.”
 

Redo patients are generally sicker

The propensity matching was designed to eliminate baseline differences for the outcome comparisons, but Dr. Makkar did point out that redo-TAVR patients were sicker than the native TAVR patients. For example, when compared prior to propensity matching, the STS score was higher (8.3 vs. 5.2; P < .01), more patients had atrial fibrillation (47.9% vs. 36.2%; P < .01), and more patients had a prior stroke (15.0% vs. 10.7%; P < .01).

The registry only has follow-up out to 1 year, but participating patients were matched to a claims database to capture outcomes out to 3 years. Mortality rates at long-term follow-up were not significantly different for redo vs. native TAVR (42.2% vs. 40.3% respectively; P = .98); for the entire dataset or when compared in subgroups defined by Edwards valve redo of an Edwards valve (P = .909) or an Edwards valve redo of a non-Edwards device (P = .871).

Whether an early redo, defined as 12 months after the index TAVR procedure, or a late redo, the rate of mortality ranged from approximately 16% to 18% with no significant difference between redo and native TAVR.

A moderator for the late-breaking trials session where these data were presented, Darren Mylotte, MD, a consultant in cardiology for the Galway University Hospitals, Ireland, challenged Dr. Makkar about the potential for selection bias. He said redo patients might be the ones that interventionalists feel confident about helping, making this comparison unrepresentative.

“I think that the selection bias is likely to cut both ways,” Dr. Makkar replied. For many patients with a failed TAVR, he explained that clinicians might think, “There is nothing to be done for this patient except to try a redo.”

Dr. Makkar reports financial relationships with Abbott, Cordis, Edwards Lifesciences, and Medtronic. Dr. Cribier reports a financial relationship with Edwards Lifesciences. Dr. Mylotte reports no potential conflicts of interest.

The Federal Trade Commission’s proposed regulation that would ban noncompete agreements across the country seems like potential good news for doctors. Of course, many hospitals and employers are against it. As a result, the FTC’s sweeping proposal has tongues wagging on both sides of the issue.

Many physicians are thrilled that they may soon have more control over their career and not be stuck in jobs where they feel frustrated, underpaid, or blocked in their progress.

If passed, the proposed ban would allow physicians to get a new job with a competing organization, bucking a long-standing trend that hospitals and health care systems have heavily relied on to keep staff in place. As of 2018, as many as 45% of primary care physicians had inked such agreements with their employers.

Typically, the agreements prevent physicians from practicing medicine with a new employer for a defined period within a specific geographic area. No matter how attractive an alternate offer of employment might be, doctors are bound by the agreements to say no if the offer exists in that defined area and time period.

The period for public comment on the proposed regulation ended on April 19, and there is currently no set date for a decision.

In a Medscape poll of 558 physicians, more than 9 out of 10 respondents said that they were either currently bound by a noncompete clause or that they had been bound by one in the past that had forced them to temporarily stop working, commute long distances, move to a different area, or switch fields.

The new proposal would make it illegal for an employer, such as a hospital or large group, to enter a noncompete with a worker; maintain a noncompete with a worker; or represent to a worker, under certain circumstances, that the worker is subject to a noncompete.

It also would not only ban future noncompete agreements but also retroactively invalidate existing ones. The FTC reasons that noncompete clauses could potentially increase worker earnings as well as lower health care costs by billions of dollars. If the ruling were to move forward, it would represent part of President Biden’s “worker-forward” priorities, focusing on how competition can be a good thing for employees. The President billed the FTC’s announcement as a “huge win for workers.”

In its statements on the proposed ban, the FTC claimed that it could lower consumer prices across the board by as much as $150 billion per year and return nearly $300 million to workers each year.

However, even if passed, the draft rule would keep in place nonsolicitation rules that many health care organizations have put into place. That means that, if a physician leaves an employer, he or she cannot reach out to former patients and colleagues to bring them along or invite them to switch to him or her in the new job.

Within that clause, however, the FTC has specified that if such nonsolicitation agreement has the “equivalent effect” of a noncompete, the agency would deem it such. That means, even if that rule stays, it could be contested and may be interpreted as violating the noncompete law. So there’s value in reading all the fine print should the ban move forward.
 

Could the ban bring potential downsides?

Most physicians view the potential to break free of a noncompete agreement as a victory. Peter Glennon, an employment litigation attorney with The Glennon Law Firm in Rochester, N.Y., says not so fast. “If you ask anyone if they’d prefer a noncompete agreement, of course they’re going to say no,” he said in an interview. “It sounds like a restriction, one that can hold you back.”

Mr. Glennon believes that there are actually upsides to physician noncompetes. For instance, many noncompetes come with sign-on bonuses that could potentially disappear without the agreements. There’s also the fact that when some physicians sign a noncompete agreement, they then receive pro bono training and continuing education along with marketing and promotion of their skills. Without signing a noncompete, employers may be less incentivized to provide all those benefits to their physician employers.

Those benefits – and the noncompetes – also vary by specialty, Mr. Glennon said. “In 2021, Washington, DC, banned noncompetes for doctors making less than $250,000. So, most generalists there can walk across the street and get a new job. For specialists like cardiologists or neurosurgeons, however, advanced training and marketing benefits matter, so many of them don’t want to lose noncompetes.”

Still, most physicians hope that the FTC’s ban takes hold. Manan Shah, MD, founder, and chief medical officer at Wyndly, an allergy relief startup practice, is one of them.

“Initially, it might disincentivize hospital systems from helping new physicians build up their name and practice because they might be concerned about a physician leaving and starting anew,” he said. “But in the long term, hospitals require physicians to bring their patients to them for care, so the best hospitals will always compete for the best physicians and support them as they build up their practice.”

Dr. Shah views noncompetes as overly prohibitive to physicians. “Right now, if a physician starts a job at a large hospital system and realizes they want to switch jobs, the noncompete distances are so wide they often have to move cities to continue practicing,” he said. “Picking up and starting over in a new city isn’t an option for everyone and can be especially difficult for someone with a family.”

Where Mr. Glennon argued that a physician leaving a team-based practice might harm patients, Shah takes a different perspective. “Imagine you have a doctor whom you trust and have been working with,” he said. “If something changes at their hospital and they decide to move, you literally have to find a new doctor instead of just being able to see them at another location down the street.”

Another potential burden of the noncompete agreements is that they could possibly squelch doctor’s desires to hang up their own shingle. According to Dr. Shah, the agreements make it so that if a physician wants to work independently, it’s nearly impossible to fly solo. “This is frustrating because independent practices have been shown to be more cost effective and allow patients to build better relationships with their doctors,” he claimed.

A 2016 study from Annals of Family Medicine supports that claim, at least for small general practices. Another study appearing in JAMA concurred. It does point out, however, that the cost equation is nuanced and that benefits of larger systems include more resilience to economic downturns and can provide more specialized care.
 

Will nonprofit hospitals be subject to this noncompete ban?

Further complicating the noncompete ban issue is how it might impact nonprofit institutions versus their for-profit peers. Most hospitals structured as nonprofits would be exempt from the rule because the FTC Act provides that it can enforce against “persons, partnerships, or corporations,” which are further defined as entities “organized to carry on business for their own profit or that of their members.”

The fallout from this, said Dr. Shah, is that it “would disproportionately affect health care providers, since many hospital systems are nonprofits. This is disconcerting because we know that many nonprofit systems make large profits anyway and can offer executive teams’ lucrative packages, while the nurses, assistants, and physicians providing the care are generally not well compensated.”

So far, about nine states plus Washington, D.C., have already put noncompete bans in place, and they may serve as a harbinger of things to come should the federal ban go into effect. Each varies in its specifics. Some, like Indiana, outright ban them, whereas others limit them based on variables like income and industry. “We’re seeing these states responding to local market conditions,” said Darryl Drevna, senior director of regulatory affairs at the American Medical Group Association. “Health care is a hyperlocal market. Depending on the situation, the bans adapt and respond specific to those states.”

Should the federal ban take hold, however, it will supersede whatever rules the individual states have in place.

Some opponents of the federal ban proposal question its authority to begin with, however, Mr. Glennon included. “Many people believe the FTC is overstepping,” he said. “Some people believe that Section 5 of the FTC Act does not give it the authority to police labor markets.”

Mr. Drevna noted that the FTC has taken an aggressive stance, one that will ultimately wind up in the courts. “How it works out is anyone’s guess,” he said. “Ideally, the FTC will consider the comments and concerns of groups like AMGA and realize that states are best suited to regulate in this area.”

In general, the ban’s supporters are employees/physicians; those who oppose it are their employers. Joining the AMGA in speaking out against the noncompete ban is the American Hospital Association, whereas the American College of Emergency Physicians has come out largely in support of the ban.

