MDedge Neurology

With a number of large-scale clinical trials underway and researchers on the hunt for new therapies, long COVID scientists are hopeful that this is the year patients — and doctors who care for them — will finally see improvements in treating their symptoms.

Here are five bold predictions — all based on encouraging research — that could happen in 2024. At the very least, they are promising signs of progress against a debilitating and frustrating disease.

#1: We’ll gain a better understanding of each long COVID phenotype

This past year, a wide breadth of research began showing that long COVID can be defined by a number of different disease phenotypes that present a range of symptoms.

Researchers identified four clinical phenotypes: Chronic fatigue-like syndrome, headache, and memory loss; respiratory syndrome, which includes cough and difficulty breathing; chronic pain; and neurosensorial syndrome, which causes an altered sense of taste and smell.

Identifying specific diagnostic criteria for each phenotype would lead to better health outcomes for patients instead of treating them as if it were a “one-size-fits-all disease,” said Nisha Viswanathan, MD, director of the long COVID program at UCLA Health, Los Angeles, California.

Ultimately, she hopes that this year her patients will receive treatments based on the type of long COVID they’re personally experiencing, and the symptoms they have, leading to improved health outcomes and more rapid relief.

“Many new medications are focused on different pathways of long COVID, and the challenge becomes which drug is the right drug for each treatment,” said Dr. Viswanathan.

#2: Monoclonal antibodies may change the game

We’re starting to have a better understanding that what’s been called “viral persistence” as a main cause of long COVID may potentially be treated with monoclonal antibodies. These are antibodies produced by cloning unique white blood cells to target the circulating spike proteins in the blood that hang out in viral reservoirs and cause the immune system to react as if it’s still fighting acute COVID-19.

Smaller-scale studies have already shown promising results. A January 2024 study published in The American Journal of Emergency Medicine followed three patients who completely recovered from long COVID after taking monoclonal antibodies. “Remission occurred despite dissimilar past histories, sex, age, and illness duration,” wrote the study authors.

Larger clinical trials are underway at the University of California, San Francisco, California, to test targeted monoclonal antibodies. If the results of the larger study show that monoclonal antibodies are beneficial, then it could be a game changer for a large swath of patients around the world, said David F. Putrino, PhD, who runs the long COVID clinic at Mount Sinai Health System in New York City.

“The idea is that the downstream damage caused by viral persistence will resolve itself once you wipe out the virus,” said Dr. Putrino.

#3: Paxlovid could prove effective for long COVID

The US Food and Drug Administration granted approval for Paxlovid last May for the treatment of mild to moderate COVID-19 in adults at a high risk for severe disease. The medication is made up of two drugs packaged together. The first, nirmatrelvir, works by blocking a key enzyme required for virus replication. The second, ritonavir, is an antiviral that’s been used in patients with HIV and helps boost levels of antivirals in the body.

In a large-scale trial headed up by Dr. Putrino and his team, the oral antiviral is being studied for use in the post-viral stage in patients who test negative for acute COVID-19 but have persisting symptoms of long COVID.

Similar to monoclonal antibodies, the idea is to quell viral persistence. If patients have long COVID because they can’t clear SAR-CoV-2 from their bodies, Paxlovid could help. But unlike monoclonal antibodies that quash the virus, Paxlovid stops the virus from replicating. It’s a different mechanism with the same end goal.

It’s been a controversial treatment because it’s life-changing for some patients and ineffective for others. In addition, it can cause a range of side effects such as diarrhea, nausea, vomiting, and an impaired sense of taste. The goal of the trial is to see which patients with long COVID are most likely to benefit from the treatment.

#4: Anti-inflammatories like metformin could prove useful

Many of the inflammatory markers persistent in patients with long COVID were similarly present in patients with autoimmune diseases like rheumatoid arthritis, according to a July 2023 study published in JAMA.

The hope is that anti-inflammatory medications may be used to reduce inflammation causing long COVID symptoms. But drugs used to treat rheumatoid arthritis like abatacept and infliximabcan also have serious side effects, including increased risk for infection, flu-like symptoms, and burning of the skin.

“Powerful anti-inflammatories can change a number of pathways in the immune system,” said Grace McComsey, MD, who leads the long COVID RECOVER study at University Hospitals Health System in Cleveland, Ohio. Anti-inflammatories hold promise but, Dr. McComsey said, “some are more toxic with many side effects, so even if they work, there’s still a question about who should take them.”

Still, other anti-inflammatories that could work don’t have as many side effects. For example, a study published in The Lancet Infectious Diseases found that the diabetes drug metformin reduced a patient’s risk for long COVID up to 40% when the drug was taken during the acute stage.

Metformin, compared to other anti-inflammatories (also known as immune modulators), is an inexpensive and widely available drug with relatively few side effects compared with other medications.

#5: Serotonin levels — and selective serotonin reuptake inhibitors (SSRIs) — may be keys to unlocking long COVID

One of the most groundbreaking studies of the year came last November. A study published in the journal Cell found lower circulating serotonin levels in patents with long COVID than in those who did not have the condition. The study also found that the SSRI fluoxetine improved cognitive function in rat models infected with the virus.

Researchers found that the reduction in serotonin levels was partially caused by the body’s inability to absorb tryptophan, an amino acid that’s a precursor to serotonin. Overactivated blood platelets may also have played a role.

Michael Peluso, MD, an assistant research professor of infectious medicine at the UCSF School of Medicine, San Francisco, California, hopes to take the finding a step further, investigating whether increased serotonin levels in patients with long COVID will lead to improvements in symptoms.

“What we need now is a good clinical trial to see whether altering levels of serotonin in people with long COVID will lead to symptom relief,” Dr. Peluso said last month in an interview with this news organization.

If patients show an improvement in symptoms, then the next step is looking into whether SSRIs boost serotonin levels in patients and, as a result, reduce their symptoms.

A version of this article appeared on Medscape.com.

With a number of large-scale clinical trials underway and researchers on the hunt for new therapies, long COVID scientists are hopeful that this is the year patients — and doctors who care for them — will finally see improvements in treating their symptoms.

Here are five bold predictions — all based on encouraging research — that could happen in 2024. At the very least, they are promising signs of progress against a debilitating and frustrating disease.

#1: We’ll gain a better understanding of each long COVID phenotype

This past year, a wide breadth of research began showing that long COVID can be defined by a number of different disease phenotypes that present a range of symptoms.

Researchers identified four clinical phenotypes: Chronic fatigue-like syndrome, headache, and memory loss; respiratory syndrome, which includes cough and difficulty breathing; chronic pain; and neurosensorial syndrome, which causes an altered sense of taste and smell.

Identifying specific diagnostic criteria for each phenotype would lead to better health outcomes for patients instead of treating them as if it were a “one-size-fits-all disease,” said Nisha Viswanathan, MD, director of the long COVID program at UCLA Health, Los Angeles, California.

Ultimately, she hopes that this year her patients will receive treatments based on the type of long COVID they’re personally experiencing, and the symptoms they have, leading to improved health outcomes and more rapid relief.

“Many new medications are focused on different pathways of long COVID, and the challenge becomes which drug is the right drug for each treatment,” said Dr. Viswanathan.

#2: Monoclonal antibodies may change the game

We’re starting to have a better understanding that what’s been called “viral persistence” as a main cause of long COVID may potentially be treated with monoclonal antibodies. These are antibodies produced by cloning unique white blood cells to target the circulating spike proteins in the blood that hang out in viral reservoirs and cause the immune system to react as if it’s still fighting acute COVID-19.

Smaller-scale studies have already shown promising results. A January 2024 study published in The American Journal of Emergency Medicine followed three patients who completely recovered from long COVID after taking monoclonal antibodies. “Remission occurred despite dissimilar past histories, sex, age, and illness duration,” wrote the study authors.

Larger clinical trials are underway at the University of California, San Francisco, California, to test targeted monoclonal antibodies. If the results of the larger study show that monoclonal antibodies are beneficial, then it could be a game changer for a large swath of patients around the world, said David F. Putrino, PhD, who runs the long COVID clinic at Mount Sinai Health System in New York City.

“The idea is that the downstream damage caused by viral persistence will resolve itself once you wipe out the virus,” said Dr. Putrino.

#3: Paxlovid could prove effective for long COVID

The US Food and Drug Administration granted approval for Paxlovid last May for the treatment of mild to moderate COVID-19 in adults at a high risk for severe disease. The medication is made up of two drugs packaged together. The first, nirmatrelvir, works by blocking a key enzyme required for virus replication. The second, ritonavir, is an antiviral that’s been used in patients with HIV and helps boost levels of antivirals in the body.

In a large-scale trial headed up by Dr. Putrino and his team, the oral antiviral is being studied for use in the post-viral stage in patients who test negative for acute COVID-19 but have persisting symptoms of long COVID.

Similar to monoclonal antibodies, the idea is to quell viral persistence. If patients have long COVID because they can’t clear SAR-CoV-2 from their bodies, Paxlovid could help. But unlike monoclonal antibodies that quash the virus, Paxlovid stops the virus from replicating. It’s a different mechanism with the same end goal.

It’s been a controversial treatment because it’s life-changing for some patients and ineffective for others. In addition, it can cause a range of side effects such as diarrhea, nausea, vomiting, and an impaired sense of taste. The goal of the trial is to see which patients with long COVID are most likely to benefit from the treatment.

#4: Anti-inflammatories like metformin could prove useful

Many of the inflammatory markers persistent in patients with long COVID were similarly present in patients with autoimmune diseases like rheumatoid arthritis, according to a July 2023 study published in JAMA.

The hope is that anti-inflammatory medications may be used to reduce inflammation causing long COVID symptoms. But drugs used to treat rheumatoid arthritis like abatacept and infliximabcan also have serious side effects, including increased risk for infection, flu-like symptoms, and burning of the skin.

“Powerful anti-inflammatories can change a number of pathways in the immune system,” said Grace McComsey, MD, who leads the long COVID RECOVER study at University Hospitals Health System in Cleveland, Ohio. Anti-inflammatories hold promise but, Dr. McComsey said, “some are more toxic with many side effects, so even if they work, there’s still a question about who should take them.”

