Rheumatology News

A new diagnostic tool can effectively discriminate different rheumatologic conditions and could potentially aid in the diagnosis of early inflammatory arthritis.

The algorithm — called Genetic Probability tool (G-PROB) — uses genetic information to calculate the probability of certain diseases.

University of Manchester

“At such an early stage of disease, it’s not always easy to determine what the final outcome will be with respect to final diagnosis,” said John Bowes, PhD, a senior lecturer in the division of musculoskeletal & dermatological sciences at the University of Manchester in the United Kingdom. He was a senior author of the newest study of G-PROB. “What we are hoping for here is that genetics can help [clinicians] with the decision-making process and hopefully accelerate the correct diagnosis and get individuals onto the correct treatment as early as possible.”
 

Creating the Algorithm

G-PROB was first developed by an international group of scientists with the goal of using genetic risk scores to predict the probabilities of common diagnoses for patients with early signs of arthritis, such as synovitis and joint swelling. According to the study authors, about 80% of these types of patients are eventually diagnosed with the following conditions: Rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), psoriatic arthritis (PsA), ankylosing spondylitis (AS), and gout.

The algorithm combines existing knowledge about single-nucleotide polymorphisms from prior genomic studies to create genetic risk scores — also called polygenic risk score (PRS) — for multiple diseases. Using these scores, the program then calculates the probabilities of certain diagnoses for a patient, based on the assumption that at least one disease was present.

In this first study, researchers trained the tool on simulated data and then tested it in three patient cohorts totaling about 1700 individuals from the Electronic Medical Records and Genomics database and Mass General Brigham Biobank. In the initial study, G-PROB identified a likely diagnosis in 45% of patients, with a positive predictive value (PPV) of 64%. Adding these genetic scores to clinical data improved diagnostic accuracy from 39% to 51%.
 

Validating G-PROB

But data from these biobanks may not necessarily be representative of early arthritis in patients appearing in outpatient clinics, noted Dr. Bowes. In this new study, researchers sought to independently validate the original study’s findings using data from the Norfolk Arthritis Register, a community-based, long-term observational study on inflammatory polyarthritis. The team applied G-PROB in this cohort and then compared the tool’s probabilities for common rheumatic conditions to the final clinician diagnosis.

The study ultimately included 1047 individuals with early inflammatory arthritis with genotype data. In the cohort, more than 70% (756 individuals) were diagnosed with RA. Of the remaining patients, 104 had PsA, 18 had SLE, 16 had AS, and 12 had gout. The research team also added an “other diseases” category to the algorithm. A total of 141 patients fell into this category and were diagnosed with diseases including chronic pain syndrome (52 individuals), polymyalgia rheumatica (29 individuals), and Sjögren’s syndrome (9 individuals).

G-PROB was best at excluding diagnoses: Probabilities under 5% for a single disease corresponded to a negative predictive value (NPV) of 96%. If probabilities for two diseases were both < 5%, the NPV was 94%.

For patients with a single probability above 50%, the tool had a PPV of 70.3%. In 55.7% of all patients, the disease with the highest probability ended up being the final diagnosis.

Generally, PRSs, as well as tests using biomarkers, were better at excluding diagnoses than affirming them, noted Matthew Brown, MBBS, MD, a professor of medicine at King’s College London, who was not involved with the research. If disease prevalence is low, then a test aimed at diagnosis of that disease would be better at excluding a diagnosis than affirming it, he explained.

Queensland University of Technology

Can G-PROB Improve Diagnosis?

The new study’s key contribution was that it independently validated findings from a previous study, noted Katherine Liao, MD, a rheumatologist at Brigham and Women’s Hospital in Boston, Massachusetts. She coauthored an accompanying editorial to the newest study and coauthored the original G-PROB paper.

Dr. Liao

This new study also brought up an important question about G-PROB that has yet to be tested: Will this tool help clinicians make more efficient and accurate diagnoses in practice?

A prospective trial would be necessary to begin answering this question, both Dr. Bowes and Dr. Liao agreed. For example, one clinician group would have access to G-PROB data, while another would not, and “see if that helps [the first group] make the diagnosis faster or more accurately,” Dr. Liao said.

Dr. Bowes was also interested in exploring if combining G-PROB with other clinical data would improve diagnostic performance.

“Genetics isn’t the full story,” he said. Dr. Bowes saw genetics as one additional, complementary tool in a clinician’s toolbox.

Future studies were needed to understand the clinical utility of genetic information in conjunction with current diagnostic practices, such as imaging, physical exams, and lab results, Dr. Liao and her editorial coauthors argued. 

“For example, in cardiovascular disease, the clinical utility of polygenic risk scores has been defined by their ability to improve risk stratification beyond what is already achieved with more common risk factors and measures such as cholesterol levels, smoking status, and coronary calcium scores,” Dr. Liao and her coauthors wrote. “Similarly, a polygenic risk score for breast cancer would not be clinically implemented alone for risk prediction but rather as one risk factor among others, such as hormonal and reproductive factors and prior mammographic data.”
 

Future of Genetics in Rheumatology

An additional hurdle for using tools like G-PROB was that a patient must have undergone DNA sequencing, and these data must be available to clinicians. Even a decade ago, this type of testing may have seemed unrealistic to incorporate in daily practice, Dr. Liao noted, but technological advancements continue to make genetic sequencing more accessible to the public.

There are already efforts in the United Kingdom to incorporate genetics into healthcare, including trials for PRSs and heart disease, noted Dr. Bowes, as well as large-scale studies such as Our Future Health.

“As these population-based studies expand more, a high proportion of individuals should hopefully have access to this kind of data,” he said.

Brown added that genetic testing is already used to make rheumatology diagnoses.

“[HLA] B-27 testing, for example, is an extremely commonly used test to assist in the diagnosis of ankylosing spondylitis. Is it that different to change to a PRS as opposed to a straight HLA testing? I don’t think it is,” he said.

While there would need to be systematic training for clinicians to understand how to calculate and use PRSs in daily practice, Dr. Brown did not think this adjustment would be too difficult.

“There is a lot of exceptionalism about genetics, which is actually inappropriate,” he said. “This is actually just a quantitative score that should be easy for people to interpret.”

Dr. Bowes and Dr. Brown reported no relevant financial relationships. Dr. Liao worked as a consultant for UCB.

A version of this article appeared on Medscape.com.

A new diagnostic tool can effectively discriminate different rheumatologic conditions and could potentially aid in the diagnosis of early inflammatory arthritis.

The algorithm — called Genetic Probability tool (G-PROB) — uses genetic information to calculate the probability of certain diseases.

University of Manchester

“At such an early stage of disease, it’s not always easy to determine what the final outcome will be with respect to final diagnosis,” said John Bowes, PhD, a senior lecturer in the division of musculoskeletal & dermatological sciences at the University of Manchester in the United Kingdom. He was a senior author of the newest study of G-PROB. “What we are hoping for here is that genetics can help [clinicians] with the decision-making process and hopefully accelerate the correct diagnosis and get individuals onto the correct treatment as early as possible.”
 

Creating the Algorithm

G-PROB was first developed by an international group of scientists with the goal of using genetic risk scores to predict the probabilities of common diagnoses for patients with early signs of arthritis, such as synovitis and joint swelling. According to the study authors, about 80% of these types of patients are eventually diagnosed with the following conditions: Rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), psoriatic arthritis (PsA), ankylosing spondylitis (AS), and gout.

The algorithm combines existing knowledge about single-nucleotide polymorphisms from prior genomic studies to create genetic risk scores — also called polygenic risk score (PRS) — for multiple diseases. Using these scores, the program then calculates the probabilities of certain diagnoses for a patient, based on the assumption that at least one disease was present.

In this first study, researchers trained the tool on simulated data and then tested it in three patient cohorts totaling about 1700 individuals from the Electronic Medical Records and Genomics database and Mass General Brigham Biobank. In the initial study, G-PROB identified a likely diagnosis in 45% of patients, with a positive predictive value (PPV) of 64%. Adding these genetic scores to clinical data improved diagnostic accuracy from 39% to 51%.
 

Validating G-PROB

But data from these biobanks may not necessarily be representative of early arthritis in patients appearing in outpatient clinics, noted Dr. Bowes. In this new study, researchers sought to independently validate the original study’s findings using data from the Norfolk Arthritis Register, a community-based, long-term observational study on inflammatory polyarthritis. The team applied G-PROB in this cohort and then compared the tool’s probabilities for common rheumatic conditions to the final clinician diagnosis.

The study ultimately included 1047 individuals with early inflammatory arthritis with genotype data. In the cohort, more than 70% (756 individuals) were diagnosed with RA. Of the remaining patients, 104 had PsA, 18 had SLE, 16 had AS, and 12 had gout. The research team also added an “other diseases” category to the algorithm. A total of 141 patients fell into this category and were diagnosed with diseases including chronic pain syndrome (52 individuals), polymyalgia rheumatica (29 individuals), and Sjögren’s syndrome (9 individuals).

G-PROB was best at excluding diagnoses: Probabilities under 5% for a single disease corresponded to a negative predictive value (NPV) of 96%. If probabilities for two diseases were both < 5%, the NPV was 94%.

For patients with a single probability above 50%, the tool had a PPV of 70.3%. In 55.7% of all patients, the disease with the highest probability ended up being the final diagnosis.

Generally, PRSs, as well as tests using biomarkers, were better at excluding diagnoses than affirming them, noted Matthew Brown, MBBS, MD, a professor of medicine at King’s College London, who was not involved with the research. If disease prevalence is low, then a test aimed at diagnosis of that disease would be better at excluding a diagnosis than affirming it, he explained.

Queensland University of Technology

Can G-PROB Improve Diagnosis?

The new study’s key contribution was that it independently validated findings from a previous study, noted Katherine Liao, MD, a rheumatologist at Brigham and Women’s Hospital in Boston, Massachusetts. She coauthored an accompanying editorial to the newest study and coauthored the original G-PROB paper.

Dr. Liao

This new study also brought up an important question about G-PROB that has yet to be tested: Will this tool help clinicians make more efficient and accurate diagnoses in practice?

A prospective trial would be necessary to begin answering this question, both Dr. Bowes and Dr. Liao agreed. For example, one clinician group would have access to G-PROB data, while another would not, and “see if that helps [the first group] make the diagnosis faster or more accurately,” Dr. Liao said.

Dr. Bowes was also interested in exploring if combining G-PROB with other clinical data would improve diagnostic performance.

“Genetics isn’t the full story,” he said. Dr. Bowes saw genetics as one additional, complementary tool in a clinician’s toolbox.

Future studies were needed to understand the clinical utility of genetic information in conjunction with current diagnostic practices, such as imaging, physical exams, and lab results, Dr. Liao and her editorial coauthors argued. 

“For example, in cardiovascular disease, the clinical utility of polygenic risk scores has been defined by their ability to improve risk stratification beyond what is already achieved with more common risk factors and measures such as cholesterol levels, smoking status, and coronary calcium scores,” Dr. Liao and her coauthors wrote. “Similarly, a polygenic risk score for breast cancer would not be clinically implemented alone for risk prediction but rather as one risk factor among others, such as hormonal and reproductive factors and prior mammographic data.”
 

Future of Genetics in Rheumatology

An additional hurdle for using tools like G-PROB was that a patient must have undergone DNA sequencing, and these data must be available to clinicians. Even a decade ago, this type of testing may have seemed unrealistic to incorporate in daily practice, Dr. Liao noted, but technological advancements continue to make genetic sequencing more accessible to the public.

There are already efforts in the United Kingdom to incorporate genetics into healthcare, including trials for PRSs and heart disease, noted Dr. Bowes, as well as large-scale studies such as Our Future Health.

“As these population-based studies expand more, a high proportion of individuals should hopefully have access to this kind of data,” he said.

Brown added that genetic testing is already used to make rheumatology diagnoses.

“[HLA] B-27 testing, for example, is an extremely commonly used test to assist in the diagnosis of ankylosing spondylitis. Is it that different to change to a PRS as opposed to a straight HLA testing? I don’t think it is,” he said.

While there would need to be systematic training for clinicians to understand how to calculate and use PRSs in daily practice, Dr. Brown did not think this adjustment would be too difficult.

“There is a lot of exceptionalism about genetics, which is actually inappropriate,” he said. “This is actually just a quantitative score that should be easy for people to interpret.”

Dr. Bowes and Dr. Brown reported no relevant financial relationships. Dr. Liao worked as a consultant for UCB.

A version of this article appeared on Medscape.com.

A new diagnostic tool can effectively discriminate different rheumatologic conditions and could potentially aid in the diagnosis of early inflammatory arthritis.

The algorithm — called Genetic Probability tool (G-PROB) — uses genetic information to calculate the probability of certain diseases.

University of Manchester

“At such an early stage of disease, it’s not always easy to determine what the final outcome will be with respect to final diagnosis,” said John Bowes, PhD, a senior lecturer in the division of musculoskeletal & dermatological sciences at the University of Manchester in the United Kingdom. He was a senior author of the newest study of G-PROB. “What we are hoping for here is that genetics can help [clinicians] with the decision-making process and hopefully accelerate the correct diagnosis and get individuals onto the correct treatment as early as possible.”
 

Creating the Algorithm

G-PROB was first developed by an international group of scientists with the goal of using genetic risk scores to predict the probabilities of common diagnoses for patients with early signs of arthritis, such as synovitis and joint swelling. According to the study authors, about 80% of these types of patients are eventually diagnosed with the following conditions: Rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), psoriatic arthritis (PsA), ankylosing spondylitis (AS), and gout.

The algorithm combines existing knowledge about single-nucleotide polymorphisms from prior genomic studies to create genetic risk scores — also called polygenic risk score (PRS) — for multiple diseases. Using these scores, the program then calculates the probabilities of certain diagnoses for a patient, based on the assumption that at least one disease was present.

In this first study, researchers trained the tool on simulated data and then tested it in three patient cohorts totaling about 1700 individuals from the Electronic Medical Records and Genomics database and Mass General Brigham Biobank. In the initial study, G-PROB identified a likely diagnosis in 45% of patients, with a positive predictive value (PPV) of 64%. Adding these genetic scores to clinical data improved diagnostic accuracy from 39% to 51%.
 

Validating G-PROB

But data from these biobanks may not necessarily be representative of early arthritis in patients appearing in outpatient clinics, noted Dr. Bowes. In this new study, researchers sought to independently validate the original study’s findings using data from the Norfolk Arthritis Register, a community-based, long-term observational study on inflammatory polyarthritis. The team applied G-PROB in this cohort and then compared the tool’s probabilities for common rheumatic conditions to the final clinician diagnosis.