Still, doctors like Dr. Shah remain hopeful. “I am optimistic that perhaps my colleagues will not continue to be stuck in overrestrictive noncompetes, but I am also realistic,” he said. “Hospital systems are already coming out strongly against this and they have deep pockets, so I won’t be surprised if it does not come to pass.”

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

The Federal Trade Commission’s proposed regulation that would ban noncompete agreements across the country seems like potential good news for doctors. Of course, many hospitals and employers are against it. As a result, the FTC’s sweeping proposal has tongues wagging on both sides of the issue.

Many physicians are thrilled that they may soon have more control over their career and not be stuck in jobs where they feel frustrated, underpaid, or blocked in their progress.

If passed, the proposed ban would allow physicians to get a new job with a competing organization, bucking a long-standing trend that hospitals and health care systems have heavily relied on to keep staff in place. As of 2018, as many as 45% of primary care physicians had inked such agreements with their employers.

Typically, the agreements prevent physicians from practicing medicine with a new employer for a defined period within a specific geographic area. No matter how attractive an alternate offer of employment might be, doctors are bound by the agreements to say no if the offer exists in that defined area and time period.

The period for public comment on the proposed regulation ended on April 19, and there is currently no set date for a decision.

In a Medscape poll of 558 physicians, more than 9 out of 10 respondents said that they were either currently bound by a noncompete clause or that they had been bound by one in the past that had forced them to temporarily stop working, commute long distances, move to a different area, or switch fields.

The new proposal would make it illegal for an employer, such as a hospital or large group, to enter a noncompete with a worker; maintain a noncompete with a worker; or represent to a worker, under certain circumstances, that the worker is subject to a noncompete.

It also would not only ban future noncompete agreements but also retroactively invalidate existing ones. The FTC reasons that noncompete clauses could potentially increase worker earnings as well as lower health care costs by billions of dollars. If the ruling were to move forward, it would represent part of President Biden’s “worker-forward” priorities, focusing on how competition can be a good thing for employees. The President billed the FTC’s announcement as a “huge win for workers.”

In its statements on the proposed ban, the FTC claimed that it could lower consumer prices across the board by as much as $150 billion per year and return nearly $300 million to workers each year.

However, even if passed, the draft rule would keep in place nonsolicitation rules that many health care organizations have put into place. That means that, if a physician leaves an employer, he or she cannot reach out to former patients and colleagues to bring them along or invite them to switch to him or her in the new job.

Within that clause, however, the FTC has specified that if such nonsolicitation agreement has the “equivalent effect” of a noncompete, the agency would deem it such. That means, even if that rule stays, it could be contested and may be interpreted as violating the noncompete law. So there’s value in reading all the fine print should the ban move forward.
 

Could the ban bring potential downsides?

Most physicians view the potential to break free of a noncompete agreement as a victory. Peter Glennon, an employment litigation attorney with The Glennon Law Firm in Rochester, N.Y., says not so fast. “If you ask anyone if they’d prefer a noncompete agreement, of course they’re going to say no,” he said in an interview. “It sounds like a restriction, one that can hold you back.”

Mr. Glennon believes that there are actually upsides to physician noncompetes. For instance, many noncompetes come with sign-on bonuses that could potentially disappear without the agreements. There’s also the fact that when some physicians sign a noncompete agreement, they then receive pro bono training and continuing education along with marketing and promotion of their skills. Without signing a noncompete, employers may be less incentivized to provide all those benefits to their physician employers.

Those benefits – and the noncompetes – also vary by specialty, Mr. Glennon said. “In 2021, Washington, DC, banned noncompetes for doctors making less than $250,000. So, most generalists there can walk across the street and get a new job. For specialists like cardiologists or neurosurgeons, however, advanced training and marketing benefits matter, so many of them don’t want to lose noncompetes.”

Still, most physicians hope that the FTC’s ban takes hold. Manan Shah, MD, founder, and chief medical officer at Wyndly, an allergy relief startup practice, is one of them.

“Initially, it might disincentivize hospital systems from helping new physicians build up their name and practice because they might be concerned about a physician leaving and starting anew,” he said. “But in the long term, hospitals require physicians to bring their patients to them for care, so the best hospitals will always compete for the best physicians and support them as they build up their practice.”

Dr. Shah views noncompetes as overly prohibitive to physicians. “Right now, if a physician starts a job at a large hospital system and realizes they want to switch jobs, the noncompete distances are so wide they often have to move cities to continue practicing,” he said. “Picking up and starting over in a new city isn’t an option for everyone and can be especially difficult for someone with a family.”

Where Mr. Glennon argued that a physician leaving a team-based practice might harm patients, Shah takes a different perspective. “Imagine you have a doctor whom you trust and have been working with,” he said. “If something changes at their hospital and they decide to move, you literally have to find a new doctor instead of just being able to see them at another location down the street.”

Another potential burden of the noncompete agreements is that they could possibly squelch doctor’s desires to hang up their own shingle. According to Dr. Shah, the agreements make it so that if a physician wants to work independently, it’s nearly impossible to fly solo. “This is frustrating because independent practices have been shown to be more cost effective and allow patients to build better relationships with their doctors,” he claimed.

A 2016 study from Annals of Family Medicine supports that claim, at least for small general practices. Another study appearing in JAMA concurred. It does point out, however, that the cost equation is nuanced and that benefits of larger systems include more resilience to economic downturns and can provide more specialized care.
 

Will nonprofit hospitals be subject to this noncompete ban?

Further complicating the noncompete ban issue is how it might impact nonprofit institutions versus their for-profit peers. Most hospitals structured as nonprofits would be exempt from the rule because the FTC Act provides that it can enforce against “persons, partnerships, or corporations,” which are further defined as entities “organized to carry on business for their own profit or that of their members.”

The fallout from this, said Dr. Shah, is that it “would disproportionately affect health care providers, since many hospital systems are nonprofits. This is disconcerting because we know that many nonprofit systems make large profits anyway and can offer executive teams’ lucrative packages, while the nurses, assistants, and physicians providing the care are generally not well compensated.”

So far, about nine states plus Washington, D.C., have already put noncompete bans in place, and they may serve as a harbinger of things to come should the federal ban go into effect. Each varies in its specifics. Some, like Indiana, outright ban them, whereas others limit them based on variables like income and industry. “We’re seeing these states responding to local market conditions,” said Darryl Drevna, senior director of regulatory affairs at the American Medical Group Association. “Health care is a hyperlocal market. Depending on the situation, the bans adapt and respond specific to those states.”

Should the federal ban take hold, however, it will supersede whatever rules the individual states have in place.

Some opponents of the federal ban proposal question its authority to begin with, however, Mr. Glennon included. “Many people believe the FTC is overstepping,” he said. “Some people believe that Section 5 of the FTC Act does not give it the authority to police labor markets.”

Mr. Drevna noted that the FTC has taken an aggressive stance, one that will ultimately wind up in the courts. “How it works out is anyone’s guess,” he said. “Ideally, the FTC will consider the comments and concerns of groups like AMGA and realize that states are best suited to regulate in this area.”

In general, the ban’s supporters are employees/physicians; those who oppose it are their employers. Joining the AMGA in speaking out against the noncompete ban is the American Hospital Association, whereas the American College of Emergency Physicians has come out largely in support of the ban.

Still, doctors like Dr. Shah remain hopeful. “I am optimistic that perhaps my colleagues will not continue to be stuck in overrestrictive noncompetes, but I am also realistic,” he said. “Hospital systems are already coming out strongly against this and they have deep pockets, so I won’t be surprised if it does not come to pass.”

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

The Federal Trade Commission’s proposed regulation that would ban noncompete agreements across the country seems like potential good news for doctors. Of course, many hospitals and employers are against it. As a result, the FTC’s sweeping proposal has tongues wagging on both sides of the issue.

Many physicians are thrilled that they may soon have more control over their career and not be stuck in jobs where they feel frustrated, underpaid, or blocked in their progress.

If passed, the proposed ban would allow physicians to get a new job with a competing organization, bucking a long-standing trend that hospitals and health care systems have heavily relied on to keep staff in place. As of 2018, as many as 45% of primary care physicians had inked such agreements with their employers.

Typically, the agreements prevent physicians from practicing medicine with a new employer for a defined period within a specific geographic area. No matter how attractive an alternate offer of employment might be, doctors are bound by the agreements to say no if the offer exists in that defined area and time period.

The period for public comment on the proposed regulation ended on April 19, and there is currently no set date for a decision.

In a Medscape poll of 558 physicians, more than 9 out of 10 respondents said that they were either currently bound by a noncompete clause or that they had been bound by one in the past that had forced them to temporarily stop working, commute long distances, move to a different area, or switch fields.

The new proposal would make it illegal for an employer, such as a hospital or large group, to enter a noncompete with a worker; maintain a noncompete with a worker; or represent to a worker, under certain circumstances, that the worker is subject to a noncompete.