Still, other anti-inflammatories that could work don’t have as many side effects. For example, a study published in The Lancet Infectious Diseases found that the diabetes drug metformin reduced a patient’s risk for long COVID up to 40% when the drug was taken during the acute stage.

Metformin, compared to other anti-inflammatories (also known as immune modulators), is an inexpensive and widely available drug with relatively few side effects compared with other medications.

#5: Serotonin levels — and selective serotonin reuptake inhibitors (SSRIs) — may be keys to unlocking long COVID

One of the most groundbreaking studies of the year came last November. A study published in the journal Cell found lower circulating serotonin levels in patents with long COVID than in those who did not have the condition. The study also found that the SSRI fluoxetine improved cognitive function in rat models infected with the virus.

Researchers found that the reduction in serotonin levels was partially caused by the body’s inability to absorb tryptophan, an amino acid that’s a precursor to serotonin. Overactivated blood platelets may also have played a role.

Michael Peluso, MD, an assistant research professor of infectious medicine at the UCSF School of Medicine, San Francisco, California, hopes to take the finding a step further, investigating whether increased serotonin levels in patients with long COVID will lead to improvements in symptoms.

“What we need now is a good clinical trial to see whether altering levels of serotonin in people with long COVID will lead to symptom relief,” Dr. Peluso said last month in an interview with this news organization.

If patients show an improvement in symptoms, then the next step is looking into whether SSRIs boost serotonin levels in patients and, as a result, reduce their symptoms.

A version of this article appeared on Medscape.com.

With a number of large-scale clinical trials underway and researchers on the hunt for new therapies, long COVID scientists are hopeful that this is the year patients — and doctors who care for them — will finally see improvements in treating their symptoms.

Here are five bold predictions — all based on encouraging research — that could happen in 2024. At the very least, they are promising signs of progress against a debilitating and frustrating disease.

#1: We’ll gain a better understanding of each long COVID phenotype

This past year, a wide breadth of research began showing that long COVID can be defined by a number of different disease phenotypes that present a range of symptoms.

Researchers identified four clinical phenotypes: Chronic fatigue-like syndrome, headache, and memory loss; respiratory syndrome, which includes cough and difficulty breathing; chronic pain; and neurosensorial syndrome, which causes an altered sense of taste and smell.

Identifying specific diagnostic criteria for each phenotype would lead to better health outcomes for patients instead of treating them as if it were a “one-size-fits-all disease,” said Nisha Viswanathan, MD, director of the long COVID program at UCLA Health, Los Angeles, California.

Ultimately, she hopes that this year her patients will receive treatments based on the type of long COVID they’re personally experiencing, and the symptoms they have, leading to improved health outcomes and more rapid relief.

“Many new medications are focused on different pathways of long COVID, and the challenge becomes which drug is the right drug for each treatment,” said Dr. Viswanathan.

#2: Monoclonal antibodies may change the game

We’re starting to have a better understanding that what’s been called “viral persistence” as a main cause of long COVID may potentially be treated with monoclonal antibodies. These are antibodies produced by cloning unique white blood cells to target the circulating spike proteins in the blood that hang out in viral reservoirs and cause the immune system to react as if it’s still fighting acute COVID-19.

Smaller-scale studies have already shown promising results. A January 2024 study published in The American Journal of Emergency Medicine followed three patients who completely recovered from long COVID after taking monoclonal antibodies. “Remission occurred despite dissimilar past histories, sex, age, and illness duration,” wrote the study authors.

Larger clinical trials are underway at the University of California, San Francisco, California, to test targeted monoclonal antibodies. If the results of the larger study show that monoclonal antibodies are beneficial, then it could be a game changer for a large swath of patients around the world, said David F. Putrino, PhD, who runs the long COVID clinic at Mount Sinai Health System in New York City.

“The idea is that the downstream damage caused by viral persistence will resolve itself once you wipe out the virus,” said Dr. Putrino.

#3: Paxlovid could prove effective for long COVID

The US Food and Drug Administration granted approval for Paxlovid last May for the treatment of mild to moderate COVID-19 in adults at a high risk for severe disease. The medication is made up of two drugs packaged together. The first, nirmatrelvir, works by blocking a key enzyme required for virus replication. The second, ritonavir, is an antiviral that’s been used in patients with HIV and helps boost levels of antivirals in the body.

In a large-scale trial headed up by Dr. Putrino and his team, the oral antiviral is being studied for use in the post-viral stage in patients who test negative for acute COVID-19 but have persisting symptoms of long COVID.

Similar to monoclonal antibodies, the idea is to quell viral persistence. If patients have long COVID because they can’t clear SAR-CoV-2 from their bodies, Paxlovid could help. But unlike monoclonal antibodies that quash the virus, Paxlovid stops the virus from replicating. It’s a different mechanism with the same end goal.

It’s been a controversial treatment because it’s life-changing for some patients and ineffective for others. In addition, it can cause a range of side effects such as diarrhea, nausea, vomiting, and an impaired sense of taste. The goal of the trial is to see which patients with long COVID are most likely to benefit from the treatment.

#4: Anti-inflammatories like metformin could prove useful

Many of the inflammatory markers persistent in patients with long COVID were similarly present in patients with autoimmune diseases like rheumatoid arthritis, according to a July 2023 study published in JAMA.

The hope is that anti-inflammatory medications may be used to reduce inflammation causing long COVID symptoms. But drugs used to treat rheumatoid arthritis like abatacept and infliximabcan also have serious side effects, including increased risk for infection, flu-like symptoms, and burning of the skin.

“Powerful anti-inflammatories can change a number of pathways in the immune system,” said Grace McComsey, MD, who leads the long COVID RECOVER study at University Hospitals Health System in Cleveland, Ohio. Anti-inflammatories hold promise but, Dr. McComsey said, “some are more toxic with many side effects, so even if they work, there’s still a question about who should take them.”

Still, other anti-inflammatories that could work don’t have as many side effects. For example, a study published in The Lancet Infectious Diseases found that the diabetes drug metformin reduced a patient’s risk for long COVID up to 40% when the drug was taken during the acute stage.

Metformin, compared to other anti-inflammatories (also known as immune modulators), is an inexpensive and widely available drug with relatively few side effects compared with other medications.

#5: Serotonin levels — and selective serotonin reuptake inhibitors (SSRIs) — may be keys to unlocking long COVID

One of the most groundbreaking studies of the year came last November. A study published in the journal Cell found lower circulating serotonin levels in patents with long COVID than in those who did not have the condition. The study also found that the SSRI fluoxetine improved cognitive function in rat models infected with the virus.

Researchers found that the reduction in serotonin levels was partially caused by the body’s inability to absorb tryptophan, an amino acid that’s a precursor to serotonin. Overactivated blood platelets may also have played a role.

Michael Peluso, MD, an assistant research professor of infectious medicine at the UCSF School of Medicine, San Francisco, California, hopes to take the finding a step further, investigating whether increased serotonin levels in patients with long COVID will lead to improvements in symptoms.

“What we need now is a good clinical trial to see whether altering levels of serotonin in people with long COVID will lead to symptom relief,” Dr. Peluso said last month in an interview with this news organization.

If patients show an improvement in symptoms, then the next step is looking into whether SSRIs boost serotonin levels in patients and, as a result, reduce their symptoms.

A version of this article appeared on Medscape.com.

Officials at Dana-Farber Cancer Institute are moving to retract at least six published research papers and correct 31 others amid allegations of data manipulation.

News of the investigation follows a blog post by British molecular biologist Sholto David, MD, who flagged almost 60 papers published between 1997 and 2017 that contained image manipulation and other errors. Some of the papers were published by Dana-Farber’s chief executive officer, Laurie Glimcher, MD, and chief operating officer, William Hahn, MD, on topics including multiple myeloma and immune cells.

Mr. David, who blogs about research integrity, highlighted numerous errors and irregularities, including copying and pasting images across multiple experiments to represent different days within the same experiment, sometimes rotating or stretching images.

In one case, Mr. David equated the manipulation with tactics used by “hapless Chinese papermills” and concluded that “a swathe of research coming out of [Dana-Farber] authored by the most senior researchers and managers appears to be hopelessly corrupt with errors that are obvious from just a cursory reading the papers.” 

“Imagine what mistakes might be found in the raw data if anyone was allowed to look!” he wrote.

Barrett Rollins, MD, PhD, Dana-Farber Cancer Institute’s research integrity officer, declined to comment on whether the errors represent scientific misconduct, according to STAT. Rollins told ScienceInsider that the “presence of image discrepancies in a paper is not evidence of an author’s intent to deceive.” 

Access to new artificial intelligence tools is making it easier for data sleuths, like Mr. David, to unearth data manipulation and errors. 

The current investigation closely follows two other investigations into the published work of Harvard University’s former president, Claudine Gay, and Stanford University’s former president, Marc Tessier-Lavigne, which led both to resign their posts. 

A version of this article appeared on Medscape.com.

Officials at Dana-Farber Cancer Institute are moving to retract at least six published research papers and correct 31 others amid allegations of data manipulation.

News of the investigation follows a blog post by British molecular biologist Sholto David, MD, who flagged almost 60 papers published between 1997 and 2017 that contained image manipulation and other errors. Some of the papers were published by Dana-Farber’s chief executive officer, Laurie Glimcher, MD, and chief operating officer, William Hahn, MD, on topics including multiple myeloma and immune cells.

Mr. David, who blogs about research integrity, highlighted numerous errors and irregularities, including copying and pasting images across multiple experiments to represent different days within the same experiment, sometimes rotating or stretching images.

In one case, Mr. David equated the manipulation with tactics used by “hapless Chinese papermills” and concluded that “a swathe of research coming out of [Dana-Farber] authored by the most senior researchers and managers appears to be hopelessly corrupt with errors that are obvious from just a cursory reading the papers.” 

“Imagine what mistakes might be found in the raw data if anyone was allowed to look!” he wrote.

Barrett Rollins, MD, PhD, Dana-Farber Cancer Institute’s research integrity officer, declined to comment on whether the errors represent scientific misconduct, according to STAT. Rollins told ScienceInsider that the “presence of image discrepancies in a paper is not evidence of an author’s intent to deceive.” 

Access to new artificial intelligence tools is making it easier for data sleuths, like Mr. David, to unearth data manipulation and errors. 