The study ultimately included 1047 individuals with early inflammatory arthritis with genotype data. In the cohort, more than 70% (756 individuals) were diagnosed with RA. Of the remaining patients, 104 had PsA, 18 had SLE, 16 had AS, and 12 had gout. The research team also added an “other diseases” category to the algorithm. A total of 141 patients fell into this category and were diagnosed with diseases including chronic pain syndrome (52 individuals), polymyalgia rheumatica (29 individuals), and Sjögren’s syndrome (9 individuals).

G-PROB was best at excluding diagnoses: Probabilities under 5% for a single disease corresponded to a negative predictive value (NPV) of 96%. If probabilities for two diseases were both < 5%, the NPV was 94%.

For patients with a single probability above 50%, the tool had a PPV of 70.3%. In 55.7% of all patients, the disease with the highest probability ended up being the final diagnosis.

Generally, PRSs, as well as tests using biomarkers, were better at excluding diagnoses than affirming them, noted Matthew Brown, MBBS, MD, a professor of medicine at King’s College London, who was not involved with the research. If disease prevalence is low, then a test aimed at diagnosis of that disease would be better at excluding a diagnosis than affirming it, he explained.

Queensland University of Technology

Can G-PROB Improve Diagnosis?

The new study’s key contribution was that it independently validated findings from a previous study, noted Katherine Liao, MD, a rheumatologist at Brigham and Women’s Hospital in Boston, Massachusetts. She coauthored an accompanying editorial to the newest study and coauthored the original G-PROB paper.

Dr. Liao

This new study also brought up an important question about G-PROB that has yet to be tested: Will this tool help clinicians make more efficient and accurate diagnoses in practice?

A prospective trial would be necessary to begin answering this question, both Dr. Bowes and Dr. Liao agreed. For example, one clinician group would have access to G-PROB data, while another would not, and “see if that helps [the first group] make the diagnosis faster or more accurately,” Dr. Liao said.

Dr. Bowes was also interested in exploring if combining G-PROB with other clinical data would improve diagnostic performance.

“Genetics isn’t the full story,” he said. Dr. Bowes saw genetics as one additional, complementary tool in a clinician’s toolbox.

Future studies were needed to understand the clinical utility of genetic information in conjunction with current diagnostic practices, such as imaging, physical exams, and lab results, Dr. Liao and her editorial coauthors argued. 

“For example, in cardiovascular disease, the clinical utility of polygenic risk scores has been defined by their ability to improve risk stratification beyond what is already achieved with more common risk factors and measures such as cholesterol levels, smoking status, and coronary calcium scores,” Dr. Liao and her coauthors wrote. “Similarly, a polygenic risk score for breast cancer would not be clinically implemented alone for risk prediction but rather as one risk factor among others, such as hormonal and reproductive factors and prior mammographic data.”
 

Future of Genetics in Rheumatology

An additional hurdle for using tools like G-PROB was that a patient must have undergone DNA sequencing, and these data must be available to clinicians. Even a decade ago, this type of testing may have seemed unrealistic to incorporate in daily practice, Dr. Liao noted, but technological advancements continue to make genetic sequencing more accessible to the public.

There are already efforts in the United Kingdom to incorporate genetics into healthcare, including trials for PRSs and heart disease, noted Dr. Bowes, as well as large-scale studies such as Our Future Health.

“As these population-based studies expand more, a high proportion of individuals should hopefully have access to this kind of data,” he said.

Brown added that genetic testing is already used to make rheumatology diagnoses.

“[HLA] B-27 testing, for example, is an extremely commonly used test to assist in the diagnosis of ankylosing spondylitis. Is it that different to change to a PRS as opposed to a straight HLA testing? I don’t think it is,” he said.

While there would need to be systematic training for clinicians to understand how to calculate and use PRSs in daily practice, Dr. Brown did not think this adjustment would be too difficult.

“There is a lot of exceptionalism about genetics, which is actually inappropriate,” he said. “This is actually just a quantitative score that should be easy for people to interpret.”

Dr. Bowes and Dr. Brown reported no relevant financial relationships. Dr. Liao worked as a consultant for UCB.

A version of this article appeared on Medscape.com.

It’s an appealing concept: Stop addictive behaviors for a while — think social media, video games, gambling, porn, junk food, drugs, alcohol (dry January, anyone?) — to reset your brain’s reward circuitry, so you can feel great minus the bad habits.

People call it dopamine fasting, abstinence sampling, or dopamine detox. But is shutting off the rush of that feel-good neurotransmitter really the key to kicking addictions?

TikTok influencers and Silicon Valley execs seem to think so. But so do some physicians.

Prominent among the proponents is Anna Lembke, MD, professor of psychiatry at Stanford University School of Medicine and chief of the Stanford Addiction Medicine Dual Diagnosis Clinic. There, the dopamine fast is an early intervention framework for many of her patients.

“What we have seen in those patients is that not only does craving begin to subside in about 4 weeks, but that mood and anxiety and sleep and all these other parameters and markers of good mental health also improve,” Dr. Lembke said.

Any clinician, regardless of background, can adopt this framework, the Dopamine Nation author said during her talk at the American College of Lifestyle Medicine (ACLM) conference last fall. “There is this idea in medicine that we have to leave addiction to the Betty Ford Clinic or to an addiction psychiatrist,” she told the gathering. “But there’s so much that we can do, no matter what our training and no matter our treatment setting.”  

But is dopamine fasting right for your patients? Some experts said it’s an oversimplified or even dangerous approach. Here’s what to know.

Dopamine and the Brain

From the prefrontal cortex — your brain’s control center — to the nucleus accumbens and ventral tegmental area located deep in your limbic system, dopamine bridges gaps between neurons to deliver critical messages about pleasure, reward, and motivation. 

We all have a baseline level of dopamine. Substances and behaviors we like — everything from chocolate and sex to cocaine and amphetamines — increase dopamine firing. 

“When we seek healthy rewards, like a good meal out in a restaurant or having a nice chat with friends, dopaminergic neurons fire, and dopamine is released,” said Birgitta Dresp, PhD, a cognitive psychologist and research director with the Centre National de la Recherche Scientifique in Paris. “That gives us a good feeling.”

But over time, with chronic exposure to hyperpleasurable stimuli, your brain adapts. Dopamine receptors downregulate and shrink, and your “hedonic setpoint,” or baseline happiness level, drops. You now need more of your favorite stimuli to feel as good as you did before.

This primitive brain wiring served evolutionary purposes, helping our ancestors relentlessly pursue scarce resources like food. But in our modern world full of easily accessible, novel, potent, and stimulating activities, our brains are constantly trying to compensate. Paradoxically, this constant “self-titillation” may be contributing to our national and global mental health crisis, Dr. Lembke suggested.

“Human activity has changed the world we live in,” said Dr. Lembke, “and now this ancient mechanistic structure has become a liability of sorts.”

The Dopamine Fast in Action

To reset this wiring, Dr. Lembke recommended a 4-week fast from a person’s “drug of choice.” But this isn’t the trendy tech-bro quick cure-all where you abstain from everything that brings you joy. It’s a targeted intervention usually aimed at one behavior or substance at a time. The fast allows a person to understand “the nature of the hijacked brain,” and breaking free motivates them to change habits long term, said Dr. Lembke.

Although the first 2 weeks are difficult, she found that many patients feel better and more motivated after 4 weeks.

How do you identify patients who might benefit from a dopamine fast? Start with “how much” and proceed to “why.” Instead of asking how much of a substance or behavior they indulge in per week, which can be inaccurate, Dr. Lembke uses a “timeline follow-back” technique — how much yesterday, the day before that, and so on. This can lead to an “aha” moment when they see the week’s true total, she told the ACLM conference.  

She also explored why they do it. Often patients say they are self-medicating or that the substance helps with their anxiety or depression. When people are compulsively continuing to use despite negative consequences, she might recommend a 4-week reset.

Important exceptions: Dr. Lembke did not recommend dopamine fasting to anyone who has repeatedly and unsuccessfully tried to quit a drug on their own nor anyone for whom withdrawal is life-threatening.

For people who can safely try the dopamine fast, she recommended “self-binding” strategies to help them stay the course. Consider the people, places, and things that encourage you to use, and try to avoid them. For example, delete your social media apps if you’re trying to detox from social media. Put physical distance between you and your phone. For foods and substances, keep them out of the house. 

Dr. Lembke also recommended “hormesis,” painful but productive activities like exercise. Your brain’s system for pleasure and pain are closely related, so these activities affect reward circuitry.

“You’re intentionally doing things that are hard, which doesn’t initially release dopamine, in contrast to intoxicants, but you get a gradual increase that remains elevated even after that activity is stopped, which is a nice way to get dopamine indirectly,” she said.

If patients plan to resume their “drug of choice” after the dopamine fast, Dr. Lembke helps them plan how much they will consume and when. For some, this works. Others, unfortunately, go back to using as much or more than they did before. But in many cases, she said, patients feel better and find that their “drug of choice” wasn’t serving them as well as they thought. 

Critiques of Dopamine Fasting

Dopamine fasting isn’t for everyone, and experts debate its safety and effectiveness. Here are some common concerns: 

It’s too simplistic. Peter Grinspoon, MD, a primary care physician at Massachusetts General Hospital and instructor at Harvard Medical School, said dopamine fasting isn’t really fasting — you don’t have a finite store of dopamine to conserve or deplete in a fixed amount of time. Even if you abstain from certain pleasures, your brain will still produce some dopamine.

What makes more sense, he said, is gradual “dopamine retargeting,” seeking rewards from healthy pleasurable activities.

“Addiction is a disease of isolation, and learning to take pleasure in the healthy things in life, like a nice home-cooked meal or a walk in the woods or a hug or a swim in the ocean, is exactly what addiction recovery is about,” he said. “Because once you learn to do that and to be happy, there’s no longer any room for the drug and you’re not nearly as susceptible to relapse.”

A related concern is that the dopamine system isn’t the only part of your brain that matters in addiction. “There are other bits of the brain which are much more important for controlling temptation,” said Trevor W. Robbins, PhD, professor of cognitive neuroscience and director of research at the Behavioural and Clinical Neuroscience Institute at the University of Cambridge. Dopamine plays an important role in addiction and recovery, “but to call this a dopamine fast, it’s just a trendy saying to make it sound exciting,” he said.

Empirical evidence is lacking. Without clinical trials to back it up, dopamine fasting lacks evidence on safety and effectiveness, said David Tzall, PsyD, a psychologist practicing in Brooklyn. “It sounds kind of fun, right? To think like, oh, I’ll just stop doing this for a while, and my body will correct itself,” said Dr. Tzall. “I think that’s a very dangerous thing because we don’t have enough evidence on it to think of how it can be effective or how it can be dangerous.”

Dr. Lembke “would like to see more evidence, too,” beyond clinical observation and expert consensus. Future research could also reveal who is most likely to benefit and how long the fast should last for maximum benefit.

It’s too much a one-size-fits-all approach. “Stopping a drug of choice is going to look different for a lot of people,” said Dr. Tzall. Some people can quit smoking cold turkey; others need to phase it out. Some need nicotine patches; some don’t. Some can do it alone; others need help. 

The individual’s why behind addiction is also crucial. Without their drug or habit, can they “cope with the stressors of life?” Dr. Tzall asked. They may need new strategies. And if they quit before they are ready and fail, they could end up feeling even worse than they did before.

Experts do agree on one thing: We can do more to help people who are struggling. “It’s very good that people are having discussions around tempering consumption because we clearly have a serious drug and alcohol addiction, obesity, and digital media problem,” said Dr. Lembke.

A version of this article appeared on Medscape.com.

It’s an appealing concept: Stop addictive behaviors for a while — think social media, video games, gambling, porn, junk food, drugs, alcohol (dry January, anyone?) — to reset your brain’s reward circuitry, so you can feel great minus the bad habits.

People call it dopamine fasting, abstinence sampling, or dopamine detox. But is shutting off the rush of that feel-good neurotransmitter really the key to kicking addictions?

TikTok influencers and Silicon Valley execs seem to think so. But so do some physicians.

Prominent among the proponents is Anna Lembke, MD, professor of psychiatry at Stanford University School of Medicine and chief of the Stanford Addiction Medicine Dual Diagnosis Clinic. There, the dopamine fast is an early intervention framework for many of her patients.

“What we have seen in those patients is that not only does craving begin to subside in about 4 weeks, but that mood and anxiety and sleep and all these other parameters and markers of good mental health also improve,” Dr. Lembke said.

Any clinician, regardless of background, can adopt this framework, the Dopamine Nation author said during her talk at the American College of Lifestyle Medicine (ACLM) conference last fall. “There is this idea in medicine that we have to leave addiction to the Betty Ford Clinic or to an addiction psychiatrist,” she told the gathering. “But there’s so much that we can do, no matter what our training and no matter our treatment setting.”  

But is dopamine fasting right for your patients? Some experts said it’s an oversimplified or even dangerous approach. Here’s what to know.

Dopamine and the Brain

From the prefrontal cortex — your brain’s control center — to the nucleus accumbens and ventral tegmental area located deep in your limbic system, dopamine bridges gaps between neurons to deliver critical messages about pleasure, reward, and motivation. 

We all have a baseline level of dopamine. Substances and behaviors we like — everything from chocolate and sex to cocaine and amphetamines — increase dopamine firing. 

“When we seek healthy rewards, like a good meal out in a restaurant or having a nice chat with friends, dopaminergic neurons fire, and dopamine is released,” said Birgitta Dresp, PhD, a cognitive psychologist and research director with the Centre National de la Recherche Scientifique in Paris. “That gives us a good feeling.”

But over time, with chronic exposure to hyperpleasurable stimuli, your brain adapts. Dopamine receptors downregulate and shrink, and your “hedonic setpoint,” or baseline happiness level, drops. You now need more of your favorite stimuli to feel as good as you did before.

This primitive brain wiring served evolutionary purposes, helping our ancestors relentlessly pursue scarce resources like food. But in our modern world full of easily accessible, novel, potent, and stimulating activities, our brains are constantly trying to compensate. Paradoxically, this constant “self-titillation” may be contributing to our national and global mental health crisis, Dr. Lembke suggested.

“Human activity has changed the world we live in,” said Dr. Lembke, “and now this ancient mechanistic structure has become a liability of sorts.”

The Dopamine Fast in Action

To reset this wiring, Dr. Lembke recommended a 4-week fast from a person’s “drug of choice.” But this isn’t the trendy tech-bro quick cure-all where you abstain from everything that brings you joy. It’s a targeted intervention usually aimed at one behavior or substance at a time. The fast allows a person to understand “the nature of the hijacked brain,” and breaking free motivates them to change habits long term, said Dr. Lembke.

Although the first 2 weeks are difficult, she found that many patients feel better and more motivated after 4 weeks.