It also would not only ban future noncompete agreements but also retroactively invalidate existing ones. The FTC reasons that noncompete clauses could potentially increase worker earnings as well as lower health care costs by billions of dollars. If the ruling were to move forward, it would represent part of President Biden’s “worker-forward” priorities, focusing on how competition can be a good thing for employees. The President billed the FTC’s announcement as a “huge win for workers.”

In its statements on the proposed ban, the FTC claimed that it could lower consumer prices across the board by as much as $150 billion per year and return nearly $300 million to workers each year.

However, even if passed, the draft rule would keep in place nonsolicitation rules that many health care organizations have put into place. That means that, if a physician leaves an employer, he or she cannot reach out to former patients and colleagues to bring them along or invite them to switch to him or her in the new job.

Within that clause, however, the FTC has specified that if such nonsolicitation agreement has the “equivalent effect” of a noncompete, the agency would deem it such. That means, even if that rule stays, it could be contested and may be interpreted as violating the noncompete law. So there’s value in reading all the fine print should the ban move forward.
 

Could the ban bring potential downsides?

Most physicians view the potential to break free of a noncompete agreement as a victory. Peter Glennon, an employment litigation attorney with The Glennon Law Firm in Rochester, N.Y., says not so fast. “If you ask anyone if they’d prefer a noncompete agreement, of course they’re going to say no,” he said in an interview. “It sounds like a restriction, one that can hold you back.”

Mr. Glennon believes that there are actually upsides to physician noncompetes. For instance, many noncompetes come with sign-on bonuses that could potentially disappear without the agreements. There’s also the fact that when some physicians sign a noncompete agreement, they then receive pro bono training and continuing education along with marketing and promotion of their skills. Without signing a noncompete, employers may be less incentivized to provide all those benefits to their physician employers.

Those benefits – and the noncompetes – also vary by specialty, Mr. Glennon said. “In 2021, Washington, DC, banned noncompetes for doctors making less than $250,000. So, most generalists there can walk across the street and get a new job. For specialists like cardiologists or neurosurgeons, however, advanced training and marketing benefits matter, so many of them don’t want to lose noncompetes.”

Still, most physicians hope that the FTC’s ban takes hold. Manan Shah, MD, founder, and chief medical officer at Wyndly, an allergy relief startup practice, is one of them.

“Initially, it might disincentivize hospital systems from helping new physicians build up their name and practice because they might be concerned about a physician leaving and starting anew,” he said. “But in the long term, hospitals require physicians to bring their patients to them for care, so the best hospitals will always compete for the best physicians and support them as they build up their practice.”

Dr. Shah views noncompetes as overly prohibitive to physicians. “Right now, if a physician starts a job at a large hospital system and realizes they want to switch jobs, the noncompete distances are so wide they often have to move cities to continue practicing,” he said. “Picking up and starting over in a new city isn’t an option for everyone and can be especially difficult for someone with a family.”

Where Mr. Glennon argued that a physician leaving a team-based practice might harm patients, Shah takes a different perspective. “Imagine you have a doctor whom you trust and have been working with,” he said. “If something changes at their hospital and they decide to move, you literally have to find a new doctor instead of just being able to see them at another location down the street.”

Another potential burden of the noncompete agreements is that they could possibly squelch doctor’s desires to hang up their own shingle. According to Dr. Shah, the agreements make it so that if a physician wants to work independently, it’s nearly impossible to fly solo. “This is frustrating because independent practices have been shown to be more cost effective and allow patients to build better relationships with their doctors,” he claimed.

A 2016 study from Annals of Family Medicine supports that claim, at least for small general practices. Another study appearing in JAMA concurred. It does point out, however, that the cost equation is nuanced and that benefits of larger systems include more resilience to economic downturns and can provide more specialized care.
 

Will nonprofit hospitals be subject to this noncompete ban?

Further complicating the noncompete ban issue is how it might impact nonprofit institutions versus their for-profit peers. Most hospitals structured as nonprofits would be exempt from the rule because the FTC Act provides that it can enforce against “persons, partnerships, or corporations,” which are further defined as entities “organized to carry on business for their own profit or that of their members.”

The fallout from this, said Dr. Shah, is that it “would disproportionately affect health care providers, since many hospital systems are nonprofits. This is disconcerting because we know that many nonprofit systems make large profits anyway and can offer executive teams’ lucrative packages, while the nurses, assistants, and physicians providing the care are generally not well compensated.”

So far, about nine states plus Washington, D.C., have already put noncompete bans in place, and they may serve as a harbinger of things to come should the federal ban go into effect. Each varies in its specifics. Some, like Indiana, outright ban them, whereas others limit them based on variables like income and industry. “We’re seeing these states responding to local market conditions,” said Darryl Drevna, senior director of regulatory affairs at the American Medical Group Association. “Health care is a hyperlocal market. Depending on the situation, the bans adapt and respond specific to those states.”

Should the federal ban take hold, however, it will supersede whatever rules the individual states have in place.

Some opponents of the federal ban proposal question its authority to begin with, however, Mr. Glennon included. “Many people believe the FTC is overstepping,” he said. “Some people believe that Section 5 of the FTC Act does not give it the authority to police labor markets.”

Mr. Drevna noted that the FTC has taken an aggressive stance, one that will ultimately wind up in the courts. “How it works out is anyone’s guess,” he said. “Ideally, the FTC will consider the comments and concerns of groups like AMGA and realize that states are best suited to regulate in this area.”

In general, the ban’s supporters are employees/physicians; those who oppose it are their employers. Joining the AMGA in speaking out against the noncompete ban is the American Hospital Association, whereas the American College of Emergency Physicians has come out largely in support of the ban.

Still, doctors like Dr. Shah remain hopeful. “I am optimistic that perhaps my colleagues will not continue to be stuck in overrestrictive noncompetes, but I am also realistic,” he said. “Hospital systems are already coming out strongly against this and they have deep pockets, so I won’t be surprised if it does not come to pass.”

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

Adding the immunotherapy cemiplimab to chemotherapy for patients with advanced non–small cell lung cancer (NSCLC) not only improved overall survival but also led to quality-of-life benefits, new data show.

In the trial, patients who received the PD-1 inhibitor plus platinum-doublet chemotherapy in the first-line setting reported significant improvements in pain symptoms and delay in time to deterioration, as well as improvements in disease-related symptoms, such as dyspnea, constipation, nausea, and vomiting.

Overall, “the findings support the concept that the superior efficacy and favorable safety profile of cemiplimab plus chemotherapy translate to better patient-reported outcomes compared with chemotherapy alone in patients with advanced non–small cell lung cancer, “ corresponding author Tamta Makharadze, MD, of LTD High Technology Hospital Med Center in Batumi, Georgia, said in a press release.

The delays reported in time to definitive clinically meaningful deterioration “are particularly pertinent, given the anticipated continued improvements in cancer survivorship among patients with advanced NSCLC,” the authors explained.

The research was published online May 8 in Cancer.

Quality of life is especially important for patients with advanced NSCLC, for whom the benefits of improved survival must be weighed against the potential drawbacks of treatment toxicities, which can severely impact quality of life, the authors noted.

In the initial multinational phase 3 EMPOWER-Lung 3 trial, Dr. Makharadze and colleagues randomly assigned 466 patients with stage IIIB, IIIC, or stage IV NSCLC to receive either 350 mg of cemiplimab (Libtayo, Regeneron Pharmaceuticals) every 3 weeks along with investigator’s choice of platinum‐doublet chemotherapy or placebo plus chemotherapy. Investigator’s choice of chemotherapy was either paclitaxel plus carboplatin or cisplatin, pemetrexed plus carboplatin, or cisplatin.

The researchers found that the addition of cemiplimab to chemotherapy was associated with a significant, almost 9-month improvement in overall survival. While the trial also highlighted significant improvements in quality of life, functioning, and most symptoms with cemiplimab in comparison with placebo, the current study provides more details on these patient-reported quality-of-life outcomes.

In the latest analysis, Dr. Makharadze and colleagues evaluated data on the 312 patients in the cemiplimab arm and the 154 in the placebo arm. The median age of the patients was 63 years, and most (83.9%) were men.

Patients in the cemiplimab arm reported significant improvements in pain symptoms from baseline, as measured with the European Organization for Research and Treatment of Cancer (EORTC) Quality of Life–Core 30 (QLQ‐C30) score (–4.98; P = .004).

Patients who were treated with cemiplimab also reported a significant delay in time to definitive clinically meaningful deterioration (hazard ratio [HR], 0.39; P < .0001).

Significant delays in the time to deterioration in other functioning and symptom scales favored the cemiplimab group, including dyspnea (HR, 0.54), nausea/vomiting (HR, 0.39), and constipation (HR, 0.48).

The cemiplimab group also reported significantly delayed time to deterioration in physical (HR, 0.62) and emotional functioning (HR, 0.52) compared with the placebo arm as well as significant overall improvements from baseline in global health status/quality of life scores.