The current investigation closely follows two other investigations into the published work of Harvard University’s former president, Claudine Gay, and Stanford University’s former president, Marc Tessier-Lavigne, which led both to resign their posts. 

A version of this article appeared on Medscape.com.

Officials at Dana-Farber Cancer Institute are moving to retract at least six published research papers and correct 31 others amid allegations of data manipulation.

News of the investigation follows a blog post by British molecular biologist Sholto David, MD, who flagged almost 60 papers published between 1997 and 2017 that contained image manipulation and other errors. Some of the papers were published by Dana-Farber’s chief executive officer, Laurie Glimcher, MD, and chief operating officer, William Hahn, MD, on topics including multiple myeloma and immune cells.

Mr. David, who blogs about research integrity, highlighted numerous errors and irregularities, including copying and pasting images across multiple experiments to represent different days within the same experiment, sometimes rotating or stretching images.

In one case, Mr. David equated the manipulation with tactics used by “hapless Chinese papermills” and concluded that “a swathe of research coming out of [Dana-Farber] authored by the most senior researchers and managers appears to be hopelessly corrupt with errors that are obvious from just a cursory reading the papers.” 

“Imagine what mistakes might be found in the raw data if anyone was allowed to look!” he wrote.

Barrett Rollins, MD, PhD, Dana-Farber Cancer Institute’s research integrity officer, declined to comment on whether the errors represent scientific misconduct, according to STAT. Rollins told ScienceInsider that the “presence of image discrepancies in a paper is not evidence of an author’s intent to deceive.” 

Access to new artificial intelligence tools is making it easier for data sleuths, like Mr. David, to unearth data manipulation and errors. 

The current investigation closely follows two other investigations into the published work of Harvard University’s former president, Claudine Gay, and Stanford University’s former president, Marc Tessier-Lavigne, which led both to resign their posts. 

A version of this article appeared on Medscape.com.

Adults with posttraumatic stress disorder (PTSD) have smaller cerebellums than unaffected adults, suggesting that this part of the brain may be a potential therapeutic target.

According to recent research on more than 4000 adults, cerebellum volume was significantly smaller (by about 2%) in those with PTSD than in trauma-exposed and trauma-naive controls without PTSD.

“The differences were largely within the posterior lobe, where a lot of the more cognitive functions attributed to the cerebellum seem to localize, as well as the vermis, which is linked to a lot of emotional processing functions,” lead author Ashley Huggins, PhD, said in a news release.

“If we know what areas are implicated, then we can start to focus interventions like brain stimulation on the cerebellum and potentially improve treatment outcomes,” said Dr. Huggins, who worked on the study while a postdoctoral researcher in the lab of Rajendra A. Morey, MD, at Duke University, Durham, North Carolina, and is now at the University of Arizona, Tucson.

While the cerebellum is known for its role in coordinating movement and balance, it also plays a key role in emotions and memory, which are affected by PTSD.

Smaller cerebellar volume has been observed in some adult and pediatric populations with PTSD.

However, those studies have been limited by either small sample sizes, the failure to consider key neuroanatomical subdivisions of the cerebellum, or a focus on certain populations such as veterans of sexual assault victims with PTSD.

To overcome these limitations, the researchers conducted a mega-analysis of total and subregional cerebellar volumes in a large, multicohort dataset from the Enhancing NeuroImaging Genetics through Meta-Analysis (ENIGMA)-Psychiatric Genomics Consortium PTSD workgroup that was published online on January 10, 2024, in Molecular Psychiatry.

They employed a novel, standardized ENIGMA cerebellum parcellation protocol to quantify cerebellar lobule volumes using structural MRI data from 1642 adults with PTSD and 2573 healthy controls without PTSD (88% trauma-exposed and 12% trauma-naive).

After adjustment for age, gender, and total intracranial volume, PTSD was associated with significant gray and white matter reductions of the cerebellum.

People with PTSD demonstrated smaller total cerebellum volume as well as reduced volume in subregions primarily within the posterior cerebellum, vermis, and flocculonodular cerebellum than controls.

In general, PTSD severity was more robustly associated with cerebellar volume differences than PTSD diagnosis.

Focusing purely on a “yes-or-no” categorical diagnosis didn’t always provide the clearest picture. “When we looked at PTSD severity, people who had more severe forms of the disorder had an even smaller cerebellar volume,” Dr. Huggins explained in the news release.

Novel Treatment Target

These findings add to “an emerging literature that underscores the relevance of cerebellar structure in the pathophysiology of PTSD,” the researchers noted.

They caution that despite the significant findings suggesting associations between PTSD and smaller cerebellar volumes, effect sizes were small. “As such, it is unlikely that structural cerebellar volumes alone will provide a clinically useful biomarker (eg, for individual-level prediction).”

Nonetheless, the study highlights the cerebellum as a “novel treatment target that may be leveraged to improve treatment outcomes for PTSD,” they wrote.

They noted that prior work has shown that the cerebellum is sensitive to external modulation. For example, noninvasive brain stimulation of the cerebellum has been shown to modulate cognitive, emotional, and social processes commonly disrupted in PTSD.

Commenting on this research, Cyrus A. Raji, MD, PhD, associate professor of radiology and neurology at Washington University in St. Louis, noted that this “large neuroimaging study links PTSD to cerebellar volume loss.”

“However, PTSD and traumatic brain injury frequently co-occur, and PTSD also frequently arises after TBI. Additionally, TBI is strongly linked to cerebellar volume loss,” Dr. Raji pointed out.

“Future studies need to better delineate volume loss from these conditions, especially when they are comorbid, though the expectation is these effects would be additive with TBI being the initial and most severe driving force,” Dr. Raji added.

The research had no commercial funding. Author disclosures are listed with the original article. Dr. Raji is a consultant for Brainreader, Apollo Health, Pacific Neuroscience Foundation, and Neurevolution Medicine LLC.
 

A version of this article appears on Medscape.com.

Adults with posttraumatic stress disorder (PTSD) have smaller cerebellums than unaffected adults, suggesting that this part of the brain may be a potential therapeutic target.

According to recent research on more than 4000 adults, cerebellum volume was significantly smaller (by about 2%) in those with PTSD than in trauma-exposed and trauma-naive controls without PTSD.

“The differences were largely within the posterior lobe, where a lot of the more cognitive functions attributed to the cerebellum seem to localize, as well as the vermis, which is linked to a lot of emotional processing functions,” lead author Ashley Huggins, PhD, said in a news release.

“If we know what areas are implicated, then we can start to focus interventions like brain stimulation on the cerebellum and potentially improve treatment outcomes,” said Dr. Huggins, who worked on the study while a postdoctoral researcher in the lab of Rajendra A. Morey, MD, at Duke University, Durham, North Carolina, and is now at the University of Arizona, Tucson.

While the cerebellum is known for its role in coordinating movement and balance, it also plays a key role in emotions and memory, which are affected by PTSD.

Smaller cerebellar volume has been observed in some adult and pediatric populations with PTSD.

However, those studies have been limited by either small sample sizes, the failure to consider key neuroanatomical subdivisions of the cerebellum, or a focus on certain populations such as veterans of sexual assault victims with PTSD.

To overcome these limitations, the researchers conducted a mega-analysis of total and subregional cerebellar volumes in a large, multicohort dataset from the Enhancing NeuroImaging Genetics through Meta-Analysis (ENIGMA)-Psychiatric Genomics Consortium PTSD workgroup that was published online on January 10, 2024, in Molecular Psychiatry.

They employed a novel, standardized ENIGMA cerebellum parcellation protocol to quantify cerebellar lobule volumes using structural MRI data from 1642 adults with PTSD and 2573 healthy controls without PTSD (88% trauma-exposed and 12% trauma-naive).

After adjustment for age, gender, and total intracranial volume, PTSD was associated with significant gray and white matter reductions of the cerebellum.

People with PTSD demonstrated smaller total cerebellum volume as well as reduced volume in subregions primarily within the posterior cerebellum, vermis, and flocculonodular cerebellum than controls.

In general, PTSD severity was more robustly associated with cerebellar volume differences than PTSD diagnosis.

Focusing purely on a “yes-or-no” categorical diagnosis didn’t always provide the clearest picture. “When we looked at PTSD severity, people who had more severe forms of the disorder had an even smaller cerebellar volume,” Dr. Huggins explained in the news release.

Novel Treatment Target

These findings add to “an emerging literature that underscores the relevance of cerebellar structure in the pathophysiology of PTSD,” the researchers noted.

They caution that despite the significant findings suggesting associations between PTSD and smaller cerebellar volumes, effect sizes were small. “As such, it is unlikely that structural cerebellar volumes alone will provide a clinically useful biomarker (eg, for individual-level prediction).”

Nonetheless, the study highlights the cerebellum as a “novel treatment target that may be leveraged to improve treatment outcomes for PTSD,” they wrote.

They noted that prior work has shown that the cerebellum is sensitive to external modulation. For example, noninvasive brain stimulation of the cerebellum has been shown to modulate cognitive, emotional, and social processes commonly disrupted in PTSD.

Commenting on this research, Cyrus A. Raji, MD, PhD, associate professor of radiology and neurology at Washington University in St. Louis, noted that this “large neuroimaging study links PTSD to cerebellar volume loss.”

“However, PTSD and traumatic brain injury frequently co-occur, and PTSD also frequently arises after TBI. Additionally, TBI is strongly linked to cerebellar volume loss,” Dr. Raji pointed out.

“Future studies need to better delineate volume loss from these conditions, especially when they are comorbid, though the expectation is these effects would be additive with TBI being the initial and most severe driving force,” Dr. Raji added.

The research had no commercial funding. Author disclosures are listed with the original article. Dr. Raji is a consultant for Brainreader, Apollo Health, Pacific Neuroscience Foundation, and Neurevolution Medicine LLC.
 

A version of this article appears on Medscape.com.

Adults with posttraumatic stress disorder (PTSD) have smaller cerebellums than unaffected adults, suggesting that this part of the brain may be a potential therapeutic target.

According to recent research on more than 4000 adults, cerebellum volume was significantly smaller (by about 2%) in those with PTSD than in trauma-exposed and trauma-naive controls without PTSD.

