Clinical Psychiatry News

AMSTERDAM — There is a mountain of evidence that atopic dermatitis (AD) exerts a large negative impact on quality of life, but a unique study with data from more than 30,000 individuals showed that adults whose AD started in childhood carry a far greater psychological and social burden throughout their life relative to AD starting after childhood.

These data, drawn from the ambitious Scars of Life (SOL) project, “suggest that childhood AD persisting into adulthood is its own phenotype,” reported Jonathan I. Silverberg, MD, PhD, director of clinical research, Department of Dermatology, George Washington University, Washington, DC.

Dr. Silverberg

One reasonable message from these data is that the failure to achieve adequate control of AD in children, whether by a late start of systemic agents or other reasons, results in a greater lifetime burden of disease when the burden beyond physical symptoms is measured, according to Dr. Silverberg.
 

More Than 30,000 From Five Continents Participated

In the SOL project, which was designed to analyze how the age of AD onset affects the severity of symptoms and quality of life, completed questionnaires were collected from 30,801 individuals in 27 countries on five continents. The questions, which elicited data to measure the burden of AD, were developed in association with several professional and patient associations with an interest in AD, including the National Eczema Association.

The SOL project has produced an enormous amount of data in four distinct groups, but Dr. Silverberg, speaking in a late-breaking news session at the annual congress of the European Academy of Dermatology and Venereology, focused on a comparison between the 2875 participants who had AD in childhood that has persisted into adulthood and the 7383 adults with adult-onset AD. Data from the other two subsets in SOL — AD in childhood but not in adulthood and no AD in either phase of life — are expected to fuel an extended series of publications.

In the two groups, baseline characteristics were similar with about 60% reporting moderate to severe symptoms and a median age of about 37 years. The proportion of women was 61% in both groups.

Using the PUSH-D questionnaire, which Dr. Silverberg described as a validated tool for gauging a sense of stigmatization, the greater burden of AD was remarkably consistent for those with childhood-onset AD vs adult-onset AD. With higher scores representing a greater sense of stigmatization, the differences in the overall score (23.0 vs 18.1; P < .0001) were highly significant as was every other domain evaluated.

For all five social behavior domains, such as avoiding contact in public and wariness of approaching people spontaneously, having AD onset in childhood persisting into adulthood produced significantly higher scores than having AD onset in adulthood, with no exceptions (P < .001 for all).
 

AD From Childhood Consistently Results in Worse Outcomes

Providing examples for some of the other 12 domains, Dr. Silverberg maintained that feelings of shame and psychological discomfort were always greater in adults with AD persistent since childhood vs AD starting in adulthood. The P values for these outcomes, such as experiencing bias at work or reporting a sense that others avoided them, were typically highly significant (P < .001).

Compared with those whose AD started in adulthood, “adults with atopic eczema that started during childhood have significantly more difficulties in their life, including occupational relationships, daily life, personal life, and partner or family relationships,” Dr. Silverberg reported.

He said that the data were controlled for multiple confounders, particularly greater severity of AD. He acknowledged that childhood onset might be considered a surrogate for more severe disease, but the data were controlled for this possibility.

Despite the fact that there are “thousands of studies across all age groups showing the burden of AD,” Dr. Silverberg considers these data to be unique by emphasizing the burden of chronicity rather than the impact of AD in any single moment in time.

For those with chronic AD from childhood, “the effect is not just on physical health but a deep negative influence on psychological and social aspects of life,” Dr. Silverberg said, suggesting that the independent effects of chronicity might be worth studying across other dermatologic diseases.

“Regulatory agencies focus on what you can do in that moment of time, losing the bigger picture of how patients are affected chronically,” he said, adding that this is an area of clinical research that should be further explored.

What the data further suggest “is that the earlier we intervene, the more likely patients will do better long term,” he said.
 

Data Provide Evidence of Systemic Therapy in Kids

For Gudrun Ratzinger, MD, of the Department of Dermatology and Venerology at the Medical University of Innsbruck in Austria, these are valuable data.

“When I prescribe systemic therapies to children, I often get resistance from the healthcare system and even other colleagues,” said Dr. Ratzinger, who was asked to comment on the results. “We are at a teaching hospital, but I often find that when patients return to their home physician, the systemic therapies are stopped.”

In her own practice, she believes the most effective therapies should be introduced in children and adults when complete control is not achieved on first-line drugs. “These data are very helpful for me in explaining to others the importance of effective treatment of atopic dermatitis in children,” she said.

Dr. Silverberg reported financial relationships with more than 40 pharmaceutical companies, including those that make drugs for AD. Dr. Ratzinger reported financial relationships with AbbVie, Almirall, Boehringer Ingelheim, Eli Lilly, Janssen, Leo Pharma, Novartis, Pelpharma, Pfizer, and UCB.

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

AMSTERDAM — There is a mountain of evidence that atopic dermatitis (AD) exerts a large negative impact on quality of life, but a unique study with data from more than 30,000 individuals showed that adults whose AD started in childhood carry a far greater psychological and social burden throughout their life relative to AD starting after childhood.

These data, drawn from the ambitious Scars of Life (SOL) project, “suggest that childhood AD persisting into adulthood is its own phenotype,” reported Jonathan I. Silverberg, MD, PhD, director of clinical research, Department of Dermatology, George Washington University, Washington, DC.

Dr. Silverberg

One reasonable message from these data is that the failure to achieve adequate control of AD in children, whether by a late start of systemic agents or other reasons, results in a greater lifetime burden of disease when the burden beyond physical symptoms is measured, according to Dr. Silverberg.
 

More Than 30,000 From Five Continents Participated

In the SOL project, which was designed to analyze how the age of AD onset affects the severity of symptoms and quality of life, completed questionnaires were collected from 30,801 individuals in 27 countries on five continents. The questions, which elicited data to measure the burden of AD, were developed in association with several professional and patient associations with an interest in AD, including the National Eczema Association.

The SOL project has produced an enormous amount of data in four distinct groups, but Dr. Silverberg, speaking in a late-breaking news session at the annual congress of the European Academy of Dermatology and Venereology, focused on a comparison between the 2875 participants who had AD in childhood that has persisted into adulthood and the 7383 adults with adult-onset AD. Data from the other two subsets in SOL — AD in childhood but not in adulthood and no AD in either phase of life — are expected to fuel an extended series of publications.

In the two groups, baseline characteristics were similar with about 60% reporting moderate to severe symptoms and a median age of about 37 years. The proportion of women was 61% in both groups.

Using the PUSH-D questionnaire, which Dr. Silverberg described as a validated tool for gauging a sense of stigmatization, the greater burden of AD was remarkably consistent for those with childhood-onset AD vs adult-onset AD. With higher scores representing a greater sense of stigmatization, the differences in the overall score (23.0 vs 18.1; P < .0001) were highly significant as was every other domain evaluated.

For all five social behavior domains, such as avoiding contact in public and wariness of approaching people spontaneously, having AD onset in childhood persisting into adulthood produced significantly higher scores than having AD onset in adulthood, with no exceptions (P < .001 for all).
 

AD From Childhood Consistently Results in Worse Outcomes

Providing examples for some of the other 12 domains, Dr. Silverberg maintained that feelings of shame and psychological discomfort were always greater in adults with AD persistent since childhood vs AD starting in adulthood. The P values for these outcomes, such as experiencing bias at work or reporting a sense that others avoided them, were typically highly significant (P < .001).

Compared with those whose AD started in adulthood, “adults with atopic eczema that started during childhood have significantly more difficulties in their life, including occupational relationships, daily life, personal life, and partner or family relationships,” Dr. Silverberg reported.

He said that the data were controlled for multiple confounders, particularly greater severity of AD. He acknowledged that childhood onset might be considered a surrogate for more severe disease, but the data were controlled for this possibility.

Despite the fact that there are “thousands of studies across all age groups showing the burden of AD,” Dr. Silverberg considers these data to be unique by emphasizing the burden of chronicity rather than the impact of AD in any single moment in time.

For those with chronic AD from childhood, “the effect is not just on physical health but a deep negative influence on psychological and social aspects of life,” Dr. Silverberg said, suggesting that the independent effects of chronicity might be worth studying across other dermatologic diseases.

“Regulatory agencies focus on what you can do in that moment of time, losing the bigger picture of how patients are affected chronically,” he said, adding that this is an area of clinical research that should be further explored.

What the data further suggest “is that the earlier we intervene, the more likely patients will do better long term,” he said.
 

Data Provide Evidence of Systemic Therapy in Kids

For Gudrun Ratzinger, MD, of the Department of Dermatology and Venerology at the Medical University of Innsbruck in Austria, these are valuable data.

“When I prescribe systemic therapies to children, I often get resistance from the healthcare system and even other colleagues,” said Dr. Ratzinger, who was asked to comment on the results. “We are at a teaching hospital, but I often find that when patients return to their home physician, the systemic therapies are stopped.”

In her own practice, she believes the most effective therapies should be introduced in children and adults when complete control is not achieved on first-line drugs. “These data are very helpful for me in explaining to others the importance of effective treatment of atopic dermatitis in children,” she said.

Dr. Silverberg reported financial relationships with more than 40 pharmaceutical companies, including those that make drugs for AD. Dr. Ratzinger reported financial relationships with AbbVie, Almirall, Boehringer Ingelheim, Eli Lilly, Janssen, Leo Pharma, Novartis, Pelpharma, Pfizer, and UCB.

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

AMSTERDAM — There is a mountain of evidence that atopic dermatitis (AD) exerts a large negative impact on quality of life, but a unique study with data from more than 30,000 individuals showed that adults whose AD started in childhood carry a far greater psychological and social burden throughout their life relative to AD starting after childhood.

These data, drawn from the ambitious Scars of Life (SOL) project, “suggest that childhood AD persisting into adulthood is its own phenotype,” reported Jonathan I. Silverberg, MD, PhD, director of clinical research, Department of Dermatology, George Washington University, Washington, DC.

Dr. Silverberg

One reasonable message from these data is that the failure to achieve adequate control of AD in children, whether by a late start of systemic agents or other reasons, results in a greater lifetime burden of disease when the burden beyond physical symptoms is measured, according to Dr. Silverberg.
 

More Than 30,000 From Five Continents Participated

In the SOL project, which was designed to analyze how the age of AD onset affects the severity of symptoms and quality of life, completed questionnaires were collected from 30,801 individuals in 27 countries on five continents. The questions, which elicited data to measure the burden of AD, were developed in association with several professional and patient associations with an interest in AD, including the National Eczema Association.

The SOL project has produced an enormous amount of data in four distinct groups, but Dr. Silverberg, speaking in a late-breaking news session at the annual congress of the European Academy of Dermatology and Venereology, focused on a comparison between the 2875 participants who had AD in childhood that has persisted into adulthood and the 7383 adults with adult-onset AD. Data from the other two subsets in SOL — AD in childhood but not in adulthood and no AD in either phase of life — are expected to fuel an extended series of publications.

In the two groups, baseline characteristics were similar with about 60% reporting moderate to severe symptoms and a median age of about 37 years. The proportion of women was 61% in both groups.

Using the PUSH-D questionnaire, which Dr. Silverberg described as a validated tool for gauging a sense of stigmatization, the greater burden of AD was remarkably consistent for those with childhood-onset AD vs adult-onset AD. With higher scores representing a greater sense of stigmatization, the differences in the overall score (23.0 vs 18.1; P < .0001) were highly significant as was every other domain evaluated.

For all five social behavior domains, such as avoiding contact in public and wariness of approaching people spontaneously, having AD onset in childhood persisting into adulthood produced significantly higher scores than having AD onset in adulthood, with no exceptions (P < .001 for all).
 

AD From Childhood Consistently Results in Worse Outcomes

Providing examples for some of the other 12 domains, Dr. Silverberg maintained that feelings of shame and psychological discomfort were always greater in adults with AD persistent since childhood vs AD starting in adulthood. The P values for these outcomes, such as experiencing bias at work or reporting a sense that others avoided them, were typically highly significant (P < .001).

Compared with those whose AD started in adulthood, “adults with atopic eczema that started during childhood have significantly more difficulties in their life, including occupational relationships, daily life, personal life, and partner or family relationships,” Dr. Silverberg reported.

He said that the data were controlled for multiple confounders, particularly greater severity of AD. He acknowledged that childhood onset might be considered a surrogate for more severe disease, but the data were controlled for this possibility.

Despite the fact that there are “thousands of studies across all age groups showing the burden of AD,” Dr. Silverberg considers these data to be unique by emphasizing the burden of chronicity rather than the impact of AD in any single moment in time.

For those with chronic AD from childhood, “the effect is not just on physical health but a deep negative influence on psychological and social aspects of life,” Dr. Silverberg said, suggesting that the independent effects of chronicity might be worth studying across other dermatologic diseases.

“Regulatory agencies focus on what you can do in that moment of time, losing the bigger picture of how patients are affected chronically,” he said, adding that this is an area of clinical research that should be further explored.

What the data further suggest “is that the earlier we intervene, the more likely patients will do better long term,” he said.
 

Data Provide Evidence of Systemic Therapy in Kids

For Gudrun Ratzinger, MD, of the Department of Dermatology and Venerology at the Medical University of Innsbruck in Austria, these are valuable data.

“When I prescribe systemic therapies to children, I often get resistance from the healthcare system and even other colleagues,” said Dr. Ratzinger, who was asked to comment on the results. “We are at a teaching hospital, but I often find that when patients return to their home physician, the systemic therapies are stopped.”

In her own practice, she believes the most effective therapies should be introduced in children and adults when complete control is not achieved on first-line drugs. “These data are very helpful for me in explaining to others the importance of effective treatment of atopic dermatitis in children,” she said.

Dr. Silverberg reported financial relationships with more than 40 pharmaceutical companies, including those that make drugs for AD. Dr. Ratzinger reported financial relationships with AbbVie, Almirall, Boehringer Ingelheim, Eli Lilly, Janssen, Leo Pharma, Novartis, Pelpharma, Pfizer, and UCB.

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

MILAN — Recent research allaying concerns about suicidality linked to glucagon-like peptide 1 (GLP-1) receptor agonists, along with evidence of these agents’ potential psychiatric and cognitive benefits, has prompted the lead investigator of a major analysis to urge researchers to explore the potential of these drugs for mental illness.

“So far, we’ve been talking about the safety from a neuropsychiatric perspective in diabetes, but there is also the safety and benefit in people with mental disorders,” Riccardo De Giorgi, MD, PhD, from the Department of Psychiatry, University of Oxford in England, said in an interview.

The results of the meta-analysis were previously reported by this news organization and reviewed by Dr. De Giorgi at the 37th European College of Neuropsychopharmacology (ECNP) Congress. Dr. De Giorgi broached whether GLP-1 inhibitors such as semaglutide might also offer the same benefits in patients without diabetes as they do in those with diabetes, in terms of cognitive deficits and substance use or mood disorders.

Noting that GLP-1s are not approved for psychiatric disorders, Dr. De Giorgi said it can’t be assumed that the “metabolic or maybe even more general mechanisms that are being modified with these medications in diabetes or even in obesity are the same for people with psychiatric disorders. We’re talking about very different things. From a clinical perspective, you could do real harm,” he told this news organization.

Yet Dr. De Giorgi emphasized the importance of exploring the potential benefits of these medications in psychiatry.

“From a research perspective ... I am very worried about missing an opportunity here. This happened with rimonabant, a cannabis medication that was used for weight loss back in 2012 and was withdrawn quite dramatically in Europe immediately after licensing because it increased suicide risk. Since then, nobody has been touching the cannabinoid system, and that’s a shame because in psychiatry, we don’t have that much we can work on. So we don’t want to miss an opportunity with the GLP-1 system — that’s why we need to be cautious and look at safety first,” he said.
 

Signal of Efficacy?

Dr. De Giorgi’s research suggested several potential neurobiological effects of GLP-1 inhibition in diabetes research.

“There was a bit of a signal specifically for the big three dementias — vascular, Lewy Body, and frontotemporal — although there was not enough power,” he reported. “We also saw a reduced risk in nicotine misuse, especially amongst other substance use disorders ... and finally a more tentative association for reduced depression.”

He noted that GLP-1s for psychiatric illness likely have limitations and may not cure mental disorders but could help specific subsets of patients. Rather than aiming for large-scale studies, the focus should be on small, incremental studies to advance the research.

Asked by the session chair, John Cryan, PhD, from University College Cork in Ireland, and chair of the ECNP Scientific Committee whether improvement in patients’ mood could be attributed to weight loss, Dr. De Giorgi replied no.

“We now have quite a lot of studies that show that if there is an effect or association it is seen quite a bit earlier than any weight loss. Remember, weight loss takes quite a lot of time, and at quite high doses, but more provocatively, even if that’s the case, does it matter? We as psychiatrists do worry that we need to disentangle these things, but they don’t do that in cardiology, for example. If they see a benefit in mortality they don’t really care if it’s specifically an effect on heart failure or ischemic disease,” said Dr. De Giorgi.

Regardless of their neuropsychiatric potential, the cardiometabolic benefits of GLP-1 inhibitors are sorely needed in the psychiatric population, noted two experts in a recent JAMA Psychiatry viewpoint article.

Sri Mahavir Agarwal, MD, PhD, and Margaret Hahn, MD, PhD, from the University of Toronto and the Schizophrenia Division at the Centre for Addiction and Mental Health, in Toronto, Ontario, Canada, pointed out that “individuals with severe mental illness (SMI) have exceedingly high rates of metabolic comorbidity; three of four are overweight or obese, whereas the prevalence of type 2 diabetes (T2D) is several-fold higher than in the general population. Consequently, individuals with SMI die 15-20 years earlier from cardiovascular disease (CVD) than do those in the general population with CVD,” they noted.

“The arrival of semaglutide has infused significant enthusiasm in the field of mental health research. The proximal effects of weight and related CV comorbidities are significant in themselves. It is plausible that semaglutide could act through neurogenesis or secondary benefits of improving metabolic health on other important outcomes, such as cognitive health and quality of life, thereby filling an unmet need in the treatment of SMI,” Dr. Agarwal and Dr. Hahn added.
 

An Exciting Opportunity

Current research investigating GLP-1s in psychiatry and neurology is increasingly focused on neuroinflammation, said Dr. De Giorgi.

Research shows significant evidence that certain medications may help reduce dysfunctional inflammatory processes linked to various cognitive and psychiatric disorders, he added.

Many patients with established psychiatric conditions also have physical health issues, which contribute to increased mortality risk, said Dr. De Giorgi. It’s crucial to understand that, if these treatments improve mortality outcomes for psychiatric patients, the specific mechanisms involved are secondary to the results. Psychiatrists must be equipped to prescribe, manage, and initiate these therapies.