No significant improvements in patient-reported outcomes favoring the placebo group were observed on any quality-of-life metric evaluated using the symptom scales.

As for study limitations, the authors said that although about 86% of patients in both arms completed at least one question at baseline and post baseline, “the results may have overrepresented the patients who did well in both treatment arms because patients who progressed no longer completed the questionnaires.”

Nevertheless, the results “show that the favorable efficacy achieved with cemiplimab plus chemotherapy over placebo plus chemotherapy is accompanied by significant overall improvement in pain and significant delay in [time to definitive clinically meaningful deterioration] in multiple patient‐reported cancer‐related and lung cancer–specific functions and symptoms,” the authors concluded.

The study was sponsored by Regeneron Pharmaceuticals and Sanofi.
 

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

Adding the immunotherapy cemiplimab to chemotherapy for patients with advanced non–small cell lung cancer (NSCLC) not only improved overall survival but also led to quality-of-life benefits, new data show.

In the trial, patients who received the PD-1 inhibitor plus platinum-doublet chemotherapy in the first-line setting reported significant improvements in pain symptoms and delay in time to deterioration, as well as improvements in disease-related symptoms, such as dyspnea, constipation, nausea, and vomiting.

Overall, “the findings support the concept that the superior efficacy and favorable safety profile of cemiplimab plus chemotherapy translate to better patient-reported outcomes compared with chemotherapy alone in patients with advanced non–small cell lung cancer, “ corresponding author Tamta Makharadze, MD, of LTD High Technology Hospital Med Center in Batumi, Georgia, said in a press release.

The delays reported in time to definitive clinically meaningful deterioration “are particularly pertinent, given the anticipated continued improvements in cancer survivorship among patients with advanced NSCLC,” the authors explained.

The research was published online May 8 in Cancer.

Quality of life is especially important for patients with advanced NSCLC, for whom the benefits of improved survival must be weighed against the potential drawbacks of treatment toxicities, which can severely impact quality of life, the authors noted.

In the initial multinational phase 3 EMPOWER-Lung 3 trial, Dr. Makharadze and colleagues randomly assigned 466 patients with stage IIIB, IIIC, or stage IV NSCLC to receive either 350 mg of cemiplimab (Libtayo, Regeneron Pharmaceuticals) every 3 weeks along with investigator’s choice of platinum‐doublet chemotherapy or placebo plus chemotherapy. Investigator’s choice of chemotherapy was either paclitaxel plus carboplatin or cisplatin, pemetrexed plus carboplatin, or cisplatin.

The researchers found that the addition of cemiplimab to chemotherapy was associated with a significant, almost 9-month improvement in overall survival. While the trial also highlighted significant improvements in quality of life, functioning, and most symptoms with cemiplimab in comparison with placebo, the current study provides more details on these patient-reported quality-of-life outcomes.

In the latest analysis, Dr. Makharadze and colleagues evaluated data on the 312 patients in the cemiplimab arm and the 154 in the placebo arm. The median age of the patients was 63 years, and most (83.9%) were men.

Patients in the cemiplimab arm reported significant improvements in pain symptoms from baseline, as measured with the European Organization for Research and Treatment of Cancer (EORTC) Quality of Life–Core 30 (QLQ‐C30) score (–4.98; P = .004).

Patients who were treated with cemiplimab also reported a significant delay in time to definitive clinically meaningful deterioration (hazard ratio [HR], 0.39; P < .0001).

Significant delays in the time to deterioration in other functioning and symptom scales favored the cemiplimab group, including dyspnea (HR, 0.54), nausea/vomiting (HR, 0.39), and constipation (HR, 0.48).

The cemiplimab group also reported significantly delayed time to deterioration in physical (HR, 0.62) and emotional functioning (HR, 0.52) compared with the placebo arm as well as significant overall improvements from baseline in global health status/quality of life scores.

No significant improvements in patient-reported outcomes favoring the placebo group were observed on any quality-of-life metric evaluated using the symptom scales.

As for study limitations, the authors said that although about 86% of patients in both arms completed at least one question at baseline and post baseline, “the results may have overrepresented the patients who did well in both treatment arms because patients who progressed no longer completed the questionnaires.”

Nevertheless, the results “show that the favorable efficacy achieved with cemiplimab plus chemotherapy over placebo plus chemotherapy is accompanied by significant overall improvement in pain and significant delay in [time to definitive clinically meaningful deterioration] in multiple patient‐reported cancer‐related and lung cancer–specific functions and symptoms,” the authors concluded.

The study was sponsored by Regeneron Pharmaceuticals and Sanofi.
 

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

Adding the immunotherapy cemiplimab to chemotherapy for patients with advanced non–small cell lung cancer (NSCLC) not only improved overall survival but also led to quality-of-life benefits, new data show.

In the trial, patients who received the PD-1 inhibitor plus platinum-doublet chemotherapy in the first-line setting reported significant improvements in pain symptoms and delay in time to deterioration, as well as improvements in disease-related symptoms, such as dyspnea, constipation, nausea, and vomiting.

Overall, “the findings support the concept that the superior efficacy and favorable safety profile of cemiplimab plus chemotherapy translate to better patient-reported outcomes compared with chemotherapy alone in patients with advanced non–small cell lung cancer, “ corresponding author Tamta Makharadze, MD, of LTD High Technology Hospital Med Center in Batumi, Georgia, said in a press release.

The delays reported in time to definitive clinically meaningful deterioration “are particularly pertinent, given the anticipated continued improvements in cancer survivorship among patients with advanced NSCLC,” the authors explained.

The research was published online May 8 in Cancer.

Quality of life is especially important for patients with advanced NSCLC, for whom the benefits of improved survival must be weighed against the potential drawbacks of treatment toxicities, which can severely impact quality of life, the authors noted.

In the initial multinational phase 3 EMPOWER-Lung 3 trial, Dr. Makharadze and colleagues randomly assigned 466 patients with stage IIIB, IIIC, or stage IV NSCLC to receive either 350 mg of cemiplimab (Libtayo, Regeneron Pharmaceuticals) every 3 weeks along with investigator’s choice of platinum‐doublet chemotherapy or placebo plus chemotherapy. Investigator’s choice of chemotherapy was either paclitaxel plus carboplatin or cisplatin, pemetrexed plus carboplatin, or cisplatin.

The researchers found that the addition of cemiplimab to chemotherapy was associated with a significant, almost 9-month improvement in overall survival. While the trial also highlighted significant improvements in quality of life, functioning, and most symptoms with cemiplimab in comparison with placebo, the current study provides more details on these patient-reported quality-of-life outcomes.

In the latest analysis, Dr. Makharadze and colleagues evaluated data on the 312 patients in the cemiplimab arm and the 154 in the placebo arm. The median age of the patients was 63 years, and most (83.9%) were men.

Patients in the cemiplimab arm reported significant improvements in pain symptoms from baseline, as measured with the European Organization for Research and Treatment of Cancer (EORTC) Quality of Life–Core 30 (QLQ‐C30) score (–4.98; P = .004).

Patients who were treated with cemiplimab also reported a significant delay in time to definitive clinically meaningful deterioration (hazard ratio [HR], 0.39; P < .0001).

Significant delays in the time to deterioration in other functioning and symptom scales favored the cemiplimab group, including dyspnea (HR, 0.54), nausea/vomiting (HR, 0.39), and constipation (HR, 0.48).

The cemiplimab group also reported significantly delayed time to deterioration in physical (HR, 0.62) and emotional functioning (HR, 0.52) compared with the placebo arm as well as significant overall improvements from baseline in global health status/quality of life scores.

No significant improvements in patient-reported outcomes favoring the placebo group were observed on any quality-of-life metric evaluated using the symptom scales.

As for study limitations, the authors said that although about 86% of patients in both arms completed at least one question at baseline and post baseline, “the results may have overrepresented the patients who did well in both treatment arms because patients who progressed no longer completed the questionnaires.”

Nevertheless, the results “show that the favorable efficacy achieved with cemiplimab plus chemotherapy over placebo plus chemotherapy is accompanied by significant overall improvement in pain and significant delay in [time to definitive clinically meaningful deterioration] in multiple patient‐reported cancer‐related and lung cancer–specific functions and symptoms,” the authors concluded.

The study was sponsored by Regeneron Pharmaceuticals and Sanofi.
 

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

Higher body mass index and changes in BMI over time may increase a person’s risk for gastrointestinal cancer, according to new data from the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial.

The researchers found that being overweight or obese in early and middle adulthood was associated with an increased risk for colorectal cancer (CRC) and noncolorectal GI cancers. Maintaining or increasing BMI over time among overweight or obese individuals was also associated with an increased GI cancer risk.