How do you identify patients who might benefit from a dopamine fast? Start with “how much” and proceed to “why.” Instead of asking how much of a substance or behavior they indulge in per week, which can be inaccurate, Dr. Lembke uses a “timeline follow-back” technique — how much yesterday, the day before that, and so on. This can lead to an “aha” moment when they see the week’s true total, she told the ACLM conference.  

She also explored why they do it. Often patients say they are self-medicating or that the substance helps with their anxiety or depression. When people are compulsively continuing to use despite negative consequences, she might recommend a 4-week reset.

Important exceptions: Dr. Lembke did not recommend dopamine fasting to anyone who has repeatedly and unsuccessfully tried to quit a drug on their own nor anyone for whom withdrawal is life-threatening.

For people who can safely try the dopamine fast, she recommended “self-binding” strategies to help them stay the course. Consider the people, places, and things that encourage you to use, and try to avoid them. For example, delete your social media apps if you’re trying to detox from social media. Put physical distance between you and your phone. For foods and substances, keep them out of the house. 

Dr. Lembke also recommended “hormesis,” painful but productive activities like exercise. Your brain’s system for pleasure and pain are closely related, so these activities affect reward circuitry.

“You’re intentionally doing things that are hard, which doesn’t initially release dopamine, in contrast to intoxicants, but you get a gradual increase that remains elevated even after that activity is stopped, which is a nice way to get dopamine indirectly,” she said.

If patients plan to resume their “drug of choice” after the dopamine fast, Dr. Lembke helps them plan how much they will consume and when. For some, this works. Others, unfortunately, go back to using as much or more than they did before. But in many cases, she said, patients feel better and find that their “drug of choice” wasn’t serving them as well as they thought. 

Critiques of Dopamine Fasting

Dopamine fasting isn’t for everyone, and experts debate its safety and effectiveness. Here are some common concerns: 

It’s too simplistic. Peter Grinspoon, MD, a primary care physician at Massachusetts General Hospital and instructor at Harvard Medical School, said dopamine fasting isn’t really fasting — you don’t have a finite store of dopamine to conserve or deplete in a fixed amount of time. Even if you abstain from certain pleasures, your brain will still produce some dopamine.

What makes more sense, he said, is gradual “dopamine retargeting,” seeking rewards from healthy pleasurable activities.

“Addiction is a disease of isolation, and learning to take pleasure in the healthy things in life, like a nice home-cooked meal or a walk in the woods or a hug or a swim in the ocean, is exactly what addiction recovery is about,” he said. “Because once you learn to do that and to be happy, there’s no longer any room for the drug and you’re not nearly as susceptible to relapse.”

A related concern is that the dopamine system isn’t the only part of your brain that matters in addiction. “There are other bits of the brain which are much more important for controlling temptation,” said Trevor W. Robbins, PhD, professor of cognitive neuroscience and director of research at the Behavioural and Clinical Neuroscience Institute at the University of Cambridge. Dopamine plays an important role in addiction and recovery, “but to call this a dopamine fast, it’s just a trendy saying to make it sound exciting,” he said.

Empirical evidence is lacking. Without clinical trials to back it up, dopamine fasting lacks evidence on safety and effectiveness, said David Tzall, PsyD, a psychologist practicing in Brooklyn. “It sounds kind of fun, right? To think like, oh, I’ll just stop doing this for a while, and my body will correct itself,” said Dr. Tzall. “I think that’s a very dangerous thing because we don’t have enough evidence on it to think of how it can be effective or how it can be dangerous.”

Dr. Lembke “would like to see more evidence, too,” beyond clinical observation and expert consensus. Future research could also reveal who is most likely to benefit and how long the fast should last for maximum benefit.

It’s too much a one-size-fits-all approach. “Stopping a drug of choice is going to look different for a lot of people,” said Dr. Tzall. Some people can quit smoking cold turkey; others need to phase it out. Some need nicotine patches; some don’t. Some can do it alone; others need help. 

The individual’s why behind addiction is also crucial. Without their drug or habit, can they “cope with the stressors of life?” Dr. Tzall asked. They may need new strategies. And if they quit before they are ready and fail, they could end up feeling even worse than they did before.

Experts do agree on one thing: We can do more to help people who are struggling. “It’s very good that people are having discussions around tempering consumption because we clearly have a serious drug and alcohol addiction, obesity, and digital media problem,” said Dr. Lembke.

A version of this article appeared on Medscape.com.

It’s an appealing concept: Stop addictive behaviors for a while — think social media, video games, gambling, porn, junk food, drugs, alcohol (dry January, anyone?) — to reset your brain’s reward circuitry, so you can feel great minus the bad habits.

People call it dopamine fasting, abstinence sampling, or dopamine detox. But is shutting off the rush of that feel-good neurotransmitter really the key to kicking addictions?

TikTok influencers and Silicon Valley execs seem to think so. But so do some physicians.

Prominent among the proponents is Anna Lembke, MD, professor of psychiatry at Stanford University School of Medicine and chief of the Stanford Addiction Medicine Dual Diagnosis Clinic. There, the dopamine fast is an early intervention framework for many of her patients.

“What we have seen in those patients is that not only does craving begin to subside in about 4 weeks, but that mood and anxiety and sleep and all these other parameters and markers of good mental health also improve,” Dr. Lembke said.

Any clinician, regardless of background, can adopt this framework, the Dopamine Nation author said during her talk at the American College of Lifestyle Medicine (ACLM) conference last fall. “There is this idea in medicine that we have to leave addiction to the Betty Ford Clinic or to an addiction psychiatrist,” she told the gathering. “But there’s so much that we can do, no matter what our training and no matter our treatment setting.”  

But is dopamine fasting right for your patients? Some experts said it’s an oversimplified or even dangerous approach. Here’s what to know.

Dopamine and the Brain

From the prefrontal cortex — your brain’s control center — to the nucleus accumbens and ventral tegmental area located deep in your limbic system, dopamine bridges gaps between neurons to deliver critical messages about pleasure, reward, and motivation. 

We all have a baseline level of dopamine. Substances and behaviors we like — everything from chocolate and sex to cocaine and amphetamines — increase dopamine firing. 

“When we seek healthy rewards, like a good meal out in a restaurant or having a nice chat with friends, dopaminergic neurons fire, and dopamine is released,” said Birgitta Dresp, PhD, a cognitive psychologist and research director with the Centre National de la Recherche Scientifique in Paris. “That gives us a good feeling.”

But over time, with chronic exposure to hyperpleasurable stimuli, your brain adapts. Dopamine receptors downregulate and shrink, and your “hedonic setpoint,” or baseline happiness level, drops. You now need more of your favorite stimuli to feel as good as you did before.

This primitive brain wiring served evolutionary purposes, helping our ancestors relentlessly pursue scarce resources like food. But in our modern world full of easily accessible, novel, potent, and stimulating activities, our brains are constantly trying to compensate. Paradoxically, this constant “self-titillation” may be contributing to our national and global mental health crisis, Dr. Lembke suggested.

“Human activity has changed the world we live in,” said Dr. Lembke, “and now this ancient mechanistic structure has become a liability of sorts.”

The Dopamine Fast in Action

To reset this wiring, Dr. Lembke recommended a 4-week fast from a person’s “drug of choice.” But this isn’t the trendy tech-bro quick cure-all where you abstain from everything that brings you joy. It’s a targeted intervention usually aimed at one behavior or substance at a time. The fast allows a person to understand “the nature of the hijacked brain,” and breaking free motivates them to change habits long term, said Dr. Lembke.

Although the first 2 weeks are difficult, she found that many patients feel better and more motivated after 4 weeks.

How do you identify patients who might benefit from a dopamine fast? Start with “how much” and proceed to “why.” Instead of asking how much of a substance or behavior they indulge in per week, which can be inaccurate, Dr. Lembke uses a “timeline follow-back” technique — how much yesterday, the day before that, and so on. This can lead to an “aha” moment when they see the week’s true total, she told the ACLM conference.  

She also explored why they do it. Often patients say they are self-medicating or that the substance helps with their anxiety or depression. When people are compulsively continuing to use despite negative consequences, she might recommend a 4-week reset.

Important exceptions: Dr. Lembke did not recommend dopamine fasting to anyone who has repeatedly and unsuccessfully tried to quit a drug on their own nor anyone for whom withdrawal is life-threatening.

For people who can safely try the dopamine fast, she recommended “self-binding” strategies to help them stay the course. Consider the people, places, and things that encourage you to use, and try to avoid them. For example, delete your social media apps if you’re trying to detox from social media. Put physical distance between you and your phone. For foods and substances, keep them out of the house. 

Dr. Lembke also recommended “hormesis,” painful but productive activities like exercise. Your brain’s system for pleasure and pain are closely related, so these activities affect reward circuitry.

“You’re intentionally doing things that are hard, which doesn’t initially release dopamine, in contrast to intoxicants, but you get a gradual increase that remains elevated even after that activity is stopped, which is a nice way to get dopamine indirectly,” she said.

If patients plan to resume their “drug of choice” after the dopamine fast, Dr. Lembke helps them plan how much they will consume and when. For some, this works. Others, unfortunately, go back to using as much or more than they did before. But in many cases, she said, patients feel better and find that their “drug of choice” wasn’t serving them as well as they thought. 

Critiques of Dopamine Fasting

Dopamine fasting isn’t for everyone, and experts debate its safety and effectiveness. Here are some common concerns: 

It’s too simplistic. Peter Grinspoon, MD, a primary care physician at Massachusetts General Hospital and instructor at Harvard Medical School, said dopamine fasting isn’t really fasting — you don’t have a finite store of dopamine to conserve or deplete in a fixed amount of time. Even if you abstain from certain pleasures, your brain will still produce some dopamine.

What makes more sense, he said, is gradual “dopamine retargeting,” seeking rewards from healthy pleasurable activities.

“Addiction is a disease of isolation, and learning to take pleasure in the healthy things in life, like a nice home-cooked meal or a walk in the woods or a hug or a swim in the ocean, is exactly what addiction recovery is about,” he said. “Because once you learn to do that and to be happy, there’s no longer any room for the drug and you’re not nearly as susceptible to relapse.”

A related concern is that the dopamine system isn’t the only part of your brain that matters in addiction. “There are other bits of the brain which are much more important for controlling temptation,” said Trevor W. Robbins, PhD, professor of cognitive neuroscience and director of research at the Behavioural and Clinical Neuroscience Institute at the University of Cambridge. Dopamine plays an important role in addiction and recovery, “but to call this a dopamine fast, it’s just a trendy saying to make it sound exciting,” he said.

Empirical evidence is lacking. Without clinical trials to back it up, dopamine fasting lacks evidence on safety and effectiveness, said David Tzall, PsyD, a psychologist practicing in Brooklyn. “It sounds kind of fun, right? To think like, oh, I’ll just stop doing this for a while, and my body will correct itself,” said Dr. Tzall. “I think that’s a very dangerous thing because we don’t have enough evidence on it to think of how it can be effective or how it can be dangerous.”

Dr. Lembke “would like to see more evidence, too,” beyond clinical observation and expert consensus. Future research could also reveal who is most likely to benefit and how long the fast should last for maximum benefit.

It’s too much a one-size-fits-all approach. “Stopping a drug of choice is going to look different for a lot of people,” said Dr. Tzall. Some people can quit smoking cold turkey; others need to phase it out. Some need nicotine patches; some don’t. Some can do it alone; others need help. 

The individual’s why behind addiction is also crucial. Without their drug or habit, can they “cope with the stressors of life?” Dr. Tzall asked. They may need new strategies. And if they quit before they are ready and fail, they could end up feeling even worse than they did before.

Experts do agree on one thing: We can do more to help people who are struggling. “It’s very good that people are having discussions around tempering consumption because we clearly have a serious drug and alcohol addiction, obesity, and digital media problem,” said Dr. Lembke.

A version of this article appeared on Medscape.com.

TOPLINE:

A combination of remote, supervised aerobic training, resistance training, and a hypocaloric diet significantly improved cardiovascular risk factors in adults with rheumatoid arthritis (RA) and overweight or obesity.

METHODOLOGY:

• The researchers recruited 24 adults aged 60-80 years with RA who met criteria for overweight or obesity; participants were randomized to a Supervised Weight Loss and Exercise Training (SWET) or Counseling Health as Treatment (CHAT) program for 16 weeks.
• The SWET intervention included remote supervision of aerobic training of 150 minutes/week moderate-to-vigorous intensity, 2 days per week of resistance training, and a hypocaloric diet based on a weight loss goal of 7% of body weight. The CHAT patients served as controls and completed two lifestyle counseling sessions followed by monthly check-ins.
• The primary outcome was change in a composite measure of cardiovascular risk based on metabolic syndrome z-score (MSSc), a continuous weighted score of five metabolic syndrome components: Waist circumference, mean arterial blood pressure, fasting glucose, triglycerides, and high-density lipoprotein cholesterol.

TAKEAWAY:

• Both groups showed improvement in the primary outcome of MSSc, with absolute changes from baseline of −1.67 for the SWET group and −1.34 for the CHAT group (P < .01 for both).
• Participants in the SWET group showed significantly more improvement in secondary outcome measures of body weight, fat mass, and disease activity score in 28 joints based on C-reactive protein (DAS28-CRP), as well as greater improvement in patient-reported physical and mental health, physical function, and fatigue, than those in the CHAT group, but the CHAT group improved significantly compared with their baseline.
• The strongest specific effects for the different components of the intervention were those of aerobic training on physical function and fatigue, resistance training on DAS28-CRP, and weight loss on MSSc.
• Neither group experienced significant changes in lean mass, absolute peak V02, unilateral isometric knee extension, or bilateral grip strength.

IN PRACTICE:

“Findings from our study indicate, at a minimum, integrating even 2 hours of healthy lifestyle counseling may improve RA management, let alone demonstrate the substantial impact that can be provided by a comprehensive, remotely supervised lifestyle intervention,” the researchers wrote.

SOURCE:

The lead author on the study was Brian J. Andonian, MD, of Duke University, Durham, North Carolina. The study was published online in ACR Open Rheumatology.

LIMITATIONS:

The small sample size was a limitation of the study findings, as was the lack of blinding and high level of motivation in the CHAT group, who had greater improvements than expected in weight loss and increased physical activity; the study also was conducted during the COVID-19 pandemic, with potential physical and mental effects on participants who tested positive during the study period.

DISCLOSURES:

The study was supported by the US National Institute of Arthritis and Musculoskeletal and Skin Diseases and the Claude D. Pepper Older Americans Independence Center of the US National Institute on Aging.

A version of this article appeared on Medscape.com.

TOPLINE:

A combination of remote, supervised aerobic training, resistance training, and a hypocaloric diet significantly improved cardiovascular risk factors in adults with rheumatoid arthritis (RA) and overweight or obesity.