“The differences were largely within the posterior lobe, where a lot of the more cognitive functions attributed to the cerebellum seem to localize, as well as the vermis, which is linked to a lot of emotional processing functions,” lead author Ashley Huggins, PhD, said in a news release.

“If we know what areas are implicated, then we can start to focus interventions like brain stimulation on the cerebellum and potentially improve treatment outcomes,” said Dr. Huggins, who worked on the study while a postdoctoral researcher in the lab of Rajendra A. Morey, MD, at Duke University, Durham, North Carolina, and is now at the University of Arizona, Tucson.

While the cerebellum is known for its role in coordinating movement and balance, it also plays a key role in emotions and memory, which are affected by PTSD.

Smaller cerebellar volume has been observed in some adult and pediatric populations with PTSD.

However, those studies have been limited by either small sample sizes, the failure to consider key neuroanatomical subdivisions of the cerebellum, or a focus on certain populations such as veterans of sexual assault victims with PTSD.

To overcome these limitations, the researchers conducted a mega-analysis of total and subregional cerebellar volumes in a large, multicohort dataset from the Enhancing NeuroImaging Genetics through Meta-Analysis (ENIGMA)-Psychiatric Genomics Consortium PTSD workgroup that was published online on January 10, 2024, in Molecular Psychiatry.

They employed a novel, standardized ENIGMA cerebellum parcellation protocol to quantify cerebellar lobule volumes using structural MRI data from 1642 adults with PTSD and 2573 healthy controls without PTSD (88% trauma-exposed and 12% trauma-naive).

After adjustment for age, gender, and total intracranial volume, PTSD was associated with significant gray and white matter reductions of the cerebellum.

People with PTSD demonstrated smaller total cerebellum volume as well as reduced volume in subregions primarily within the posterior cerebellum, vermis, and flocculonodular cerebellum than controls.

In general, PTSD severity was more robustly associated with cerebellar volume differences than PTSD diagnosis.

Focusing purely on a “yes-or-no” categorical diagnosis didn’t always provide the clearest picture. “When we looked at PTSD severity, people who had more severe forms of the disorder had an even smaller cerebellar volume,” Dr. Huggins explained in the news release.

Novel Treatment Target

These findings add to “an emerging literature that underscores the relevance of cerebellar structure in the pathophysiology of PTSD,” the researchers noted.

They caution that despite the significant findings suggesting associations between PTSD and smaller cerebellar volumes, effect sizes were small. “As such, it is unlikely that structural cerebellar volumes alone will provide a clinically useful biomarker (eg, for individual-level prediction).”

Nonetheless, the study highlights the cerebellum as a “novel treatment target that may be leveraged to improve treatment outcomes for PTSD,” they wrote.

They noted that prior work has shown that the cerebellum is sensitive to external modulation. For example, noninvasive brain stimulation of the cerebellum has been shown to modulate cognitive, emotional, and social processes commonly disrupted in PTSD.

Commenting on this research, Cyrus A. Raji, MD, PhD, associate professor of radiology and neurology at Washington University in St. Louis, noted that this “large neuroimaging study links PTSD to cerebellar volume loss.”

“However, PTSD and traumatic brain injury frequently co-occur, and PTSD also frequently arises after TBI. Additionally, TBI is strongly linked to cerebellar volume loss,” Dr. Raji pointed out.

“Future studies need to better delineate volume loss from these conditions, especially when they are comorbid, though the expectation is these effects would be additive with TBI being the initial and most severe driving force,” Dr. Raji added.

The research had no commercial funding. Author disclosures are listed with the original article. Dr. Raji is a consultant for Brainreader, Apollo Health, Pacific Neuroscience Foundation, and Neurevolution Medicine LLC.
 

A version of this article appears on Medscape.com.

TOPLINE: 

Pet ownership is associated with slower cognitive decline in seniors who live alone, a new longitudinal cohort study showed. Investigators note the findings are important because previous research suggests older adults who live alone are at higher risk for dementia.

METHODOLOGY:

• Investigators analyzed data on 7945 participants aged 50 years and older (56% female; mean age, 66 years) from the English Longitudinal Study of Ageing (ELSA) and determined whether they lived alone or had a pet.
• Every couple of years for the next 8 years after baseline, participants were assessed for verbal cognition, verbal memory, and verbal fluency. Information about covariates including age, sex, employment status, educational level, and health was also collected.
• 35% of participants were pet owners, and 27% lived alone.

TAKEAWAY: 

• Pet owners who lived alone had a slower rate of decline in verbal cognition (P = .009), verbal memory (P = .04), and verbal fluency (P = .03) compared with those without pets who lived alone.
• Stratified analysis showed that pet ownership was associated with slower rates of decline in composite verbal cognition, verbal memory, and verbal fluency but only among those who lived alone (all P < .001).
• There was no significant difference in rates of decline in composite verbal cognition, verbal memory, or verbal fluency between pet owners living alone and pet owners living with others.

IN PRACTICE:

“Pet ownership completely offset the associations of living alone with declining rates in verbal memory, verbal fluency, and composite verbal cognition. Our findings provide innovative insights for developing public health policies to slow cognitive decline in older adults living alone,” the authors wrote. 

SOURCE:

Ciyong Lu, PhD, of Sun Yat-sen University in Guangzhou, China, led the study, which was published online on December 26, 2023, in JAMA Network Open.

LIMITATIONS:

Whereas cognitive function includes multiple components, the study only assessed verbal memory and verbal fluency. Also, the study did not gather information on the duration of pet ownership after baseline.

DISCLOSURES:

The investigators reported no disclosures.
 

A version of this article appeared on Medscape.com.

TOPLINE: 

Pet ownership is associated with slower cognitive decline in seniors who live alone, a new longitudinal cohort study showed. Investigators note the findings are important because previous research suggests older adults who live alone are at higher risk for dementia.

METHODOLOGY:

• Investigators analyzed data on 7945 participants aged 50 years and older (56% female; mean age, 66 years) from the English Longitudinal Study of Ageing (ELSA) and determined whether they lived alone or had a pet.
• Every couple of years for the next 8 years after baseline, participants were assessed for verbal cognition, verbal memory, and verbal fluency. Information about covariates including age, sex, employment status, educational level, and health was also collected.
• 35% of participants were pet owners, and 27% lived alone.

TAKEAWAY: 

• Pet owners who lived alone had a slower rate of decline in verbal cognition (P = .009), verbal memory (P = .04), and verbal fluency (P = .03) compared with those without pets who lived alone.
• Stratified analysis showed that pet ownership was associated with slower rates of decline in composite verbal cognition, verbal memory, and verbal fluency but only among those who lived alone (all P < .001).
• There was no significant difference in rates of decline in composite verbal cognition, verbal memory, or verbal fluency between pet owners living alone and pet owners living with others.

IN PRACTICE:

“Pet ownership completely offset the associations of living alone with declining rates in verbal memory, verbal fluency, and composite verbal cognition. Our findings provide innovative insights for developing public health policies to slow cognitive decline in older adults living alone,” the authors wrote. 

SOURCE:

Ciyong Lu, PhD, of Sun Yat-sen University in Guangzhou, China, led the study, which was published online on December 26, 2023, in JAMA Network Open.

LIMITATIONS:

Whereas cognitive function includes multiple components, the study only assessed verbal memory and verbal fluency. Also, the study did not gather information on the duration of pet ownership after baseline.

DISCLOSURES:

The investigators reported no disclosures.
 

A version of this article appeared on Medscape.com.

TOPLINE: 

Pet ownership is associated with slower cognitive decline in seniors who live alone, a new longitudinal cohort study showed. Investigators note the findings are important because previous research suggests older adults who live alone are at higher risk for dementia.

METHODOLOGY:

• Investigators analyzed data on 7945 participants aged 50 years and older (56% female; mean age, 66 years) from the English Longitudinal Study of Ageing (ELSA) and determined whether they lived alone or had a pet.
• Every couple of years for the next 8 years after baseline, participants were assessed for verbal cognition, verbal memory, and verbal fluency. Information about covariates including age, sex, employment status, educational level, and health was also collected.
• 35% of participants were pet owners, and 27% lived alone.

TAKEAWAY: 

• Pet owners who lived alone had a slower rate of decline in verbal cognition (P = .009), verbal memory (P = .04), and verbal fluency (P = .03) compared with those without pets who lived alone.
• Stratified analysis showed that pet ownership was associated with slower rates of decline in composite verbal cognition, verbal memory, and verbal fluency but only among those who lived alone (all P < .001).
• There was no significant difference in rates of decline in composite verbal cognition, verbal memory, or verbal fluency between pet owners living alone and pet owners living with others.

IN PRACTICE:

“Pet ownership completely offset the associations of living alone with declining rates in verbal memory, verbal fluency, and composite verbal cognition. Our findings provide innovative insights for developing public health policies to slow cognitive decline in older adults living alone,” the authors wrote. 

SOURCE:

Ciyong Lu, PhD, of Sun Yat-sen University in Guangzhou, China, led the study, which was published online on December 26, 2023, in JAMA Network Open.

LIMITATIONS:

Whereas cognitive function includes multiple components, the study only assessed verbal memory and verbal fluency. Also, the study did not gather information on the duration of pet ownership after baseline.

DISCLOSURES:

The investigators reported no disclosures.
 

A version of this article appeared on Medscape.com.

Mr. Smith was once a nice guy.

These days, unfortunately, he’s anything but. The ravages of a neurodegenerative disease have left him demented, impulsive, and agitated.

His family is trying to find placement for him, and in the meantime I’m doing my best to keep his behavior controlled. Like many things in medicine, this is as much art as science. A tablet of this, a capsule of that, increase this slightly, add something for PRN use ... a witch’s brew of modern medicine.

Because of his worsening, his wife was calling us several times a week with updates, not in an annoying way but in an “I need help” way. I began answering the phone myself if I saw her number come up, because it was easier and faster for me to deal with her directly, and I knew she wasn’t calling for fun.

A few months ago I stopped a medication that didn’t seem to be doing much and started a different one.

And then things went quiet. His wife’s calls went from 3-4 a week to none.

This worried me. I mean, maybe the new medicine was working. ... but the sudden silence was deafening.

One week went by, then two ... I did a Google search to make sure he and his wife hadn’t died or been in the news.

Of course, I could have picked up the phone and called his wife, but why tempt fate?