“While trials involving psychosis patients are ongoing, we are making progress and should seize this opportunity” said Dr. De Giorgi.

Dr. Cryan agreed: “I think we’ll get there. What these drugs have shown is that you can, through a single mechanism, have multitude effects related to brain-body interactions, and why not focus that on mood and anxiety and cognitive performance? It’s exciting no matter what. We now need to do longitudinal, cross-sectional, placebo-controlled trials in specific patient populations.”

This study received funding from the National Institute for Health and Care Research Oxford Health Biomedical Research Centre and Medical Research Council. Dr. De Giorgi’s coauthors reported receiving funding for other work from Novo Nordisk, Five Lives, Cognetivity Ltd., Cognex, P1vital, Lundbeck, Servier, UCB, Zogenix, Johnson & Johnson, and Syndesi. Dr. Cryan reported no relevant disclosures.

A version of this article appeared on Medscape.com.

MILAN — Recent research allaying concerns about suicidality linked to glucagon-like peptide 1 (GLP-1) receptor agonists, along with evidence of these agents’ potential psychiatric and cognitive benefits, has prompted the lead investigator of a major analysis to urge researchers to explore the potential of these drugs for mental illness.

“So far, we’ve been talking about the safety from a neuropsychiatric perspective in diabetes, but there is also the safety and benefit in people with mental disorders,” Riccardo De Giorgi, MD, PhD, from the Department of Psychiatry, University of Oxford in England, said in an interview.

The results of the meta-analysis were previously reported by this news organization and reviewed by Dr. De Giorgi at the 37th European College of Neuropsychopharmacology (ECNP) Congress. Dr. De Giorgi broached whether GLP-1 inhibitors such as semaglutide might also offer the same benefits in patients without diabetes as they do in those with diabetes, in terms of cognitive deficits and substance use or mood disorders.

Noting that GLP-1s are not approved for psychiatric disorders, Dr. De Giorgi said it can’t be assumed that the “metabolic or maybe even more general mechanisms that are being modified with these medications in diabetes or even in obesity are the same for people with psychiatric disorders. We’re talking about very different things. From a clinical perspective, you could do real harm,” he told this news organization.

Yet Dr. De Giorgi emphasized the importance of exploring the potential benefits of these medications in psychiatry.

“From a research perspective ... I am very worried about missing an opportunity here. This happened with rimonabant, a cannabis medication that was used for weight loss back in 2012 and was withdrawn quite dramatically in Europe immediately after licensing because it increased suicide risk. Since then, nobody has been touching the cannabinoid system, and that’s a shame because in psychiatry, we don’t have that much we can work on. So we don’t want to miss an opportunity with the GLP-1 system — that’s why we need to be cautious and look at safety first,” he said.
 

Signal of Efficacy?

Dr. De Giorgi’s research suggested several potential neurobiological effects of GLP-1 inhibition in diabetes research.

“There was a bit of a signal specifically for the big three dementias — vascular, Lewy Body, and frontotemporal — although there was not enough power,” he reported. “We also saw a reduced risk in nicotine misuse, especially amongst other substance use disorders ... and finally a more tentative association for reduced depression.”

He noted that GLP-1s for psychiatric illness likely have limitations and may not cure mental disorders but could help specific subsets of patients. Rather than aiming for large-scale studies, the focus should be on small, incremental studies to advance the research.

Asked by the session chair, John Cryan, PhD, from University College Cork in Ireland, and chair of the ECNP Scientific Committee whether improvement in patients’ mood could be attributed to weight loss, Dr. De Giorgi replied no.

“We now have quite a lot of studies that show that if there is an effect or association it is seen quite a bit earlier than any weight loss. Remember, weight loss takes quite a lot of time, and at quite high doses, but more provocatively, even if that’s the case, does it matter? We as psychiatrists do worry that we need to disentangle these things, but they don’t do that in cardiology, for example. If they see a benefit in mortality they don’t really care if it’s specifically an effect on heart failure or ischemic disease,” said Dr. De Giorgi.

Regardless of their neuropsychiatric potential, the cardiometabolic benefits of GLP-1 inhibitors are sorely needed in the psychiatric population, noted two experts in a recent JAMA Psychiatry viewpoint article.

Sri Mahavir Agarwal, MD, PhD, and Margaret Hahn, MD, PhD, from the University of Toronto and the Schizophrenia Division at the Centre for Addiction and Mental Health, in Toronto, Ontario, Canada, pointed out that “individuals with severe mental illness (SMI) have exceedingly high rates of metabolic comorbidity; three of four are overweight or obese, whereas the prevalence of type 2 diabetes (T2D) is several-fold higher than in the general population. Consequently, individuals with SMI die 15-20 years earlier from cardiovascular disease (CVD) than do those in the general population with CVD,” they noted.

“The arrival of semaglutide has infused significant enthusiasm in the field of mental health research. The proximal effects of weight and related CV comorbidities are significant in themselves. It is plausible that semaglutide could act through neurogenesis or secondary benefits of improving metabolic health on other important outcomes, such as cognitive health and quality of life, thereby filling an unmet need in the treatment of SMI,” Dr. Agarwal and Dr. Hahn added.
 

An Exciting Opportunity

Current research investigating GLP-1s in psychiatry and neurology is increasingly focused on neuroinflammation, said Dr. De Giorgi.

Research shows significant evidence that certain medications may help reduce dysfunctional inflammatory processes linked to various cognitive and psychiatric disorders, he added.

Many patients with established psychiatric conditions also have physical health issues, which contribute to increased mortality risk, said Dr. De Giorgi. It’s crucial to understand that, if these treatments improve mortality outcomes for psychiatric patients, the specific mechanisms involved are secondary to the results. Psychiatrists must be equipped to prescribe, manage, and initiate these therapies.

“While trials involving psychosis patients are ongoing, we are making progress and should seize this opportunity” said Dr. De Giorgi.

Dr. Cryan agreed: “I think we’ll get there. What these drugs have shown is that you can, through a single mechanism, have multitude effects related to brain-body interactions, and why not focus that on mood and anxiety and cognitive performance? It’s exciting no matter what. We now need to do longitudinal, cross-sectional, placebo-controlled trials in specific patient populations.”

This study received funding from the National Institute for Health and Care Research Oxford Health Biomedical Research Centre and Medical Research Council. Dr. De Giorgi’s coauthors reported receiving funding for other work from Novo Nordisk, Five Lives, Cognetivity Ltd., Cognex, P1vital, Lundbeck, Servier, UCB, Zogenix, Johnson & Johnson, and Syndesi. Dr. Cryan reported no relevant disclosures.

A version of this article appeared on Medscape.com.

MILAN — Recent research allaying concerns about suicidality linked to glucagon-like peptide 1 (GLP-1) receptor agonists, along with evidence of these agents’ potential psychiatric and cognitive benefits, has prompted the lead investigator of a major analysis to urge researchers to explore the potential of these drugs for mental illness.

“So far, we’ve been talking about the safety from a neuropsychiatric perspective in diabetes, but there is also the safety and benefit in people with mental disorders,” Riccardo De Giorgi, MD, PhD, from the Department of Psychiatry, University of Oxford in England, said in an interview.

The results of the meta-analysis were previously reported by this news organization and reviewed by Dr. De Giorgi at the 37th European College of Neuropsychopharmacology (ECNP) Congress. Dr. De Giorgi broached whether GLP-1 inhibitors such as semaglutide might also offer the same benefits in patients without diabetes as they do in those with diabetes, in terms of cognitive deficits and substance use or mood disorders.

Noting that GLP-1s are not approved for psychiatric disorders, Dr. De Giorgi said it can’t be assumed that the “metabolic or maybe even more general mechanisms that are being modified with these medications in diabetes or even in obesity are the same for people with psychiatric disorders. We’re talking about very different things. From a clinical perspective, you could do real harm,” he told this news organization.

Yet Dr. De Giorgi emphasized the importance of exploring the potential benefits of these medications in psychiatry.

“From a research perspective ... I am very worried about missing an opportunity here. This happened with rimonabant, a cannabis medication that was used for weight loss back in 2012 and was withdrawn quite dramatically in Europe immediately after licensing because it increased suicide risk. Since then, nobody has been touching the cannabinoid system, and that’s a shame because in psychiatry, we don’t have that much we can work on. So we don’t want to miss an opportunity with the GLP-1 system — that’s why we need to be cautious and look at safety first,” he said.
 

Signal of Efficacy?

Dr. De Giorgi’s research suggested several potential neurobiological effects of GLP-1 inhibition in diabetes research.

“There was a bit of a signal specifically for the big three dementias — vascular, Lewy Body, and frontotemporal — although there was not enough power,” he reported. “We also saw a reduced risk in nicotine misuse, especially amongst other substance use disorders ... and finally a more tentative association for reduced depression.”

He noted that GLP-1s for psychiatric illness likely have limitations and may not cure mental disorders but could help specific subsets of patients. Rather than aiming for large-scale studies, the focus should be on small, incremental studies to advance the research.

Asked by the session chair, John Cryan, PhD, from University College Cork in Ireland, and chair of the ECNP Scientific Committee whether improvement in patients’ mood could be attributed to weight loss, Dr. De Giorgi replied no.

“We now have quite a lot of studies that show that if there is an effect or association it is seen quite a bit earlier than any weight loss. Remember, weight loss takes quite a lot of time, and at quite high doses, but more provocatively, even if that’s the case, does it matter? We as psychiatrists do worry that we need to disentangle these things, but they don’t do that in cardiology, for example. If they see a benefit in mortality they don’t really care if it’s specifically an effect on heart failure or ischemic disease,” said Dr. De Giorgi.

Regardless of their neuropsychiatric potential, the cardiometabolic benefits of GLP-1 inhibitors are sorely needed in the psychiatric population, noted two experts in a recent JAMA Psychiatry viewpoint article.

Sri Mahavir Agarwal, MD, PhD, and Margaret Hahn, MD, PhD, from the University of Toronto and the Schizophrenia Division at the Centre for Addiction and Mental Health, in Toronto, Ontario, Canada, pointed out that “individuals with severe mental illness (SMI) have exceedingly high rates of metabolic comorbidity; three of four are overweight or obese, whereas the prevalence of type 2 diabetes (T2D) is several-fold higher than in the general population. Consequently, individuals with SMI die 15-20 years earlier from cardiovascular disease (CVD) than do those in the general population with CVD,” they noted.

“The arrival of semaglutide has infused significant enthusiasm in the field of mental health research. The proximal effects of weight and related CV comorbidities are significant in themselves. It is plausible that semaglutide could act through neurogenesis or secondary benefits of improving metabolic health on other important outcomes, such as cognitive health and quality of life, thereby filling an unmet need in the treatment of SMI,” Dr. Agarwal and Dr. Hahn added.
 

An Exciting Opportunity

Current research investigating GLP-1s in psychiatry and neurology is increasingly focused on neuroinflammation, said Dr. De Giorgi.

Research shows significant evidence that certain medications may help reduce dysfunctional inflammatory processes linked to various cognitive and psychiatric disorders, he added.

Many patients with established psychiatric conditions also have physical health issues, which contribute to increased mortality risk, said Dr. De Giorgi. It’s crucial to understand that, if these treatments improve mortality outcomes for psychiatric patients, the specific mechanisms involved are secondary to the results. Psychiatrists must be equipped to prescribe, manage, and initiate these therapies.

“While trials involving psychosis patients are ongoing, we are making progress and should seize this opportunity” said Dr. De Giorgi.

Dr. Cryan agreed: “I think we’ll get there. What these drugs have shown is that you can, through a single mechanism, have multitude effects related to brain-body interactions, and why not focus that on mood and anxiety and cognitive performance? It’s exciting no matter what. We now need to do longitudinal, cross-sectional, placebo-controlled trials in specific patient populations.”

This study received funding from the National Institute for Health and Care Research Oxford Health Biomedical Research Centre and Medical Research Council. Dr. De Giorgi’s coauthors reported receiving funding for other work from Novo Nordisk, Five Lives, Cognetivity Ltd., Cognex, P1vital, Lundbeck, Servier, UCB, Zogenix, Johnson & Johnson, and Syndesi. Dr. Cryan reported no relevant disclosures.

A version of this article appeared on Medscape.com.

Our dermatology department is composed of 25 doctors spread across 4 offices. It can be difficult to sustain cohesion so we have a few rituals to help hold us together. One is the morning huddle. This is a stand-up meeting lasting 3-5 minutes at 8:42 a.m. (just before the 8:45 a.m. patients). Led by our staff, huddle is a quick review of the priorities, issues, and celebrations across our department. While enthusiastically celebrating a staff member’s promotion one morning, a patient swung open the exam door and shouted, “What’s going on out here?! I’m sitting here waiting!” before slamming the door closed again. “Well, that was unnecessary,” our morning lead interjected as she went to reprimand him.

His behavior was easily recognizable to any doctor with children. It was an emotional outburst we call a tantrum. Although a graphic of tantrums by age would show a steep curve that drops precipitously after 4-years-old (please God, I hope), it persists throughout life. Even adults have tantrums. After? When I broke my pinky toe saving the family from flaming tornadoes a few weeks ago (I ran into the sofa), I flung the ice bag across the room in frustration. “You’ve a right to be mad,” my wife said returning the ice to where I was elevating my foot. She was spot on, it is understandable that I would be angry. It will be weeks before I can run again. And also my toe was broken. Both things were true.

Dr. Benabio

“Two things are true” is a technique for managing tantrums in toddlers. I first learned of it from Dr. Becky Kennedy, a clinical psychologist specializing in family therapy. She has a popular podcast called “Good Inside” based on her book of the same name. Her approach is to use positive psychology with an emphasis on connecting with children to not only shape behavior, but also to help them learn to manage their emotions. I read her book to level up dad skills and realized many of her principles are applicable to various types of relationships. Instead of viewing behaviors as an end, she instead recommends using them as an opportunity to probe for understanding. When someone exhibits poor behavior rather than assume they are being a jerk, try to find the most generous interpretation of what just happened. Assume they are doing the best they can. When my 4-year-old obstinately refused to go to bed despite the usual colored night lights and bedtime rituals, it seemed she was being a typical tantrum-y toddler. The more I insisted — lights-out! the more she resisted. It wasn’t until I asked why that I learned she was worried that the trash truck was going to come overnight. What seemed like just a behavioral problem, time for bed, was actually an opportunity for her to be seen and for us to connect.

I was finishing up with a patient last week when my medical assistant interrupted to advise my next patient was leaving. I walked out to see her storm into the corridor heading for the exit. “I am sorry, you must be quite frustrated having to wait for me.” “Yes, you don’t respect my time,” she said loudly enough for everyone pretending to not notice. I coaxed her back into the room and sat down. After apologizing for her wait and explaining it was because an urgent patient had been added to my schedule, she calmed down and allowed me to continue. At her previous visit, I had biopsied a firm dermal papule on her upper abdomen that turned out to be metastatic breast cancer. She was treated years ago and believed she was in complete remission. Now she was alone, terrified, and wanted her full appointment with me. Because I was running late, she assumed I wouldn’t have the time for her. It was an opportunity for me to connect with her and help her feel safe. I would have missed that opportunity if I had labeled her as just another angry “Karen” brassly asserting herself.

Dr. Kennedy talks a lot in her book about taking the “Most generous interpretation” of whatever behavioral issue arises. Take the time to validate what they are feeling and empathize as best as we can. Acknowledge that it’s normal to be angry and also these are the truths we have to work with. Two truths commonly appear in these emotional episodes. One, the immutable facts, for example, insurance doesn’t cover that drug, and two, your right to be frustrated by that. Above all, remember you, the doctor, are good inside as is your discourteous patient, disaffected staff member or sometimes mendacious teenager. “All good decisions start with feeling secure and nothing feels more secure than being recognized for the good people we are,” says Dr. Kennedy. True I believe even if we sometimes slam the door.

Dr. Benabio is chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on X. Write to him at [email protected].

Our dermatology department is composed of 25 doctors spread across 4 offices. It can be difficult to sustain cohesion so we have a few rituals to help hold us together. One is the morning huddle. This is a stand-up meeting lasting 3-5 minutes at 8:42 a.m. (just before the 8:45 a.m. patients). Led by our staff, huddle is a quick review of the priorities, issues, and celebrations across our department. While enthusiastically celebrating a staff member’s promotion one morning, a patient swung open the exam door and shouted, “What’s going on out here?! I’m sitting here waiting!” before slamming the door closed again. “Well, that was unnecessary,” our morning lead interjected as she went to reprimand him.

His behavior was easily recognizable to any doctor with children. It was an emotional outburst we call a tantrum. Although a graphic of tantrums by age would show a steep curve that drops precipitously after 4-years-old (please God, I hope), it persists throughout life. Even adults have tantrums. After? When I broke my pinky toe saving the family from flaming tornadoes a few weeks ago (I ran into the sofa), I flung the ice bag across the room in frustration. “You’ve a right to be mad,” my wife said returning the ice to where I was elevating my foot. She was spot on, it is understandable that I would be angry. It will be weeks before I can run again. And also my toe was broken. Both things were true.

Dr. Benabio

“Two things are true” is a technique for managing tantrums in toddlers. I first learned of it from Dr. Becky Kennedy, a clinical psychologist specializing in family therapy. She has a popular podcast called “Good Inside” based on her book of the same name. Her approach is to use positive psychology with an emphasis on connecting with children to not only shape behavior, but also to help them learn to manage their emotions. I read her book to level up dad skills and realized many of her principles are applicable to various types of relationships. Instead of viewing behaviors as an end, she instead recommends using them as an opportunity to probe for understanding. When someone exhibits poor behavior rather than assume they are being a jerk, try to find the most generous interpretation of what just happened. Assume they are doing the best they can. When my 4-year-old obstinately refused to go to bed despite the usual colored night lights and bedtime rituals, it seemed she was being a typical tantrum-y toddler. The more I insisted — lights-out! the more she resisted. It wasn’t until I asked why that I learned she was worried that the trash truck was going to come overnight. What seemed like just a behavioral problem, time for bed, was actually an opportunity for her to be seen and for us to connect.

I was finishing up with a patient last week when my medical assistant interrupted to advise my next patient was leaving. I walked out to see her storm into the corridor heading for the exit. “I am sorry, you must be quite frustrated having to wait for me.” “Yes, you don’t respect my time,” she said loudly enough for everyone pretending to not notice. I coaxed her back into the room and sat down. After apologizing for her wait and explaining it was because an urgent patient had been added to my schedule, she calmed down and allowed me to continue. At her previous visit, I had biopsied a firm dermal papule on her upper abdomen that turned out to be metastatic breast cancer. She was treated years ago and believed she was in complete remission. Now she was alone, terrified, and wanted her full appointment with me. Because I was running late, she assumed I wouldn’t have the time for her. It was an opportunity for me to connect with her and help her feel safe. I would have missed that opportunity if I had labeled her as just another angry “Karen” brassly asserting herself.