METHODOLOGY:

• The researchers recruited 24 adults aged 60-80 years with RA who met criteria for overweight or obesity; participants were randomized to a Supervised Weight Loss and Exercise Training (SWET) or Counseling Health as Treatment (CHAT) program for 16 weeks.
• The SWET intervention included remote supervision of aerobic training of 150 minutes/week moderate-to-vigorous intensity, 2 days per week of resistance training, and a hypocaloric diet based on a weight loss goal of 7% of body weight. The CHAT patients served as controls and completed two lifestyle counseling sessions followed by monthly check-ins.
• The primary outcome was change in a composite measure of cardiovascular risk based on metabolic syndrome z-score (MSSc), a continuous weighted score of five metabolic syndrome components: Waist circumference, mean arterial blood pressure, fasting glucose, triglycerides, and high-density lipoprotein cholesterol.

TAKEAWAY:

• Both groups showed improvement in the primary outcome of MSSc, with absolute changes from baseline of −1.67 for the SWET group and −1.34 for the CHAT group (P < .01 for both).
• Participants in the SWET group showed significantly more improvement in secondary outcome measures of body weight, fat mass, and disease activity score in 28 joints based on C-reactive protein (DAS28-CRP), as well as greater improvement in patient-reported physical and mental health, physical function, and fatigue, than those in the CHAT group, but the CHAT group improved significantly compared with their baseline.
• The strongest specific effects for the different components of the intervention were those of aerobic training on physical function and fatigue, resistance training on DAS28-CRP, and weight loss on MSSc.
• Neither group experienced significant changes in lean mass, absolute peak V02, unilateral isometric knee extension, or bilateral grip strength.

IN PRACTICE:

“Findings from our study indicate, at a minimum, integrating even 2 hours of healthy lifestyle counseling may improve RA management, let alone demonstrate the substantial impact that can be provided by a comprehensive, remotely supervised lifestyle intervention,” the researchers wrote.

SOURCE:

The lead author on the study was Brian J. Andonian, MD, of Duke University, Durham, North Carolina. The study was published online in ACR Open Rheumatology.

LIMITATIONS:

The small sample size was a limitation of the study findings, as was the lack of blinding and high level of motivation in the CHAT group, who had greater improvements than expected in weight loss and increased physical activity; the study also was conducted during the COVID-19 pandemic, with potential physical and mental effects on participants who tested positive during the study period.

DISCLOSURES:

The study was supported by the US National Institute of Arthritis and Musculoskeletal and Skin Diseases and the Claude D. Pepper Older Americans Independence Center of the US National Institute on Aging.

A version of this article appeared on Medscape.com.

TOPLINE:

A combination of remote, supervised aerobic training, resistance training, and a hypocaloric diet significantly improved cardiovascular risk factors in adults with rheumatoid arthritis (RA) and overweight or obesity.

METHODOLOGY:

• The researchers recruited 24 adults aged 60-80 years with RA who met criteria for overweight or obesity; participants were randomized to a Supervised Weight Loss and Exercise Training (SWET) or Counseling Health as Treatment (CHAT) program for 16 weeks.
• The SWET intervention included remote supervision of aerobic training of 150 minutes/week moderate-to-vigorous intensity, 2 days per week of resistance training, and a hypocaloric diet based on a weight loss goal of 7% of body weight. The CHAT patients served as controls and completed two lifestyle counseling sessions followed by monthly check-ins.
• The primary outcome was change in a composite measure of cardiovascular risk based on metabolic syndrome z-score (MSSc), a continuous weighted score of five metabolic syndrome components: Waist circumference, mean arterial blood pressure, fasting glucose, triglycerides, and high-density lipoprotein cholesterol.

TAKEAWAY:

• Both groups showed improvement in the primary outcome of MSSc, with absolute changes from baseline of −1.67 for the SWET group and −1.34 for the CHAT group (P < .01 for both).
• Participants in the SWET group showed significantly more improvement in secondary outcome measures of body weight, fat mass, and disease activity score in 28 joints based on C-reactive protein (DAS28-CRP), as well as greater improvement in patient-reported physical and mental health, physical function, and fatigue, than those in the CHAT group, but the CHAT group improved significantly compared with their baseline.
• The strongest specific effects for the different components of the intervention were those of aerobic training on physical function and fatigue, resistance training on DAS28-CRP, and weight loss on MSSc.
• Neither group experienced significant changes in lean mass, absolute peak V02, unilateral isometric knee extension, or bilateral grip strength.

IN PRACTICE:

“Findings from our study indicate, at a minimum, integrating even 2 hours of healthy lifestyle counseling may improve RA management, let alone demonstrate the substantial impact that can be provided by a comprehensive, remotely supervised lifestyle intervention,” the researchers wrote.

SOURCE:

The lead author on the study was Brian J. Andonian, MD, of Duke University, Durham, North Carolina. The study was published online in ACR Open Rheumatology.

LIMITATIONS:

The small sample size was a limitation of the study findings, as was the lack of blinding and high level of motivation in the CHAT group, who had greater improvements than expected in weight loss and increased physical activity; the study also was conducted during the COVID-19 pandemic, with potential physical and mental effects on participants who tested positive during the study period.

DISCLOSURES:

The study was supported by the US National Institute of Arthritis and Musculoskeletal and Skin Diseases and the Claude D. Pepper Older Americans Independence Center of the US National Institute on Aging.

A version of this article appeared on Medscape.com.

About 20% of US physicians took less than 1 week of vacation in the previous year, a new study found. When doctors did go on vacation, 70% reported working on their days off to handle patient-related tasks.

Burnout was more likely among doctors who worked more during vacations and lacked coverage in responding to electronic health messages from patients, according to the cross-sectional study, which was published on January 12, 2024, in JAMA Network Open.“It’s important to provide physicians with adequate time to disconnect from work and recharge,” said study coauthor Tait Shanafelt, MD, chief wellness officer at Stanford Medicine, in an interview.

The study’s conclusion that most US physicians work on their days off “is a marker of inadequate staffing, suboptimal teamwork, and poorly designed coverage systems,” he added. “Simply allocating people a number of vacation days is not enough.”

According to Dr. Shanafelt, there’s been little research into vacation’s impact on physician well-being. However, it is clear that work overload and exhaustion are major problems among American physicians. “Inadequate time off may magnify these challenges.”

Research suggests that physicians suffer more burnout than other US workers even after adjusting for confounders, he said. Extensive evidence shows that burnout in physicians contributes to medical errors and erodes quality of care and patient satisfaction, he added.

For the new study, researchers mailed surveys to 3671 members of the American Medical Association from 2020 to 2021, and 1162 (31.7%) responded. Another 6348 (7.1%) responded to an email survey sent to 90,000 physicians. An analysis suggested the respondents were representative of all US practicing physicians. 

Among 3024 respondents who responded to a subsurvey about vacations, about 40% took more than 15 days of vacation over the past year, about 40% took 6-15 days, and about 20% took 5 or fewer days. 

Fewer than half of physicians said their electronic health record (EHR) inboxes were fully covered by others while they were away. About 70% said they worked while on vacation, with nearly 15% working an hour or more each day.

Emergency physicians were the least likely and anesthesiologists were the most likely to take at least 15 days of vacation per year, according to the study. 

Women were more likely than men to work 30 or more minutes a day on vacation. Physicians aged 65 years and older were more likely to take 15 or more days of vacation per year than those under 35 years.

An adjusted analysis linked complete EHR inbox coverage to lower odds of taking time during vacation to work (odds ratio [OR], 0.68; 95% CI, 0.57-0.80).

“For many, difficulty finding clinical coverage, lack of EHR inbox coverage, and returning to an overwhelming backlog of EHR inbox work at were identified as barriers to taking vacation,” Dr. Shanafelt said.

Researchers linked lower rates of burnout to taking more than 3 weeks of vacation per year (OR, 0.59-0.66, depending on time spent; 95% CI, 0.40-0.98) vs none. They also linked less burnout to full EHR inbox coverage while on vacation (OR, 0.74; 95% CI, 0.63-0.88) and more burnout to spending 30 minutes or more on work while on a typical vacation day (OR, 1.58-1.97, depending on time spent; 95% CI, 1.22-2.77). 

Study limitations include the low participation rate and lack of insight into causation. It’s not clear how burnout and less vacation time are related and whether one causes the other, Shanafelt said. “It is possible there are a number of interacting factors rather than a simple, linear relationship.”

In an interview, Lazar J. Greenfield, Jr., MD, PhD, professor and chairman of neurology at UConn Health, Farmington, Connecticut, said his department encourages clinicians to plan vacations well ahead of time, and “we make a real strong effort to make sure that people are fully covered and someone has their Epic inbox.”

Dr. Greenfield, who wasn’t involved in the new study, recommended that physicians plan active vacations, so they have less downtime to catch up on work matters. But he acknowledged that stepping away from emails can be difficult, especially when physicians fear pileups of work upon their return or don’t want to annoy patients with tardy responses.

“They have a hard time disengaging from their moral obligations to patients,” he said. “Another issue, particularly in my field of neurology, is that there’s a lot of subspecialties. Finding somebody with the exact subspecialty and expertise to cover a very specific patient population they treat can be really hard.”

The Stanford WellMD Center, Mayo Clinic Department of Medicine Program on Physician Well-being, and American Medical Association funded the study.

Dr. Shanafelt discloses coinventing the Well-Being Index and its derivatives with another study author; Mayo Clinic licensed the Well-Being Index and pays them royalties outside the submitted work. Dr. Shanafelt also reported support for grand rounds, lectures, and advising for healthcare organizations outside the submitted work. Other authors reported personal fees from Marvin Behavioral Health and grants from the National Institute of Nursing Research, National Science Foundation, and Med Ed Solutions. 

Dr. Greenfield had no disclosures.

A version of this article appeared on Medscape.com. 

About 20% of US physicians took less than 1 week of vacation in the previous year, a new study found. When doctors did go on vacation, 70% reported working on their days off to handle patient-related tasks.

Burnout was more likely among doctors who worked more during vacations and lacked coverage in responding to electronic health messages from patients, according to the cross-sectional study, which was published on January 12, 2024, in JAMA Network Open.“It’s important to provide physicians with adequate time to disconnect from work and recharge,” said study coauthor Tait Shanafelt, MD, chief wellness officer at Stanford Medicine, in an interview.

The study’s conclusion that most US physicians work on their days off “is a marker of inadequate staffing, suboptimal teamwork, and poorly designed coverage systems,” he added. “Simply allocating people a number of vacation days is not enough.”

According to Dr. Shanafelt, there’s been little research into vacation’s impact on physician well-being. However, it is clear that work overload and exhaustion are major problems among American physicians. “Inadequate time off may magnify these challenges.”

Research suggests that physicians suffer more burnout than other US workers even after adjusting for confounders, he said. Extensive evidence shows that burnout in physicians contributes to medical errors and erodes quality of care and patient satisfaction, he added.

For the new study, researchers mailed surveys to 3671 members of the American Medical Association from 2020 to 2021, and 1162 (31.7%) responded. Another 6348 (7.1%) responded to an email survey sent to 90,000 physicians. An analysis suggested the respondents were representative of all US practicing physicians. 

Among 3024 respondents who responded to a subsurvey about vacations, about 40% took more than 15 days of vacation over the past year, about 40% took 6-15 days, and about 20% took 5 or fewer days. 

Fewer than half of physicians said their electronic health record (EHR) inboxes were fully covered by others while they were away. About 70% said they worked while on vacation, with nearly 15% working an hour or more each day.

Emergency physicians were the least likely and anesthesiologists were the most likely to take at least 15 days of vacation per year, according to the study. 

Women were more likely than men to work 30 or more minutes a day on vacation. Physicians aged 65 years and older were more likely to take 15 or more days of vacation per year than those under 35 years.

An adjusted analysis linked complete EHR inbox coverage to lower odds of taking time during vacation to work (odds ratio [OR], 0.68; 95% CI, 0.57-0.80).

“For many, difficulty finding clinical coverage, lack of EHR inbox coverage, and returning to an overwhelming backlog of EHR inbox work at were identified as barriers to taking vacation,” Dr. Shanafelt said.

Researchers linked lower rates of burnout to taking more than 3 weeks of vacation per year (OR, 0.59-0.66, depending on time spent; 95% CI, 0.40-0.98) vs none. They also linked less burnout to full EHR inbox coverage while on vacation (OR, 0.74; 95% CI, 0.63-0.88) and more burnout to spending 30 minutes or more on work while on a typical vacation day (OR, 1.58-1.97, depending on time spent; 95% CI, 1.22-2.77). 

Study limitations include the low participation rate and lack of insight into causation. It’s not clear how burnout and less vacation time are related and whether one causes the other, Shanafelt said. “It is possible there are a number of interacting factors rather than a simple, linear relationship.”

In an interview, Lazar J. Greenfield, Jr., MD, PhD, professor and chairman of neurology at UConn Health, Farmington, Connecticut, said his department encourages clinicians to plan vacations well ahead of time, and “we make a real strong effort to make sure that people are fully covered and someone has their Epic inbox.”

Dr. Greenfield, who wasn’t involved in the new study, recommended that physicians plan active vacations, so they have less downtime to catch up on work matters. But he acknowledged that stepping away from emails can be difficult, especially when physicians fear pileups of work upon their return or don’t want to annoy patients with tardy responses.

“They have a hard time disengaging from their moral obligations to patients,” he said. “Another issue, particularly in my field of neurology, is that there’s a lot of subspecialties. Finding somebody with the exact subspecialty and expertise to cover a very specific patient population they treat can be really hard.”

The Stanford WellMD Center, Mayo Clinic Department of Medicine Program on Physician Well-being, and American Medical Association funded the study.

Dr. Shanafelt discloses coinventing the Well-Being Index and its derivatives with another study author; Mayo Clinic licensed the Well-Being Index and pays them royalties outside the submitted work. Dr. Shanafelt also reported support for grand rounds, lectures, and advising for healthcare organizations outside the submitted work. Other authors reported personal fees from Marvin Behavioral Health and grants from the National Institute of Nursing Research, National Science Foundation, and Med Ed Solutions. 

Dr. Greenfield had no disclosures.

A version of this article appeared on Medscape.com. 

About 20% of US physicians took less than 1 week of vacation in the previous year, a new study found. When doctors did go on vacation, 70% reported working on their days off to handle patient-related tasks.

Burnout was more likely among doctors who worked more during vacations and lacked coverage in responding to electronic health messages from patients, according to the cross-sectional study, which was published on January 12, 2024, in JAMA Network Open.“It’s important to provide physicians with adequate time to disconnect from work and recharge,” said study coauthor Tait Shanafelt, MD, chief wellness officer at Stanford Medicine, in an interview.

The study’s conclusion that most US physicians work on their days off “is a marker of inadequate staffing, suboptimal teamwork, and poorly designed coverage systems,” he added. “Simply allocating people a number of vacation days is not enough.”