Three weeks ... I was sure my MA, who handles far more calls than I do, had probably noticed this, too.

It would have been easy to mention it, but even with 16 years of school and 5 years of medical training, not to mention 3,000-4,000 years of hard-earned science behind me, there was the old grade school notion of jinxing myself. To say something is to invite trouble.

Four weeks. Finally, his wife called in and reached my MA. The medication had been working, but now was wearing off and the dose needed to be adjusted. So we did that.

Afterward I mentioned the time lapse to my MA, that I’d been afraid of jinxing it by saying something to her, and she told me she’d been thinking the same thing.

Funny when you think about it. We’re both educated people, believers in science, and (I hope) intelligent. We’re living in a (by human standards) technologically advanced time.

Yet, the old superstitions are still there, the idea that we somehow have magical control over time, space, random chance, and the actions of others by not talking about a phone call (or the lack of one).

Surprisingly (or maybe not), this is pretty normal. When on call we never say “quiet,” for fear of enraging the mysterious Call Gods. If needed, we use “the Q word.”

We still try not to walk under ladders, avoid stepping on sidewalk cracks, carry good luck charms, cross fingers, and fight over wishbones.

Superstitions such as saying “bless you” or “gesundheit” when someone sneezes are so ingrained into us that they’re now part of good manners and polite society.

I’ve worked in quite a few hospitals over the years. Not one of them had a room on any floor that ended in 13, always jumping from 12 to 14.

Civilization is roughly 10,000-15,000 years old. We have the internet and can travel to (relatively nearby) space and back. We have probes exploring — and even leaving — our solar system.

But it’s one thing to say a superstition is silly. It’s another to actually convince your primeval self of it.

I’m going to knock on wood now.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Mr. Smith was once a nice guy.

These days, unfortunately, he’s anything but. The ravages of a neurodegenerative disease have left him demented, impulsive, and agitated.

His family is trying to find placement for him, and in the meantime I’m doing my best to keep his behavior controlled. Like many things in medicine, this is as much art as science. A tablet of this, a capsule of that, increase this slightly, add something for PRN use ... a witch’s brew of modern medicine.

Because of his worsening, his wife was calling us several times a week with updates, not in an annoying way but in an “I need help” way. I began answering the phone myself if I saw her number come up, because it was easier and faster for me to deal with her directly, and I knew she wasn’t calling for fun.

A few months ago I stopped a medication that didn’t seem to be doing much and started a different one.

And then things went quiet. His wife’s calls went from 3-4 a week to none.

This worried me. I mean, maybe the new medicine was working. ... but the sudden silence was deafening.

One week went by, then two ... I did a Google search to make sure he and his wife hadn’t died or been in the news.

Of course, I could have picked up the phone and called his wife, but why tempt fate?

Three weeks ... I was sure my MA, who handles far more calls than I do, had probably noticed this, too.

It would have been easy to mention it, but even with 16 years of school and 5 years of medical training, not to mention 3,000-4,000 years of hard-earned science behind me, there was the old grade school notion of jinxing myself. To say something is to invite trouble.

Four weeks. Finally, his wife called in and reached my MA. The medication had been working, but now was wearing off and the dose needed to be adjusted. So we did that.

Afterward I mentioned the time lapse to my MA, that I’d been afraid of jinxing it by saying something to her, and she told me she’d been thinking the same thing.

Funny when you think about it. We’re both educated people, believers in science, and (I hope) intelligent. We’re living in a (by human standards) technologically advanced time.

Yet, the old superstitions are still there, the idea that we somehow have magical control over time, space, random chance, and the actions of others by not talking about a phone call (or the lack of one).

Surprisingly (or maybe not), this is pretty normal. When on call we never say “quiet,” for fear of enraging the mysterious Call Gods. If needed, we use “the Q word.”

We still try not to walk under ladders, avoid stepping on sidewalk cracks, carry good luck charms, cross fingers, and fight over wishbones.

Superstitions such as saying “bless you” or “gesundheit” when someone sneezes are so ingrained into us that they’re now part of good manners and polite society.

I’ve worked in quite a few hospitals over the years. Not one of them had a room on any floor that ended in 13, always jumping from 12 to 14.

Civilization is roughly 10,000-15,000 years old. We have the internet and can travel to (relatively nearby) space and back. We have probes exploring — and even leaving — our solar system.

But it’s one thing to say a superstition is silly. It’s another to actually convince your primeval self of it.

I’m going to knock on wood now.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Mr. Smith was once a nice guy.

These days, unfortunately, he’s anything but. The ravages of a neurodegenerative disease have left him demented, impulsive, and agitated.

His family is trying to find placement for him, and in the meantime I’m doing my best to keep his behavior controlled. Like many things in medicine, this is as much art as science. A tablet of this, a capsule of that, increase this slightly, add something for PRN use ... a witch’s brew of modern medicine.

Because of his worsening, his wife was calling us several times a week with updates, not in an annoying way but in an “I need help” way. I began answering the phone myself if I saw her number come up, because it was easier and faster for me to deal with her directly, and I knew she wasn’t calling for fun.

A few months ago I stopped a medication that didn’t seem to be doing much and started a different one.

And then things went quiet. His wife’s calls went from 3-4 a week to none.

This worried me. I mean, maybe the new medicine was working. ... but the sudden silence was deafening.

One week went by, then two ... I did a Google search to make sure he and his wife hadn’t died or been in the news.

Of course, I could have picked up the phone and called his wife, but why tempt fate?

Three weeks ... I was sure my MA, who handles far more calls than I do, had probably noticed this, too.

It would have been easy to mention it, but even with 16 years of school and 5 years of medical training, not to mention 3,000-4,000 years of hard-earned science behind me, there was the old grade school notion of jinxing myself. To say something is to invite trouble.

Four weeks. Finally, his wife called in and reached my MA. The medication had been working, but now was wearing off and the dose needed to be adjusted. So we did that.

Afterward I mentioned the time lapse to my MA, that I’d been afraid of jinxing it by saying something to her, and she told me she’d been thinking the same thing.

Funny when you think about it. We’re both educated people, believers in science, and (I hope) intelligent. We’re living in a (by human standards) technologically advanced time.

Yet, the old superstitions are still there, the idea that we somehow have magical control over time, space, random chance, and the actions of others by not talking about a phone call (or the lack of one).

Surprisingly (or maybe not), this is pretty normal. When on call we never say “quiet,” for fear of enraging the mysterious Call Gods. If needed, we use “the Q word.”

We still try not to walk under ladders, avoid stepping on sidewalk cracks, carry good luck charms, cross fingers, and fight over wishbones.

Superstitions such as saying “bless you” or “gesundheit” when someone sneezes are so ingrained into us that they’re now part of good manners and polite society.

I’ve worked in quite a few hospitals over the years. Not one of them had a room on any floor that ended in 13, always jumping from 12 to 14.

Civilization is roughly 10,000-15,000 years old. We have the internet and can travel to (relatively nearby) space and back. We have probes exploring — and even leaving — our solar system.

But it’s one thing to say a superstition is silly. It’s another to actually convince your primeval self of it.

I’m going to knock on wood now.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

A wearable, soft, robotic device could help patients with Parkinson’s disease (PD) walk without experiencing freezing of gait (FoG), early research suggested.

The robotic apparel, worn around the hips and thighs, gently pushes the hips as the leg swings, facilitating a longer stride and preventing FoG, a common disorder in PD that affects nearly all patients over the disease course.

The small, proof-of-concept study included one person with PD. But investigators noted the reduction in freezing and falls and improvement in walking distance and speed was dramatic. Incidence of FoG decreased from 63% to just 6% when the patient wore the robotic garment outdoors. Wearing the device indoors eliminated freezing altogether.

“We demonstrate proof-of-concept that FoG can be averted using a soft robotic device — a machine that aims to apply physical assistance to movement with minimal restriction, a fundamentally different approach to rigid exoskeletons,” lead investigators Conor Walsh, PhD, and Terry Ellis, PhD, PT, told this news organization.

Walsh is a professor at Harvard John A. Paulson School of Engineering and Applied Sciences in Boston, and Ellis is a professor and chair of the physical therapy department and director of the Center for Neurorehabilitation, Boston University, Boston, Massachusetts.

The study was published online on January 5, 2024, in Nature Medicine.

Disabling Disturbance

From a biomechanical perspective, FoG is manifested by an overt breakdown in spatial and temporal mechanics of walking. The impaired limb coordination occurs during the “swing phase” of the gait cycle.

There are currently no interventions that prevent FoG. Available treatment interventions include pharmacotherapy, such as dopamine replacement; deep brain stimulation (DBS) of the subthalamic nucleus; and behavioral interventions, such as cueing strategies. All have shown only modest effects in reducing FoG and, in some cases, might even worsen it, the investigators noted.

“This challenge led us to become interested in leveraging soft wearable robots to deliver mechanical cues to disrupt aberrant gait mechanics and prevent FOG in people with PD,” Dr. Walsh and Dr. Ellis said.

“Wearable robots” have been used to augment kinematics in neurologic conditions, such as stroke, cerebral palsy, and spinal cord injury. Harnessing this technology to address FoG required “a collaboration between engineers, rehabilitation scientists, physical therapists, biomechanists, and apparel designers,” the researchers said.

The wearable robotic device uses cable-driven actuators, which enable physical movement by converting electrical energy into mechanical force, and sensors worn around the waist and thighs. Using motion data collected by the sensors, algorithms estimate the phase of the walking cycle and generate assistive forces in concert with biological muscles.

Real-World Testing

The researchers tested the robotic garment on a 73-year-old man with idiopathic PD of 10-year duration. The man’s ongoing pharmacologic treatment included 1.5 tablets of 25- to 100-mg carbidopa/levodopa taken four times per day, one tablet of 100-mg amantadine twice per day, and one tablet of 200-mg entacapone taken four times per day.

He had also undergone DBS to the globus pallidus internus and utilized behavioral strategies. Despite these interventions, he continued to endure more than 10 episodes of FoG per day and numerous falls.

The patient tended to use walls to stabilize himself when walking. Freezing episodes were observed mostly when he walked in open hallways, turned, walked outdoors, and when he tried to walk and talk simultaneously.