Dr. Kennedy talks a lot in her book about taking the “Most generous interpretation” of whatever behavioral issue arises. Take the time to validate what they are feeling and empathize as best as we can. Acknowledge that it’s normal to be angry and also these are the truths we have to work with. Two truths commonly appear in these emotional episodes. One, the immutable facts, for example, insurance doesn’t cover that drug, and two, your right to be frustrated by that. Above all, remember you, the doctor, are good inside as is your discourteous patient, disaffected staff member or sometimes mendacious teenager. “All good decisions start with feeling secure and nothing feels more secure than being recognized for the good people we are,” says Dr. Kennedy. True I believe even if we sometimes slam the door.

Dr. Benabio is chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on X. Write to him at [email protected].

Our dermatology department is composed of 25 doctors spread across 4 offices. It can be difficult to sustain cohesion so we have a few rituals to help hold us together. One is the morning huddle. This is a stand-up meeting lasting 3-5 minutes at 8:42 a.m. (just before the 8:45 a.m. patients). Led by our staff, huddle is a quick review of the priorities, issues, and celebrations across our department. While enthusiastically celebrating a staff member’s promotion one morning, a patient swung open the exam door and shouted, “What’s going on out here?! I’m sitting here waiting!” before slamming the door closed again. “Well, that was unnecessary,” our morning lead interjected as she went to reprimand him.

His behavior was easily recognizable to any doctor with children. It was an emotional outburst we call a tantrum. Although a graphic of tantrums by age would show a steep curve that drops precipitously after 4-years-old (please God, I hope), it persists throughout life. Even adults have tantrums. After? When I broke my pinky toe saving the family from flaming tornadoes a few weeks ago (I ran into the sofa), I flung the ice bag across the room in frustration. “You’ve a right to be mad,” my wife said returning the ice to where I was elevating my foot. She was spot on, it is understandable that I would be angry. It will be weeks before I can run again. And also my toe was broken. Both things were true.

Dr. Benabio

“Two things are true” is a technique for managing tantrums in toddlers. I first learned of it from Dr. Becky Kennedy, a clinical psychologist specializing in family therapy. She has a popular podcast called “Good Inside” based on her book of the same name. Her approach is to use positive psychology with an emphasis on connecting with children to not only shape behavior, but also to help them learn to manage their emotions. I read her book to level up dad skills and realized many of her principles are applicable to various types of relationships. Instead of viewing behaviors as an end, she instead recommends using them as an opportunity to probe for understanding. When someone exhibits poor behavior rather than assume they are being a jerk, try to find the most generous interpretation of what just happened. Assume they are doing the best they can. When my 4-year-old obstinately refused to go to bed despite the usual colored night lights and bedtime rituals, it seemed she was being a typical tantrum-y toddler. The more I insisted — lights-out! the more she resisted. It wasn’t until I asked why that I learned she was worried that the trash truck was going to come overnight. What seemed like just a behavioral problem, time for bed, was actually an opportunity for her to be seen and for us to connect.

I was finishing up with a patient last week when my medical assistant interrupted to advise my next patient was leaving. I walked out to see her storm into the corridor heading for the exit. “I am sorry, you must be quite frustrated having to wait for me.” “Yes, you don’t respect my time,” she said loudly enough for everyone pretending to not notice. I coaxed her back into the room and sat down. After apologizing for her wait and explaining it was because an urgent patient had been added to my schedule, she calmed down and allowed me to continue. At her previous visit, I had biopsied a firm dermal papule on her upper abdomen that turned out to be metastatic breast cancer. She was treated years ago and believed she was in complete remission. Now she was alone, terrified, and wanted her full appointment with me. Because I was running late, she assumed I wouldn’t have the time for her. It was an opportunity for me to connect with her and help her feel safe. I would have missed that opportunity if I had labeled her as just another angry “Karen” brassly asserting herself.

Dr. Kennedy talks a lot in her book about taking the “Most generous interpretation” of whatever behavioral issue arises. Take the time to validate what they are feeling and empathize as best as we can. Acknowledge that it’s normal to be angry and also these are the truths we have to work with. Two truths commonly appear in these emotional episodes. One, the immutable facts, for example, insurance doesn’t cover that drug, and two, your right to be frustrated by that. Above all, remember you, the doctor, are good inside as is your discourteous patient, disaffected staff member or sometimes mendacious teenager. “All good decisions start with feeling secure and nothing feels more secure than being recognized for the good people we are,” says Dr. Kennedy. True I believe even if we sometimes slam the door.

Dr. Benabio is chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on X. Write to him at [email protected].

TOPLINE:

Treatment-resistant major depression (TRD) is associated with a 17% higher risk for all-cause mortality than non-TRD major depressive disorder (MDD), a new study shows. The increased mortality risk was driven largely by suicide and accidental overdose, which were nearly twice as high among people whose depression didn’t improve after two treatments. 

METHODOLOGY:

• Data on 176,942 individuals diagnosed with MDD and treated with an antidepressant (median age at diagnosis, 40 years; 63% women) were obtained from Finnish nationwide registers.
• About 11% of the participants had TRD, defined as having more than two adequate treatment trials of at least 28 days, each within 2 years from the index antidepressant prescription.
• The outcomes were all-cause and cause-specific mortality, with demographic characteristics, psychiatric comorbidities, and treatment history included as covariates.
• The median follow-up period was 8.9 years.

TAKEAWAY:

• Median time to TRD was 8 months, and 959 and 7662 deaths were observed in the TRD and non-TRD groups, respectively.
• All-cause mortality was 17% higher among patients with TRD than among those with non-TRD (adjusted hazard ratio [aHR], 1.17; 95% CI, 1.09-1.25) because of higher mortality to external causes.
• Mortalities because of suicides (aHR, 1.90; 95% CI, 1.64-2.20) and accidental poisonings (aHR, 1.81; 95% CI, 1.48-2.22) were almost double in the TRD group, compared with the non-TRD group.
• No significant difference in mortality due to natural causes was observed between the TRD and non-TRD groups.

IN PRACTICE:

“The markedly increased mortality due to suicides and accidental overdoses suggests that persons with TRD may experience higher-intensity symptoms and more severe suicidal ideation than persons with non-TRD major depression,” the study authors wrote.

SOURCE:

The study was led by Tapio T. Gustafsson, University of Eastern Finland, Niuvanniemi Hospital, Kuopio, Finland. It was published online on September 11, 2024, in The Journal of Affective Disorders.

LIMITATIONS:

The definition of TRD lacked consensus. The study used routine data to define TRD, which may not have captured all relevant clinical nuances. Additionally, the reasons for medication changes were unavailable.

DISCLOSURES:

This study was funded by Johnson & Johnson Innovative Medicine and Niuvanniemi Hospital, with support from the Finnish Ministry of Social Affairs and Health. Several authors disclosed financial relationships with various pharmaceutical companies, and two are employees of Johnson & Johnson Innovative Medicine.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Treatment-resistant major depression (TRD) is associated with a 17% higher risk for all-cause mortality than non-TRD major depressive disorder (MDD), a new study shows. The increased mortality risk was driven largely by suicide and accidental overdose, which were nearly twice as high among people whose depression didn’t improve after two treatments. 

METHODOLOGY:

• Data on 176,942 individuals diagnosed with MDD and treated with an antidepressant (median age at diagnosis, 40 years; 63% women) were obtained from Finnish nationwide registers.
• About 11% of the participants had TRD, defined as having more than two adequate treatment trials of at least 28 days, each within 2 years from the index antidepressant prescription.
• The outcomes were all-cause and cause-specific mortality, with demographic characteristics, psychiatric comorbidities, and treatment history included as covariates.
• The median follow-up period was 8.9 years.

TAKEAWAY:

• Median time to TRD was 8 months, and 959 and 7662 deaths were observed in the TRD and non-TRD groups, respectively.
• All-cause mortality was 17% higher among patients with TRD than among those with non-TRD (adjusted hazard ratio [aHR], 1.17; 95% CI, 1.09-1.25) because of higher mortality to external causes.
• Mortalities because of suicides (aHR, 1.90; 95% CI, 1.64-2.20) and accidental poisonings (aHR, 1.81; 95% CI, 1.48-2.22) were almost double in the TRD group, compared with the non-TRD group.
• No significant difference in mortality due to natural causes was observed between the TRD and non-TRD groups.

IN PRACTICE:

“The markedly increased mortality due to suicides and accidental overdoses suggests that persons with TRD may experience higher-intensity symptoms and more severe suicidal ideation than persons with non-TRD major depression,” the study authors wrote.

SOURCE:

The study was led by Tapio T. Gustafsson, University of Eastern Finland, Niuvanniemi Hospital, Kuopio, Finland. It was published online on September 11, 2024, in The Journal of Affective Disorders.

LIMITATIONS:

The definition of TRD lacked consensus. The study used routine data to define TRD, which may not have captured all relevant clinical nuances. Additionally, the reasons for medication changes were unavailable.

DISCLOSURES:

This study was funded by Johnson & Johnson Innovative Medicine and Niuvanniemi Hospital, with support from the Finnish Ministry of Social Affairs and Health. Several authors disclosed financial relationships with various pharmaceutical companies, and two are employees of Johnson & Johnson Innovative Medicine.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Treatment-resistant major depression (TRD) is associated with a 17% higher risk for all-cause mortality than non-TRD major depressive disorder (MDD), a new study shows. The increased mortality risk was driven largely by suicide and accidental overdose, which were nearly twice as high among people whose depression didn’t improve after two treatments. 

METHODOLOGY:

• Data on 176,942 individuals diagnosed with MDD and treated with an antidepressant (median age at diagnosis, 40 years; 63% women) were obtained from Finnish nationwide registers.
• About 11% of the participants had TRD, defined as having more than two adequate treatment trials of at least 28 days, each within 2 years from the index antidepressant prescription.
• The outcomes were all-cause and cause-specific mortality, with demographic characteristics, psychiatric comorbidities, and treatment history included as covariates.
• The median follow-up period was 8.9 years.

TAKEAWAY:

• Median time to TRD was 8 months, and 959 and 7662 deaths were observed in the TRD and non-TRD groups, respectively.
• All-cause mortality was 17% higher among patients with TRD than among those with non-TRD (adjusted hazard ratio [aHR], 1.17; 95% CI, 1.09-1.25) because of higher mortality to external causes.
• Mortalities because of suicides (aHR, 1.90; 95% CI, 1.64-2.20) and accidental poisonings (aHR, 1.81; 95% CI, 1.48-2.22) were almost double in the TRD group, compared with the non-TRD group.
• No significant difference in mortality due to natural causes was observed between the TRD and non-TRD groups.

IN PRACTICE:

“The markedly increased mortality due to suicides and accidental overdoses suggests that persons with TRD may experience higher-intensity symptoms and more severe suicidal ideation than persons with non-TRD major depression,” the study authors wrote.

SOURCE:

The study was led by Tapio T. Gustafsson, University of Eastern Finland, Niuvanniemi Hospital, Kuopio, Finland. It was published online on September 11, 2024, in The Journal of Affective Disorders.

LIMITATIONS:

The definition of TRD lacked consensus. The study used routine data to define TRD, which may not have captured all relevant clinical nuances. Additionally, the reasons for medication changes were unavailable.

DISCLOSURES:

This study was funded by Johnson & Johnson Innovative Medicine and Niuvanniemi Hospital, with support from the Finnish Ministry of Social Affairs and Health. Several authors disclosed financial relationships with various pharmaceutical companies, and two are employees of Johnson & Johnson Innovative Medicine.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

COPENHAGEN — A higher cumulative genetic burden for depression is associated with an increased risk for relapse and worsening disability in people with multiple sclerosis (MS), early results of a new study showed.

Unlike the previous research, the current analysis used polygenic risk scores for depression, which summarize the estimated effect of genetic variants to determine the potential association with MS disease activity, so results are less likely to be explained by reverse causality.

This study increases awareness of the link between depression and MS, said study investigator Kaarina Kowalec, PhD, assistant professor, College of Pharmacy, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada. “We’re starting to understand how depression affects relapses and disability progression in MS,” she said.

The findings were presented at the 2024 ECTRIMS annual meeting.
 

Common Comorbidity

Depression is a common comorbidity in patients with MS and is associated with increased relapse and disability progression. Depression risk is partly polygenic in nature, involving numerous common genetic variants, said Dr. Kowalec.

The case-control study included 3420 relapsing-onset MS cases of European ancestry from four existing cohorts in three countries.

The Canadian cohort included those enrolled in a prospective longitudinal study of psychiatric comorbidity in chronic immune-mediated inflammatory disease (IMID), including MS; the Swedish cohort was an MS registry (SSReg) that encompasses 64 MS clinics (the cohort was split into two groups); and the US cohort was enrolled in a clinical trial of combined therapy with interferon and glatiramer acetate (CombiRx) in patients with MS.

The median follow-up in these cohorts ranged from 3 to 5 years.

Not surprisingly, most participants were women (from 71% in one of the Swedish cohorts to 83% in the Canadian cohort), and the age at MS onset ranged from 29 years in the Canadian cohort to 35 years in one of the Swedish cohorts.

The median baseline Expanded Disability Status Scale (EDSS) score was higher in the Canadian cohort (3.5) than in the Swedish (1.5) and US (2.0) cohorts, “reflective of the Canadian cohort being slightly more progressed,” said Dr. Kowalec.
 

Inherited Variants

To measure depression heritability, researchers generated a polygenic risk score in whole-genome imputed genotypes. The score reflects the number of inherited common genetic variants, weighted by effect sizes.

Researchers investigated the association between depression polygenic risk scores (top 20% vs. bottom 80%) with annualized relapse rate and worsening disability in MS measured by the rate of change in EDSS score. In the US cohort, they also explored the association between depression polygenic risk scores and time to relapse and confirmed EDSS worsening.

Covariates included use of disease-modifying therapy, age, sex, and the first five genetic ancestry principal components. The latter was done to capture residual stratification by genetic ancestry, although Dr. Kowalec stressed analyses were done only in those of European ancestry.

Investigators found a higher depression polygenic risk score was associated with relapse risk (incident rate ratio, 1.23; 95% CI, 1.01-1.49).

“Essentially, for every one standard deviation increase in the depression polygenic score, we found a significant increased hazard of 23% for experiencing a relapse over the follow-up period,” said Dr. Kowalec, who is also affiliated with the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.

She noted the Canadian cohort did not have many relapses, while the US and Swedish cohorts “had an increased rate.”

Other analyses examined the risk of having a relapse or worsening disability. Every one SD increase in the depression polygenic risk score was significantly associated with a 2.2 greater risk of experiencing relapse (hazard ratio [HR], 2.20; 95% CI, 1.35-3.60) and a 51% increased risk for confirmed EDSS progression (HR, 1.51; 95% CI, 1.03-2.22).
 

‘An Ideal Marker’

Use of polygenetic risk scores reduces the possibility of reverse causation, noted Dr. Kowalec. “These markers are fixed at birth and don’t change over your lifespan, so they’re really an ideal marker.”

The results suggest polygenetic risk scores represent a potential biomarker for risk stratification in people with MS, said Dr. Kowalec. Although depression polygenic risk scores are not currently available in clinical practice, “I would hope this would change in the next 3-4 years,” she said.

Asked by a delegate if confounding by a third variable is possible, Dr. Kowalec said because genetic markers don’t change over time, there is a hint that the direction is causal and that depression is driving the outcome. However, she added, further confirmation is needed.

Dr. Kowalec noted that there were no data on antidepressant use but noted that about half of the Canadian and US cohorts — and likely the same number in the Swedish cohorts — self-reported depression.

A limitation of the study was that it included only participants of European ancestry.
 

Clinical Implications Unclear

Commenting on the research, Lauren Gluck, MD, program director, Montefiore Multiple Sclerosis Center, Bronx, New York, described the study as “fascinating” but noted that it’s unclear how to use this new information in clinical practice.

“Clinicians frequently ask people with MS about mood symptoms and offer interventions like antidepressants and referrals to therapists. However, genetic testing is not routine, so we don’t yet know who to target based on these data.”

Preexisting depression or more severe depression could be viewed as a “red flag” for risk for more disease activity in the future, she said.

“This could encourage clinicians to use more highly effective therapy in these patients, similar to our strategies for people with MS with frequent attacks and more disease burden on MRIs.”

The study received support from the Consortium of Multiple Sclerosis Centers and the Congressionally Directed Medical Research Programs, Department of Defense.

Dr. Kowalec reported no relevant conflicts of interest.
 

A version of this article appeared on Medscape.com.

COPENHAGEN — A higher cumulative genetic burden for depression is associated with an increased risk for relapse and worsening disability in people with multiple sclerosis (MS), early results of a new study showed.

Unlike the previous research, the current analysis used polygenic risk scores for depression, which summarize the estimated effect of genetic variants to determine the potential association with MS disease activity, so results are less likely to be explained by reverse causality.

This study increases awareness of the link between depression and MS, said study investigator Kaarina Kowalec, PhD, assistant professor, College of Pharmacy, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada. “We’re starting to understand how depression affects relapses and disability progression in MS,” she said.

The findings were presented at the 2024 ECTRIMS annual meeting.
 

Common Comorbidity

Depression is a common comorbidity in patients with MS and is associated with increased relapse and disability progression. Depression risk is partly polygenic in nature, involving numerous common genetic variants, said Dr. Kowalec.

The case-control study included 3420 relapsing-onset MS cases of European ancestry from four existing cohorts in three countries.

The Canadian cohort included those enrolled in a prospective longitudinal study of psychiatric comorbidity in chronic immune-mediated inflammatory disease (IMID), including MS; the Swedish cohort was an MS registry (SSReg) that encompasses 64 MS clinics (the cohort was split into two groups); and the US cohort was enrolled in a clinical trial of combined therapy with interferon and glatiramer acetate (CombiRx) in patients with MS.

The median follow-up in these cohorts ranged from 3 to 5 years.

Not surprisingly, most participants were women (from 71% in one of the Swedish cohorts to 83% in the Canadian cohort), and the age at MS onset ranged from 29 years in the Canadian cohort to 35 years in one of the Swedish cohorts.

The median baseline Expanded Disability Status Scale (EDSS) score was higher in the Canadian cohort (3.5) than in the Swedish (1.5) and US (2.0) cohorts, “reflective of the Canadian cohort being slightly more progressed,” said Dr. Kowalec.
 