According to Dr. Shanafelt, there’s been little research into vacation’s impact on physician well-being. However, it is clear that work overload and exhaustion are major problems among American physicians. “Inadequate time off may magnify these challenges.”

Research suggests that physicians suffer more burnout than other US workers even after adjusting for confounders, he said. Extensive evidence shows that burnout in physicians contributes to medical errors and erodes quality of care and patient satisfaction, he added.

For the new study, researchers mailed surveys to 3671 members of the American Medical Association from 2020 to 2021, and 1162 (31.7%) responded. Another 6348 (7.1%) responded to an email survey sent to 90,000 physicians. An analysis suggested the respondents were representative of all US practicing physicians. 

Among 3024 respondents who responded to a subsurvey about vacations, about 40% took more than 15 days of vacation over the past year, about 40% took 6-15 days, and about 20% took 5 or fewer days. 

Fewer than half of physicians said their electronic health record (EHR) inboxes were fully covered by others while they were away. About 70% said they worked while on vacation, with nearly 15% working an hour or more each day.

Emergency physicians were the least likely and anesthesiologists were the most likely to take at least 15 days of vacation per year, according to the study. 

Women were more likely than men to work 30 or more minutes a day on vacation. Physicians aged 65 years and older were more likely to take 15 or more days of vacation per year than those under 35 years.

An adjusted analysis linked complete EHR inbox coverage to lower odds of taking time during vacation to work (odds ratio [OR], 0.68; 95% CI, 0.57-0.80).

“For many, difficulty finding clinical coverage, lack of EHR inbox coverage, and returning to an overwhelming backlog of EHR inbox work at were identified as barriers to taking vacation,” Dr. Shanafelt said.

Researchers linked lower rates of burnout to taking more than 3 weeks of vacation per year (OR, 0.59-0.66, depending on time spent; 95% CI, 0.40-0.98) vs none. They also linked less burnout to full EHR inbox coverage while on vacation (OR, 0.74; 95% CI, 0.63-0.88) and more burnout to spending 30 minutes or more on work while on a typical vacation day (OR, 1.58-1.97, depending on time spent; 95% CI, 1.22-2.77). 

Study limitations include the low participation rate and lack of insight into causation. It’s not clear how burnout and less vacation time are related and whether one causes the other, Shanafelt said. “It is possible there are a number of interacting factors rather than a simple, linear relationship.”

In an interview, Lazar J. Greenfield, Jr., MD, PhD, professor and chairman of neurology at UConn Health, Farmington, Connecticut, said his department encourages clinicians to plan vacations well ahead of time, and “we make a real strong effort to make sure that people are fully covered and someone has their Epic inbox.”

Dr. Greenfield, who wasn’t involved in the new study, recommended that physicians plan active vacations, so they have less downtime to catch up on work matters. But he acknowledged that stepping away from emails can be difficult, especially when physicians fear pileups of work upon their return or don’t want to annoy patients with tardy responses.

“They have a hard time disengaging from their moral obligations to patients,” he said. “Another issue, particularly in my field of neurology, is that there’s a lot of subspecialties. Finding somebody with the exact subspecialty and expertise to cover a very specific patient population they treat can be really hard.”

The Stanford WellMD Center, Mayo Clinic Department of Medicine Program on Physician Well-being, and American Medical Association funded the study.

Dr. Shanafelt discloses coinventing the Well-Being Index and its derivatives with another study author; Mayo Clinic licensed the Well-Being Index and pays them royalties outside the submitted work. Dr. Shanafelt also reported support for grand rounds, lectures, and advising for healthcare organizations outside the submitted work. Other authors reported personal fees from Marvin Behavioral Health and grants from the National Institute of Nursing Research, National Science Foundation, and Med Ed Solutions. 

Dr. Greenfield had no disclosures.

A version of this article appeared on Medscape.com. 

Prophylactic treatment with zoledronic acid (ZA) in individuals at high genetic risk for Paget disease of the bone (PDB) can prevent the development or progression of the condition, according to a new study. The authors argued that the positive results from the trial suggest that individuals with a familial history of PDB should undergo genetic screening.

“If it’s positive, you should be able to have a bone scan and take it from there,” senior author Stuart Ralston, MBChB, MD, professor of rheumatology at the University of Edinburgh (Scotland), said in an interview.

Dr. Ralston

PDB is a chronic skeletal growth disorder that affects an estimated 1-3 million people in the United States and is most prevalent in individuals over 65 years old. Symptoms of the disease may not present until later stages when there is already skeletal damage that cannot be resolved by medications. Earlier intervention in individuals who have not yet shown signs of the condition could potentially halt disease progression, Dr. Ralston said.

Genetics plays a substantial role in PDB, especially pathogenic variants of the gene SQSTM1. An estimated 40%-50% of people with a familial history of PDB have these variants, according to the study, which are associated with earlier PDB onset and more severe disease.

However, it was unclear if early interventions in these higher-risk individuals may result in better health outcomes.

In this new study, published on December 20, 2023, in Annals of the Rheumatic Diseases, researchers recruited participants through family members already diagnosed with PDB who received treatment at outpatient clinics. Over 1400 individuals with PDB underwent genetic testing for pathogenic SQSTM1 variants. If they tested positive, their first-degree relatives — primarily children — were offered the same genetic test. In total, 350 relatives tested positive for these pathogenic SQSTM1 variants, and of these individuals, 222 agreed to participate in the trial.

At the beginning of the study, all participants received a radionuclide bone scan to screen for bone lesions. They also underwent testing for the bone resorption marker type I collagen C-terminal telopeptides (CTX) and the bone formation marker procollagen type I amino-terminal propeptide (P1NP).

Participants were then randomized to receive either a single intravenous infusion of 5 mg of ZA or placebo treatment. Researchers followed up with participants annually for a median of 84 months (7 years), and then baseline assessments were repeated.

A total of 90 individuals in the ZA treatment group and 90 individuals in the placebo group completed the trial.

Participants were, on average, 50 years old at the beginning of the study. In the ZA group, nine individuals had lesions detected in bone scans at baseline, compared with just one at the study’s end. In the placebo group, 12 individuals had detectable lesions at baseline, compared with 11 individuals at the study’s end.

While the proportion of individuals with lesions was similar between the two groups, there were about twice as many lesions overall in the placebo group, compared with the ZA group (29 vs 15), which researchers said was by chance. All but two lesions disappeared in the ZA group, compared with 26 lesions remaining in the placebo group (P < .0001).

“The bone scan reversal of abnormalities was amazing,” said Ralston, where eight of nine patients with lesions in the ZA group “had their bone scan evidence completely wiped out,” he said. “That’s a very powerful result.”

Both CTX and P1NP concentrations fell in the ZA group at 12 months and remained significantly lower than the placebo group throughout the study (P < .0001 for each).

Overall, the researchers reported that eight individuals in the placebo group and no individuals in the ZA group had a poor outcome, defined as new bone lesions or lesions that were unchanged or progressed (odds ratio, 0.08; P = .003). Two individuals in the placebo group developed lesions during the study, compared with none in the ZA group, but this difference was not statistically significant.

Importantly, there were no differences in adverse events between the two groups.

While only a small number of people in the study had legions — around 9% of participants — the effect of ZA is “dramatic,” Linda A. Russell, MD, director of the Osteoporosis and Metabolic Bone Health Center at the Hospital for Special Surgery in New York City, told this news organization.

While clinicians primarily diagnose PDB with X-rays or an alkaline phosphatase blood test, testing for SQSTM1 is a new way to understand if someone is at higher risk for the disease, she said.

“Now, it seems like [the test] is fairly easily available, so probably it’s something we can begin to incorporate into our armamentarium,” Dr. Russell said.

Individuals who test positive for pathogenic variants of SQSTM1 could then get a bone scan, while those who tested negative may not need any additional testing, she added.

Dr. Ralston and coauthors noted that the effect size shown in this study is similar to that of studies examining adjuvant bisphosphonate therapy for postmenopausal women with early breast cancer. That practice, they write, is now a part of the standard of care.

“We believe that a similar approach is now justified in people with a family history of PDB who test positive for SQSTM1 mutations,” they wrote.

However, it is not clear if all individuals with pathogenic SQSTM1 should receive ZA treatment or if treatment should be given to only those with bone lesions.

“Future research to gather the views of people with a family history of PDB will help to inform the most appropriate way forward,” the authors wrote.

The UK Medical Research Council and Arthritis Research UK funded the trial. Zoledronic acid and a placebo were supplied by Novartis. Dr. Ralston reported funding to his institution from Kyowa Kirin, UCB, the Paget’s Association, and the Royal Osteoporosis Society. Some coauthors reported financial relationships with pharmaceutical companies outside the trial. Dr. Russell had no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

Prophylactic treatment with zoledronic acid (ZA) in individuals at high genetic risk for Paget disease of the bone (PDB) can prevent the development or progression of the condition, according to a new study. The authors argued that the positive results from the trial suggest that individuals with a familial history of PDB should undergo genetic screening.

“If it’s positive, you should be able to have a bone scan and take it from there,” senior author Stuart Ralston, MBChB, MD, professor of rheumatology at the University of Edinburgh (Scotland), said in an interview.

Dr. Ralston

PDB is a chronic skeletal growth disorder that affects an estimated 1-3 million people in the United States and is most prevalent in individuals over 65 years old. Symptoms of the disease may not present until later stages when there is already skeletal damage that cannot be resolved by medications. Earlier intervention in individuals who have not yet shown signs of the condition could potentially halt disease progression, Dr. Ralston said.

Genetics plays a substantial role in PDB, especially pathogenic variants of the gene SQSTM1. An estimated 40%-50% of people with a familial history of PDB have these variants, according to the study, which are associated with earlier PDB onset and more severe disease.

However, it was unclear if early interventions in these higher-risk individuals may result in better health outcomes.

In this new study, published on December 20, 2023, in Annals of the Rheumatic Diseases, researchers recruited participants through family members already diagnosed with PDB who received treatment at outpatient clinics. Over 1400 individuals with PDB underwent genetic testing for pathogenic SQSTM1 variants. If they tested positive, their first-degree relatives — primarily children — were offered the same genetic test. In total, 350 relatives tested positive for these pathogenic SQSTM1 variants, and of these individuals, 222 agreed to participate in the trial.

At the beginning of the study, all participants received a radionuclide bone scan to screen for bone lesions. They also underwent testing for the bone resorption marker type I collagen C-terminal telopeptides (CTX) and the bone formation marker procollagen type I amino-terminal propeptide (P1NP).

Participants were then randomized to receive either a single intravenous infusion of 5 mg of ZA or placebo treatment. Researchers followed up with participants annually for a median of 84 months (7 years), and then baseline assessments were repeated.

A total of 90 individuals in the ZA treatment group and 90 individuals in the placebo group completed the trial.

Participants were, on average, 50 years old at the beginning of the study. In the ZA group, nine individuals had lesions detected in bone scans at baseline, compared with just one at the study’s end. In the placebo group, 12 individuals had detectable lesions at baseline, compared with 11 individuals at the study’s end.

While the proportion of individuals with lesions was similar between the two groups, there were about twice as many lesions overall in the placebo group, compared with the ZA group (29 vs 15), which researchers said was by chance. All but two lesions disappeared in the ZA group, compared with 26 lesions remaining in the placebo group (P < .0001).

“The bone scan reversal of abnormalities was amazing,” said Ralston, where eight of nine patients with lesions in the ZA group “had their bone scan evidence completely wiped out,” he said. “That’s a very powerful result.”

Both CTX and P1NP concentrations fell in the ZA group at 12 months and remained significantly lower than the placebo group throughout the study (P < .0001 for each).

Overall, the researchers reported that eight individuals in the placebo group and no individuals in the ZA group had a poor outcome, defined as new bone lesions or lesions that were unchanged or progressed (odds ratio, 0.08; P = .003). Two individuals in the placebo group developed lesions during the study, compared with none in the ZA group, but this difference was not statistically significant.

Importantly, there were no differences in adverse events between the two groups.

While only a small number of people in the study had legions — around 9% of participants — the effect of ZA is “dramatic,” Linda A. Russell, MD, director of the Osteoporosis and Metabolic Bone Health Center at the Hospital for Special Surgery in New York City, told this news organization.

While clinicians primarily diagnose PDB with X-rays or an alkaline phosphatase blood test, testing for SQSTM1 is a new way to understand if someone is at higher risk for the disease, she said.

“Now, it seems like [the test] is fairly easily available, so probably it’s something we can begin to incorporate into our armamentarium,” Dr. Russell said.

Individuals who test positive for pathogenic variants of SQSTM1 could then get a bone scan, while those who tested negative may not need any additional testing, she added.

Dr. Ralston and coauthors noted that the effect size shown in this study is similar to that of studies examining adjuvant bisphosphonate therapy for postmenopausal women with early breast cancer. That practice, they write, is now a part of the standard of care.

“We believe that a similar approach is now justified in people with a family history of PDB who test positive for SQSTM1 mutations,” they wrote.

However, it is not clear if all individuals with pathogenic SQSTM1 should receive ZA treatment or if treatment should be given to only those with bone lesions.

“Future research to gather the views of people with a family history of PDB will help to inform the most appropriate way forward,” the authors wrote.

The UK Medical Research Council and Arthritis Research UK funded the trial. Zoledronic acid and a placebo were supplied by Novartis. Dr. Ralston reported funding to his institution from Kyowa Kirin, UCB, the Paget’s Association, and the Royal Osteoporosis Society. Some coauthors reported financial relationships with pharmaceutical companies outside the trial. Dr. Russell had no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

Prophylactic treatment with zoledronic acid (ZA) in individuals at high genetic risk for Paget disease of the bone (PDB) can prevent the development or progression of the condition, according to a new study. The authors argued that the positive results from the trial suggest that individuals with a familial history of PDB should undergo genetic screening.

“If it’s positive, you should be able to have a bone scan and take it from there,” senior author Stuart Ralston, MBChB, MD, professor of rheumatology at the University of Edinburgh (Scotland), said in an interview.

Dr. Ralston

PDB is a chronic skeletal growth disorder that affects an estimated 1-3 million people in the United States and is most prevalent in individuals over 65 years old. Symptoms of the disease may not present until later stages when there is already skeletal damage that cannot be resolved by medications. Earlier intervention in individuals who have not yet shown signs of the condition could potentially halt disease progression, Dr. Ralston said.

Genetics plays a substantial role in PDB, especially pathogenic variants of the gene SQSTM1. An estimated 40%-50% of people with a familial history of PDB have these variants, according to the study, which are associated with earlier PDB onset and more severe disease.

However, it was unclear if early interventions in these higher-risk individuals may result in better health outcomes.