The research was conducted over a 6-month period, with a total of five study sessions that consisted of walking trials. Four were administered in the laboratory. The fifth was conducted in a real-world outdoor community setting.

During the first visit, a biomechanical analysis of walking was performed under single-task conditions during the medication-on phase.

Testing was usually conducted during medication-on phase and under single-task conditions. But testing conditions also included attention-demanding dual tasks and single-task walking during the medication-off phase.

The researchers compared the effects of the assistance of the robotic apparel to no apparel and with the apparel turned off. They measured the percentage of time spent freezing and the total distance walked.

Robust Response

The participant demonstrated a “robust response” to the robotic apparel. With the garment’s assistance, FoG was eliminated when worn indoors, and walking distance increased by 55%. The participant walked faster and had a 25% reduction in gait variability.

These beneficial effects were repeated across multiple days as well as different types of provoking conditions and environmental contexts. When the device was tried outdoors, FoG decreased from 63% to 6% of the time. The patient was also able to simultaneously walk and talk without freezing.

“When the device assisted with hip flexion during the terminal stance phase of walking (when lifting the toe), FoG was instantaneously eliminated during inner walking, accompanied by clinically significant improvement in walking speeds and distance,” Dr. Walsh and Dr. Ellis reported.

The approach “suggests the potential benefits of a ‘bottom-up’ rather than a ‘top-down’ solution to treating gait freezing,” they commented. “We see that restoring almost-normal biomechanics alters the peripheral dynamics of gait and may influence the central processing of gait control.”

Bringing Hope

Rebecca Gilbert MD, PhD, chief mission officer, American Parkinson Disease Association, said this new approach is “exciting.”

Whether the benefits will be as robust in other people with PD “remains to be seen,” said Dr. Gilbert, who was not involved with the study.

“The paper states that multiple experimental variables utilizing the device could potentially be adjusted to serve different people with PD, and these will need to be tested in clinical trials as well,” Dr. Gilbert said.

Additionally, “the device itself is complex and may be challenging to get on and off without help, which may limit its usability in the community,” Dr. Gilbert noted.

Although more work is needed, the study “represents a remarkable proof of concept that brings hope to those with FoG,” she added.

These “promising findings prompt further investigation to validate the effects of the robotic apparel on a broader range of individuals with PD experiencing FoG and across various FoG phenotypes and environments and task contexts, complemented with FoG metrics that include quantification of the severity of the freezing episodes,” Walsh and Ellis added.

This study was based on work supported by the National Science Foundation, the National Institutes of Health, and the Massachusetts Technology Collaborative, Collaborative Research and Development Matching Grant. This work was also partially funded by the John A. Paulson School of Engineering and Applied Sciences at Harvard University as well as received financial support from the Samsung Scholarship.
 

A version of this article appeared on Medscape.com.

A wearable, soft, robotic device could help patients with Parkinson’s disease (PD) walk without experiencing freezing of gait (FoG), early research suggested.

The robotic apparel, worn around the hips and thighs, gently pushes the hips as the leg swings, facilitating a longer stride and preventing FoG, a common disorder in PD that affects nearly all patients over the disease course.

The small, proof-of-concept study included one person with PD. But investigators noted the reduction in freezing and falls and improvement in walking distance and speed was dramatic. Incidence of FoG decreased from 63% to just 6% when the patient wore the robotic garment outdoors. Wearing the device indoors eliminated freezing altogether.

“We demonstrate proof-of-concept that FoG can be averted using a soft robotic device — a machine that aims to apply physical assistance to movement with minimal restriction, a fundamentally different approach to rigid exoskeletons,” lead investigators Conor Walsh, PhD, and Terry Ellis, PhD, PT, told this news organization.

Walsh is a professor at Harvard John A. Paulson School of Engineering and Applied Sciences in Boston, and Ellis is a professor and chair of the physical therapy department and director of the Center for Neurorehabilitation, Boston University, Boston, Massachusetts.

The study was published online on January 5, 2024, in Nature Medicine.

Disabling Disturbance

From a biomechanical perspective, FoG is manifested by an overt breakdown in spatial and temporal mechanics of walking. The impaired limb coordination occurs during the “swing phase” of the gait cycle.

There are currently no interventions that prevent FoG. Available treatment interventions include pharmacotherapy, such as dopamine replacement; deep brain stimulation (DBS) of the subthalamic nucleus; and behavioral interventions, such as cueing strategies. All have shown only modest effects in reducing FoG and, in some cases, might even worsen it, the investigators noted.

“This challenge led us to become interested in leveraging soft wearable robots to deliver mechanical cues to disrupt aberrant gait mechanics and prevent FOG in people with PD,” Dr. Walsh and Dr. Ellis said.

“Wearable robots” have been used to augment kinematics in neurologic conditions, such as stroke, cerebral palsy, and spinal cord injury. Harnessing this technology to address FoG required “a collaboration between engineers, rehabilitation scientists, physical therapists, biomechanists, and apparel designers,” the researchers said.

The wearable robotic device uses cable-driven actuators, which enable physical movement by converting electrical energy into mechanical force, and sensors worn around the waist and thighs. Using motion data collected by the sensors, algorithms estimate the phase of the walking cycle and generate assistive forces in concert with biological muscles.

Real-World Testing

The researchers tested the robotic garment on a 73-year-old man with idiopathic PD of 10-year duration. The man’s ongoing pharmacologic treatment included 1.5 tablets of 25- to 100-mg carbidopa/levodopa taken four times per day, one tablet of 100-mg amantadine twice per day, and one tablet of 200-mg entacapone taken four times per day.

He had also undergone DBS to the globus pallidus internus and utilized behavioral strategies. Despite these interventions, he continued to endure more than 10 episodes of FoG per day and numerous falls.

The patient tended to use walls to stabilize himself when walking. Freezing episodes were observed mostly when he walked in open hallways, turned, walked outdoors, and when he tried to walk and talk simultaneously.

The research was conducted over a 6-month period, with a total of five study sessions that consisted of walking trials. Four were administered in the laboratory. The fifth was conducted in a real-world outdoor community setting.

During the first visit, a biomechanical analysis of walking was performed under single-task conditions during the medication-on phase.

Testing was usually conducted during medication-on phase and under single-task conditions. But testing conditions also included attention-demanding dual tasks and single-task walking during the medication-off phase.

The researchers compared the effects of the assistance of the robotic apparel to no apparel and with the apparel turned off. They measured the percentage of time spent freezing and the total distance walked.

Robust Response

The participant demonstrated a “robust response” to the robotic apparel. With the garment’s assistance, FoG was eliminated when worn indoors, and walking distance increased by 55%. The participant walked faster and had a 25% reduction in gait variability.

These beneficial effects were repeated across multiple days as well as different types of provoking conditions and environmental contexts. When the device was tried outdoors, FoG decreased from 63% to 6% of the time. The patient was also able to simultaneously walk and talk without freezing.

“When the device assisted with hip flexion during the terminal stance phase of walking (when lifting the toe), FoG was instantaneously eliminated during inner walking, accompanied by clinically significant improvement in walking speeds and distance,” Dr. Walsh and Dr. Ellis reported.

The approach “suggests the potential benefits of a ‘bottom-up’ rather than a ‘top-down’ solution to treating gait freezing,” they commented. “We see that restoring almost-normal biomechanics alters the peripheral dynamics of gait and may influence the central processing of gait control.”

Bringing Hope

Rebecca Gilbert MD, PhD, chief mission officer, American Parkinson Disease Association, said this new approach is “exciting.”

Whether the benefits will be as robust in other people with PD “remains to be seen,” said Dr. Gilbert, who was not involved with the study.

“The paper states that multiple experimental variables utilizing the device could potentially be adjusted to serve different people with PD, and these will need to be tested in clinical trials as well,” Dr. Gilbert said.

Additionally, “the device itself is complex and may be challenging to get on and off without help, which may limit its usability in the community,” Dr. Gilbert noted.

Although more work is needed, the study “represents a remarkable proof of concept that brings hope to those with FoG,” she added.

These “promising findings prompt further investigation to validate the effects of the robotic apparel on a broader range of individuals with PD experiencing FoG and across various FoG phenotypes and environments and task contexts, complemented with FoG metrics that include quantification of the severity of the freezing episodes,” Walsh and Ellis added.

This study was based on work supported by the National Science Foundation, the National Institutes of Health, and the Massachusetts Technology Collaborative, Collaborative Research and Development Matching Grant. This work was also partially funded by the John A. Paulson School of Engineering and Applied Sciences at Harvard University as well as received financial support from the Samsung Scholarship.
 

A version of this article appeared on Medscape.com.

A wearable, soft, robotic device could help patients with Parkinson’s disease (PD) walk without experiencing freezing of gait (FoG), early research suggested.

The robotic apparel, worn around the hips and thighs, gently pushes the hips as the leg swings, facilitating a longer stride and preventing FoG, a common disorder in PD that affects nearly all patients over the disease course.

The small, proof-of-concept study included one person with PD. But investigators noted the reduction in freezing and falls and improvement in walking distance and speed was dramatic. Incidence of FoG decreased from 63% to just 6% when the patient wore the robotic garment outdoors. Wearing the device indoors eliminated freezing altogether.

“We demonstrate proof-of-concept that FoG can be averted using a soft robotic device — a machine that aims to apply physical assistance to movement with minimal restriction, a fundamentally different approach to rigid exoskeletons,” lead investigators Conor Walsh, PhD, and Terry Ellis, PhD, PT, told this news organization.

Walsh is a professor at Harvard John A. Paulson School of Engineering and Applied Sciences in Boston, and Ellis is a professor and chair of the physical therapy department and director of the Center for Neurorehabilitation, Boston University, Boston, Massachusetts.

The study was published online on January 5, 2024, in Nature Medicine.

Disabling Disturbance

From a biomechanical perspective, FoG is manifested by an overt breakdown in spatial and temporal mechanics of walking. The impaired limb coordination occurs during the “swing phase” of the gait cycle.

There are currently no interventions that prevent FoG. Available treatment interventions include pharmacotherapy, such as dopamine replacement; deep brain stimulation (DBS) of the subthalamic nucleus; and behavioral interventions, such as cueing strategies. All have shown only modest effects in reducing FoG and, in some cases, might even worsen it, the investigators noted.