Aspirin use did not significantly modify these associations, suggesting that aspirin may not be as effective for cancer prevention among overweight or obese individuals.

The results provide “relatively consistent messaging that overweight or obesity from early to later adulthood as well as BMI increases throughout adulthood were associated with increased risk of GI cancers, especially CRC,” the authors of an editorial accompanying the study wrote.

These “important findings highlight the unmet need to identify the critical time window linking adiposity and GI cancer,” said editorialists Mengyao Shi, MBBS, MPD, and Yin Cao, ScD, MPH, of Washington University in St. Louis.

The analysis was published online in JAMA Network Open. 

A growing body of evidence has revealed a strong association between obesity and GI cancers, with chronic inflammation being a likely cause. As rates of overweight and obesity continue to grow, better understanding of the association between obesity and cancer has become increasingly important.

In the analysis, Holli A. Loomans-Kropp, PhD, MPH, with Ohio State University, Columbus, and Asad Umar, PhD, DVM, with the National Cancer Institute, Rockville, Md., explored associations between BMI in early adulthood (age 20), middle adulthood (age 50) and later adulthood (age 55 and over) and GI cancer risk in 135,161 adults from the PLCO Cancer Screening Trial.

BMI was determined using self-reported height and weight at each age time point. The median age at enrollment was 62 years, and 50% of participants were women. Overweight BMI was 25.0-29.9 kg/m² and obese BMI was 30 or higher.

During as many as 21 years of follow-up, 2,803 individuals developed CRC and 2,285 developed non-CRC GI cancers (esophageal, liver, gastric, and pancreatic).

Overweight BMI in early, middle, and later adulthood was associated with an increased risk of CRC (hazard ratio, 1.23 for early and middle years; HR, 1.21 for later years). Obese BMI in middle and later adulthood was also associated with increased risk of CRC (HR, 1.55 and 1.39, respectively). 

The authors observed similar associations between BMI in middle and later adulthood and overall GI and non-CRC GI risk.

“When modeled continuously, we observed 2%-4% increased risk of both CRC and noncolorectal GI cancer with each 1-unit increase in BMI across all time points,” the researchers said.

Their data also suggest that BMI over time may be associated with GI cancer risk. Adults who exhibited no change in overweight or obese BMIs between early and later adulthood and those who exhibited increases in BMI from underweight or normal in early adulthood to overweight or obese BMI in later adulthood had a significantly higher risk for CRC and noncolorectal GI cancer.

Among frequent aspirin users, those with overweight or obese BMIs in early, middle, and later adulthood still had an increased risk for CRC and noncolorectal GI cancer (hazard ratios, 1.44, 1.45, and 1.43, respectively).

The finding that regular weekly aspirin use did not modify GI cancer risk suggests that obesity may alter the cancer-preventive effect of aspirin, the researchers suggested. Individuals with obesity may need to increase aspirin frequency or dosage to see an effect, but upping the dose comes with its own risks, including GI bleeding.

Overall, until now, most epidemiologic studies have examined BMI at one time point, “missing the opportunity to delineate the contribution of adiposity throughout the life course,” Dr. Shi and Dr. Cao wrote.

“As we continue to investigate precision-based interventions to intercept the link between obesity and cancer, it is imperative to reiterate the importance of maintaining a healthy weight and lifestyle from an early age and incorporate it widely into cancer prevention strategies at all levels with immediate implementation,” the editorialists concluded.

This study was supported in part by funds from Ohio State University and the NIH. The study authors reported no relevant financial relationships. Dr. Cao has received personal fees from Geneoscopy for consulting.

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

Higher body mass index and changes in BMI over time may increase a person’s risk for gastrointestinal cancer, according to new data from the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial.

The researchers found that being overweight or obese in early and middle adulthood was associated with an increased risk for colorectal cancer (CRC) and noncolorectal GI cancers. Maintaining or increasing BMI over time among overweight or obese individuals was also associated with an increased GI cancer risk.

Aspirin use did not significantly modify these associations, suggesting that aspirin may not be as effective for cancer prevention among overweight or obese individuals.

The results provide “relatively consistent messaging that overweight or obesity from early to later adulthood as well as BMI increases throughout adulthood were associated with increased risk of GI cancers, especially CRC,” the authors of an editorial accompanying the study wrote.

These “important findings highlight the unmet need to identify the critical time window linking adiposity and GI cancer,” said editorialists Mengyao Shi, MBBS, MPD, and Yin Cao, ScD, MPH, of Washington University in St. Louis.

The analysis was published online in JAMA Network Open. 

A growing body of evidence has revealed a strong association between obesity and GI cancers, with chronic inflammation being a likely cause. As rates of overweight and obesity continue to grow, better understanding of the association between obesity and cancer has become increasingly important.

In the analysis, Holli A. Loomans-Kropp, PhD, MPH, with Ohio State University, Columbus, and Asad Umar, PhD, DVM, with the National Cancer Institute, Rockville, Md., explored associations between BMI in early adulthood (age 20), middle adulthood (age 50) and later adulthood (age 55 and over) and GI cancer risk in 135,161 adults from the PLCO Cancer Screening Trial.

BMI was determined using self-reported height and weight at each age time point. The median age at enrollment was 62 years, and 50% of participants were women. Overweight BMI was 25.0-29.9 kg/m² and obese BMI was 30 or higher.

During as many as 21 years of follow-up, 2,803 individuals developed CRC and 2,285 developed non-CRC GI cancers (esophageal, liver, gastric, and pancreatic).

Overweight BMI in early, middle, and later adulthood was associated with an increased risk of CRC (hazard ratio, 1.23 for early and middle years; HR, 1.21 for later years). Obese BMI in middle and later adulthood was also associated with increased risk of CRC (HR, 1.55 and 1.39, respectively). 

The authors observed similar associations between BMI in middle and later adulthood and overall GI and non-CRC GI risk.

“When modeled continuously, we observed 2%-4% increased risk of both CRC and noncolorectal GI cancer with each 1-unit increase in BMI across all time points,” the researchers said.

Their data also suggest that BMI over time may be associated with GI cancer risk. Adults who exhibited no change in overweight or obese BMIs between early and later adulthood and those who exhibited increases in BMI from underweight or normal in early adulthood to overweight or obese BMI in later adulthood had a significantly higher risk for CRC and noncolorectal GI cancer.

Among frequent aspirin users, those with overweight or obese BMIs in early, middle, and later adulthood still had an increased risk for CRC and noncolorectal GI cancer (hazard ratios, 1.44, 1.45, and 1.43, respectively).

The finding that regular weekly aspirin use did not modify GI cancer risk suggests that obesity may alter the cancer-preventive effect of aspirin, the researchers suggested. Individuals with obesity may need to increase aspirin frequency or dosage to see an effect, but upping the dose comes with its own risks, including GI bleeding.

Overall, until now, most epidemiologic studies have examined BMI at one time point, “missing the opportunity to delineate the contribution of adiposity throughout the life course,” Dr. Shi and Dr. Cao wrote.

“As we continue to investigate precision-based interventions to intercept the link between obesity and cancer, it is imperative to reiterate the importance of maintaining a healthy weight and lifestyle from an early age and incorporate it widely into cancer prevention strategies at all levels with immediate implementation,” the editorialists concluded.

This study was supported in part by funds from Ohio State University and the NIH. The study authors reported no relevant financial relationships. Dr. Cao has received personal fees from Geneoscopy for consulting.

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

Higher body mass index and changes in BMI over time may increase a person’s risk for gastrointestinal cancer, according to new data from the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial.

The researchers found that being overweight or obese in early and middle adulthood was associated with an increased risk for colorectal cancer (CRC) and noncolorectal GI cancers. Maintaining or increasing BMI over time among overweight or obese individuals was also associated with an increased GI cancer risk.

Aspirin use did not significantly modify these associations, suggesting that aspirin may not be as effective for cancer prevention among overweight or obese individuals.

The results provide “relatively consistent messaging that overweight or obesity from early to later adulthood as well as BMI increases throughout adulthood were associated with increased risk of GI cancers, especially CRC,” the authors of an editorial accompanying the study wrote.

These “important findings highlight the unmet need to identify the critical time window linking adiposity and GI cancer,” said editorialists Mengyao Shi, MBBS, MPD, and Yin Cao, ScD, MPH, of Washington University in St. Louis.

The analysis was published online in JAMA Network Open. 

A growing body of evidence has revealed a strong association between obesity and GI cancers, with chronic inflammation being a likely cause. As rates of overweight and obesity continue to grow, better understanding of the association between obesity and cancer has become increasingly important.

In the analysis, Holli A. Loomans-Kropp, PhD, MPH, with Ohio State University, Columbus, and Asad Umar, PhD, DVM, with the National Cancer Institute, Rockville, Md., explored associations between BMI in early adulthood (age 20), middle adulthood (age 50) and later adulthood (age 55 and over) and GI cancer risk in 135,161 adults from the PLCO Cancer Screening Trial.