In this new study, published on December 20, 2023, in Annals of the Rheumatic Diseases, researchers recruited participants through family members already diagnosed with PDB who received treatment at outpatient clinics. Over 1400 individuals with PDB underwent genetic testing for pathogenic SQSTM1 variants. If they tested positive, their first-degree relatives — primarily children — were offered the same genetic test. In total, 350 relatives tested positive for these pathogenic SQSTM1 variants, and of these individuals, 222 agreed to participate in the trial.

At the beginning of the study, all participants received a radionuclide bone scan to screen for bone lesions. They also underwent testing for the bone resorption marker type I collagen C-terminal telopeptides (CTX) and the bone formation marker procollagen type I amino-terminal propeptide (P1NP).

Participants were then randomized to receive either a single intravenous infusion of 5 mg of ZA or placebo treatment. Researchers followed up with participants annually for a median of 84 months (7 years), and then baseline assessments were repeated.

A total of 90 individuals in the ZA treatment group and 90 individuals in the placebo group completed the trial.

Participants were, on average, 50 years old at the beginning of the study. In the ZA group, nine individuals had lesions detected in bone scans at baseline, compared with just one at the study’s end. In the placebo group, 12 individuals had detectable lesions at baseline, compared with 11 individuals at the study’s end.

While the proportion of individuals with lesions was similar between the two groups, there were about twice as many lesions overall in the placebo group, compared with the ZA group (29 vs 15), which researchers said was by chance. All but two lesions disappeared in the ZA group, compared with 26 lesions remaining in the placebo group (P < .0001).

“The bone scan reversal of abnormalities was amazing,” said Ralston, where eight of nine patients with lesions in the ZA group “had their bone scan evidence completely wiped out,” he said. “That’s a very powerful result.”

Both CTX and P1NP concentrations fell in the ZA group at 12 months and remained significantly lower than the placebo group throughout the study (P < .0001 for each).

Overall, the researchers reported that eight individuals in the placebo group and no individuals in the ZA group had a poor outcome, defined as new bone lesions or lesions that were unchanged or progressed (odds ratio, 0.08; P = .003). Two individuals in the placebo group developed lesions during the study, compared with none in the ZA group, but this difference was not statistically significant.

Importantly, there were no differences in adverse events between the two groups.

While only a small number of people in the study had legions — around 9% of participants — the effect of ZA is “dramatic,” Linda A. Russell, MD, director of the Osteoporosis and Metabolic Bone Health Center at the Hospital for Special Surgery in New York City, told this news organization.

While clinicians primarily diagnose PDB with X-rays or an alkaline phosphatase blood test, testing for SQSTM1 is a new way to understand if someone is at higher risk for the disease, she said.

“Now, it seems like [the test] is fairly easily available, so probably it’s something we can begin to incorporate into our armamentarium,” Dr. Russell said.

Individuals who test positive for pathogenic variants of SQSTM1 could then get a bone scan, while those who tested negative may not need any additional testing, she added.

Dr. Ralston and coauthors noted that the effect size shown in this study is similar to that of studies examining adjuvant bisphosphonate therapy for postmenopausal women with early breast cancer. That practice, they write, is now a part of the standard of care.

“We believe that a similar approach is now justified in people with a family history of PDB who test positive for SQSTM1 mutations,” they wrote.

However, it is not clear if all individuals with pathogenic SQSTM1 should receive ZA treatment or if treatment should be given to only those with bone lesions.

“Future research to gather the views of people with a family history of PDB will help to inform the most appropriate way forward,” the authors wrote.

The UK Medical Research Council and Arthritis Research UK funded the trial. Zoledronic acid and a placebo were supplied by Novartis. Dr. Ralston reported funding to his institution from Kyowa Kirin, UCB, the Paget’s Association, and the Royal Osteoporosis Society. Some coauthors reported financial relationships with pharmaceutical companies outside the trial. Dr. Russell had no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

An influential panel is seeking an increase in Medicare’s 2025 payments for clinicians, adding to pressure on Congress to reconsider how the largest US purchaser of health services pays for office visits and related care of the nation’s older citizens and those with disabilities.

The Medicare Payment Advisory Commission (MedPAC) on Thursday voted unanimously in favor of a two-part recommendation on changes to the 2025 physician fee schedule:

• An increase in the base rate equal to half of the projected change in the Medicare Economic Index (MEI). Recent estimates have projected a 2.6% increase in MEI for 2025, which is intended to show how inflation affects the costs of running a medical practice.
• The creation of a safety-net add-on payment under the physician fee schedule to cover care of people with low incomes.

These recommendations echo the calls MedPAC made in a 2023 report to Congress. 

Lawmakers and the Centers for Medicare and Medicaid Services (CMS) rely on MedPAC’s work in deciding how much to pay for services. About 1.3 million clinicians bill Medicare for their work, including about 670,000 physicians.

Thursday’s MedPAC vote comes amid continuing uncertainty about how much the federal government will actually pay clinicians this year through the physician fee schedule.

There are serious efforts underway to undo cuts already demanded by previously passed federal law. In an email, Rep. Larry Buchson, MD, (R-IN) said he remains committed to “eliminating the full 3.37% cut this year while also working toward a permanent solution to halt the downward spiral of physician reimbursement.”

“The Medicare payment cut to physicians will impede patients’ access to care and further accelerate the current path toward consolidation, physician burnout, and closure of medical practices,” Buchson told this news organization. “It’s past time that Congress provides much needed and deserved stability for America’s doctors.”

Congress this month is attempting to complete overdue budget legislation needed to fund federal operations for fiscal 2024, which began October 1, 2023. The pending expiration of a short-term stopgap continuing resolution could provide a vehicle that could also carry legislation that would address the physician fee schedule.

In a Thursday statement, Jesse M. Ehrenfeld, MD, MPH, president of the American Medical Association, commended MedPAC for its recommendations and urged lawmakers to act.

“Long-term reforms from Congress are overdue to close the unsustainable gap between what Medicare pays physicians and the actual costs of delivering high-quality care,” Dr. Ehrenfeld said. “When adjusted for inflation in practice costs, Medicare physician pay declined 26% from 2001 to 2023.”
 

Continual Struggles

Congress has struggled for years in its attempts to set Medicare payments for office visits and other services covered by the physician fee schedule. A 1990s budget law set the stage for what proved to be untenable reductions in payment through the sustainable growth rate mechanism.

Between 2003 through April 2014, lawmakers passed “doc-fix” legislation 17 times to block the slated cuts, according to the Congressional Research Service. In 2015, Congress passed an intended overhaul of the physician fee schedule through the Medicare Access and CHIP Reauthorization Act (MACRA). As part of this law, Congress eliminated a base automatic inflation adjuster for the physician fee schedule.

In recent years, Congress has acted repeatedly to address MACRA’s mandates for flat base pay. MedPAC and members of both parties in Congress have called for a broad new look at how Medicare pays physicians. 

At Thursday’s meeting, MedPAC member Lawrence Casalino, MD, PhD, MPH, noted that the struggles to keep up with inflation and the “unpredictability of what the payment rates are going to be from year to year really do affect physician morale.”

A version of this article appeared on Medscape.com.

An influential panel is seeking an increase in Medicare’s 2025 payments for clinicians, adding to pressure on Congress to reconsider how the largest US purchaser of health services pays for office visits and related care of the nation’s older citizens and those with disabilities.

The Medicare Payment Advisory Commission (MedPAC) on Thursday voted unanimously in favor of a two-part recommendation on changes to the 2025 physician fee schedule:

• An increase in the base rate equal to half of the projected change in the Medicare Economic Index (MEI). Recent estimates have projected a 2.6% increase in MEI for 2025, which is intended to show how inflation affects the costs of running a medical practice.
• The creation of a safety-net add-on payment under the physician fee schedule to cover care of people with low incomes.

These recommendations echo the calls MedPAC made in a 2023 report to Congress. 

Lawmakers and the Centers for Medicare and Medicaid Services (CMS) rely on MedPAC’s work in deciding how much to pay for services. About 1.3 million clinicians bill Medicare for their work, including about 670,000 physicians.

Thursday’s MedPAC vote comes amid continuing uncertainty about how much the federal government will actually pay clinicians this year through the physician fee schedule.

There are serious efforts underway to undo cuts already demanded by previously passed federal law. In an email, Rep. Larry Buchson, MD, (R-IN) said he remains committed to “eliminating the full 3.37% cut this year while also working toward a permanent solution to halt the downward spiral of physician reimbursement.”

“The Medicare payment cut to physicians will impede patients’ access to care and further accelerate the current path toward consolidation, physician burnout, and closure of medical practices,” Buchson told this news organization. “It’s past time that Congress provides much needed and deserved stability for America’s doctors.”

Congress this month is attempting to complete overdue budget legislation needed to fund federal operations for fiscal 2024, which began October 1, 2023. The pending expiration of a short-term stopgap continuing resolution could provide a vehicle that could also carry legislation that would address the physician fee schedule.

In a Thursday statement, Jesse M. Ehrenfeld, MD, MPH, president of the American Medical Association, commended MedPAC for its recommendations and urged lawmakers to act.

“Long-term reforms from Congress are overdue to close the unsustainable gap between what Medicare pays physicians and the actual costs of delivering high-quality care,” Dr. Ehrenfeld said. “When adjusted for inflation in practice costs, Medicare physician pay declined 26% from 2001 to 2023.”
 

Continual Struggles

Congress has struggled for years in its attempts to set Medicare payments for office visits and other services covered by the physician fee schedule. A 1990s budget law set the stage for what proved to be untenable reductions in payment through the sustainable growth rate mechanism.

Between 2003 through April 2014, lawmakers passed “doc-fix” legislation 17 times to block the slated cuts, according to the Congressional Research Service. In 2015, Congress passed an intended overhaul of the physician fee schedule through the Medicare Access and CHIP Reauthorization Act (MACRA). As part of this law, Congress eliminated a base automatic inflation adjuster for the physician fee schedule.

In recent years, Congress has acted repeatedly to address MACRA’s mandates for flat base pay. MedPAC and members of both parties in Congress have called for a broad new look at how Medicare pays physicians. 

At Thursday’s meeting, MedPAC member Lawrence Casalino, MD, PhD, MPH, noted that the struggles to keep up with inflation and the “unpredictability of what the payment rates are going to be from year to year really do affect physician morale.”

A version of this article appeared on Medscape.com.

An influential panel is seeking an increase in Medicare’s 2025 payments for clinicians, adding to pressure on Congress to reconsider how the largest US purchaser of health services pays for office visits and related care of the nation’s older citizens and those with disabilities.

The Medicare Payment Advisory Commission (MedPAC) on Thursday voted unanimously in favor of a two-part recommendation on changes to the 2025 physician fee schedule:

• An increase in the base rate equal to half of the projected change in the Medicare Economic Index (MEI). Recent estimates have projected a 2.6% increase in MEI for 2025, which is intended to show how inflation affects the costs of running a medical practice.
• The creation of a safety-net add-on payment under the physician fee schedule to cover care of people with low incomes.

These recommendations echo the calls MedPAC made in a 2023 report to Congress. 

Lawmakers and the Centers for Medicare and Medicaid Services (CMS) rely on MedPAC’s work in deciding how much to pay for services. About 1.3 million clinicians bill Medicare for their work, including about 670,000 physicians.

Thursday’s MedPAC vote comes amid continuing uncertainty about how much the federal government will actually pay clinicians this year through the physician fee schedule.

There are serious efforts underway to undo cuts already demanded by previously passed federal law. In an email, Rep. Larry Buchson, MD, (R-IN) said he remains committed to “eliminating the full 3.37% cut this year while also working toward a permanent solution to halt the downward spiral of physician reimbursement.”

“The Medicare payment cut to physicians will impede patients’ access to care and further accelerate the current path toward consolidation, physician burnout, and closure of medical practices,” Buchson told this news organization. “It’s past time that Congress provides much needed and deserved stability for America’s doctors.”

Congress this month is attempting to complete overdue budget legislation needed to fund federal operations for fiscal 2024, which began October 1, 2023. The pending expiration of a short-term stopgap continuing resolution could provide a vehicle that could also carry legislation that would address the physician fee schedule.

In a Thursday statement, Jesse M. Ehrenfeld, MD, MPH, president of the American Medical Association, commended MedPAC for its recommendations and urged lawmakers to act.

“Long-term reforms from Congress are overdue to close the unsustainable gap between what Medicare pays physicians and the actual costs of delivering high-quality care,” Dr. Ehrenfeld said. “When adjusted for inflation in practice costs, Medicare physician pay declined 26% from 2001 to 2023.”
 

Continual Struggles

Congress has struggled for years in its attempts to set Medicare payments for office visits and other services covered by the physician fee schedule. A 1990s budget law set the stage for what proved to be untenable reductions in payment through the sustainable growth rate mechanism.

Between 2003 through April 2014, lawmakers passed “doc-fix” legislation 17 times to block the slated cuts, according to the Congressional Research Service. In 2015, Congress passed an intended overhaul of the physician fee schedule through the Medicare Access and CHIP Reauthorization Act (MACRA). As part of this law, Congress eliminated a base automatic inflation adjuster for the physician fee schedule.

In recent years, Congress has acted repeatedly to address MACRA’s mandates for flat base pay. MedPAC and members of both parties in Congress have called for a broad new look at how Medicare pays physicians. 

At Thursday’s meeting, MedPAC member Lawrence Casalino, MD, PhD, MPH, noted that the struggles to keep up with inflation and the “unpredictability of what the payment rates are going to be from year to year really do affect physician morale.”

A version of this article appeared on Medscape.com.

TOPLINE:

Adults using medical cannabis for chronic pain, especially those with cancer or cardiometabolic disease, have a slightly elevated risk of developing arrhythmia, mainly atrial fibrillation/flutter, a Danish registry study suggested. Cannabis use has been associated with increased cardiovascular (CV) risk, but data on CV side effects with use of medical cannabis for chronic pain are limited.

METHODOLOGY:

• To investigate, researchers identified 5391 patients with chronic pain (median age 59; 63% women) initiating first-time treatment with medical cannabis during 2018-2021 and matched them (1:5) to 26,941 control patients on age, sex, chronic pain diagnosis, and concomitant use of other noncannabis pain medication.
• They calculated and compared absolute risks for first-time arrhythmia (atrial fibrillation/flutter, conduction disorders, paroxysmal tachycardias, and ventricular arrhythmias) and acute coronary syndrome (ACS) between groups.

TAKEAWAY:

• Within 180 days, 42 medical cannabis users and 107 control participants developed arrhythmia, most commonly atrial fibrillation/flutter.
• Medical cannabis users had a slightly elevated risk for new-onset arrhythmia compared with nonusers (180-day absolute risk, 0.8% vs 0.4%).
• The 180-day risk ratio with cannabis use was 2.07 (95% CI, 1.34-2.80), and the 1-year risk ratio was 1.36 (95% CI, 1.00-1.73).
• Adults with cancer or cardiometabolic disease had the highest risk for arrhythmia with cannabis use (180-day absolute risk difference, 1.1% and 0.8%). There was no significant association between medical cannabis use and ACS risk.