“This challenge led us to become interested in leveraging soft wearable robots to deliver mechanical cues to disrupt aberrant gait mechanics and prevent FOG in people with PD,” Dr. Walsh and Dr. Ellis said.

“Wearable robots” have been used to augment kinematics in neurologic conditions, such as stroke, cerebral palsy, and spinal cord injury. Harnessing this technology to address FoG required “a collaboration between engineers, rehabilitation scientists, physical therapists, biomechanists, and apparel designers,” the researchers said.

The wearable robotic device uses cable-driven actuators, which enable physical movement by converting electrical energy into mechanical force, and sensors worn around the waist and thighs. Using motion data collected by the sensors, algorithms estimate the phase of the walking cycle and generate assistive forces in concert with biological muscles.

Real-World Testing

The researchers tested the robotic garment on a 73-year-old man with idiopathic PD of 10-year duration. The man’s ongoing pharmacologic treatment included 1.5 tablets of 25- to 100-mg carbidopa/levodopa taken four times per day, one tablet of 100-mg amantadine twice per day, and one tablet of 200-mg entacapone taken four times per day.

He had also undergone DBS to the globus pallidus internus and utilized behavioral strategies. Despite these interventions, he continued to endure more than 10 episodes of FoG per day and numerous falls.

The patient tended to use walls to stabilize himself when walking. Freezing episodes were observed mostly when he walked in open hallways, turned, walked outdoors, and when he tried to walk and talk simultaneously.

The research was conducted over a 6-month period, with a total of five study sessions that consisted of walking trials. Four were administered in the laboratory. The fifth was conducted in a real-world outdoor community setting.

During the first visit, a biomechanical analysis of walking was performed under single-task conditions during the medication-on phase.

Testing was usually conducted during medication-on phase and under single-task conditions. But testing conditions also included attention-demanding dual tasks and single-task walking during the medication-off phase.

The researchers compared the effects of the assistance of the robotic apparel to no apparel and with the apparel turned off. They measured the percentage of time spent freezing and the total distance walked.

Robust Response

The participant demonstrated a “robust response” to the robotic apparel. With the garment’s assistance, FoG was eliminated when worn indoors, and walking distance increased by 55%. The participant walked faster and had a 25% reduction in gait variability.

These beneficial effects were repeated across multiple days as well as different types of provoking conditions and environmental contexts. When the device was tried outdoors, FoG decreased from 63% to 6% of the time. The patient was also able to simultaneously walk and talk without freezing.

“When the device assisted with hip flexion during the terminal stance phase of walking (when lifting the toe), FoG was instantaneously eliminated during inner walking, accompanied by clinically significant improvement in walking speeds and distance,” Dr. Walsh and Dr. Ellis reported.

The approach “suggests the potential benefits of a ‘bottom-up’ rather than a ‘top-down’ solution to treating gait freezing,” they commented. “We see that restoring almost-normal biomechanics alters the peripheral dynamics of gait and may influence the central processing of gait control.”

Bringing Hope

Rebecca Gilbert MD, PhD, chief mission officer, American Parkinson Disease Association, said this new approach is “exciting.”

Whether the benefits will be as robust in other people with PD “remains to be seen,” said Dr. Gilbert, who was not involved with the study.

“The paper states that multiple experimental variables utilizing the device could potentially be adjusted to serve different people with PD, and these will need to be tested in clinical trials as well,” Dr. Gilbert said.

Additionally, “the device itself is complex and may be challenging to get on and off without help, which may limit its usability in the community,” Dr. Gilbert noted.

Although more work is needed, the study “represents a remarkable proof of concept that brings hope to those with FoG,” she added.

These “promising findings prompt further investigation to validate the effects of the robotic apparel on a broader range of individuals with PD experiencing FoG and across various FoG phenotypes and environments and task contexts, complemented with FoG metrics that include quantification of the severity of the freezing episodes,” Walsh and Ellis added.

This study was based on work supported by the National Science Foundation, the National Institutes of Health, and the Massachusetts Technology Collaborative, Collaborative Research and Development Matching Grant. This work was also partially funded by the John A. Paulson School of Engineering and Applied Sciences at Harvard University as well as received financial support from the Samsung Scholarship.
 

A version of this article appeared on Medscape.com.

This interview was recorded Dec. 8, 2023. The transcript has been edited for clarity.

Kathrin LaFaver, MD: I have the pleasure of talking with Dr. Elizabeth Loder today. Dr. Loder is the vice chair of academic affairs in the department of neurology and a staff physician at Graham Headache Center at Brigham and Women’s Hospital in Boston. She’s also a professor of neurology at Harvard Medical School and has been a mentor to many headache specialists in the field.

We’ll be talking about the topic of sexism in medicine.

Elizabeth W. Loder, MD, MPH: Thank you so much, Dr. LaFaver. I’m very pleased to be here to talk about something that I think is very important.

Dr. LaFaver: Dr. Loder, you were a speaker at our Women in Neurology third annual conference in Florida, giving a talk on this very topic, sexism in medicine. It was very helpful, especially for many younger women entering the field of neurology, to hear that some of the experiences they’re having are not unique to them, but unfortunately remain a more systemic issue.

To get us started, could you define sexism in medicine for us, and how you got interested in this topic?
 

Sexism Can Be Subtle

Dr. Loder: You’re absolutely right. Sexism is still there. It might be a bit more subtle than it used to be at the beginning of my career, but it’s definitely still there. It’s nice for women, particularly those entering the field, to know that they’re not alone.

What is sexism? Well, it’s generally considered to be prejudice or discrimination against someone based on their sex or gender. One thing that’s important to remember is it’s not always extremely obvious. It’s not always intentional. I think most of us, I’d include myself in that, have sexist views. We may not always be aware of them. This is part of the unconscious bias that many of us have been trained to think.

As one example, we’re socialized — or I certainly was — to think of doctors as male. When a patient says, “I saw a cardiologist,” in my mind, I think that that person might have been male. Sometimes, I will ask, “What did he say?” That’s an example of sexism.

Sexism can be internalized. It can come from any source. We’re all implicated in it. I think that’s very important to remember. This is not a case of them doing something to us. This is something that is much more widespread and engendered in the society that we live in.

Dr. LaFaver: I think that’s really important to realize. Could you mention some other examples, specifically in the field of neurology, that you have encountered?

Dr. Loder: Certainly, looking over my own career — and I’m at a point now where I can look at early, mid, and late career — things were, of course, very different when I began. I would say that sexism was much more overt.

Very early in my career, I experienced a large amount of hostility from a boss. I ended up having to leave. This was, I believe, based on my sex. It turned out that leaving was a good thing for me, but it was a very unpleasant experience.

I also became a leader in my professional society. During my path to leadership and seeing other women attempt to make progress within the organization, I certainly saw behavior that I would characterize as rooted in sexism. To its credit, though, the professional society to which I belong, I think, has become one of the most progressive societies out there. The women within have been able to affect quite a bit of change in that professional organization.

I dealt with a case of sexual harassment in my own division when I was a division chief, which gave me insight into institutional policies and procedures meant to deal with situations like that, which, I think, leave something to be desired. That’s changing.

Now, I work in academic affairs, and I see how likely or unlikely people, based on their sex, are to put themselves forward for promotion, how likely they are to believe in their own capabilities. I also work as a medical journal editor, and I see generally that women are more hesitant to proclaim themselves experts and to accept invitations to provide or write editorial commentary. Sometimes, they do not perceive themselves as being expert enough to do so. I have seen many of these things over my career.

Dr. LaFaver: Thank you for sharing. I think it’s important to realize that it›s not just unidirectional but sometimes affects women and kind of goes both ways.

As you mentioned, these issues are not always overt. In recent years, microaggressions has become more of a term that has been used. Could you talk a bit about that? What are the microaggressions and how do they affect women?
 

Microaggressions and Migraine Mavens

Dr. Loder: The term microaggression has become very popular, and I think many people find it somewhat irritating. That, to me, is inherent in what a microaggression is. Microaggressions, by definition, are small things. It’s hard to prove that they were rooted in sexism. Sometimes, there’s a large amount of ambiguity about it. It can be as simple as inviting a pregnant woman to sit down because you perceive that she needs to sit, commenting on somebody’s shoes, or things like that.

Often, they’re unintentional. Sometimes, they come from a place of what we might term benevolent sexism, people trying to be helpful to a woman because they perceive that she’s weaker or she might not be able to do something, or maybe she has family responsibilities. They think that they’re being helpful. These things happen when we perceive people to be different in some way, as women are perceived to be different in terms of their responsibilities in the home or different in terms of what we expect from them in the workplace.

The problem with microaggressions is because they’re small, each one of them, I think the temptation is often to say, “Oh you know, they didn’t mean it. It’s not that big a deal. It was just a comment on your shoes.” If a woman brings that up, she’s often made to feel, sometimes by other women, that she should just chill out. This isn’t a big deal.

The problem is that they may not be a big deal in and of themselves, but when they are repeated over a long period of time, they can really sap somebody’s confidence in herself, make her question her own competence, and can have a cumulative effect that is very negative.

Although I think many people are skeptical about microaggressions as an important contribution to how women do in the workplace and in other settings, they are, in my opinion, important. I’ll just emphasize again that they come from everywhere, including other women and colleagues who mean to be helpful.

Dr. LaFaver: I know you have led a team of headache specialists and wrote a fantastic article about navigating sexism at work and what not to say to your female colleagues. Could you share some tips for them to navigate sexism at work and, specifically, as it applies to our careers in medicine.

Dr. Loder: Thank you for calling out that article. It actually grew organically out of a Facebook group that I started called Migraine Mavens. I’ve worked in the headache field throughout my career, and I experienced something that, to me, was kind of discouraging that I felt was sexist within our field. I just thought, What can I do? I thought, Well, maybe there’s some strength to be had in sharing this with other women, and maybe we should have our own social media community, so I formed this group.

After I gave a talk at the American Headache Society about sexism in the headache field, one of the members sent me a message saying, “Your talk was very timely. Immediately after you gave this talk, somebody stopped me in the hall and said, ‘Congratulations on your leadership position in the society, but are you really sure you can do this because you’ve got young children at home?’ Your talk was very needed.”