Inherited Variants

To measure depression heritability, researchers generated a polygenic risk score in whole-genome imputed genotypes. The score reflects the number of inherited common genetic variants, weighted by effect sizes.

Researchers investigated the association between depression polygenic risk scores (top 20% vs. bottom 80%) with annualized relapse rate and worsening disability in MS measured by the rate of change in EDSS score. In the US cohort, they also explored the association between depression polygenic risk scores and time to relapse and confirmed EDSS worsening.

Covariates included use of disease-modifying therapy, age, sex, and the first five genetic ancestry principal components. The latter was done to capture residual stratification by genetic ancestry, although Dr. Kowalec stressed analyses were done only in those of European ancestry.

Investigators found a higher depression polygenic risk score was associated with relapse risk (incident rate ratio, 1.23; 95% CI, 1.01-1.49).

“Essentially, for every one standard deviation increase in the depression polygenic score, we found a significant increased hazard of 23% for experiencing a relapse over the follow-up period,” said Dr. Kowalec, who is also affiliated with the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.

She noted the Canadian cohort did not have many relapses, while the US and Swedish cohorts “had an increased rate.”

Other analyses examined the risk of having a relapse or worsening disability. Every one SD increase in the depression polygenic risk score was significantly associated with a 2.2 greater risk of experiencing relapse (hazard ratio [HR], 2.20; 95% CI, 1.35-3.60) and a 51% increased risk for confirmed EDSS progression (HR, 1.51; 95% CI, 1.03-2.22).
 

‘An Ideal Marker’

Use of polygenetic risk scores reduces the possibility of reverse causation, noted Dr. Kowalec. “These markers are fixed at birth and don’t change over your lifespan, so they’re really an ideal marker.”

The results suggest polygenetic risk scores represent a potential biomarker for risk stratification in people with MS, said Dr. Kowalec. Although depression polygenic risk scores are not currently available in clinical practice, “I would hope this would change in the next 3-4 years,” she said.

Asked by a delegate if confounding by a third variable is possible, Dr. Kowalec said because genetic markers don’t change over time, there is a hint that the direction is causal and that depression is driving the outcome. However, she added, further confirmation is needed.

Dr. Kowalec noted that there were no data on antidepressant use but noted that about half of the Canadian and US cohorts — and likely the same number in the Swedish cohorts — self-reported depression.

A limitation of the study was that it included only participants of European ancestry.
 

Clinical Implications Unclear

Commenting on the research, Lauren Gluck, MD, program director, Montefiore Multiple Sclerosis Center, Bronx, New York, described the study as “fascinating” but noted that it’s unclear how to use this new information in clinical practice.

“Clinicians frequently ask people with MS about mood symptoms and offer interventions like antidepressants and referrals to therapists. However, genetic testing is not routine, so we don’t yet know who to target based on these data.”

Preexisting depression or more severe depression could be viewed as a “red flag” for risk for more disease activity in the future, she said.

“This could encourage clinicians to use more highly effective therapy in these patients, similar to our strategies for people with MS with frequent attacks and more disease burden on MRIs.”

The study received support from the Consortium of Multiple Sclerosis Centers and the Congressionally Directed Medical Research Programs, Department of Defense.

Dr. Kowalec reported no relevant conflicts of interest.
 

A version of this article appeared on Medscape.com.

COPENHAGEN — A higher cumulative genetic burden for depression is associated with an increased risk for relapse and worsening disability in people with multiple sclerosis (MS), early results of a new study showed.

Unlike the previous research, the current analysis used polygenic risk scores for depression, which summarize the estimated effect of genetic variants to determine the potential association with MS disease activity, so results are less likely to be explained by reverse causality.

This study increases awareness of the link between depression and MS, said study investigator Kaarina Kowalec, PhD, assistant professor, College of Pharmacy, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada. “We’re starting to understand how depression affects relapses and disability progression in MS,” she said.

The findings were presented at the 2024 ECTRIMS annual meeting.
 

Common Comorbidity

Depression is a common comorbidity in patients with MS and is associated with increased relapse and disability progression. Depression risk is partly polygenic in nature, involving numerous common genetic variants, said Dr. Kowalec.

The case-control study included 3420 relapsing-onset MS cases of European ancestry from four existing cohorts in three countries.

The Canadian cohort included those enrolled in a prospective longitudinal study of psychiatric comorbidity in chronic immune-mediated inflammatory disease (IMID), including MS; the Swedish cohort was an MS registry (SSReg) that encompasses 64 MS clinics (the cohort was split into two groups); and the US cohort was enrolled in a clinical trial of combined therapy with interferon and glatiramer acetate (CombiRx) in patients with MS.

The median follow-up in these cohorts ranged from 3 to 5 years.

Not surprisingly, most participants were women (from 71% in one of the Swedish cohorts to 83% in the Canadian cohort), and the age at MS onset ranged from 29 years in the Canadian cohort to 35 years in one of the Swedish cohorts.

The median baseline Expanded Disability Status Scale (EDSS) score was higher in the Canadian cohort (3.5) than in the Swedish (1.5) and US (2.0) cohorts, “reflective of the Canadian cohort being slightly more progressed,” said Dr. Kowalec.
 

Inherited Variants

To measure depression heritability, researchers generated a polygenic risk score in whole-genome imputed genotypes. The score reflects the number of inherited common genetic variants, weighted by effect sizes.

Researchers investigated the association between depression polygenic risk scores (top 20% vs. bottom 80%) with annualized relapse rate and worsening disability in MS measured by the rate of change in EDSS score. In the US cohort, they also explored the association between depression polygenic risk scores and time to relapse and confirmed EDSS worsening.

Covariates included use of disease-modifying therapy, age, sex, and the first five genetic ancestry principal components. The latter was done to capture residual stratification by genetic ancestry, although Dr. Kowalec stressed analyses were done only in those of European ancestry.

Investigators found a higher depression polygenic risk score was associated with relapse risk (incident rate ratio, 1.23; 95% CI, 1.01-1.49).

“Essentially, for every one standard deviation increase in the depression polygenic score, we found a significant increased hazard of 23% for experiencing a relapse over the follow-up period,” said Dr. Kowalec, who is also affiliated with the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.

She noted the Canadian cohort did not have many relapses, while the US and Swedish cohorts “had an increased rate.”

Other analyses examined the risk of having a relapse or worsening disability. Every one SD increase in the depression polygenic risk score was significantly associated with a 2.2 greater risk of experiencing relapse (hazard ratio [HR], 2.20; 95% CI, 1.35-3.60) and a 51% increased risk for confirmed EDSS progression (HR, 1.51; 95% CI, 1.03-2.22).
 

‘An Ideal Marker’

Use of polygenetic risk scores reduces the possibility of reverse causation, noted Dr. Kowalec. “These markers are fixed at birth and don’t change over your lifespan, so they’re really an ideal marker.”

The results suggest polygenetic risk scores represent a potential biomarker for risk stratification in people with MS, said Dr. Kowalec. Although depression polygenic risk scores are not currently available in clinical practice, “I would hope this would change in the next 3-4 years,” she said.

Asked by a delegate if confounding by a third variable is possible, Dr. Kowalec said because genetic markers don’t change over time, there is a hint that the direction is causal and that depression is driving the outcome. However, she added, further confirmation is needed.

Dr. Kowalec noted that there were no data on antidepressant use but noted that about half of the Canadian and US cohorts — and likely the same number in the Swedish cohorts — self-reported depression.

A limitation of the study was that it included only participants of European ancestry.
 

Clinical Implications Unclear

Commenting on the research, Lauren Gluck, MD, program director, Montefiore Multiple Sclerosis Center, Bronx, New York, described the study as “fascinating” but noted that it’s unclear how to use this new information in clinical practice.

“Clinicians frequently ask people with MS about mood symptoms and offer interventions like antidepressants and referrals to therapists. However, genetic testing is not routine, so we don’t yet know who to target based on these data.”

Preexisting depression or more severe depression could be viewed as a “red flag” for risk for more disease activity in the future, she said.

“This could encourage clinicians to use more highly effective therapy in these patients, similar to our strategies for people with MS with frequent attacks and more disease burden on MRIs.”

The study received support from the Consortium of Multiple Sclerosis Centers and the Congressionally Directed Medical Research Programs, Department of Defense.

Dr. Kowalec reported no relevant conflicts of interest.
 

A version of this article appeared on Medscape.com.

As a psychiatrist specializing in eating disorders, Kim Dennis, MD, has seen firsthand the complex relationship between obesity treatment and mental health in adolescents.

Now, with the rising popularity of medications like Ozempic for weight loss, she fears she will care for more teens with eating disorders who are seeking glucagon-like peptide 1 (GLP-1) agonists or who have developed a disorder while taking them.

“We haven’t seen patients yet, but I’m sure they are on their way,” said Dr. Dennis, a clinical assistant professor in the Department of Psychiatry at the University of Illinois College of Medicine in Chicago. She is also the cofounder and chief medical officer of SunCloud Health, an outpatient eating disorder treatment center in Illinois.

Dr. Dennis’ concerns reflect a growing unease among eating disorder specialists as obesity medications gain traction for adolescent use. A recent study published in JAMA Pediatrics showed nearly 80% of teens in treatment for obesity reported symptoms of disordered eating at the outset of an intervention. These included signs of binge eating and loss of control.

The randomized clinical trial, conducted from 2018 to 2023, examined 141 adolescents with obesity undergoing interventions like low-energy diets or intermittent energy restriction. Almost half scored as having risk for an undiagnosed eating disorder, as defined by the Eating Disorder Examination Questionnaire (EDE-Q).

At the end of the intervention, many teens continued to have symptoms of disordered eating, while a smaller group was newly scored as having a risk for an eating disorder.
 

Weight Loss and Eating Disorders: A Balancing Act

The findings illuminate a significant challenge for pediatricians and primary care clinicians: Balancing effective weight management with the risk of exacerbating or triggering eating disorders, said Hiba Jebeile, PhD, a research dietitian at The Children’s Hospital at Westmead in Australia, and the study’s lead author. Adding weight loss medication on top of the equation can further complicate care.

“It is helpful for obesity and eating disorder services to work together, with clear referral pathways, to manage these adolescents,” Dr. Jebeile said.

The US Food and Drug Administration approved semaglutide for weight loss in adolescents aged 12-17 years in December 2020. One study found that the number of adolescents prescribed GLP-1 receptor agonists (GLP-1 RAs) for type 2 diabetes and weight management rose from 8722 to 60,567 between 2020 and 2023 — a nearly sevenfold increase.

“The number of adolescents taking these medications is going up because they work,” said Suzanne Cuda, MD, medical director of Alamo City Healthy Kids and Families, a medical weight management clinic in San Antonio. The medications have been shown to treat type 2 diabetes, lower blood pressure, and reduce the risk for cardiovascular diseases.

“The younger you are, the better the outcome,” Dr. Cuda said.

How GLP-1 agonists may affect adolescents in the long run is not yet clear. Existing studies on GLP-1 medications in patients with eating disorders have shown mixed results. Some studies indicate that the drugs decrease binge episodes for those with binge eating disorder or bulimia nervosa. However, these studies had small sample sizes and measured only short-term effects, leaving long-term outcomes and risks unknown.

Traditional treatments for eating disorders emphasize regular eating patterns, body acceptance, addressing weight stigma, and improving attunement to hunger and fullness cues — approaches that may conflict with the effects of GLP-1 agonists. These drugs suppress appetite, alter metabolic signals, and may unintentionally reinforce weight loss as a primary goal, creating a potential disconnect between the aims of recovery from eating disorders and the biologic effects of the medication, experts said.

Dr. Cuda said she has cared for adolescents with diagnosed eating disorders in her practice who are seeking GLP-1 agonists. She said she first works with patients to treat the underlying disorder before prescribing medication.

“One of the concerns is the extreme reductions in calories that could be induced by GLP-1 RA in children and adolescents,” she said. Unlike adults, adolescents use caloric energy not just for physical activity but also for growing and developing, she said.

“They can’t catch up on that growth and development,” she added.
 

Advice for Screening and Monitoring

The National Eating Disorders Association raised concerns about the potential misuse of these medications and their potential to exacerbate eating disorder behaviors in people who are already at a higher risk of developing one of the conditions, including those with existing mental health disorders, stress, who have already dieted, and who have experienced weight-centric bullying.

Clinicians should be on the lookout for patients seeking GLP-1s who present with symptoms of an eating disorder that may be less apparent, such as picky eating, insomnia or difficulty sleeping, or, for girls, irregular menstrual periods, Dr. Dennis said. These patients may be more likely to go undiagnosed or misdiagnosed. Research also suggests that people of color are less likely to be diagnosed or receive specialty care for eating disorders.

Discussions between patients and clinicians about obesity treatment prior to prescribing provide a crucial opportunity to screen and monitor for disordered eating, which Dr. Dennis said does not universally occur currently.

Dr. Dennis recommended initial assessments using validated screening tools like the EDE-Q and the Center for Epidemiologic Studies Depression Scale Revised, 10-Item Version.

Ongoing monitoring throughout treatment is essential, with initial monthly check-ins that include dietary counseling to detect subtle changes in eating behaviors or attitudes toward food and body image, Dr. Cuda said.

The Obesity Medicine Association (OMA) has stressed the importance of a collaborative approach involving connections with mental health professionals specializing in eating disorders and dietitians.

“If you have a chance to send them to an obesity medicine specialist, you should do that,” said Dr. Cuda, who coauthored the OMA statement. “It’s impractical to expect a primary care physician to do everything: Screen for dietary disorders, do a full dietary counseling, follow up on their activity.”

For patients showing signs of disordered eating, clinicians should avoid recommending restrictive dietary approaches, like cutting out food groups such as carbohydrates or a restricted calorie goal. Instead, they can suggest focusing on healthier lifestyle habits and referring to a psychotherapist, the experts said. Clinicians also should be prepared to adjust or pause GLP-1 agonists if disordered eating disorder symptoms worsen.

“I think a weight-agnostic approach where the focus of care is not weight loss but increase in health protective behaviors and nutritional intake is safest for all kids, especially those with eating disorders or eating disorder risk factors,” Dr. Dennis said.

Various authors of the eating disorder study reported receiving grants, advisory board fees, and speaker fees from entities including the National Health and Medical Research Council of Australia, Eli Lilly, Novo Nordisk, Nu-Mega Ingredients, and the National Institutes of Health, among others.
 

A version of this article appeared on Medscape.com.

As a psychiatrist specializing in eating disorders, Kim Dennis, MD, has seen firsthand the complex relationship between obesity treatment and mental health in adolescents.

Now, with the rising popularity of medications like Ozempic for weight loss, she fears she will care for more teens with eating disorders who are seeking glucagon-like peptide 1 (GLP-1) agonists or who have developed a disorder while taking them.

“We haven’t seen patients yet, but I’m sure they are on their way,” said Dr. Dennis, a clinical assistant professor in the Department of Psychiatry at the University of Illinois College of Medicine in Chicago. She is also the cofounder and chief medical officer of SunCloud Health, an outpatient eating disorder treatment center in Illinois.

Dr. Dennis’ concerns reflect a growing unease among eating disorder specialists as obesity medications gain traction for adolescent use. A recent study published in JAMA Pediatrics showed nearly 80% of teens in treatment for obesity reported symptoms of disordered eating at the outset of an intervention. These included signs of binge eating and loss of control.

The randomized clinical trial, conducted from 2018 to 2023, examined 141 adolescents with obesity undergoing interventions like low-energy diets or intermittent energy restriction. Almost half scored as having risk for an undiagnosed eating disorder, as defined by the Eating Disorder Examination Questionnaire (EDE-Q).

At the end of the intervention, many teens continued to have symptoms of disordered eating, while a smaller group was newly scored as having a risk for an eating disorder.
 

Weight Loss and Eating Disorders: A Balancing Act

The findings illuminate a significant challenge for pediatricians and primary care clinicians: Balancing effective weight management with the risk of exacerbating or triggering eating disorders, said Hiba Jebeile, PhD, a research dietitian at The Children’s Hospital at Westmead in Australia, and the study’s lead author. Adding weight loss medication on top of the equation can further complicate care.

“It is helpful for obesity and eating disorder services to work together, with clear referral pathways, to manage these adolescents,” Dr. Jebeile said.

The US Food and Drug Administration approved semaglutide for weight loss in adolescents aged 12-17 years in December 2020. One study found that the number of adolescents prescribed GLP-1 receptor agonists (GLP-1 RAs) for type 2 diabetes and weight management rose from 8722 to 60,567 between 2020 and 2023 — a nearly sevenfold increase.

“The number of adolescents taking these medications is going up because they work,” said Suzanne Cuda, MD, medical director of Alamo City Healthy Kids and Families, a medical weight management clinic in San Antonio. The medications have been shown to treat type 2 diabetes, lower blood pressure, and reduce the risk for cardiovascular diseases.

“The younger you are, the better the outcome,” Dr. Cuda said.

How GLP-1 agonists may affect adolescents in the long run is not yet clear. Existing studies on GLP-1 medications in patients with eating disorders have shown mixed results. Some studies indicate that the drugs decrease binge episodes for those with binge eating disorder or bulimia nervosa. However, these studies had small sample sizes and measured only short-term effects, leaving long-term outcomes and risks unknown.

Traditional treatments for eating disorders emphasize regular eating patterns, body acceptance, addressing weight stigma, and improving attunement to hunger and fullness cues — approaches that may conflict with the effects of GLP-1 agonists. These drugs suppress appetite, alter metabolic signals, and may unintentionally reinforce weight loss as a primary goal, creating a potential disconnect between the aims of recovery from eating disorders and the biologic effects of the medication, experts said.

Dr. Cuda said she has cared for adolescents with diagnosed eating disorders in her practice who are seeking GLP-1 agonists. She said she first works with patients to treat the underlying disorder before prescribing medication.

“One of the concerns is the extreme reductions in calories that could be induced by GLP-1 RA in children and adolescents,” she said. Unlike adults, adolescents use caloric energy not just for physical activity but also for growing and developing, she said.

“They can’t catch up on that growth and development,” she added.
 

Advice for Screening and Monitoring

The National Eating Disorders Association raised concerns about the potential misuse of these medications and their potential to exacerbate eating disorder behaviors in people who are already at a higher risk of developing one of the conditions, including those with existing mental health disorders, stress, who have already dieted, and who have experienced weight-centric bullying.

Clinicians should be on the lookout for patients seeking GLP-1s who present with symptoms of an eating disorder that may be less apparent, such as picky eating, insomnia or difficulty sleeping, or, for girls, irregular menstrual periods, Dr. Dennis said. These patients may be more likely to go undiagnosed or misdiagnosed. Research also suggests that people of color are less likely to be diagnosed or receive specialty care for eating disorders.