IN PRACTICE:

“With the investigated cohort’s low age and low prevalence of comorbidity in mind, the notable relative risk increase of new-onset arrhythmia, mainly driven by atrial fibrillation/flutter, could be a reason for concern, albeit the absolute risks in this study population were modest,” the authors wrote.

“Medical cannabis may not be a ‘one-size-fits-all’ therapeutic option for certain medical conditions and should be contextualized based on patient comorbidities and potential vulnerability to side effects,” added the author of an editorial.

SOURCE:

The study, led by Anders Holt, MD, Copenhagen University and Herlev-Gentofte Hospital, Hellerup, Denmark, was published online on January 11, 2024, in the European Heart Journal, with an editorial by Robert Page II, PharmD, MSPH, University of Colorado, Aurora.

LIMITATIONS:

Residual confounding is possible. The registers lack information on disease severity, clinical measures, blood tests, and lifestyle factors. The route of cannabis administration was not known.

DISCLOSURES:

The study was funded by external and independent medical research grants. Holt had no relevant disclosures. Some coauthors reported research grants and speakers’ fees from various drug companies.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Adults using medical cannabis for chronic pain, especially those with cancer or cardiometabolic disease, have a slightly elevated risk of developing arrhythmia, mainly atrial fibrillation/flutter, a Danish registry study suggested. Cannabis use has been associated with increased cardiovascular (CV) risk, but data on CV side effects with use of medical cannabis for chronic pain are limited.

METHODOLOGY:

• To investigate, researchers identified 5391 patients with chronic pain (median age 59; 63% women) initiating first-time treatment with medical cannabis during 2018-2021 and matched them (1:5) to 26,941 control patients on age, sex, chronic pain diagnosis, and concomitant use of other noncannabis pain medication.
• They calculated and compared absolute risks for first-time arrhythmia (atrial fibrillation/flutter, conduction disorders, paroxysmal tachycardias, and ventricular arrhythmias) and acute coronary syndrome (ACS) between groups.

TAKEAWAY:

• Within 180 days, 42 medical cannabis users and 107 control participants developed arrhythmia, most commonly atrial fibrillation/flutter.
• Medical cannabis users had a slightly elevated risk for new-onset arrhythmia compared with nonusers (180-day absolute risk, 0.8% vs 0.4%).
• The 180-day risk ratio with cannabis use was 2.07 (95% CI, 1.34-2.80), and the 1-year risk ratio was 1.36 (95% CI, 1.00-1.73).
• Adults with cancer or cardiometabolic disease had the highest risk for arrhythmia with cannabis use (180-day absolute risk difference, 1.1% and 0.8%). There was no significant association between medical cannabis use and ACS risk.

IN PRACTICE:

“With the investigated cohort’s low age and low prevalence of comorbidity in mind, the notable relative risk increase of new-onset arrhythmia, mainly driven by atrial fibrillation/flutter, could be a reason for concern, albeit the absolute risks in this study population were modest,” the authors wrote.

“Medical cannabis may not be a ‘one-size-fits-all’ therapeutic option for certain medical conditions and should be contextualized based on patient comorbidities and potential vulnerability to side effects,” added the author of an editorial.

SOURCE:

The study, led by Anders Holt, MD, Copenhagen University and Herlev-Gentofte Hospital, Hellerup, Denmark, was published online on January 11, 2024, in the European Heart Journal, with an editorial by Robert Page II, PharmD, MSPH, University of Colorado, Aurora.

LIMITATIONS:

Residual confounding is possible. The registers lack information on disease severity, clinical measures, blood tests, and lifestyle factors. The route of cannabis administration was not known.

DISCLOSURES:

The study was funded by external and independent medical research grants. Holt had no relevant disclosures. Some coauthors reported research grants and speakers’ fees from various drug companies.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Adults using medical cannabis for chronic pain, especially those with cancer or cardiometabolic disease, have a slightly elevated risk of developing arrhythmia, mainly atrial fibrillation/flutter, a Danish registry study suggested. Cannabis use has been associated with increased cardiovascular (CV) risk, but data on CV side effects with use of medical cannabis for chronic pain are limited.

METHODOLOGY:

• To investigate, researchers identified 5391 patients with chronic pain (median age 59; 63% women) initiating first-time treatment with medical cannabis during 2018-2021 and matched them (1:5) to 26,941 control patients on age, sex, chronic pain diagnosis, and concomitant use of other noncannabis pain medication.
• They calculated and compared absolute risks for first-time arrhythmia (atrial fibrillation/flutter, conduction disorders, paroxysmal tachycardias, and ventricular arrhythmias) and acute coronary syndrome (ACS) between groups.

TAKEAWAY:

• Within 180 days, 42 medical cannabis users and 107 control participants developed arrhythmia, most commonly atrial fibrillation/flutter.
• Medical cannabis users had a slightly elevated risk for new-onset arrhythmia compared with nonusers (180-day absolute risk, 0.8% vs 0.4%).
• The 180-day risk ratio with cannabis use was 2.07 (95% CI, 1.34-2.80), and the 1-year risk ratio was 1.36 (95% CI, 1.00-1.73).
• Adults with cancer or cardiometabolic disease had the highest risk for arrhythmia with cannabis use (180-day absolute risk difference, 1.1% and 0.8%). There was no significant association between medical cannabis use and ACS risk.

IN PRACTICE:

“With the investigated cohort’s low age and low prevalence of comorbidity in mind, the notable relative risk increase of new-onset arrhythmia, mainly driven by atrial fibrillation/flutter, could be a reason for concern, albeit the absolute risks in this study population were modest,” the authors wrote.

“Medical cannabis may not be a ‘one-size-fits-all’ therapeutic option for certain medical conditions and should be contextualized based on patient comorbidities and potential vulnerability to side effects,” added the author of an editorial.

SOURCE:

The study, led by Anders Holt, MD, Copenhagen University and Herlev-Gentofte Hospital, Hellerup, Denmark, was published online on January 11, 2024, in the European Heart Journal, with an editorial by Robert Page II, PharmD, MSPH, University of Colorado, Aurora.

LIMITATIONS:

Residual confounding is possible. The registers lack information on disease severity, clinical measures, blood tests, and lifestyle factors. The route of cannabis administration was not known.

DISCLOSURES:

The study was funded by external and independent medical research grants. Holt had no relevant disclosures. Some coauthors reported research grants and speakers’ fees from various drug companies.
 

A version of this article appeared on Medscape.com.

Infection with COVID-19 conferred a nearly twofold risk of developing alopecia areata (AA), results from a large analysis of Korean patients demonstrated.

“There is a growing number of reports on new onset, exacerbation, and recurrence of AA after COVID-19,” corresponding author Jin Park, MD, PhD, of the department of dermatology at Jeonbuk National University Medical School, South Korea, and colleagues wrote in a research letter published online January 10, 2024, in JAMA Dermatology. “However, evidence supporting an association between COVID-19 and AA is limited.”

To investigate the association between COVID-19 and AA, the researchers used data from the Korea Disease Control and Prevention Agency–COVID-19–National Health Insurance Service cohort to conduct a propensity score–matched, nationwide, population-based cohort study from October 8, 2020, to September 30, 2021. They used Cox proportional hazards regression to calculate the incidence, prevalence, and adjusted hazard ratios (AHRs) for AA.

The cohort consisted of 259,369 patients with COVID-19 and 259,369 uninfected controls. The researchers observed an increased risk of telogen effluvium in patients with COVID-19 compared with the uninfected controls (AHR, 6.40; 95% CI, 4.92-8.33), while the incidence of epidermal cysts, benign skin tumors, and other negative control outcomes did not differ between groups.

Meanwhile, the incidence of AA in patients with COVID-19 was significantly higher compared with the uninfected controls (43.19 per 10,000 person-years [PY]), regardless of clinical subtype. This translated into an AHR of 1.82 (95% CI, 1.60-2.07). In other findings, the incidence of patchy AA and alopecia totalis and alopecia universalis (AT/AU) was 35.94 and 7.24 per 10,000 PY in patients with COVID-19 compared with 19.43 and 4.18 per 10,000 PY in uninfected controls, respectively.

“These findings support the possible role of COVID-19 in AA occurrence and exacerbation, although other environmental factors, such as psychological stress, may have also contributed to AA development during the pandemic,” the authors concluded. “Plausible mechanisms of AA following COVID-19 include antigenic molecular mimicry between SARS-CoV-2 and hair follicle autoantigens, cytokine shifting, and bystander activation.”

They acknowledged certain limitations of the analysis, including the potential for detection or misclassification bias and the fact that it did not evaluate causality between the two conditions.

Shari Lipner, MD, PhD, associate professor of dermatology at Weill Cornell Medicine, New York, who was asked to comment on the study, said that strengths of the study include the large sample size, and the use of positive and negative outcome controls, and that the incidence and prevalence of AA in Korea was stable during the prepandemic period. “A weakness of the study is that all alopecia areata cases may not have necessarily been confirmed,” Dr. Lipner told this news organization.

“Based on this study, dermatologists may consider AA in the differential diagnosis for a patient presenting with hair loss with recent COVID-19 diagnosis,” she added, noting that the potential for prevention of AA flares is also a reason to recommend COVID-19 vaccination for patients with a history of AA.

Christine Ko, MD, professor of dermatology and pathology at Yale University, New Haven, Connecticut, who was also asked to comment on the study, said that while the analysis suggests a definite epidemiologic association between COVID-19 and AA, “any causal relationship needs further study.” She added that she has no specific advice for patients who develop AA following a COVID-19 infection. “Any conversation about AA can be difficult because there is no way to prognosticate if someone will just have one small, localized area of hair loss,” or several small areas, versus loss of all hair on the head or even the body as well, Dr. Ko explained.

The study was supported with grants from the National Research Foundation of the Korean Government and the Ministry of Health and Welfare, Republic of Korea. The authors, as well as Dr. Lipner and Dr. Ko, reported having no relevant disclosures.

Infection with COVID-19 conferred a nearly twofold risk of developing alopecia areata (AA), results from a large analysis of Korean patients demonstrated.

“There is a growing number of reports on new onset, exacerbation, and recurrence of AA after COVID-19,” corresponding author Jin Park, MD, PhD, of the department of dermatology at Jeonbuk National University Medical School, South Korea, and colleagues wrote in a research letter published online January 10, 2024, in JAMA Dermatology. “However, evidence supporting an association between COVID-19 and AA is limited.”

To investigate the association between COVID-19 and AA, the researchers used data from the Korea Disease Control and Prevention Agency–COVID-19–National Health Insurance Service cohort to conduct a propensity score–matched, nationwide, population-based cohort study from October 8, 2020, to September 30, 2021. They used Cox proportional hazards regression to calculate the incidence, prevalence, and adjusted hazard ratios (AHRs) for AA.

The cohort consisted of 259,369 patients with COVID-19 and 259,369 uninfected controls. The researchers observed an increased risk of telogen effluvium in patients with COVID-19 compared with the uninfected controls (AHR, 6.40; 95% CI, 4.92-8.33), while the incidence of epidermal cysts, benign skin tumors, and other negative control outcomes did not differ between groups.

Meanwhile, the incidence of AA in patients with COVID-19 was significantly higher compared with the uninfected controls (43.19 per 10,000 person-years [PY]), regardless of clinical subtype. This translated into an AHR of 1.82 (95% CI, 1.60-2.07). In other findings, the incidence of patchy AA and alopecia totalis and alopecia universalis (AT/AU) was 35.94 and 7.24 per 10,000 PY in patients with COVID-19 compared with 19.43 and 4.18 per 10,000 PY in uninfected controls, respectively.

“These findings support the possible role of COVID-19 in AA occurrence and exacerbation, although other environmental factors, such as psychological stress, may have also contributed to AA development during the pandemic,” the authors concluded. “Plausible mechanisms of AA following COVID-19 include antigenic molecular mimicry between SARS-CoV-2 and hair follicle autoantigens, cytokine shifting, and bystander activation.”

They acknowledged certain limitations of the analysis, including the potential for detection or misclassification bias and the fact that it did not evaluate causality between the two conditions.

Shari Lipner, MD, PhD, associate professor of dermatology at Weill Cornell Medicine, New York, who was asked to comment on the study, said that strengths of the study include the large sample size, and the use of positive and negative outcome controls, and that the incidence and prevalence of AA in Korea was stable during the prepandemic period. “A weakness of the study is that all alopecia areata cases may not have necessarily been confirmed,” Dr. Lipner told this news organization.

“Based on this study, dermatologists may consider AA in the differential diagnosis for a patient presenting with hair loss with recent COVID-19 diagnosis,” she added, noting that the potential for prevention of AA flares is also a reason to recommend COVID-19 vaccination for patients with a history of AA.

Christine Ko, MD, professor of dermatology and pathology at Yale University, New Haven, Connecticut, who was also asked to comment on the study, said that while the analysis suggests a definite epidemiologic association between COVID-19 and AA, “any causal relationship needs further study.” She added that she has no specific advice for patients who develop AA following a COVID-19 infection. “Any conversation about AA can be difficult because there is no way to prognosticate if someone will just have one small, localized area of hair loss,” or several small areas, versus loss of all hair on the head or even the body as well, Dr. Ko explained.

The study was supported with grants from the National Research Foundation of the Korean Government and the Ministry of Health and Welfare, Republic of Korea. The authors, as well as Dr. Lipner and Dr. Ko, reported having no relevant disclosures.

Infection with COVID-19 conferred a nearly twofold risk of developing alopecia areata (AA), results from a large analysis of Korean patients demonstrated.

“There is a growing number of reports on new onset, exacerbation, and recurrence of AA after COVID-19,” corresponding author Jin Park, MD, PhD, of the department of dermatology at Jeonbuk National University Medical School, South Korea, and colleagues wrote in a research letter published online January 10, 2024, in JAMA Dermatology. “However, evidence supporting an association between COVID-19 and AA is limited.”

To investigate the association between COVID-19 and AA, the researchers used data from the Korea Disease Control and Prevention Agency–COVID-19–National Health Insurance Service cohort to conduct a propensity score–matched, nationwide, population-based cohort study from October 8, 2020, to September 30, 2021. They used Cox proportional hazards regression to calculate the incidence, prevalence, and adjusted hazard ratios (AHRs) for AA.

The cohort consisted of 259,369 patients with COVID-19 and 259,369 uninfected controls. The researchers observed an increased risk of telogen effluvium in patients with COVID-19 compared with the uninfected controls (AHR, 6.40; 95% CI, 4.92-8.33), while the incidence of epidermal cysts, benign skin tumors, and other negative control outcomes did not differ between groups.