BMI was determined using self-reported height and weight at each age time point. The median age at enrollment was 62 years, and 50% of participants were women. Overweight BMI was 25.0-29.9 kg/m² and obese BMI was 30 or higher.

During as many as 21 years of follow-up, 2,803 individuals developed CRC and 2,285 developed non-CRC GI cancers (esophageal, liver, gastric, and pancreatic).

Overweight BMI in early, middle, and later adulthood was associated with an increased risk of CRC (hazard ratio, 1.23 for early and middle years; HR, 1.21 for later years). Obese BMI in middle and later adulthood was also associated with increased risk of CRC (HR, 1.55 and 1.39, respectively). 

The authors observed similar associations between BMI in middle and later adulthood and overall GI and non-CRC GI risk.

“When modeled continuously, we observed 2%-4% increased risk of both CRC and noncolorectal GI cancer with each 1-unit increase in BMI across all time points,” the researchers said.

Their data also suggest that BMI over time may be associated with GI cancer risk. Adults who exhibited no change in overweight or obese BMIs between early and later adulthood and those who exhibited increases in BMI from underweight or normal in early adulthood to overweight or obese BMI in later adulthood had a significantly higher risk for CRC and noncolorectal GI cancer.

Among frequent aspirin users, those with overweight or obese BMIs in early, middle, and later adulthood still had an increased risk for CRC and noncolorectal GI cancer (hazard ratios, 1.44, 1.45, and 1.43, respectively).

The finding that regular weekly aspirin use did not modify GI cancer risk suggests that obesity may alter the cancer-preventive effect of aspirin, the researchers suggested. Individuals with obesity may need to increase aspirin frequency or dosage to see an effect, but upping the dose comes with its own risks, including GI bleeding.

Overall, until now, most epidemiologic studies have examined BMI at one time point, “missing the opportunity to delineate the contribution of adiposity throughout the life course,” Dr. Shi and Dr. Cao wrote.

“As we continue to investigate precision-based interventions to intercept the link between obesity and cancer, it is imperative to reiterate the importance of maintaining a healthy weight and lifestyle from an early age and incorporate it widely into cancer prevention strategies at all levels with immediate implementation,” the editorialists concluded.

This study was supported in part by funds from Ohio State University and the NIH. The study authors reported no relevant financial relationships. Dr. Cao has received personal fees from Geneoscopy for consulting.

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

Stroke is a “disease of disparities,” with racial and ethnic inequities in incidence, prevalence, treatment, and outcomes, and research is needed to identify structural or “upstream” interventions to address the problem, the American Heart Association says in a new scientific statement.

“There are enormous inequities in stroke care, which lead to significant gaps in functional outcomes after stroke for people from historically disenfranchised racial and ethnic groups, including Black, Hispanic, and Indigenous peoples,” writing group chair Amytis Towfighi, MD, professor of neurology, University of Southern California, Los Angeles, says in a news release.

“While research has historically focused on describing these inequities, it is critical to develop and test interventions to address them,” Dr. Towfighi adds.

The scientific statement was published online in the journal Stroke.

It follows a 2020 AHA presidential advisory that declared structural racism a fundamental driver of poor health and early death from heart disease and stroke.

Dr. Towfighi and colleagues reviewed the literature on interventions to address racial and ethnic inequities to identify gaps and areas for future research.

They note that various interventions have shown promise in reducing inequities across the stroke continuum of care.

For example, data suggest that careful attention to stroke preparedness among patients, caregivers, and emergency medical services can reduce inequities in getting people suspected of having a stroke to the emergency department quickly, with delivery of prompt treatment.

However, insufficient research attention has been paid to reducing inequities in rehabilitation, recovery, and social reintegration, the writing group says.

In addition, most studies have addressed patient-level factors, such as medication adherence, health literacy, and health behaviors, but not upstream social factors such as structural racism, housing, income, food security, and access to care, which also affect stroke incidence, care, and outcomes.

“Combating the effects of systemic racism will involve upstream interventions, including policy changes, place-based interventions, and engaging with the health care systems that serve predominantly historically disenfranchised populations and the communities they serve, understanding the barriers, and collaboratively developing solutions to address barriers,” the writing group says.

Further research is needed across the stroke continuum of care to tackle racial and ethnic inequities in stroke care and improve outcomes, they say.

“It’s critical for historically disenfranchised communities to participate in research so that researchers may collaborate in addressing the communities’ needs and concerns,” Bernadette Boden-Albala, DrPH, MPH, vice chair of the writing group, says in the news release.

“Opportunities include working with community stakeholder groups and community organizations to advocate for partnerships with hospitals, academic medical centers, local colleges and universities; or joining community advisory boards and volunteering with the American Heart Association,” Dr. Boden-Albala adds.

Dr. Towfighi encourages health care professionals to “think outside the ‘stroke box.’ Sustainable, effective interventions to address inequities will likely require collaboration with patients, their communities, policymakers, and other sectors.”

The scientific statement was prepared by the volunteer writing group on behalf of the AHA Stroke Council, the Council on Cardiovascular and Stroke Nursing, the Council on Cardiovascular Radiology and Intervention, the Council on Clinical Cardiology, the Council on Hypertension, the Council on the Kidney in Cardiovascular Disease, and the Council on Peripheral Vascular Disease.

The research had no commercial funding.
 

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

Stroke is a “disease of disparities,” with racial and ethnic inequities in incidence, prevalence, treatment, and outcomes, and research is needed to identify structural or “upstream” interventions to address the problem, the American Heart Association says in a new scientific statement.

“There are enormous inequities in stroke care, which lead to significant gaps in functional outcomes after stroke for people from historically disenfranchised racial and ethnic groups, including Black, Hispanic, and Indigenous peoples,” writing group chair Amytis Towfighi, MD, professor of neurology, University of Southern California, Los Angeles, says in a news release.

“While research has historically focused on describing these inequities, it is critical to develop and test interventions to address them,” Dr. Towfighi adds.

The scientific statement was published online in the journal Stroke.

It follows a 2020 AHA presidential advisory that declared structural racism a fundamental driver of poor health and early death from heart disease and stroke.

Dr. Towfighi and colleagues reviewed the literature on interventions to address racial and ethnic inequities to identify gaps and areas for future research.

They note that various interventions have shown promise in reducing inequities across the stroke continuum of care.

For example, data suggest that careful attention to stroke preparedness among patients, caregivers, and emergency medical services can reduce inequities in getting people suspected of having a stroke to the emergency department quickly, with delivery of prompt treatment.

However, insufficient research attention has been paid to reducing inequities in rehabilitation, recovery, and social reintegration, the writing group says.

In addition, most studies have addressed patient-level factors, such as medication adherence, health literacy, and health behaviors, but not upstream social factors such as structural racism, housing, income, food security, and access to care, which also affect stroke incidence, care, and outcomes.

“Combating the effects of systemic racism will involve upstream interventions, including policy changes, place-based interventions, and engaging with the health care systems that serve predominantly historically disenfranchised populations and the communities they serve, understanding the barriers, and collaboratively developing solutions to address barriers,” the writing group says.

Further research is needed across the stroke continuum of care to tackle racial and ethnic inequities in stroke care and improve outcomes, they say.

“It’s critical for historically disenfranchised communities to participate in research so that researchers may collaborate in addressing the communities’ needs and concerns,” Bernadette Boden-Albala, DrPH, MPH, vice chair of the writing group, says in the news release.

“Opportunities include working with community stakeholder groups and community organizations to advocate for partnerships with hospitals, academic medical centers, local colleges and universities; or joining community advisory boards and volunteering with the American Heart Association,” Dr. Boden-Albala adds.

Dr. Towfighi encourages health care professionals to “think outside the ‘stroke box.’ Sustainable, effective interventions to address inequities will likely require collaboration with patients, their communities, policymakers, and other sectors.”

The scientific statement was prepared by the volunteer writing group on behalf of the AHA Stroke Council, the Council on Cardiovascular and Stroke Nursing, the Council on Cardiovascular Radiology and Intervention, the Council on Clinical Cardiology, the Council on Hypertension, the Council on the Kidney in Cardiovascular Disease, and the Council on Peripheral Vascular Disease.

The research had no commercial funding.
 

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

Stroke is a “disease of disparities,” with racial and ethnic inequities in incidence, prevalence, treatment, and outcomes, and research is needed to identify structural or “upstream” interventions to address the problem, the American Heart Association says in a new scientific statement.

“There are enormous inequities in stroke care, which lead to significant gaps in functional outcomes after stroke for people from historically disenfranchised racial and ethnic groups, including Black, Hispanic, and Indigenous peoples,” writing group chair Amytis Towfighi, MD, professor of neurology, University of Southern California, Los Angeles, says in a news release.