Discussions between patients and clinicians about obesity treatment prior to prescribing provide a crucial opportunity to screen and monitor for disordered eating, which Dr. Dennis said does not universally occur currently.

Dr. Dennis recommended initial assessments using validated screening tools like the EDE-Q and the Center for Epidemiologic Studies Depression Scale Revised, 10-Item Version.

Ongoing monitoring throughout treatment is essential, with initial monthly check-ins that include dietary counseling to detect subtle changes in eating behaviors or attitudes toward food and body image, Dr. Cuda said.

The Obesity Medicine Association (OMA) has stressed the importance of a collaborative approach involving connections with mental health professionals specializing in eating disorders and dietitians.

“If you have a chance to send them to an obesity medicine specialist, you should do that,” said Dr. Cuda, who coauthored the OMA statement. “It’s impractical to expect a primary care physician to do everything: Screen for dietary disorders, do a full dietary counseling, follow up on their activity.”

For patients showing signs of disordered eating, clinicians should avoid recommending restrictive dietary approaches, like cutting out food groups such as carbohydrates or a restricted calorie goal. Instead, they can suggest focusing on healthier lifestyle habits and referring to a psychotherapist, the experts said. Clinicians also should be prepared to adjust or pause GLP-1 agonists if disordered eating disorder symptoms worsen.

“I think a weight-agnostic approach where the focus of care is not weight loss but increase in health protective behaviors and nutritional intake is safest for all kids, especially those with eating disorders or eating disorder risk factors,” Dr. Dennis said.

Various authors of the eating disorder study reported receiving grants, advisory board fees, and speaker fees from entities including the National Health and Medical Research Council of Australia, Eli Lilly, Novo Nordisk, Nu-Mega Ingredients, and the National Institutes of Health, among others.
 

A version of this article appeared on Medscape.com.

As a psychiatrist specializing in eating disorders, Kim Dennis, MD, has seen firsthand the complex relationship between obesity treatment and mental health in adolescents.

Now, with the rising popularity of medications like Ozempic for weight loss, she fears she will care for more teens with eating disorders who are seeking glucagon-like peptide 1 (GLP-1) agonists or who have developed a disorder while taking them.

“We haven’t seen patients yet, but I’m sure they are on their way,” said Dr. Dennis, a clinical assistant professor in the Department of Psychiatry at the University of Illinois College of Medicine in Chicago. She is also the cofounder and chief medical officer of SunCloud Health, an outpatient eating disorder treatment center in Illinois.

Dr. Dennis’ concerns reflect a growing unease among eating disorder specialists as obesity medications gain traction for adolescent use. A recent study published in JAMA Pediatrics showed nearly 80% of teens in treatment for obesity reported symptoms of disordered eating at the outset of an intervention. These included signs of binge eating and loss of control.

The randomized clinical trial, conducted from 2018 to 2023, examined 141 adolescents with obesity undergoing interventions like low-energy diets or intermittent energy restriction. Almost half scored as having risk for an undiagnosed eating disorder, as defined by the Eating Disorder Examination Questionnaire (EDE-Q).

At the end of the intervention, many teens continued to have symptoms of disordered eating, while a smaller group was newly scored as having a risk for an eating disorder.
 

Weight Loss and Eating Disorders: A Balancing Act

The findings illuminate a significant challenge for pediatricians and primary care clinicians: Balancing effective weight management with the risk of exacerbating or triggering eating disorders, said Hiba Jebeile, PhD, a research dietitian at The Children’s Hospital at Westmead in Australia, and the study’s lead author. Adding weight loss medication on top of the equation can further complicate care.

“It is helpful for obesity and eating disorder services to work together, with clear referral pathways, to manage these adolescents,” Dr. Jebeile said.

The US Food and Drug Administration approved semaglutide for weight loss in adolescents aged 12-17 years in December 2020. One study found that the number of adolescents prescribed GLP-1 receptor agonists (GLP-1 RAs) for type 2 diabetes and weight management rose from 8722 to 60,567 between 2020 and 2023 — a nearly sevenfold increase.

“The number of adolescents taking these medications is going up because they work,” said Suzanne Cuda, MD, medical director of Alamo City Healthy Kids and Families, a medical weight management clinic in San Antonio. The medications have been shown to treat type 2 diabetes, lower blood pressure, and reduce the risk for cardiovascular diseases.

“The younger you are, the better the outcome,” Dr. Cuda said.

How GLP-1 agonists may affect adolescents in the long run is not yet clear. Existing studies on GLP-1 medications in patients with eating disorders have shown mixed results. Some studies indicate that the drugs decrease binge episodes for those with binge eating disorder or bulimia nervosa. However, these studies had small sample sizes and measured only short-term effects, leaving long-term outcomes and risks unknown.

Traditional treatments for eating disorders emphasize regular eating patterns, body acceptance, addressing weight stigma, and improving attunement to hunger and fullness cues — approaches that may conflict with the effects of GLP-1 agonists. These drugs suppress appetite, alter metabolic signals, and may unintentionally reinforce weight loss as a primary goal, creating a potential disconnect between the aims of recovery from eating disorders and the biologic effects of the medication, experts said.

Dr. Cuda said she has cared for adolescents with diagnosed eating disorders in her practice who are seeking GLP-1 agonists. She said she first works with patients to treat the underlying disorder before prescribing medication.

“One of the concerns is the extreme reductions in calories that could be induced by GLP-1 RA in children and adolescents,” she said. Unlike adults, adolescents use caloric energy not just for physical activity but also for growing and developing, she said.

“They can’t catch up on that growth and development,” she added.
 

Advice for Screening and Monitoring

The National Eating Disorders Association raised concerns about the potential misuse of these medications and their potential to exacerbate eating disorder behaviors in people who are already at a higher risk of developing one of the conditions, including those with existing mental health disorders, stress, who have already dieted, and who have experienced weight-centric bullying.

Clinicians should be on the lookout for patients seeking GLP-1s who present with symptoms of an eating disorder that may be less apparent, such as picky eating, insomnia or difficulty sleeping, or, for girls, irregular menstrual periods, Dr. Dennis said. These patients may be more likely to go undiagnosed or misdiagnosed. Research also suggests that people of color are less likely to be diagnosed or receive specialty care for eating disorders.

Discussions between patients and clinicians about obesity treatment prior to prescribing provide a crucial opportunity to screen and monitor for disordered eating, which Dr. Dennis said does not universally occur currently.

Dr. Dennis recommended initial assessments using validated screening tools like the EDE-Q and the Center for Epidemiologic Studies Depression Scale Revised, 10-Item Version.

Ongoing monitoring throughout treatment is essential, with initial monthly check-ins that include dietary counseling to detect subtle changes in eating behaviors or attitudes toward food and body image, Dr. Cuda said.

The Obesity Medicine Association (OMA) has stressed the importance of a collaborative approach involving connections with mental health professionals specializing in eating disorders and dietitians.

“If you have a chance to send them to an obesity medicine specialist, you should do that,” said Dr. Cuda, who coauthored the OMA statement. “It’s impractical to expect a primary care physician to do everything: Screen for dietary disorders, do a full dietary counseling, follow up on their activity.”

For patients showing signs of disordered eating, clinicians should avoid recommending restrictive dietary approaches, like cutting out food groups such as carbohydrates or a restricted calorie goal. Instead, they can suggest focusing on healthier lifestyle habits and referring to a psychotherapist, the experts said. Clinicians also should be prepared to adjust or pause GLP-1 agonists if disordered eating disorder symptoms worsen.

“I think a weight-agnostic approach where the focus of care is not weight loss but increase in health protective behaviors and nutritional intake is safest for all kids, especially those with eating disorders or eating disorder risk factors,” Dr. Dennis said.

Various authors of the eating disorder study reported receiving grants, advisory board fees, and speaker fees from entities including the National Health and Medical Research Council of Australia, Eli Lilly, Novo Nordisk, Nu-Mega Ingredients, and the National Institutes of Health, among others.
 

A version of this article appeared on Medscape.com.

The Food and Drug Administration (FDA) plans to scrutinize the safety and efficacy of lab-developed tests — those designed, manufactured, and used in a single laboratory — far more thoroughly in the future.

Under a rule finalized in April, the FDA will treat facilities that develop and use lab tests as manufacturers and regulate tests as medical devices. That means that most lab tests will need an FDA review before going on sale.

The FDA will also impose new quality standards, requiring test manufacturers to report adverse events and create a registry of lab tests under the new rule, which will be phased in over 4 years.

FDA officials have been concerned for years about the reliability of commercial lab tests, which have ballooned into a multibillion-dollar industry.

Consumer groups have long urged the FDA to regulate lab tests more strictly, arguing that the lack of scrutiny allows doctors and patients to be exploited by bad actors such as Theranos, which falsely claimed that its tests could diagnose multiple diseases with a single drop of blood.

“When it comes to some of these tests that doctors are recommending for patients, many doctors are just crossing their fingers and relying on the representation of the company because nobody is checking” to verify a manufacturer’s claims, said Joshua Sharfstein, MD, vice dean for public health practice and community engagement at the Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland.
 

Nearly 12,000 Labs Making Medical Tests

Although the FDA estimates there are nearly 12,000 labs manufacturing medical tests, agency officials said they don’t know how many tests are being marketed. The FDA already requires that home test kits marketed directly to consumers, such as those used to detect COVID-19, get clearance from the agency before being sold.

“There’s plenty of time for industry to get its act together to develop the data that it might need to make a premarket application,” said Peter Lurie, MD, PhD, a former associate commissioner at the FDA. In 2015, Dr. Lurie led a report outlining some of the dangers of unregulated lab tests.

For the average physician who orders lab tests, nothing is going to immediately change because of the final rule, said Dr. Lurie, now president of the Center for Science in the Public Interest, a nonprofit consumer watchdog.

“Tomorrow, this will look just the same as it does today,” Dr. Lurie said. “For the next 3 years, the companies will be scurrying behind the scenes to comply with the early stages of implementation. But most of that will be invisible to the average practitioner.”

Dr. Lurie predicted the FDA will focus its scrutiny on tests that pose the greatest potential risk to patients, such as ones used to diagnose serious diseases or guide treatment for life-threatening conditions. “The least significant tests will likely get very limited, if any, scrutiny,” said Dr. Lurie, adding that the FDA will likely issue guidance about how it plans to define low- and high-risk tests. “My suspicion is that it will be probably a small minority of products that are subject to full premarket approval.”
 

Lab Industry Groups Push Back

But imposing new rules with the potential to affect an industry’s bottom line is no easy task.

The American Clinical Laboratory Association, which represents the lab industry, said in a statement that the FDA rule will “limit access to scores of critical tests, increase healthcare costs, and undermine innovation in new diagnostics.” Another industry group, the Association for Molecular Pathology, has warned of “significant and harmful disruption to laboratory medicine.”

The two associations have filed separate lawsuits, charging that the FDA overstepped the authority granted by Congress. In their lawsuits, groups claim that lab tests are professional services, not manufactured products. The groups noted that the Centers for Medicare & Medicaid Services (CMS) already inspects lab facilities. CMS does not assess the tests’ quality or reliability.

A recent Supreme Court decision could make those lawsuits more likely to succeed, said David Simon, JD, LLM, PhD, an assistant professor of law at the Northeastern University School of Law, Boston, Massachusetts.

In the case of Loper Bright Enterprises v. Raimondo, decided in June, justices overturned a long-standing precedent known as Chevron deference, which required courts to defer to federal agencies when interpreting ambiguous laws. That means that courts no longer have to accept the FDA’s definition of a device, Dr. Simon said.

“Because judges may have more active roles in defining agency authority, federal agencies may have correspondingly less robust roles in policymaking,” Dr. Simon wrote in an editorial coauthored with Michael J. Young, MD, MPhil, of Harvard Medical School, Boston.

The Supreme Court ruling could pressure Congress to more clearly define FDA’s ruling in regulating lab tests, Dr. Simon and Dr. Young wrote.

Members of Congress first introduced a bill to clarify the FDA’s role in regulating lab tests, called the VALID Act, in 2020. The bill stalled and, despite efforts to revive it, still hasn’t passed.

FDA officials have said they remain “open to working with Congress,” noting that any future legislation about lab-developed tests would supersede their current policy.

In an interview, Dr. Simon noted the FDA significantly narrowed the scope of the final rule in response to comments from critics who objected to an earlier version of the policy proposed in 2023. The final rule carves out several categories of tests that won’t need to apply for “premarket review.”

Notably, a “grandfather clause” will allow some lab tests already on the market to continue being sold without undergoing FDA’s premarket review process. In explaining the exemption, FDA officials said they did not want doctors and patients to lose access to tests on which they rely. But Dr. Lurie noted that because the FDA views all these tests as under its jurisdiction, the agency could opt to take a closer look “at a very old device that is causing a problem today.”

The FDA also will exempt tests approved by New York State’s Clinical Laboratory Evaluation Program, which conducts its own stringent reviews. And the FDA will continue to allow hospitals to develop tests for patients within their healthcare system without going through the FDA approval process, if no FDA-approved tests are available.

Hospital-based tests play a critical role in treating infectious diseases, said Amesh Adalja, MD, an infectious diseases specialist and senior scholar at the Johns Hopkins Center for Health Security. For example, a large research hospital treating a patient with cytomegalovirus may need to develop its own test to determine whether the infection is resistant to antiviral drugs, Dr. Adalja said.

“With novel infectious disease outbreaks, researchers are able to move quickly to make diagnostic tests months and months before commercial laboratories are able to get through regulatory processes,” Dr. Adalja said.

To help scientists respond quickly to emergencies, the FDA published special guidance for labs that develop unauthorized lab tests for disease outbreaks.

Medical groups such as the American Hospital Association and Infectious Diseases Society of America remain concerned about the burden of complying with new regulations.

“Many vital tests developed in hospitals and health systems may be subjected to unnecessary and costly paperwork,” said Stacey Hughes, executive vice president of the American Hospital Association, in a statement.

Other groups, such as the American Society of Clinical Oncology, praised the new FDA policy. In comments submitted to the FDA in 2023, the cancer group said it “emphatically supports” requiring lab tests to undergo FDA review.

“We appreciate FDA action to modernize oversight of these tests and are hopeful this rule will increase focus on the need to balance rapid diagnostic innovation with patient safety and access” Everett Vokes, MD, the group’s board chair, said in a statement released after the FDA’s final rule was published.

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

The Food and Drug Administration (FDA) plans to scrutinize the safety and efficacy of lab-developed tests — those designed, manufactured, and used in a single laboratory — far more thoroughly in the future.

Under a rule finalized in April, the FDA will treat facilities that develop and use lab tests as manufacturers and regulate tests as medical devices. That means that most lab tests will need an FDA review before going on sale.

The FDA will also impose new quality standards, requiring test manufacturers to report adverse events and create a registry of lab tests under the new rule, which will be phased in over 4 years.

FDA officials have been concerned for years about the reliability of commercial lab tests, which have ballooned into a multibillion-dollar industry.

Consumer groups have long urged the FDA to regulate lab tests more strictly, arguing that the lack of scrutiny allows doctors and patients to be exploited by bad actors such as Theranos, which falsely claimed that its tests could diagnose multiple diseases with a single drop of blood.

“When it comes to some of these tests that doctors are recommending for patients, many doctors are just crossing their fingers and relying on the representation of the company because nobody is checking” to verify a manufacturer’s claims, said Joshua Sharfstein, MD, vice dean for public health practice and community engagement at the Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland.
 

Nearly 12,000 Labs Making Medical Tests

Although the FDA estimates there are nearly 12,000 labs manufacturing medical tests, agency officials said they don’t know how many tests are being marketed. The FDA already requires that home test kits marketed directly to consumers, such as those used to detect COVID-19, get clearance from the agency before being sold.

“There’s plenty of time for industry to get its act together to develop the data that it might need to make a premarket application,” said Peter Lurie, MD, PhD, a former associate commissioner at the FDA. In 2015, Dr. Lurie led a report outlining some of the dangers of unregulated lab tests.

For the average physician who orders lab tests, nothing is going to immediately change because of the final rule, said Dr. Lurie, now president of the Center for Science in the Public Interest, a nonprofit consumer watchdog.

“Tomorrow, this will look just the same as it does today,” Dr. Lurie said. “For the next 3 years, the companies will be scurrying behind the scenes to comply with the early stages of implementation. But most of that will be invisible to the average practitioner.”

Dr. Lurie predicted the FDA will focus its scrutiny on tests that pose the greatest potential risk to patients, such as ones used to diagnose serious diseases or guide treatment for life-threatening conditions. “The least significant tests will likely get very limited, if any, scrutiny,” said Dr. Lurie, adding that the FDA will likely issue guidance about how it plans to define low- and high-risk tests. “My suspicion is that it will be probably a small minority of products that are subject to full premarket approval.”
 

Lab Industry Groups Push Back

But imposing new rules with the potential to affect an industry’s bottom line is no easy task.

The American Clinical Laboratory Association, which represents the lab industry, said in a statement that the FDA rule will “limit access to scores of critical tests, increase healthcare costs, and undermine innovation in new diagnostics.” Another industry group, the Association for Molecular Pathology, has warned of “significant and harmful disruption to laboratory medicine.”

The two associations have filed separate lawsuits, charging that the FDA overstepped the authority granted by Congress. In their lawsuits, groups claim that lab tests are professional services, not manufactured products. The groups noted that the Centers for Medicare & Medicaid Services (CMS) already inspects lab facilities. CMS does not assess the tests’ quality or reliability.

A recent Supreme Court decision could make those lawsuits more likely to succeed, said David Simon, JD, LLM, PhD, an assistant professor of law at the Northeastern University School of Law, Boston, Massachusetts.

In the case of Loper Bright Enterprises v. Raimondo, decided in June, justices overturned a long-standing precedent known as Chevron deference, which required courts to defer to federal agencies when interpreting ambiguous laws. That means that courts no longer have to accept the FDA’s definition of a device, Dr. Simon said.

“Because judges may have more active roles in defining agency authority, federal agencies may have correspondingly less robust roles in policymaking,” Dr. Simon wrote in an editorial coauthored with Michael J. Young, MD, MPhil, of Harvard Medical School, Boston.

The Supreme Court ruling could pressure Congress to more clearly define FDA’s ruling in regulating lab tests, Dr. Simon and Dr. Young wrote.

Members of Congress first introduced a bill to clarify the FDA’s role in regulating lab tests, called the VALID Act, in 2020. The bill stalled and, despite efforts to revive it, still hasn’t passed.

FDA officials have said they remain “open to working with Congress,” noting that any future legislation about lab-developed tests would supersede their current policy.