Meanwhile, the incidence of AA in patients with COVID-19 was significantly higher compared with the uninfected controls (43.19 per 10,000 person-years [PY]), regardless of clinical subtype. This translated into an AHR of 1.82 (95% CI, 1.60-2.07). In other findings, the incidence of patchy AA and alopecia totalis and alopecia universalis (AT/AU) was 35.94 and 7.24 per 10,000 PY in patients with COVID-19 compared with 19.43 and 4.18 per 10,000 PY in uninfected controls, respectively.

“These findings support the possible role of COVID-19 in AA occurrence and exacerbation, although other environmental factors, such as psychological stress, may have also contributed to AA development during the pandemic,” the authors concluded. “Plausible mechanisms of AA following COVID-19 include antigenic molecular mimicry between SARS-CoV-2 and hair follicle autoantigens, cytokine shifting, and bystander activation.”

They acknowledged certain limitations of the analysis, including the potential for detection or misclassification bias and the fact that it did not evaluate causality between the two conditions.

Shari Lipner, MD, PhD, associate professor of dermatology at Weill Cornell Medicine, New York, who was asked to comment on the study, said that strengths of the study include the large sample size, and the use of positive and negative outcome controls, and that the incidence and prevalence of AA in Korea was stable during the prepandemic period. “A weakness of the study is that all alopecia areata cases may not have necessarily been confirmed,” Dr. Lipner told this news organization.

“Based on this study, dermatologists may consider AA in the differential diagnosis for a patient presenting with hair loss with recent COVID-19 diagnosis,” she added, noting that the potential for prevention of AA flares is also a reason to recommend COVID-19 vaccination for patients with a history of AA.

Christine Ko, MD, professor of dermatology and pathology at Yale University, New Haven, Connecticut, who was also asked to comment on the study, said that while the analysis suggests a definite epidemiologic association between COVID-19 and AA, “any causal relationship needs further study.” She added that she has no specific advice for patients who develop AA following a COVID-19 infection. “Any conversation about AA can be difficult because there is no way to prognosticate if someone will just have one small, localized area of hair loss,” or several small areas, versus loss of all hair on the head or even the body as well, Dr. Ko explained.

The study was supported with grants from the National Research Foundation of the Korean Government and the Ministry of Health and Welfare, Republic of Korea. The authors, as well as Dr. Lipner and Dr. Ko, reported having no relevant disclosures.

Exposure to endocrine-disrupting chemicals (EDCs) via daily use of plastics is a major contributor to the overall disease burden in the United States and the associated costs to society amount to more than 1% of the gross domestic product, revealed a large-scale analysis.

The research, published in the Journal of the Endocrine Society, indicated that taken together, the disease burden attributable to EDCs used in the manufacture of plastics added up to almost $250 billion in 2018 alone.

“The diseases due to plastics run the entire life course from preterm birth to obesity, heart disease, and cancers,” commented lead author Leonardo Trasande, MD, MPP, Jim G. Hendrick, MD Professor of Pediatrics, Department of Pediatrics, NYU Langone Medical Center, New York, in a release.

“Our study drives home the need to address chemicals used in plastic materials” through global treaties and other policy initiatives, he said, so as to “reduce these costs” in line with reductions in exposure to the chemicals.

Co-author Michael Belliveau, Executive Director at Defend Our Health in Portland, ME, agreed, saying: “We can reduce these health costs and the prevalence of chronic endocrine diseases such as diabetes and obesity if governments and companies enact policies that minimize exposure to EDCs to protect public health and the environment.”

Plastics may contain any one of a number of EDCs, such as polybrominated diphenylethers in flame retardant additives, phthalates in food packaging, bisphenols in can linings, and perfluoroalkyl and polyfluoroalkyl substances (PFAS) in nonstick cooking utensils.

These chemicals have been shown to leach and disturb the body’s hormone systems, increasing the risk for cancer, diabetes, reproductive disorders, neurological impairments in developing fetuses and children, and even death.

In March 2022, the United Nations Environment Assembly committed to a global plastics treaty to “end plastic pollution and forge an international legally binding agreement by 2024” that “addresses the full life cycle of plastic, including its production, design and disposal.”

Minimizing EDC Exposure

But what can doctors tell their patients today to help them reduce their exposure to EDCs?

“There are safe and simple steps that people can take to limit their exposure to the chemicals of greatest concern,” Dr. Trasande told this news organization.

This can be partly achieved by reducing plastic use down to its essentials. “To use an example, when you are flying, fill up a stainless steel container after clearing security. At home, use glass or stainless steel” rather than plastic bottles or containers.

In particular, “avoiding microwaving plastic is important,” Dr. Trasande said, “even if a container says it’s microwave-safe.”

He warned that “many chemicals used in plastic are not covalently bound, and heat facilitates leaching into food. Microscopic contaminants can also get into food when you microwave plastic.”

Dr. Trasande also suggests limiting canned food consumption and avoiding cleaning plastic food containers in machine dishwashers.

Calculating the Disease Burden

To accurately assess the “the tradeoffs involved in the ongoing reliance on plastic production as a source of economic productivity,” the current researchers calculated the attributable disease burden and cost related to EDCs used in plastic materials in the United States in 2018.

Building on previously published analyses, they used industry reports, publications by national and international governing bodies, and peer-reviewed publications to determine the usage of each type of EDC and its attributable disease and disability burden.

This plastic-related fraction (PRF) of disease burden was then used to calculate an updated cost estimate for each EDC, based on the assumption that the disease burden is directly proportional to its exposure.

They found that for bisphenol A, 97.5% of its use, and therefore its estimated PRF of disease burden, was related to the manufacture of plastics, while this figure was 98%-100% for phthalates. For PDBE, 98% of its use was in plastics vs 93% for PFAS.

The researchers then estimated that the total plastic-attributable disease burden in the United States in 2018 cost the nation $249 billion, or 1.22% of the gross domestic product. Of this, $159 billion was linked to PDBE exposure, which is associated with diseases such as cancer.

Moreover, $1.02 billion plastic-attributable disease burden was associated with bisphenol A exposure, which can have potentially harmful health effects on the immune system; followed by $66.7 billion due to phthalates, which are linked to preterm birth, reduced sperm count, and childhood obesity; and $22.4 billion due to PFAS, which are associated with kidney failure and gestational diabetes.

The study was supported by the National Institutes of Health and the Passport Foundation.

Dr. Trasande declared relationships with Audible, Houghton Mifflin, Paidos, and Kobunsha, none of which relate to the present manuscript.

No other financial relationships were declared.

A version of this article appeared on Medscape.com.

Exposure to endocrine-disrupting chemicals (EDCs) via daily use of plastics is a major contributor to the overall disease burden in the United States and the associated costs to society amount to more than 1% of the gross domestic product, revealed a large-scale analysis.

The research, published in the Journal of the Endocrine Society, indicated that taken together, the disease burden attributable to EDCs used in the manufacture of plastics added up to almost $250 billion in 2018 alone.

“The diseases due to plastics run the entire life course from preterm birth to obesity, heart disease, and cancers,” commented lead author Leonardo Trasande, MD, MPP, Jim G. Hendrick, MD Professor of Pediatrics, Department of Pediatrics, NYU Langone Medical Center, New York, in a release.

“Our study drives home the need to address chemicals used in plastic materials” through global treaties and other policy initiatives, he said, so as to “reduce these costs” in line with reductions in exposure to the chemicals.

Co-author Michael Belliveau, Executive Director at Defend Our Health in Portland, ME, agreed, saying: “We can reduce these health costs and the prevalence of chronic endocrine diseases such as diabetes and obesity if governments and companies enact policies that minimize exposure to EDCs to protect public health and the environment.”

Plastics may contain any one of a number of EDCs, such as polybrominated diphenylethers in flame retardant additives, phthalates in food packaging, bisphenols in can linings, and perfluoroalkyl and polyfluoroalkyl substances (PFAS) in nonstick cooking utensils.

These chemicals have been shown to leach and disturb the body’s hormone systems, increasing the risk for cancer, diabetes, reproductive disorders, neurological impairments in developing fetuses and children, and even death.

In March 2022, the United Nations Environment Assembly committed to a global plastics treaty to “end plastic pollution and forge an international legally binding agreement by 2024” that “addresses the full life cycle of plastic, including its production, design and disposal.”

Minimizing EDC Exposure

But what can doctors tell their patients today to help them reduce their exposure to EDCs?

“There are safe and simple steps that people can take to limit their exposure to the chemicals of greatest concern,” Dr. Trasande told this news organization.

This can be partly achieved by reducing plastic use down to its essentials. “To use an example, when you are flying, fill up a stainless steel container after clearing security. At home, use glass or stainless steel” rather than plastic bottles or containers.

In particular, “avoiding microwaving plastic is important,” Dr. Trasande said, “even if a container says it’s microwave-safe.”

He warned that “many chemicals used in plastic are not covalently bound, and heat facilitates leaching into food. Microscopic contaminants can also get into food when you microwave plastic.”

Dr. Trasande also suggests limiting canned food consumption and avoiding cleaning plastic food containers in machine dishwashers.

Calculating the Disease Burden

To accurately assess the “the tradeoffs involved in the ongoing reliance on plastic production as a source of economic productivity,” the current researchers calculated the attributable disease burden and cost related to EDCs used in plastic materials in the United States in 2018.

Building on previously published analyses, they used industry reports, publications by national and international governing bodies, and peer-reviewed publications to determine the usage of each type of EDC and its attributable disease and disability burden.

This plastic-related fraction (PRF) of disease burden was then used to calculate an updated cost estimate for each EDC, based on the assumption that the disease burden is directly proportional to its exposure.

They found that for bisphenol A, 97.5% of its use, and therefore its estimated PRF of disease burden, was related to the manufacture of plastics, while this figure was 98%-100% for phthalates. For PDBE, 98% of its use was in plastics vs 93% for PFAS.

The researchers then estimated that the total plastic-attributable disease burden in the United States in 2018 cost the nation $249 billion, or 1.22% of the gross domestic product. Of this, $159 billion was linked to PDBE exposure, which is associated with diseases such as cancer.

Moreover, $1.02 billion plastic-attributable disease burden was associated with bisphenol A exposure, which can have potentially harmful health effects on the immune system; followed by $66.7 billion due to phthalates, which are linked to preterm birth, reduced sperm count, and childhood obesity; and $22.4 billion due to PFAS, which are associated with kidney failure and gestational diabetes.

The study was supported by the National Institutes of Health and the Passport Foundation.

Dr. Trasande declared relationships with Audible, Houghton Mifflin, Paidos, and Kobunsha, none of which relate to the present manuscript.

No other financial relationships were declared.

A version of this article appeared on Medscape.com.

Exposure to endocrine-disrupting chemicals (EDCs) via daily use of plastics is a major contributor to the overall disease burden in the United States and the associated costs to society amount to more than 1% of the gross domestic product, revealed a large-scale analysis.

The research, published in the Journal of the Endocrine Society, indicated that taken together, the disease burden attributable to EDCs used in the manufacture of plastics added up to almost $250 billion in 2018 alone.

“The diseases due to plastics run the entire life course from preterm birth to obesity, heart disease, and cancers,” commented lead author Leonardo Trasande, MD, MPP, Jim G. Hendrick, MD Professor of Pediatrics, Department of Pediatrics, NYU Langone Medical Center, New York, in a release.

“Our study drives home the need to address chemicals used in plastic materials” through global treaties and other policy initiatives, he said, so as to “reduce these costs” in line with reductions in exposure to the chemicals.

Co-author Michael Belliveau, Executive Director at Defend Our Health in Portland, ME, agreed, saying: “We can reduce these health costs and the prevalence of chronic endocrine diseases such as diabetes and obesity if governments and companies enact policies that minimize exposure to EDCs to protect public health and the environment.”

Plastics may contain any one of a number of EDCs, such as polybrominated diphenylethers in flame retardant additives, phthalates in food packaging, bisphenols in can linings, and perfluoroalkyl and polyfluoroalkyl substances (PFAS) in nonstick cooking utensils.

These chemicals have been shown to leach and disturb the body’s hormone systems, increasing the risk for cancer, diabetes, reproductive disorders, neurological impairments in developing fetuses and children, and even death.

In March 2022, the United Nations Environment Assembly committed to a global plastics treaty to “end plastic pollution and forge an international legally binding agreement by 2024” that “addresses the full life cycle of plastic, including its production, design and disposal.”

Minimizing EDC Exposure

But what can doctors tell their patients today to help them reduce their exposure to EDCs?

“There are safe and simple steps that people can take to limit their exposure to the chemicals of greatest concern,” Dr. Trasande told this news organization.

This can be partly achieved by reducing plastic use down to its essentials. “To use an example, when you are flying, fill up a stainless steel container after clearing security. At home, use glass or stainless steel” rather than plastic bottles or containers.

In particular, “avoiding microwaving plastic is important,” Dr. Trasande said, “even if a container says it’s microwave-safe.”

He warned that “many chemicals used in plastic are not covalently bound, and heat facilitates leaching into food. Microscopic contaminants can also get into food when you microwave plastic.”

Dr. Trasande also suggests limiting canned food consumption and avoiding cleaning plastic food containers in machine dishwashers.

Calculating the Disease Burden

To accurately assess the “the tradeoffs involved in the ongoing reliance on plastic production as a source of economic productivity,” the current researchers calculated the attributable disease burden and cost related to EDCs used in plastic materials in the United States in 2018.

Building on previously published analyses, they used industry reports, publications by national and international governing bodies, and peer-reviewed publications to determine the usage of each type of EDC and its attributable disease and disability burden.

This plastic-related fraction (PRF) of disease burden was then used to calculate an updated cost estimate for each EDC, based on the assumption that the disease burden is directly proportional to its exposure.

They found that for bisphenol A, 97.5% of its use, and therefore its estimated PRF of disease burden, was related to the manufacture of plastics, while this figure was 98%-100% for phthalates. For PDBE, 98% of its use was in plastics vs 93% for PFAS.

The researchers then estimated that the total plastic-attributable disease burden in the United States in 2018 cost the nation $249 billion, or 1.22% of the gross domestic product. Of this, $159 billion was linked to PDBE exposure, which is associated with diseases such as cancer.

Moreover, $1.02 billion plastic-attributable disease burden was associated with bisphenol A exposure, which can have potentially harmful health effects on the immune system; followed by $66.7 billion due to phthalates, which are linked to preterm birth, reduced sperm count, and childhood obesity; and $22.4 billion due to PFAS, which are associated with kidney failure and gestational diabetes.

The study was supported by the National Institutes of Health and the Passport Foundation.

Dr. Trasande declared relationships with Audible, Houghton Mifflin, Paidos, and Kobunsha, none of which relate to the present manuscript.

No other financial relationships were declared.

A version of this article appeared on Medscape.com.