“While research has historically focused on describing these inequities, it is critical to develop and test interventions to address them,” Dr. Towfighi adds.

The scientific statement was published online in the journal Stroke.

It follows a 2020 AHA presidential advisory that declared structural racism a fundamental driver of poor health and early death from heart disease and stroke.

Dr. Towfighi and colleagues reviewed the literature on interventions to address racial and ethnic inequities to identify gaps and areas for future research.

They note that various interventions have shown promise in reducing inequities across the stroke continuum of care.

For example, data suggest that careful attention to stroke preparedness among patients, caregivers, and emergency medical services can reduce inequities in getting people suspected of having a stroke to the emergency department quickly, with delivery of prompt treatment.

However, insufficient research attention has been paid to reducing inequities in rehabilitation, recovery, and social reintegration, the writing group says.

In addition, most studies have addressed patient-level factors, such as medication adherence, health literacy, and health behaviors, but not upstream social factors such as structural racism, housing, income, food security, and access to care, which also affect stroke incidence, care, and outcomes.

“Combating the effects of systemic racism will involve upstream interventions, including policy changes, place-based interventions, and engaging with the health care systems that serve predominantly historically disenfranchised populations and the communities they serve, understanding the barriers, and collaboratively developing solutions to address barriers,” the writing group says.

Further research is needed across the stroke continuum of care to tackle racial and ethnic inequities in stroke care and improve outcomes, they say.

“It’s critical for historically disenfranchised communities to participate in research so that researchers may collaborate in addressing the communities’ needs and concerns,” Bernadette Boden-Albala, DrPH, MPH, vice chair of the writing group, says in the news release.

“Opportunities include working with community stakeholder groups and community organizations to advocate for partnerships with hospitals, academic medical centers, local colleges and universities; or joining community advisory boards and volunteering with the American Heart Association,” Dr. Boden-Albala adds.

Dr. Towfighi encourages health care professionals to “think outside the ‘stroke box.’ Sustainable, effective interventions to address inequities will likely require collaboration with patients, their communities, policymakers, and other sectors.”

The scientific statement was prepared by the volunteer writing group on behalf of the AHA Stroke Council, the Council on Cardiovascular and Stroke Nursing, the Council on Cardiovascular Radiology and Intervention, the Council on Clinical Cardiology, the Council on Hypertension, the Council on the Kidney in Cardiovascular Disease, and the Council on Peripheral Vascular Disease.

The research had no commercial funding.
 

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

The history and findings in this case are suggestive of chronic kidney disease (CKD).

CKD affects between 8% and 16% of the population worldwide. Risk factors for CKD are numerous and include T2D, hypertension, and prediabetes. Diabetes is the leading cause of CKD. Up to 40% of patients with diabetes develop diabetic kidney disease, which can progress to end-stage renal disease (ESRD) requiring dialysis or kidney transplantation. In fact, diabetic kidney disease is the top cause of ESRD in the United States.

Diagnostic criteria for CKD include elevated urinary albumin excretion (albuminuria) and/or eGFR < 60 mL/1.73 m² that persists for more than 3 months. The normal presentation of diabetic kidney disease includes long-standing diabetes, retinopathy, albuminuria without gross hematuria, and gradually progressive decline of eGFR. However, signs of diabetic kidney disease may be present in patients at diagnosis or without retinopathy in T2D. Reduced eGFR without albuminuria has been frequently reported in both type 1 diabetes (T1D) and T2D and is becoming increasingly common as the prevalence of diabetes rises in the United States.

Chronic kidney disease is usually identified through routine screening with serum chemistry profile and urine studies or as an incidental finding. Less often, patients may present with symptoms, such as gross hematuria, "foamy urine" (a sign of albuminuria), nocturia, flank pain, or decreased urine output. In advanced cases, patients may report fatigue, poor appetite, nausea, vomiting, a metallic taste, unintentional weight loss, pruritus, changes in mental status, dyspnea, and/or peripheral edema.

The American Diabetes Association (ADA) 2023 Standards of Care in Diabetes describes five stages of CKD. Stages 1-2 are defined by evidence of high albuminuria with eGFR ≥ 60 mL/min/1.73 m², while stages 3-5 are defined by progressively lower ranges of eGFR. Of note, at any eGFR, the degree of albuminuria is associated with risk for cardiovascular disease, CKD progression, and mortality. Thus, as noted by the ADA Standards, both eGFR and albuminuria should be used to guide treatment decisions; additionally, eGFR levels are essential for modifying drug dosages or restrictions of use, and the degree of albuminuria should influence selection of antihypertensive agents and glucose-lowering medications.

According to the ADA 2023 Standards of Care in Diabetes, for people with non–dialysis-dependent CKD, dietary protein intake should be ∼0.8 g/kg body weight per day (the recommended daily allowance), as this level has been shown to slow GFR decline compared with higher levels of dietary protein intake, with evidence of a greater effect over time. Conversely, higher levels of dietary protein intake (> 20% of daily calories from protein or > 1.3 g/kg/d) have been associated with increased albuminuria, more rapid kidney function loss, and cardiovascular disease mortality. For patients on dialysis, higher levels of dietary protein intake should be considered, because malnutrition is a significant problem in some of these patients.

Urinary excretion of sodium and potassium may be impaired in patients with reduced eGFR. Thus, restriction of dietary sodium to < 2300 mg/d may help to control blood pressure and reduce cardiovascular risk, and restriction of dietary potassium may be necessary to control serum potassium concentration. 

Intensive glycemic control with the goal of achieving near-normoglycemia has been shown to delay the onset and progression of albuminuria and reduced eGFR in patients with diabetes. Insulin alone was used to lower blood glucose in the Diabetes Control and Complications Trial (DCCT)/Epidemiology of Diabetes Interventions and Complications (EDIC) study of T1D while a variety of agents were used in clinical trials of T2D, supporting the conclusion that glycemic control itself helps prevent CKD and its progression. However, the presence of CKD affects the risks and benefits of intensive glycemic control and several glucose-lowering medications. In the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial of T2D, increased adverse effects of intensive glycemic control (hypoglycemia and mortality) were seen among patients with kidney disease at baseline. Moreover, it may take at least 2 years to see improved eGFR outcomes as an effect of intensive glycemic control. Therefore, in some patients with prevalent CKD and substantial comorbidity, target A1c levels may be less intensive.

According to guidance from the US Food and Drug Administration, eGFR should be monitored while taking metformin and metformin is contraindicated in patients with an eGFR < 30 mL/min/1.73 m². Clinicians should assess the benefits and risks of continuing treatment when eGFR falls to < 45 mL/min/1.73 m². 

The ADA recommends that sodium–glucose cotransporter 2 inhibitors be given to all patients with stage 3 CKD or higher and T2D, regardless of glycemic control, as they have been shown to delay CKD progression and reduce heart failure risk independent of glycemic control. Glucagon-like peptide 1 receptor agonists (GLP-1 RAs) also have direct effects on the kidney and have been reported to improve renal outcomes compared with placebo. In patients for whom cardiovascular risk is a predominant problem, the ADA suggests using GLP-1 RAs for cardiovascular risk reduction.

Comprehensive guidance on the management of CKD in patients with T2D is available in the ADA 2023 Standards of Care in Diabetes.

Romesh K. Khardori, MD, PhD, Professor, Department of Internal Medicine, Division of Diabetes, Endocrine, and Metabolic Disorders, Eastern Virginia Medical School; EVMS Medical Group, Norfolk, Virginia

Romesh K. Khardori, MD, PhD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

The history and findings in this case are suggestive of chronic kidney disease (CKD).

CKD affects between 8% and 16% of the population worldwide. Risk factors for CKD are numerous and include T2D, hypertension, and prediabetes. Diabetes is the leading cause of CKD. Up to 40% of patients with diabetes develop diabetic kidney disease, which can progress to end-stage renal disease (ESRD) requiring dialysis or kidney transplantation. In fact, diabetic kidney disease is the top cause of ESRD in the United States.

Diagnostic criteria for CKD include elevated urinary albumin excretion (albuminuria) and/or eGFR < 60 mL/1.73 m² that persists for more than 3 months. The normal presentation of diabetic kidney disease includes long-standing diabetes, retinopathy, albuminuria without gross hematuria, and gradually progressive decline of eGFR. However, signs of diabetic kidney disease may be present in patients at diagnosis or without retinopathy in T2D. Reduced eGFR without albuminuria has been frequently reported in both type 1 diabetes (T1D) and T2D and is becoming increasingly common as the prevalence of diabetes rises in the United States.

Chronic kidney disease is usually identified through routine screening with serum chemistry profile and urine studies or as an incidental finding. Less often, patients may present with symptoms, such as gross hematuria, "foamy urine" (a sign of albuminuria), nocturia, flank pain, or decreased urine output. In advanced cases, patients may report fatigue, poor appetite, nausea, vomiting, a metallic taste, unintentional weight loss, pruritus, changes in mental status, dyspnea, and/or peripheral edema.