In an interview, Dr. Simon noted the FDA significantly narrowed the scope of the final rule in response to comments from critics who objected to an earlier version of the policy proposed in 2023. The final rule carves out several categories of tests that won’t need to apply for “premarket review.”

Notably, a “grandfather clause” will allow some lab tests already on the market to continue being sold without undergoing FDA’s premarket review process. In explaining the exemption, FDA officials said they did not want doctors and patients to lose access to tests on which they rely. But Dr. Lurie noted that because the FDA views all these tests as under its jurisdiction, the agency could opt to take a closer look “at a very old device that is causing a problem today.”

The FDA also will exempt tests approved by New York State’s Clinical Laboratory Evaluation Program, which conducts its own stringent reviews. And the FDA will continue to allow hospitals to develop tests for patients within their healthcare system without going through the FDA approval process, if no FDA-approved tests are available.

Hospital-based tests play a critical role in treating infectious diseases, said Amesh Adalja, MD, an infectious diseases specialist and senior scholar at the Johns Hopkins Center for Health Security. For example, a large research hospital treating a patient with cytomegalovirus may need to develop its own test to determine whether the infection is resistant to antiviral drugs, Dr. Adalja said.

“With novel infectious disease outbreaks, researchers are able to move quickly to make diagnostic tests months and months before commercial laboratories are able to get through regulatory processes,” Dr. Adalja said.

To help scientists respond quickly to emergencies, the FDA published special guidance for labs that develop unauthorized lab tests for disease outbreaks.

Medical groups such as the American Hospital Association and Infectious Diseases Society of America remain concerned about the burden of complying with new regulations.

“Many vital tests developed in hospitals and health systems may be subjected to unnecessary and costly paperwork,” said Stacey Hughes, executive vice president of the American Hospital Association, in a statement.

Other groups, such as the American Society of Clinical Oncology, praised the new FDA policy. In comments submitted to the FDA in 2023, the cancer group said it “emphatically supports” requiring lab tests to undergo FDA review.

“We appreciate FDA action to modernize oversight of these tests and are hopeful this rule will increase focus on the need to balance rapid diagnostic innovation with patient safety and access” Everett Vokes, MD, the group’s board chair, said in a statement released after the FDA’s final rule was published.

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

The Food and Drug Administration (FDA) plans to scrutinize the safety and efficacy of lab-developed tests — those designed, manufactured, and used in a single laboratory — far more thoroughly in the future.

Under a rule finalized in April, the FDA will treat facilities that develop and use lab tests as manufacturers and regulate tests as medical devices. That means that most lab tests will need an FDA review before going on sale.

The FDA will also impose new quality standards, requiring test manufacturers to report adverse events and create a registry of lab tests under the new rule, which will be phased in over 4 years.

FDA officials have been concerned for years about the reliability of commercial lab tests, which have ballooned into a multibillion-dollar industry.

Consumer groups have long urged the FDA to regulate lab tests more strictly, arguing that the lack of scrutiny allows doctors and patients to be exploited by bad actors such as Theranos, which falsely claimed that its tests could diagnose multiple diseases with a single drop of blood.

“When it comes to some of these tests that doctors are recommending for patients, many doctors are just crossing their fingers and relying on the representation of the company because nobody is checking” to verify a manufacturer’s claims, said Joshua Sharfstein, MD, vice dean for public health practice and community engagement at the Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland.
 

Nearly 12,000 Labs Making Medical Tests

Although the FDA estimates there are nearly 12,000 labs manufacturing medical tests, agency officials said they don’t know how many tests are being marketed. The FDA already requires that home test kits marketed directly to consumers, such as those used to detect COVID-19, get clearance from the agency before being sold.

“There’s plenty of time for industry to get its act together to develop the data that it might need to make a premarket application,” said Peter Lurie, MD, PhD, a former associate commissioner at the FDA. In 2015, Dr. Lurie led a report outlining some of the dangers of unregulated lab tests.

For the average physician who orders lab tests, nothing is going to immediately change because of the final rule, said Dr. Lurie, now president of the Center for Science in the Public Interest, a nonprofit consumer watchdog.

“Tomorrow, this will look just the same as it does today,” Dr. Lurie said. “For the next 3 years, the companies will be scurrying behind the scenes to comply with the early stages of implementation. But most of that will be invisible to the average practitioner.”

Dr. Lurie predicted the FDA will focus its scrutiny on tests that pose the greatest potential risk to patients, such as ones used to diagnose serious diseases or guide treatment for life-threatening conditions. “The least significant tests will likely get very limited, if any, scrutiny,” said Dr. Lurie, adding that the FDA will likely issue guidance about how it plans to define low- and high-risk tests. “My suspicion is that it will be probably a small minority of products that are subject to full premarket approval.”
 

Lab Industry Groups Push Back

But imposing new rules with the potential to affect an industry’s bottom line is no easy task.

The American Clinical Laboratory Association, which represents the lab industry, said in a statement that the FDA rule will “limit access to scores of critical tests, increase healthcare costs, and undermine innovation in new diagnostics.” Another industry group, the Association for Molecular Pathology, has warned of “significant and harmful disruption to laboratory medicine.”

The two associations have filed separate lawsuits, charging that the FDA overstepped the authority granted by Congress. In their lawsuits, groups claim that lab tests are professional services, not manufactured products. The groups noted that the Centers for Medicare & Medicaid Services (CMS) already inspects lab facilities. CMS does not assess the tests’ quality or reliability.

A recent Supreme Court decision could make those lawsuits more likely to succeed, said David Simon, JD, LLM, PhD, an assistant professor of law at the Northeastern University School of Law, Boston, Massachusetts.

In the case of Loper Bright Enterprises v. Raimondo, decided in June, justices overturned a long-standing precedent known as Chevron deference, which required courts to defer to federal agencies when interpreting ambiguous laws. That means that courts no longer have to accept the FDA’s definition of a device, Dr. Simon said.

“Because judges may have more active roles in defining agency authority, federal agencies may have correspondingly less robust roles in policymaking,” Dr. Simon wrote in an editorial coauthored with Michael J. Young, MD, MPhil, of Harvard Medical School, Boston.

The Supreme Court ruling could pressure Congress to more clearly define FDA’s ruling in regulating lab tests, Dr. Simon and Dr. Young wrote.

Members of Congress first introduced a bill to clarify the FDA’s role in regulating lab tests, called the VALID Act, in 2020. The bill stalled and, despite efforts to revive it, still hasn’t passed.

FDA officials have said they remain “open to working with Congress,” noting that any future legislation about lab-developed tests would supersede their current policy.

In an interview, Dr. Simon noted the FDA significantly narrowed the scope of the final rule in response to comments from critics who objected to an earlier version of the policy proposed in 2023. The final rule carves out several categories of tests that won’t need to apply for “premarket review.”

Notably, a “grandfather clause” will allow some lab tests already on the market to continue being sold without undergoing FDA’s premarket review process. In explaining the exemption, FDA officials said they did not want doctors and patients to lose access to tests on which they rely. But Dr. Lurie noted that because the FDA views all these tests as under its jurisdiction, the agency could opt to take a closer look “at a very old device that is causing a problem today.”

The FDA also will exempt tests approved by New York State’s Clinical Laboratory Evaluation Program, which conducts its own stringent reviews. And the FDA will continue to allow hospitals to develop tests for patients within their healthcare system without going through the FDA approval process, if no FDA-approved tests are available.

Hospital-based tests play a critical role in treating infectious diseases, said Amesh Adalja, MD, an infectious diseases specialist and senior scholar at the Johns Hopkins Center for Health Security. For example, a large research hospital treating a patient with cytomegalovirus may need to develop its own test to determine whether the infection is resistant to antiviral drugs, Dr. Adalja said.

“With novel infectious disease outbreaks, researchers are able to move quickly to make diagnostic tests months and months before commercial laboratories are able to get through regulatory processes,” Dr. Adalja said.

To help scientists respond quickly to emergencies, the FDA published special guidance for labs that develop unauthorized lab tests for disease outbreaks.

Medical groups such as the American Hospital Association and Infectious Diseases Society of America remain concerned about the burden of complying with new regulations.

“Many vital tests developed in hospitals and health systems may be subjected to unnecessary and costly paperwork,” said Stacey Hughes, executive vice president of the American Hospital Association, in a statement.

Other groups, such as the American Society of Clinical Oncology, praised the new FDA policy. In comments submitted to the FDA in 2023, the cancer group said it “emphatically supports” requiring lab tests to undergo FDA review.

“We appreciate FDA action to modernize oversight of these tests and are hopeful this rule will increase focus on the need to balance rapid diagnostic innovation with patient safety and access” Everett Vokes, MD, the group’s board chair, said in a statement released after the FDA’s final rule was published.

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

MILAN — Psilocybin leads to a better overall outcome in the treatment of moderate to severe major depressive disorder (MDD) than the selective serotonin reuptake inhibitor (SSRI) escitalopram, results of the first long-term comparison of the two treatments suggest.

“This is the first work to compare the long-term effects of these two drugs in the context of overall well-being, not just freedom from depression,” study investigator Tommaso Barba, PhD candidate at Imperial College London in England, said in a press release. “Psilocybin outperformed escitalopram in several measures of well-being, meaning in life, work, and social functioning.”

Findings from the 6-month follow-up study of a phase 2 double-blind, randomized, controlled trial were presented at the 37th European College of Neuropsychopharmacology (ECNP) Congress and published simultaneously in The Lancet eClinicalMedicine

Addressing a Treatment ‘Mismatch’

The findings are important because they address “a mismatch” between what psychiatrists and what patients think is important, Mr. Barba said in an interview.

“Psychiatrists really focus on negative symptoms of depression. So, if you are not sad anymore, if your sleep or appetite is not impaired, they think you’re better. But if you look at what patients define as important, they say it’s the degree in which their life is meaningful, in which they can connect with people around them, in which they can function in everyday life,” Mr. Barba said.

“The study suggests that psilocybin therapy might be a more holistic treatment option for depression,” added co–first author David Erritzoe, MD, PhD, clinical director and deputy head of the Centre for Psychedelic Research, Imperial College London. “This could make a substantial difference in the overall happiness and daily activities of those suffering from depression, providing a more joined-up approach to mental health treatment.”

The initial single-center study included 59 adults with MDD (mean age, 41 years) who were randomized to receive either psilocybin or escitalopram over a 6-week period. The psilocybin arm (n = 30) received two 25-mg oral doses of psilocybin therapy (PT), and the escitalopram arm (n = 29) received 10-20 mg of daily escitalopram plus two (placebo-like) 1-mg doses of psilocybin (ET). Both groups received psychological support.

Based on change in depression scores on the 16-item Quick Inventory of Depressive Symptomatology–Self-Report (QIDS-SR-16) at week 6, the initial study results suggested noninferiority between the two treatments in terms of depressive symptoms (primary outcome), but superiority of PT for secondary outcomes including “well-being, anhedonia, social functioning, sexual functioning, and related variables, with fewer side effects compared to ET,” the researchers noted.

The new 6-month follow-up findings, with monthly questionnaires and no additional study treatment or psychiatric treatment restrictions, measured the QIDS-SR-16, plus Work and Social Adjustment Scale (WSAS), Meaning in Life Questionnaire, Flourishing Scale (FS), and Watts Connectedness Scale (WCS).

Again, both groups maintained similar results on the QIDS-SR-16, with slightly greater reductions in depressive symptoms for PT in the first month (positive false discovery rate [pFDR] = 0.021), but not thereafter.

At both 3 and 6 months, there were greater improvements in WSAS scores for the PT group (pFDR < 0.001 and pFDR = 0.01, respectively), and also greater improvements in meaning in life across all follow-up timepoints (pFDR < 0.001).

There was also greater improvement in the PT group regarding WCS at both 3 and 6 months (pFDR = 0.02, and pFDR = 0.04) and comparable FS improvements for both groups across all timepoints.

Confounding follow-up interventions may have muddied the results, with 30.7% of PT participants and 43.5% of ET participants receiving an additional intervention during this period.

The researchers conclude that while a short course of SSRIs combined with intensive therapeutic support (around 20 hours) “might be enough to induce sustained antidepressant effects,” patients treated with psilocybin showed greater improvements in general functioning, connectedness, and meaning in life.

Although not reassessed in the follow-up, the initial study showed that adverse events, particularly sexual functioning, favored psilocybin, said Mr. Barba. “The two treatments seemed to go in opposite directions with psilocybin seeming to improve it and the antidepressant to suppress it. Other side effects associated with psilocybin were less diverse — mainly headaches at the end of the day — but with escitalopram they were way more diverse and more impairing.”

Although many therapists may be unfamiliar with psilocybin-assisted psychotherapy, “it’s not a difficult skill to master. It might require some specialization, but I think if you’re a good psychotherapist, you can learn how to implement psilocybin into your practice,” he said.

“Normally the journey is quite inward, so patients do not require active support during the psychedelic experience [around 6 hours]. Sometimes they do require some hand-holding, or helping them to ‘let go’, or breathing exercises. The important part is the integration work that comes afterwards,” Mr. Barba added.

He said he envisions a therapy program that involves “psychiatrists working together with psychotherapists. The psychotherapists would be more in charge of the active guiding, and the psychiatrist would do the prescribing, with the follow-up psychological support on Zoom.”

He added a word of caution for therapists that “psilocybin requires active confrontation of painful, negative emotions and people who take this drug need to be open and prepared for the idea that they are going into a state where they may probably end up crying and confronting whatever they are maybe running away from in their lives. Not everyone may want to do this.”
 

A New Treatment Paradigm?

In a comment, Johan Lundberg, MD, PhD, adjunct professor of psychiatry at the Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden, said the study addresses a key outstanding question about the long-term effects of one or two doses of psilocybin.

“It’s a 6-month follow-up of a short treatment intervention, so in that sense, it’s of high interest. It has been talked about that psilocybin might have a long-term effect, but this is the first study that has followed this for a longer term.”

But Dr. Lundberg also pointed out that one shortcoming of the study is the diversity of treatments following the intervention.

“They didn’t have control over whether patients received other treatments or when they started. So, that is a key concern. But they transparently reported that, and we do know there was a difference in reported ability to perform activities of daily life, and that is important.”

He added that if psilocybin is eventually approved, it would likely come with an education package for providers — “which is already the case with other treatments like ECT [electroconvulsive therapy] or TMS [transcranial magnetic stimulation] — you have to learn how to do it.”

James Rucker, MD, PhD, psychiatrist and senior clinical lecturer at King’s College London, who was not involved in the research, also noted that they have tended to attribute differences observed in this study to comparative differences between the drugs themselves.

However, he noted, it is also possible that the results reflect biased reporting between groups. This is more likely here because studies involving psilocybin tend to attract those with positive preconceptions about psilocybin and negative preconceptions about conventional antidepressants, and study participants were unblinded during the long-term follow-up phase, so knew which condition they were allocated to.

“This said, the nature of depression varies hugely between individuals, and this calls for the development of a similarly varied suite of treatment paradigms. Psilocybin therapy is certainly a different paradigm of treatment to escitalopram. The observation of similar levels of effectiveness to antidepressants here is encouraging to see alongside the much larger trials of psilocybin currently underway here in the UK, Europe, and the US,” Dr. Rucker added.

This work was supported by The Alexander Mosley Charitable Trust and by the founding partners of Imperial College London’s Centre for Psychedelic Research.

Mr. Barba reported having received consulting fees from Adamo Bioscience. Both Dr. Lundberg and Dr. Rucker are involved in psilocybin research, but neither reported financial links.

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

MILAN — Psilocybin leads to a better overall outcome in the treatment of moderate to severe major depressive disorder (MDD) than the selective serotonin reuptake inhibitor (SSRI) escitalopram, results of the first long-term comparison of the two treatments suggest.

“This is the first work to compare the long-term effects of these two drugs in the context of overall well-being, not just freedom from depression,” study investigator Tommaso Barba, PhD candidate at Imperial College London in England, said in a press release. “Psilocybin outperformed escitalopram in several measures of well-being, meaning in life, work, and social functioning.”

Findings from the 6-month follow-up study of a phase 2 double-blind, randomized, controlled trial were presented at the 37th European College of Neuropsychopharmacology (ECNP) Congress and published simultaneously in The Lancet eClinicalMedicine

Addressing a Treatment ‘Mismatch’

The findings are important because they address “a mismatch” between what psychiatrists and what patients think is important, Mr. Barba said in an interview.

“Psychiatrists really focus on negative symptoms of depression. So, if you are not sad anymore, if your sleep or appetite is not impaired, they think you’re better. But if you look at what patients define as important, they say it’s the degree in which their life is meaningful, in which they can connect with people around them, in which they can function in everyday life,” Mr. Barba said.

“The study suggests that psilocybin therapy might be a more holistic treatment option for depression,” added co–first author David Erritzoe, MD, PhD, clinical director and deputy head of the Centre for Psychedelic Research, Imperial College London. “This could make a substantial difference in the overall happiness and daily activities of those suffering from depression, providing a more joined-up approach to mental health treatment.”

The initial single-center study included 59 adults with MDD (mean age, 41 years) who were randomized to receive either psilocybin or escitalopram over a 6-week period. The psilocybin arm (n = 30) received two 25-mg oral doses of psilocybin therapy (PT), and the escitalopram arm (n = 29) received 10-20 mg of daily escitalopram plus two (placebo-like) 1-mg doses of psilocybin (ET). Both groups received psychological support.

Based on change in depression scores on the 16-item Quick Inventory of Depressive Symptomatology–Self-Report (QIDS-SR-16) at week 6, the initial study results suggested noninferiority between the two treatments in terms of depressive symptoms (primary outcome), but superiority of PT for secondary outcomes including “well-being, anhedonia, social functioning, sexual functioning, and related variables, with fewer side effects compared to ET,” the researchers noted.

The new 6-month follow-up findings, with monthly questionnaires and no additional study treatment or psychiatric treatment restrictions, measured the QIDS-SR-16, plus Work and Social Adjustment Scale (WSAS), Meaning in Life Questionnaire, Flourishing Scale (FS), and Watts Connectedness Scale (WCS).

Again, both groups maintained similar results on the QIDS-SR-16, with slightly greater reductions in depressive symptoms for PT in the first month (positive false discovery rate [pFDR] = 0.021), but not thereafter.

At both 3 and 6 months, there were greater improvements in WSAS scores for the PT group (pFDR < 0.001 and pFDR = 0.01, respectively), and also greater improvements in meaning in life across all follow-up timepoints (pFDR < 0.001).

There was also greater improvement in the PT group regarding WCS at both 3 and 6 months (pFDR = 0.02, and pFDR = 0.04) and comparable FS improvements for both groups across all timepoints.

Confounding follow-up interventions may have muddied the results, with 30.7% of PT participants and 43.5% of ET participants receiving an additional intervention during this period.

The researchers conclude that while a short course of SSRIs combined with intensive therapeutic support (around 20 hours) “might be enough to induce sustained antidepressant effects,” patients treated with psilocybin showed greater improvements in general functioning, connectedness, and meaning in life.

Although not reassessed in the follow-up, the initial study showed that adverse events, particularly sexual functioning, favored psilocybin, said Mr. Barba. “The two treatments seemed to go in opposite directions with psilocybin seeming to improve it and the antidepressant to suppress it. Other side effects associated with psilocybin were less diverse — mainly headaches at the end of the day — but with escitalopram they were way more diverse and more impairing.”

Although many therapists may be unfamiliar with psilocybin-assisted psychotherapy, “it’s not a difficult skill to master. It might require some specialization, but I think if you’re a good psychotherapist, you can learn how to implement psilocybin into your practice,” he said.

“Normally the journey is quite inward, so patients do not require active support during the psychedelic experience [around 6 hours]. Sometimes they do require some hand-holding, or helping them to ‘let go’, or breathing exercises. The important part is the integration work that comes afterwards,” Mr. Barba added.

He said he envisions a therapy program that involves “psychiatrists working together with psychotherapists. The psychotherapists would be more in charge of the active guiding, and the psychiatrist would do the prescribing, with the follow-up psychological support on Zoom.”

He added a word of caution for therapists that “psilocybin requires active confrontation of painful, negative emotions and people who take this drug need to be open and prepared for the idea that they are going into a state where they may probably end up crying and confronting whatever they are maybe running away from in their lives. Not everyone may want to do this.”
 

A New Treatment Paradigm?

In a comment, Johan Lundberg, MD, PhD, adjunct professor of psychiatry at the Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden, said the study addresses a key outstanding question about the long-term effects of one or two doses of psilocybin.

“It’s a 6-month follow-up of a short treatment intervention, so in that sense, it’s of high interest. It has been talked about that psilocybin might have a long-term effect, but this is the first study that has followed this for a longer term.”

But Dr. Lundberg also pointed out that one shortcoming of the study is the diversity of treatments following the intervention.

“They didn’t have control over whether patients received other treatments or when they started. So, that is a key concern. But they transparently reported that, and we do know there was a difference in reported ability to perform activities of daily life, and that is important.”

He added that if psilocybin is eventually approved, it would likely come with an education package for providers — “which is already the case with other treatments like ECT [electroconvulsive therapy] or TMS [transcranial magnetic stimulation] — you have to learn how to do it.”

James Rucker, MD, PhD, psychiatrist and senior clinical lecturer at King’s College London, who was not involved in the research, also noted that they have tended to attribute differences observed in this study to comparative differences between the drugs themselves.

However, he noted, it is also possible that the results reflect biased reporting between groups. This is more likely here because studies involving psilocybin tend to attract those with positive preconceptions about psilocybin and negative preconceptions about conventional antidepressants, and study participants were unblinded during the long-term follow-up phase, so knew which condition they were allocated to.

“This said, the nature of depression varies hugely between individuals, and this calls for the development of a similarly varied suite of treatment paradigms. Psilocybin therapy is certainly a different paradigm of treatment to escitalopram. The observation of similar levels of effectiveness to antidepressants here is encouraging to see alongside the much larger trials of psilocybin currently underway here in the UK, Europe, and the US,” Dr. Rucker added.

This work was supported by The Alexander Mosley Charitable Trust and by the founding partners of Imperial College London’s Centre for Psychedelic Research.

Mr. Barba reported having received consulting fees from Adamo Bioscience. Both Dr. Lundberg and Dr. Rucker are involved in psilocybin research, but neither reported financial links.

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

MILAN — Psilocybin leads to a better overall outcome in the treatment of moderate to severe major depressive disorder (MDD) than the selective serotonin reuptake inhibitor (SSRI) escitalopram, results of the first long-term comparison of the two treatments suggest.

“This is the first work to compare the long-term effects of these two drugs in the context of overall well-being, not just freedom from depression,” study investigator Tommaso Barba, PhD candidate at Imperial College London in England, said in a press release. “Psilocybin outperformed escitalopram in several measures of well-being, meaning in life, work, and social functioning.”

Findings from the 6-month follow-up study of a phase 2 double-blind, randomized, controlled trial were presented at the 37th European College of Neuropsychopharmacology (ECNP) Congress and published simultaneously in The Lancet eClinicalMedicine

Addressing a Treatment ‘Mismatch’

The findings are important because they address “a mismatch” between what psychiatrists and what patients think is important, Mr. Barba said in an interview.

“Psychiatrists really focus on negative symptoms of depression. So, if you are not sad anymore, if your sleep or appetite is not impaired, they think you’re better. But if you look at what patients define as important, they say it’s the degree in which their life is meaningful, in which they can connect with people around them, in which they can function in everyday life,” Mr. Barba said.

“The study suggests that psilocybin therapy might be a more holistic treatment option for depression,” added co–first author David Erritzoe, MD, PhD, clinical director and deputy head of the Centre for Psychedelic Research, Imperial College London. “This could make a substantial difference in the overall happiness and daily activities of those suffering from depression, providing a more joined-up approach to mental health treatment.”

The initial single-center study included 59 adults with MDD (mean age, 41 years) who were randomized to receive either psilocybin or escitalopram over a 6-week period. The psilocybin arm (n = 30) received two 25-mg oral doses of psilocybin therapy (PT), and the escitalopram arm (n = 29) received 10-20 mg of daily escitalopram plus two (placebo-like) 1-mg doses of psilocybin (ET). Both groups received psychological support.

Based on change in depression scores on the 16-item Quick Inventory of Depressive Symptomatology–Self-Report (QIDS-SR-16) at week 6, the initial study results suggested noninferiority between the two treatments in terms of depressive symptoms (primary outcome), but superiority of PT for secondary outcomes including “well-being, anhedonia, social functioning, sexual functioning, and related variables, with fewer side effects compared to ET,” the researchers noted.

The new 6-month follow-up findings, with monthly questionnaires and no additional study treatment or psychiatric treatment restrictions, measured the QIDS-SR-16, plus Work and Social Adjustment Scale (WSAS), Meaning in Life Questionnaire, Flourishing Scale (FS), and Watts Connectedness Scale (WCS).

Again, both groups maintained similar results on the QIDS-SR-16, with slightly greater reductions in depressive symptoms for PT in the first month (positive false discovery rate [pFDR] = 0.021), but not thereafter.

At both 3 and 6 months, there were greater improvements in WSAS scores for the PT group (pFDR < 0.001 and pFDR = 0.01, respectively), and also greater improvements in meaning in life across all follow-up timepoints (pFDR < 0.001).

There was also greater improvement in the PT group regarding WCS at both 3 and 6 months (pFDR = 0.02, and pFDR = 0.04) and comparable FS improvements for both groups across all timepoints.

Confounding follow-up interventions may have muddied the results, with 30.7% of PT participants and 43.5% of ET participants receiving an additional intervention during this period.

The researchers conclude that while a short course of SSRIs combined with intensive therapeutic support (around 20 hours) “might be enough to induce sustained antidepressant effects,” patients treated with psilocybin showed greater improvements in general functioning, connectedness, and meaning in life.

Although not reassessed in the follow-up, the initial study showed that adverse events, particularly sexual functioning, favored psilocybin, said Mr. Barba. “The two treatments seemed to go in opposite directions with psilocybin seeming to improve it and the antidepressant to suppress it. Other side effects associated with psilocybin were less diverse — mainly headaches at the end of the day — but with escitalopram they were way more diverse and more impairing.”

Although many therapists may be unfamiliar with psilocybin-assisted psychotherapy, “it’s not a difficult skill to master. It might require some specialization, but I think if you’re a good psychotherapist, you can learn how to implement psilocybin into your practice,” he said.

“Normally the journey is quite inward, so patients do not require active support during the psychedelic experience [around 6 hours]. Sometimes they do require some hand-holding, or helping them to ‘let go’, or breathing exercises. The important part is the integration work that comes afterwards,” Mr. Barba added.

He said he envisions a therapy program that involves “psychiatrists working together with psychotherapists. The psychotherapists would be more in charge of the active guiding, and the psychiatrist would do the prescribing, with the follow-up psychological support on Zoom.”

He added a word of caution for therapists that “psilocybin requires active confrontation of painful, negative emotions and people who take this drug need to be open and prepared for the idea that they are going into a state where they may probably end up crying and confronting whatever they are maybe running away from in their lives. Not everyone may want to do this.”
 

A New Treatment Paradigm?

In a comment, Johan Lundberg, MD, PhD, adjunct professor of psychiatry at the Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden, said the study addresses a key outstanding question about the long-term effects of one or two doses of psilocybin.

“It’s a 6-month follow-up of a short treatment intervention, so in that sense, it’s of high interest. It has been talked about that psilocybin might have a long-term effect, but this is the first study that has followed this for a longer term.”

But Dr. Lundberg also pointed out that one shortcoming of the study is the diversity of treatments following the intervention.

“They didn’t have control over whether patients received other treatments or when they started. So, that is a key concern. But they transparently reported that, and we do know there was a difference in reported ability to perform activities of daily life, and that is important.”

He added that if psilocybin is eventually approved, it would likely come with an education package for providers — “which is already the case with other treatments like ECT [electroconvulsive therapy] or TMS [transcranial magnetic stimulation] — you have to learn how to do it.”

James Rucker, MD, PhD, psychiatrist and senior clinical lecturer at King’s College London, who was not involved in the research, also noted that they have tended to attribute differences observed in this study to comparative differences between the drugs themselves.

However, he noted, it is also possible that the results reflect biased reporting between groups. This is more likely here because studies involving psilocybin tend to attract those with positive preconceptions about psilocybin and negative preconceptions about conventional antidepressants, and study participants were unblinded during the long-term follow-up phase, so knew which condition they were allocated to.

“This said, the nature of depression varies hugely between individuals, and this calls for the development of a similarly varied suite of treatment paradigms. Psilocybin therapy is certainly a different paradigm of treatment to escitalopram. The observation of similar levels of effectiveness to antidepressants here is encouraging to see alongside the much larger trials of psilocybin currently underway here in the UK, Europe, and the US,” Dr. Rucker added.

This work was supported by The Alexander Mosley Charitable Trust and by the founding partners of Imperial College London’s Centre for Psychedelic Research.

Mr. Barba reported having received consulting fees from Adamo Bioscience. Both Dr. Lundberg and Dr. Rucker are involved in psilocybin research, but neither reported financial links.

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

This transcript has been edited for clarity. 

There’s a very interesting story in the medical press. A few years ago, a plastic surgeon named Edmond Cabbabe was preparing to do a follow-up cosmetic procedure on his wife at Mercy Hospital South, which is a big hospital in the St. Louis, Missouri, area.

He put her on the operating schedule, and he had done that when he had performed the original operation on her. On the day of the surgery, he got a call from the hospital saying the procedure was canceled. They said that the hospital’s policy, maybe a new one, would not allow doctors to operate on family members.

This physician was a past president of the Missouri State Medical Association. I think he was also on the board or president of the American Medical Association (AMA) Foundation. This was a physician not only in a skilled area where he felt confident he could take care of his wife, but also someone who was prominent in medical politics and medical policy.

The AMA forever has had a policy that says don’t treat relatives. This physician basically said, I think that policy is too restrictive, too cautious, and it doesn’t make much sense to continue to say that you can’t treat family and friends.

By implication, he was saying, I know exactly what I’m doing in my field and I know exactly what I’m doing with her procedure. I should have a right to perform it. I think I do a great job and I’d be best for her.

If you look at medical boards, every once in a while in some state, someone is brought up on a charge of doing different things with family members and saying that they’re going to get censured. They don’t usually lose their license, but they get a reprimand or get told that is just not ethical to do.

I think, in the long run, the policy about not treating your family and friends makes sense. The problem is, as is well known from the social sciences and psychology, people get biased when they deal with those they care about, love, and hold close to them.

It’s hard for the doctor to be objective when dealing with people that they really like or love. It’s also difficult for patients because they may not want to bring up something or they are uncomfortable talking with a doctor who’s a family member or close friend. They may not want to complain. They may be a little bit embarrassed about things. It just adds an emotional edge, I think, that’s difficult.

All that said, do I know doctors who regularly prescribe, say, an ointment for something that’s itchy or some kind of a pill when allergy season breaks out? I do. Do I think they’re acting in a horribly unethical manner? I don’t.

You need some judgment here. There are absolutely minor things where objectivity, fear, and anxiety are not in play. You’re going to be able to prescribe the routine thing for the routine itch without worrying too much about whether it’s a stranger, a friend, or your daughter.

What sorts of things am I really talking about when I say that minor variability ought to be allowed? It’s one thing when someone has poison ivy and they’re going to need some kind of standard medicine to treat it. A very different area that’s much more dangerous, and one I would avoid, is in the mental health field, and for that matter, the pain field.

It’s tempting to say: “Oh, my relative is just having a bad time. I’ll give her a little bit of antidepressant medicine,” or “They seem to be having pain after an operation or something, and I’m going to give them a little bit of pain meds just to get them through.”

Those areas are flying red flags. It’s easy to abuse and easy for someone to become a user and manipulate a friend or a doctor who’s a relative into getting things that another doctor wouldn’t be giving. I think that’s the space where you’ve got to exercise extreme caution.

Time and again, when those people get called up in front of the boards for treating relatives, it’s in those spaces of mental health, anxiety, and pain control. Again, when you know that there’s a likelihood of abuse, I think that’s the place where the line has to hold. Don’t treat the relative. Don’t treat the friend.

At the end of the day, I wouldn’t change the AMA policy. I think we should keep it in place and morally try to discourage doctors from caring for those they’re close to or they have emotional ties to.

At the same time, as with all ethical situations, there has to be a little bit of wiggle room for those super-minor cases where it just makes sense to say: “You don’t have to go find somebody else to do this. I can prescribe this ointment or this minor thing for you. No one’s objectivity is going to be soured, and you’re not going to feel in any way at risk because I’m going to prescribe this for you.”

Common sense ought to prevail. The default position is don’t do it; however, maybe with a tiny bit of space for what’s minor, what’s routine, and what really does just save people some inconvenience, there I might just give a little.

Dr. Caplan, Director, Division of Medical Ethics, New York University Langone Medical Center, New York City, has disclosed relationships with Johnson & Johnson’s Panel for Compassionate Drug Use and Medscape.

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

This transcript has been edited for clarity. 

There’s a very interesting story in the medical press. A few years ago, a plastic surgeon named Edmond Cabbabe was preparing to do a follow-up cosmetic procedure on his wife at Mercy Hospital South, which is a big hospital in the St. Louis, Missouri, area.

He put her on the operating schedule, and he had done that when he had performed the original operation on her. On the day of the surgery, he got a call from the hospital saying the procedure was canceled. They said that the hospital’s policy, maybe a new one, would not allow doctors to operate on family members.

This physician was a past president of the Missouri State Medical Association. I think he was also on the board or president of the American Medical Association (AMA) Foundation. This was a physician not only in a skilled area where he felt confident he could take care of his wife, but also someone who was prominent in medical politics and medical policy.

The AMA forever has had a policy that says don’t treat relatives. This physician basically said, I think that policy is too restrictive, too cautious, and it doesn’t make much sense to continue to say that you can’t treat family and friends.

By implication, he was saying, I know exactly what I’m doing in my field and I know exactly what I’m doing with her procedure. I should have a right to perform it. I think I do a great job and I’d be best for her.

If you look at medical boards, every once in a while in some state, someone is brought up on a charge of doing different things with family members and saying that they’re going to get censured. They don’t usually lose their license, but they get a reprimand or get told that is just not ethical to do.

I think, in the long run, the policy about not treating your family and friends makes sense. The problem is, as is well known from the social sciences and psychology, people get biased when they deal with those they care about, love, and hold close to them.

It’s hard for the doctor to be objective when dealing with people that they really like or love. It’s also difficult for patients because they may not want to bring up something or they are uncomfortable talking with a doctor who’s a family member or close friend. They may not want to complain. They may be a little bit embarrassed about things. It just adds an emotional edge, I think, that’s difficult.

All that said, do I know doctors who regularly prescribe, say, an ointment for something that’s itchy or some kind of a pill when allergy season breaks out? I do. Do I think they’re acting in a horribly unethical manner? I don’t.

You need some judgment here. There are absolutely minor things where objectivity, fear, and anxiety are not in play. You’re going to be able to prescribe the routine thing for the routine itch without worrying too much about whether it’s a stranger, a friend, or your daughter.

What sorts of things am I really talking about when I say that minor variability ought to be allowed? It’s one thing when someone has poison ivy and they’re going to need some kind of standard medicine to treat it. A very different area that’s much more dangerous, and one I would avoid, is in the mental health field, and for that matter, the pain field.

It’s tempting to say: “Oh, my relative is just having a bad time. I’ll give her a little bit of antidepressant medicine,” or “They seem to be having pain after an operation or something, and I’m going to give them a little bit of pain meds just to get them through.”

Those areas are flying red flags. It’s easy to abuse and easy for someone to become a user and manipulate a friend or a doctor who’s a relative into getting things that another doctor wouldn’t be giving. I think that’s the space where you’ve got to exercise extreme caution.

Time and again, when those people get called up in front of the boards for treating relatives, it’s in those spaces of mental health, anxiety, and pain control. Again, when you know that there’s a likelihood of abuse, I think that’s the place where the line has to hold. Don’t treat the relative. Don’t treat the friend.

At the end of the day, I wouldn’t change the AMA policy. I think we should keep it in place and morally try to discourage doctors from caring for those they’re close to or they have emotional ties to.

At the same time, as with all ethical situations, there has to be a little bit of wiggle room for those super-minor cases where it just makes sense to say: “You don’t have to go find somebody else to do this. I can prescribe this ointment or this minor thing for you. No one’s objectivity is going to be soured, and you’re not going to feel in any way at risk because I’m going to prescribe this for you.”

Common sense ought to prevail. The default position is don’t do it; however, maybe with a tiny bit of space for what’s minor, what’s routine, and what really does just save people some inconvenience, there I might just give a little.

Dr. Caplan, Director, Division of Medical Ethics, New York University Langone Medical Center, New York City, has disclosed relationships with Johnson & Johnson’s Panel for Compassionate Drug Use and Medscape.

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

This transcript has been edited for clarity. 

There’s a very interesting story in the medical press. A few years ago, a plastic surgeon named Edmond Cabbabe was preparing to do a follow-up cosmetic procedure on his wife at Mercy Hospital South, which is a big hospital in the St. Louis, Missouri, area.