The American Diabetes Association (ADA) 2023 Standards of Care in Diabetes describes five stages of CKD. Stages 1-2 are defined by evidence of high albuminuria with eGFR ≥ 60 mL/min/1.73 m², while stages 3-5 are defined by progressively lower ranges of eGFR. Of note, at any eGFR, the degree of albuminuria is associated with risk for cardiovascular disease, CKD progression, and mortality. Thus, as noted by the ADA Standards, both eGFR and albuminuria should be used to guide treatment decisions; additionally, eGFR levels are essential for modifying drug dosages or restrictions of use, and the degree of albuminuria should influence selection of antihypertensive agents and glucose-lowering medications.

According to the ADA 2023 Standards of Care in Diabetes, for people with non–dialysis-dependent CKD, dietary protein intake should be ∼0.8 g/kg body weight per day (the recommended daily allowance), as this level has been shown to slow GFR decline compared with higher levels of dietary protein intake, with evidence of a greater effect over time. Conversely, higher levels of dietary protein intake (> 20% of daily calories from protein or > 1.3 g/kg/d) have been associated with increased albuminuria, more rapid kidney function loss, and cardiovascular disease mortality. For patients on dialysis, higher levels of dietary protein intake should be considered, because malnutrition is a significant problem in some of these patients.

Urinary excretion of sodium and potassium may be impaired in patients with reduced eGFR. Thus, restriction of dietary sodium to < 2300 mg/d may help to control blood pressure and reduce cardiovascular risk, and restriction of dietary potassium may be necessary to control serum potassium concentration. 

Intensive glycemic control with the goal of achieving near-normoglycemia has been shown to delay the onset and progression of albuminuria and reduced eGFR in patients with diabetes. Insulin alone was used to lower blood glucose in the Diabetes Control and Complications Trial (DCCT)/Epidemiology of Diabetes Interventions and Complications (EDIC) study of T1D while a variety of agents were used in clinical trials of T2D, supporting the conclusion that glycemic control itself helps prevent CKD and its progression. However, the presence of CKD affects the risks and benefits of intensive glycemic control and several glucose-lowering medications. In the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial of T2D, increased adverse effects of intensive glycemic control (hypoglycemia and mortality) were seen among patients with kidney disease at baseline. Moreover, it may take at least 2 years to see improved eGFR outcomes as an effect of intensive glycemic control. Therefore, in some patients with prevalent CKD and substantial comorbidity, target A1c levels may be less intensive.

According to guidance from the US Food and Drug Administration, eGFR should be monitored while taking metformin and metformin is contraindicated in patients with an eGFR < 30 mL/min/1.73 m². Clinicians should assess the benefits and risks of continuing treatment when eGFR falls to < 45 mL/min/1.73 m². 

The ADA recommends that sodium–glucose cotransporter 2 inhibitors be given to all patients with stage 3 CKD or higher and T2D, regardless of glycemic control, as they have been shown to delay CKD progression and reduce heart failure risk independent of glycemic control. Glucagon-like peptide 1 receptor agonists (GLP-1 RAs) also have direct effects on the kidney and have been reported to improve renal outcomes compared with placebo. In patients for whom cardiovascular risk is a predominant problem, the ADA suggests using GLP-1 RAs for cardiovascular risk reduction.

Comprehensive guidance on the management of CKD in patients with T2D is available in the ADA 2023 Standards of Care in Diabetes.

Romesh K. Khardori, MD, PhD, Professor, Department of Internal Medicine, Division of Diabetes, Endocrine, and Metabolic Disorders, Eastern Virginia Medical School; EVMS Medical Group, Norfolk, Virginia

Romesh K. Khardori, MD, PhD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

The history and findings in this case are suggestive of chronic kidney disease (CKD).

CKD affects between 8% and 16% of the population worldwide. Risk factors for CKD are numerous and include T2D, hypertension, and prediabetes. Diabetes is the leading cause of CKD. Up to 40% of patients with diabetes develop diabetic kidney disease, which can progress to end-stage renal disease (ESRD) requiring dialysis or kidney transplantation. In fact, diabetic kidney disease is the top cause of ESRD in the United States.

Diagnostic criteria for CKD include elevated urinary albumin excretion (albuminuria) and/or eGFR < 60 mL/1.73 m² that persists for more than 3 months. The normal presentation of diabetic kidney disease includes long-standing diabetes, retinopathy, albuminuria without gross hematuria, and gradually progressive decline of eGFR. However, signs of diabetic kidney disease may be present in patients at diagnosis or without retinopathy in T2D. Reduced eGFR without albuminuria has been frequently reported in both type 1 diabetes (T1D) and T2D and is becoming increasingly common as the prevalence of diabetes rises in the United States.

Chronic kidney disease is usually identified through routine screening with serum chemistry profile and urine studies or as an incidental finding. Less often, patients may present with symptoms, such as gross hematuria, "foamy urine" (a sign of albuminuria), nocturia, flank pain, or decreased urine output. In advanced cases, patients may report fatigue, poor appetite, nausea, vomiting, a metallic taste, unintentional weight loss, pruritus, changes in mental status, dyspnea, and/or peripheral edema.

The American Diabetes Association (ADA) 2023 Standards of Care in Diabetes describes five stages of CKD. Stages 1-2 are defined by evidence of high albuminuria with eGFR ≥ 60 mL/min/1.73 m², while stages 3-5 are defined by progressively lower ranges of eGFR. Of note, at any eGFR, the degree of albuminuria is associated with risk for cardiovascular disease, CKD progression, and mortality. Thus, as noted by the ADA Standards, both eGFR and albuminuria should be used to guide treatment decisions; additionally, eGFR levels are essential for modifying drug dosages or restrictions of use, and the degree of albuminuria should influence selection of antihypertensive agents and glucose-lowering medications.

According to the ADA 2023 Standards of Care in Diabetes, for people with non–dialysis-dependent CKD, dietary protein intake should be ∼0.8 g/kg body weight per day (the recommended daily allowance), as this level has been shown to slow GFR decline compared with higher levels of dietary protein intake, with evidence of a greater effect over time. Conversely, higher levels of dietary protein intake (> 20% of daily calories from protein or > 1.3 g/kg/d) have been associated with increased albuminuria, more rapid kidney function loss, and cardiovascular disease mortality. For patients on dialysis, higher levels of dietary protein intake should be considered, because malnutrition is a significant problem in some of these patients.

Urinary excretion of sodium and potassium may be impaired in patients with reduced eGFR. Thus, restriction of dietary sodium to < 2300 mg/d may help to control blood pressure and reduce cardiovascular risk, and restriction of dietary potassium may be necessary to control serum potassium concentration. 

Intensive glycemic control with the goal of achieving near-normoglycemia has been shown to delay the onset and progression of albuminuria and reduced eGFR in patients with diabetes. Insulin alone was used to lower blood glucose in the Diabetes Control and Complications Trial (DCCT)/Epidemiology of Diabetes Interventions and Complications (EDIC) study of T1D while a variety of agents were used in clinical trials of T2D, supporting the conclusion that glycemic control itself helps prevent CKD and its progression. However, the presence of CKD affects the risks and benefits of intensive glycemic control and several glucose-lowering medications. In the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial of T2D, increased adverse effects of intensive glycemic control (hypoglycemia and mortality) were seen among patients with kidney disease at baseline. Moreover, it may take at least 2 years to see improved eGFR outcomes as an effect of intensive glycemic control. Therefore, in some patients with prevalent CKD and substantial comorbidity, target A1c levels may be less intensive.

According to guidance from the US Food and Drug Administration, eGFR should be monitored while taking metformin and metformin is contraindicated in patients with an eGFR < 30 mL/min/1.73 m². Clinicians should assess the benefits and risks of continuing treatment when eGFR falls to < 45 mL/min/1.73 m². 

The ADA recommends that sodium–glucose cotransporter 2 inhibitors be given to all patients with stage 3 CKD or higher and T2D, regardless of glycemic control, as they have been shown to delay CKD progression and reduce heart failure risk independent of glycemic control. Glucagon-like peptide 1 receptor agonists (GLP-1 RAs) also have direct effects on the kidney and have been reported to improve renal outcomes compared with placebo. In patients for whom cardiovascular risk is a predominant problem, the ADA suggests using GLP-1 RAs for cardiovascular risk reduction.

Comprehensive guidance on the management of CKD in patients with T2D is available in the ADA 2023 Standards of Care in Diabetes.

Romesh K. Khardori, MD, PhD, Professor, Department of Internal Medicine, Division of Diabetes, Endocrine, and Metabolic Disorders, Eastern Virginia Medical School; EVMS Medical Group, Norfolk, Virginia

Romesh K. Khardori, MD, PhD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.