He put her on the operating schedule, and he had done that when he had performed the original operation on her. On the day of the surgery, he got a call from the hospital saying the procedure was canceled. They said that the hospital’s policy, maybe a new one, would not allow doctors to operate on family members.

This physician was a past president of the Missouri State Medical Association. I think he was also on the board or president of the American Medical Association (AMA) Foundation. This was a physician not only in a skilled area where he felt confident he could take care of his wife, but also someone who was prominent in medical politics and medical policy.

The AMA forever has had a policy that says don’t treat relatives. This physician basically said, I think that policy is too restrictive, too cautious, and it doesn’t make much sense to continue to say that you can’t treat family and friends.

By implication, he was saying, I know exactly what I’m doing in my field and I know exactly what I’m doing with her procedure. I should have a right to perform it. I think I do a great job and I’d be best for her.

If you look at medical boards, every once in a while in some state, someone is brought up on a charge of doing different things with family members and saying that they’re going to get censured. They don’t usually lose their license, but they get a reprimand or get told that is just not ethical to do.

I think, in the long run, the policy about not treating your family and friends makes sense. The problem is, as is well known from the social sciences and psychology, people get biased when they deal with those they care about, love, and hold close to them.

It’s hard for the doctor to be objective when dealing with people that they really like or love. It’s also difficult for patients because they may not want to bring up something or they are uncomfortable talking with a doctor who’s a family member or close friend. They may not want to complain. They may be a little bit embarrassed about things. It just adds an emotional edge, I think, that’s difficult.

All that said, do I know doctors who regularly prescribe, say, an ointment for something that’s itchy or some kind of a pill when allergy season breaks out? I do. Do I think they’re acting in a horribly unethical manner? I don’t.

You need some judgment here. There are absolutely minor things where objectivity, fear, and anxiety are not in play. You’re going to be able to prescribe the routine thing for the routine itch without worrying too much about whether it’s a stranger, a friend, or your daughter.

What sorts of things am I really talking about when I say that minor variability ought to be allowed? It’s one thing when someone has poison ivy and they’re going to need some kind of standard medicine to treat it. A very different area that’s much more dangerous, and one I would avoid, is in the mental health field, and for that matter, the pain field.

It’s tempting to say: “Oh, my relative is just having a bad time. I’ll give her a little bit of antidepressant medicine,” or “They seem to be having pain after an operation or something, and I’m going to give them a little bit of pain meds just to get them through.”

Those areas are flying red flags. It’s easy to abuse and easy for someone to become a user and manipulate a friend or a doctor who’s a relative into getting things that another doctor wouldn’t be giving. I think that’s the space where you’ve got to exercise extreme caution.

Time and again, when those people get called up in front of the boards for treating relatives, it’s in those spaces of mental health, anxiety, and pain control. Again, when you know that there’s a likelihood of abuse, I think that’s the place where the line has to hold. Don’t treat the relative. Don’t treat the friend.

At the end of the day, I wouldn’t change the AMA policy. I think we should keep it in place and morally try to discourage doctors from caring for those they’re close to or they have emotional ties to.

At the same time, as with all ethical situations, there has to be a little bit of wiggle room for those super-minor cases where it just makes sense to say: “You don’t have to go find somebody else to do this. I can prescribe this ointment or this minor thing for you. No one’s objectivity is going to be soured, and you’re not going to feel in any way at risk because I’m going to prescribe this for you.”

Common sense ought to prevail. The default position is don’t do it; however, maybe with a tiny bit of space for what’s minor, what’s routine, and what really does just save people some inconvenience, there I might just give a little.

Dr. Caplan, Director, Division of Medical Ethics, New York University Langone Medical Center, New York City, has disclosed relationships with Johnson & Johnson’s Panel for Compassionate Drug Use and Medscape.

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

NEW YORK — Underrepresentation by gender and race in major clinical trials has been a cause for complaint for decades, but the Food and Drug Administration (FDA) has drafted a regulatory solution to this issue expected to be implemented sometime in 2025.

This initiative, known as the FDA’s Diversity Action Plan (DAP), will require plans for all pivotal and phase 3 trials to provide details in their design of how diversity will be achieved or, if there are no plans for diversity, the reason why, according to Valerie M. Harvey, MD, MPH, associate clinical professor, Edward Via College of Osteopathic Medicine, Blacksburg, Virginia. These rules will be codified, she said at the 2024 Skin of Color Update.

Once the DAP is enacted, “the sponsor must specify the rationale and goals for study enrollment by age, ethnicity, sex, and race,” she said. Furthermore, the submission to the FDA must “describe the methods to meet the diversity benchmarks.”
 

Lack of Trial Diversity Is Common Across Medicine

Although she focused on the relevance of this initiative to dermatology, Dr. Harvey said the lack of diversity in clinical trials is pervasive throughout medicine. In one survey of randomized controlled trials, less than 60% of trials even specified the race and ethnicity of the participants. In recent psoriasis trials, only 30% met a diversity definition of ≥ 20% of patients identifying as minority (Black, Hispanic, Asian, or other non-White group), said Dr. Harvey, who practices dermatology in Newport News, Virginia.

The FDA draft guidance for the DAP was released in June 2024 and is now available for submitting comments (until September 26). The plan is expected to be published in June 2025, according to Dr. Harvey. It will pertain to all pivotal and phase 3 trials enrolling 180 days after the publication date and will be relevant to all drugs and biologics as well as certain devices.

This initiative could be a critical step toward ensuring diversity in major clinical trials after years of stagnation, Dr. Harvey said, noting that despite repeated calls for more diversity in clinical trials, the literature suggests “little progress.”

However, she said that increasing diversity in clinical trials is just one step toward gathering data about the generalizability of efficacy and safety across racial and ethnic groups. A much more complex issue involves how race and ethnicity are defined in order to understand differences, if any, for efficacy and risk.

“Race is a dynamic social construct and a poor measure for biologic variation and skin color,” Dr. Harvey said. This means that work is needed to address the more complex issue of race and ethnicity stratification that will help clinicians understand the relative benefits and risks for the drugs in these trials.

Rather than differences based on genetic or other sources of biologic differences, she said, outcomes by race alone are often suspected of reflecting disparities in access to healthcare rather than a difference in therapeutic response.
 

Skin Color Is Inadequate to Define Race

When stratifying patients by race or ethnicity, Dr. Harvey said that “we have to be very, very careful in considering the study purpose and what the study question is.” A study attempting to compare benefits and risks among subgroups by race or ethnicity will require descriptors beyond skin color.

The recognized limitations of measuring skin tone as a surrogate of race are one reason for widespread interest in moving away from the Fitzpatrick skin type (FST) rating that has been widely considered a standard, according to Dr. Harvey. Several alternatives have been proposed, including the Monk Skin Tone Scale, the Individual Typology Angle, and the Eumelanin Human Skin Color Scale, but she cautioned that these are less well validated and generally have the limitations of the FST.

If skin color was ever useful for grouping individuals on the basis of shared physiology, growing rates of intermarriage and immigration have made skin color increasingly irrelevant to racial identity. If the goal is to evaluate the safety and efficacy of drugs across racial groups and ethnicities, the characterization of populations will almost certainly require multiple descriptors and biomarkers, she said.

“It is very important to have many tools for characterizing patients by skin type,” Susan Taylor, MD, professor of dermatology and vice chair for diversity, equity, and inclusion for the Department of Dermatology, University of Pennsylvania, Philadelphia, said in an interview at the meeting.

The reason is “there are limitations to all of them,” she said, noting also that the questions being asked about how and if skin color and race are relevant to therapeutic options differ by the question, such as innate response or access to care.

Dr. Taylor is part of a workshop that she said is evaluating a combination of instruments for characterizing skin color and race in ways relevant to the specific question being asked.

The solutions might differ. While simple clinical assessments involving skin color might be made with methods captured on a smartphone app, Dr. Taylor acknowledged that far more complex tools might be required to document the effect of racial or ethnic differences in drug efficacy and safety in a research setting.

Outside of a research setting, any tools that might be useful for assessing race as a variable must be practical, according to Dr. Harvey. She suggested that these must be time efficient, of reasonable cost, and most importantly, reliable.

Tools meeting these criteria do not currently exist, but Dr. Harvey said the work is underway. She expects a “top-down” collaborative approach to validate alternatives to the FST. If such tools can be developed with buy-in from the FDA, they might be particularly useful for translating trial data to patient care, she added.

Dr. Harvey reported financial relationships with AbbVie, Bristol-Myers Squibb, Janssen, Johnson & Johnson, L’Oréal, and SkinCeuticals. Dr. Taylor, president-elect of the American Academy of Dermatology, reported financial relationships with more than 25 pharmaceutical and cosmetic companies.

A version of this article appeared on Medscape.com.

NEW YORK — Underrepresentation by gender and race in major clinical trials has been a cause for complaint for decades, but the Food and Drug Administration (FDA) has drafted a regulatory solution to this issue expected to be implemented sometime in 2025.

This initiative, known as the FDA’s Diversity Action Plan (DAP), will require plans for all pivotal and phase 3 trials to provide details in their design of how diversity will be achieved or, if there are no plans for diversity, the reason why, according to Valerie M. Harvey, MD, MPH, associate clinical professor, Edward Via College of Osteopathic Medicine, Blacksburg, Virginia. These rules will be codified, she said at the 2024 Skin of Color Update.

Once the DAP is enacted, “the sponsor must specify the rationale and goals for study enrollment by age, ethnicity, sex, and race,” she said. Furthermore, the submission to the FDA must “describe the methods to meet the diversity benchmarks.”
 

Lack of Trial Diversity Is Common Across Medicine

Although she focused on the relevance of this initiative to dermatology, Dr. Harvey said the lack of diversity in clinical trials is pervasive throughout medicine. In one survey of randomized controlled trials, less than 60% of trials even specified the race and ethnicity of the participants. In recent psoriasis trials, only 30% met a diversity definition of ≥ 20% of patients identifying as minority (Black, Hispanic, Asian, or other non-White group), said Dr. Harvey, who practices dermatology in Newport News, Virginia.

The FDA draft guidance for the DAP was released in June 2024 and is now available for submitting comments (until September 26). The plan is expected to be published in June 2025, according to Dr. Harvey. It will pertain to all pivotal and phase 3 trials enrolling 180 days after the publication date and will be relevant to all drugs and biologics as well as certain devices.

This initiative could be a critical step toward ensuring diversity in major clinical trials after years of stagnation, Dr. Harvey said, noting that despite repeated calls for more diversity in clinical trials, the literature suggests “little progress.”

However, she said that increasing diversity in clinical trials is just one step toward gathering data about the generalizability of efficacy and safety across racial and ethnic groups. A much more complex issue involves how race and ethnicity are defined in order to understand differences, if any, for efficacy and risk.

“Race is a dynamic social construct and a poor measure for biologic variation and skin color,” Dr. Harvey said. This means that work is needed to address the more complex issue of race and ethnicity stratification that will help clinicians understand the relative benefits and risks for the drugs in these trials.

Rather than differences based on genetic or other sources of biologic differences, she said, outcomes by race alone are often suspected of reflecting disparities in access to healthcare rather than a difference in therapeutic response.
 

Skin Color Is Inadequate to Define Race

When stratifying patients by race or ethnicity, Dr. Harvey said that “we have to be very, very careful in considering the study purpose and what the study question is.” A study attempting to compare benefits and risks among subgroups by race or ethnicity will require descriptors beyond skin color.

The recognized limitations of measuring skin tone as a surrogate of race are one reason for widespread interest in moving away from the Fitzpatrick skin type (FST) rating that has been widely considered a standard, according to Dr. Harvey. Several alternatives have been proposed, including the Monk Skin Tone Scale, the Individual Typology Angle, and the Eumelanin Human Skin Color Scale, but she cautioned that these are less well validated and generally have the limitations of the FST.

If skin color was ever useful for grouping individuals on the basis of shared physiology, growing rates of intermarriage and immigration have made skin color increasingly irrelevant to racial identity. If the goal is to evaluate the safety and efficacy of drugs across racial groups and ethnicities, the characterization of populations will almost certainly require multiple descriptors and biomarkers, she said.

“It is very important to have many tools for characterizing patients by skin type,” Susan Taylor, MD, professor of dermatology and vice chair for diversity, equity, and inclusion for the Department of Dermatology, University of Pennsylvania, Philadelphia, said in an interview at the meeting.

The reason is “there are limitations to all of them,” she said, noting also that the questions being asked about how and if skin color and race are relevant to therapeutic options differ by the question, such as innate response or access to care.

Dr. Taylor is part of a workshop that she said is evaluating a combination of instruments for characterizing skin color and race in ways relevant to the specific question being asked.

The solutions might differ. While simple clinical assessments involving skin color might be made with methods captured on a smartphone app, Dr. Taylor acknowledged that far more complex tools might be required to document the effect of racial or ethnic differences in drug efficacy and safety in a research setting.

Outside of a research setting, any tools that might be useful for assessing race as a variable must be practical, according to Dr. Harvey. She suggested that these must be time efficient, of reasonable cost, and most importantly, reliable.

Tools meeting these criteria do not currently exist, but Dr. Harvey said the work is underway. She expects a “top-down” collaborative approach to validate alternatives to the FST. If such tools can be developed with buy-in from the FDA, they might be particularly useful for translating trial data to patient care, she added.

Dr. Harvey reported financial relationships with AbbVie, Bristol-Myers Squibb, Janssen, Johnson & Johnson, L’Oréal, and SkinCeuticals. Dr. Taylor, president-elect of the American Academy of Dermatology, reported financial relationships with more than 25 pharmaceutical and cosmetic companies.

A version of this article appeared on Medscape.com.

NEW YORK — Underrepresentation by gender and race in major clinical trials has been a cause for complaint for decades, but the Food and Drug Administration (FDA) has drafted a regulatory solution to this issue expected to be implemented sometime in 2025.

This initiative, known as the FDA’s Diversity Action Plan (DAP), will require plans for all pivotal and phase 3 trials to provide details in their design of how diversity will be achieved or, if there are no plans for diversity, the reason why, according to Valerie M. Harvey, MD, MPH, associate clinical professor, Edward Via College of Osteopathic Medicine, Blacksburg, Virginia. These rules will be codified, she said at the 2024 Skin of Color Update.

Once the DAP is enacted, “the sponsor must specify the rationale and goals for study enrollment by age, ethnicity, sex, and race,” she said. Furthermore, the submission to the FDA must “describe the methods to meet the diversity benchmarks.”
 

Lack of Trial Diversity Is Common Across Medicine

Although she focused on the relevance of this initiative to dermatology, Dr. Harvey said the lack of diversity in clinical trials is pervasive throughout medicine. In one survey of randomized controlled trials, less than 60% of trials even specified the race and ethnicity of the participants. In recent psoriasis trials, only 30% met a diversity definition of ≥ 20% of patients identifying as minority (Black, Hispanic, Asian, or other non-White group), said Dr. Harvey, who practices dermatology in Newport News, Virginia.

The FDA draft guidance for the DAP was released in June 2024 and is now available for submitting comments (until September 26). The plan is expected to be published in June 2025, according to Dr. Harvey. It will pertain to all pivotal and phase 3 trials enrolling 180 days after the publication date and will be relevant to all drugs and biologics as well as certain devices.

This initiative could be a critical step toward ensuring diversity in major clinical trials after years of stagnation, Dr. Harvey said, noting that despite repeated calls for more diversity in clinical trials, the literature suggests “little progress.”

However, she said that increasing diversity in clinical trials is just one step toward gathering data about the generalizability of efficacy and safety across racial and ethnic groups. A much more complex issue involves how race and ethnicity are defined in order to understand differences, if any, for efficacy and risk.

“Race is a dynamic social construct and a poor measure for biologic variation and skin color,” Dr. Harvey said. This means that work is needed to address the more complex issue of race and ethnicity stratification that will help clinicians understand the relative benefits and risks for the drugs in these trials.

Rather than differences based on genetic or other sources of biologic differences, she said, outcomes by race alone are often suspected of reflecting disparities in access to healthcare rather than a difference in therapeutic response.
 

Skin Color Is Inadequate to Define Race

When stratifying patients by race or ethnicity, Dr. Harvey said that “we have to be very, very careful in considering the study purpose and what the study question is.” A study attempting to compare benefits and risks among subgroups by race or ethnicity will require descriptors beyond skin color.

The recognized limitations of measuring skin tone as a surrogate of race are one reason for widespread interest in moving away from the Fitzpatrick skin type (FST) rating that has been widely considered a standard, according to Dr. Harvey. Several alternatives have been proposed, including the Monk Skin Tone Scale, the Individual Typology Angle, and the Eumelanin Human Skin Color Scale, but she cautioned that these are less well validated and generally have the limitations of the FST.

If skin color was ever useful for grouping individuals on the basis of shared physiology, growing rates of intermarriage and immigration have made skin color increasingly irrelevant to racial identity. If the goal is to evaluate the safety and efficacy of drugs across racial groups and ethnicities, the characterization of populations will almost certainly require multiple descriptors and biomarkers, she said.

“It is very important to have many tools for characterizing patients by skin type,” Susan Taylor, MD, professor of dermatology and vice chair for diversity, equity, and inclusion for the Department of Dermatology, University of Pennsylvania, Philadelphia, said in an interview at the meeting.

The reason is “there are limitations to all of them,” she said, noting also that the questions being asked about how and if skin color and race are relevant to therapeutic options differ by the question, such as innate response or access to care.

Dr. Taylor is part of a workshop that she said is evaluating a combination of instruments for characterizing skin color and race in ways relevant to the specific question being asked.

The solutions might differ. While simple clinical assessments involving skin color might be made with methods captured on a smartphone app, Dr. Taylor acknowledged that far more complex tools might be required to document the effect of racial or ethnic differences in drug efficacy and safety in a research setting.

Outside of a research setting, any tools that might be useful for assessing race as a variable must be practical, according to Dr. Harvey. She suggested that these must be time efficient, of reasonable cost, and most importantly, reliable.

Tools meeting these criteria do not currently exist, but Dr. Harvey said the work is underway. She expects a “top-down” collaborative approach to validate alternatives to the FST. If such tools can be developed with buy-in from the FDA, they might be particularly useful for translating trial data to patient care, she added.

Dr. Harvey reported financial relationships with AbbVie, Bristol-Myers Squibb, Janssen, Johnson & Johnson, L’Oréal, and SkinCeuticals. Dr. Taylor, president-elect of the American Academy of Dermatology, reported financial relationships with more than 25 pharmaceutical and cosmetic companies.

A version of this article appeared on Medscape.com.