People started just discussing within the group, “Oh, this happened to me,” “That happened to me.” We began to brainstorm what we could have done differently. When these things happen, people are not necessarily prepared for them, and later on, you lie awake thinking of what you could have said.

We decided to write a paper. It ended up being published in The Journal of Head and Face Pain, and it was based on real vignettes from people in the group. We anonymized them so that people would not recognize themselves necessarily, but they’re all real. They’re things that really happened to women in the group.

We first describe the vignette — what happened. Then we explain, for those who need the explanation, what’s wrong with it. Why is it wrong to tell somebody to smile, for example. What could you do differently? What could somebody who sees this happen do, the so-called bystander or upstander? If you witness something like that, can you help the person toward whom this problematic behavior is directed? We came up with some examples. The all-purpose thing is to say, “What did you just say?” Make them repeat it, which often helps people to realize how inappropriate it is.

This got published as an article. It became quite the subject of attention on X [formerly Twitter] and elsewhere. I guess the term going viral would apply to this. It included a large amount of real-world advice. The thing I really loved about it was that it was written by the women in the group who had experienced these things. I would characterize it as having been somewhat therapeutic. We got many messages from women in other disciplines, outside medicine, saying that this happens in oceanography, for example. I think what we described really resonated beyond the field of headache medicine and neurology.
 

Institutional Sexism

Dr. LaFaver: Looking beyond the individual person, do you have any recommendations for medical institutions to share in order to do better and maybe create an environment that is less sexist?

Dr. Loder: Yes. I think many institutions try to deal with the problem of lack of diversity, whether it›s women or other underrepresented groups, by hiring. That’s one way to go about it, but I think retention strategies are also very important, and they need to pay attention to the work environment.

Every institution now has guidelines about harassment, bullying, sexism, racism, and so on. In general though — and I’m not speaking about any particular institution — these policies and procedures are often crafted with an eye toward protecting the institution. I would advise institutions to be a bit more genuine about this, and not to think so quickly about what can we do to prevent the institution from facing a charge of sexism, or what can we do to deny or dismiss these allegations, toward thinking, what can we do to really and truly be helpful to these women? In other words, approach it from the point of view of trying to help the people involved instead of trying to help the institution. That will make a very big difference.

I also think that citizenship activities, serving on committees, doing thankless tasks behind the scenes, and clinical work, seeing patients ... Women are overrepresented among clinicians. Of course, we know that research and bringing in big grants is often prioritized over clinical care, despite what institutions may say about that in public. I think those activities should be valued more highly, both in terms of pay and in terms of academic recognition.

In regard to the issue of salary, I would encourage institutions to publish salaries or at least make them easily findable by people within the institution. I think there should be objective criteria for salary determinations. The most important thing is that I do not think that women should be expected to negotiate their salaries. Women are judged differently than men when they attempt to negotiate salaries. It often backfires for them. It also is something that many women do not feel comfortable doing.

Waiting until somebody tries to negotiate a higher salary really guarantees, embeds, and operationalizes sex differences in salaries. We need to move away from the idea that you have to be a go-getter and that you have to ask for this raise. There should be objective criteria, salaries should be revisited on a regular basis, and the kinds of activities that women do that are undervalued should be more recognized in terms of money and advancement within academia.

Dr. LaFaver: I couldn’t agree more. One of the other topics discussed at the Women in Neurology conference was mid-career development, retention, and career paths. I think it’s known that many women leave academic medicine mid-career. I think these are excellent suggestions and hopefully will help to make careers successful for men and women, without needing to worry about being treated differently or unfairly.

Thank you so much. This was a wonderful overview of this topic.

Dr. Loder: You’re welcome, Dr. LaFaver. Thank you so much for asking me to speak on this topic. I really appreciate it.

Dr. LaFaver: Thanks, everyone.

 

Dr. LaFaver is a neurologist at Saratoga Hospital Medical Group, Saratoga Springs, New York. Dr. LaFaver and Dr. Loder disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

This interview was recorded Dec. 8, 2023. The transcript has been edited for clarity.

Kathrin LaFaver, MD: I have the pleasure of talking with Dr. Elizabeth Loder today. Dr. Loder is the vice chair of academic affairs in the department of neurology and a staff physician at Graham Headache Center at Brigham and Women’s Hospital in Boston. She’s also a professor of neurology at Harvard Medical School and has been a mentor to many headache specialists in the field.

We’ll be talking about the topic of sexism in medicine.

Elizabeth W. Loder, MD, MPH: Thank you so much, Dr. LaFaver. I’m very pleased to be here to talk about something that I think is very important.

Dr. LaFaver: Dr. Loder, you were a speaker at our Women in Neurology third annual conference in Florida, giving a talk on this very topic, sexism in medicine. It was very helpful, especially for many younger women entering the field of neurology, to hear that some of the experiences they’re having are not unique to them, but unfortunately remain a more systemic issue.

To get us started, could you define sexism in medicine for us, and how you got interested in this topic?
 

Sexism Can Be Subtle

Dr. Loder: You’re absolutely right. Sexism is still there. It might be a bit more subtle than it used to be at the beginning of my career, but it’s definitely still there. It’s nice for women, particularly those entering the field, to know that they’re not alone.

What is sexism? Well, it’s generally considered to be prejudice or discrimination against someone based on their sex or gender. One thing that’s important to remember is it’s not always extremely obvious. It’s not always intentional. I think most of us, I’d include myself in that, have sexist views. We may not always be aware of them. This is part of the unconscious bias that many of us have been trained to think.

As one example, we’re socialized — or I certainly was — to think of doctors as male. When a patient says, “I saw a cardiologist,” in my mind, I think that that person might have been male. Sometimes, I will ask, “What did he say?” That’s an example of sexism.

Sexism can be internalized. It can come from any source. We’re all implicated in it. I think that’s very important to remember. This is not a case of them doing something to us. This is something that is much more widespread and engendered in the society that we live in.

Dr. LaFaver: I think that’s really important to realize. Could you mention some other examples, specifically in the field of neurology, that you have encountered?

Dr. Loder: Certainly, looking over my own career — and I’m at a point now where I can look at early, mid, and late career — things were, of course, very different when I began. I would say that sexism was much more overt.

Very early in my career, I experienced a large amount of hostility from a boss. I ended up having to leave. This was, I believe, based on my sex. It turned out that leaving was a good thing for me, but it was a very unpleasant experience.

I also became a leader in my professional society. During my path to leadership and seeing other women attempt to make progress within the organization, I certainly saw behavior that I would characterize as rooted in sexism. To its credit, though, the professional society to which I belong, I think, has become one of the most progressive societies out there. The women within have been able to affect quite a bit of change in that professional organization.

I dealt with a case of sexual harassment in my own division when I was a division chief, which gave me insight into institutional policies and procedures meant to deal with situations like that, which, I think, leave something to be desired. That’s changing.

Now, I work in academic affairs, and I see how likely or unlikely people, based on their sex, are to put themselves forward for promotion, how likely they are to believe in their own capabilities. I also work as a medical journal editor, and I see generally that women are more hesitant to proclaim themselves experts and to accept invitations to provide or write editorial commentary. Sometimes, they do not perceive themselves as being expert enough to do so. I have seen many of these things over my career.

Dr. LaFaver: Thank you for sharing. I think it’s important to realize that it›s not just unidirectional but sometimes affects women and kind of goes both ways.

As you mentioned, these issues are not always overt. In recent years, microaggressions has become more of a term that has been used. Could you talk a bit about that? What are the microaggressions and how do they affect women?
 

Microaggressions and Migraine Mavens

Dr. Loder: The term microaggression has become very popular, and I think many people find it somewhat irritating. That, to me, is inherent in what a microaggression is. Microaggressions, by definition, are small things. It’s hard to prove that they were rooted in sexism. Sometimes, there’s a large amount of ambiguity about it. It can be as simple as inviting a pregnant woman to sit down because you perceive that she needs to sit, commenting on somebody’s shoes, or things like that.

Often, they’re unintentional. Sometimes, they come from a place of what we might term benevolent sexism, people trying to be helpful to a woman because they perceive that she’s weaker or she might not be able to do something, or maybe she has family responsibilities. They think that they’re being helpful. These things happen when we perceive people to be different in some way, as women are perceived to be different in terms of their responsibilities in the home or different in terms of what we expect from them in the workplace.

The problem with microaggressions is because they’re small, each one of them, I think the temptation is often to say, “Oh you know, they didn’t mean it. It’s not that big a deal. It was just a comment on your shoes.” If a woman brings that up, she’s often made to feel, sometimes by other women, that she should just chill out. This isn’t a big deal.

The problem is that they may not be a big deal in and of themselves, but when they are repeated over a long period of time, they can really sap somebody’s confidence in herself, make her question her own competence, and can have a cumulative effect that is very negative.

Although I think many people are skeptical about microaggressions as an important contribution to how women do in the workplace and in other settings, they are, in my opinion, important. I’ll just emphasize again that they come from everywhere, including other women and colleagues who mean to be helpful.

Dr. LaFaver: I know you have led a team of headache specialists and wrote a fantastic article about navigating sexism at work and what not to say to your female colleagues. Could you share some tips for them to navigate sexism at work and, specifically, as it applies to our careers in medicine.

Dr. Loder: Thank you for calling out that article. It actually grew organically out of a Facebook group that I started called Migraine Mavens. I’ve worked in the headache field throughout my career, and I experienced something that, to me, was kind of discouraging that I felt was sexist within our field. I just thought, What can I do? I thought, Well, maybe there’s some strength to be had in sharing this with other women, and maybe we should have our own social media community, so I formed this group.

After I gave a talk at the American Headache Society about sexism in the headache field, one of the members sent me a message saying, “Your talk was very timely. Immediately after you gave this talk, somebody stopped me in the hall and said, ‘Congratulations on your leadership position in the society, but are you really sure you can do this because you’ve got young children at home?’ Your talk was very needed.”

People started just discussing within the group, “Oh, this happened to me,” “That happened to me.” We began to brainstorm what we could have done differently. When these things happen, people are not necessarily prepared for them, and later on, you lie awake thinking of what you could have said.

We decided to write a paper. It ended up being published in The Journal of Head and Face Pain, and it was based on real vignettes from people in the group. We anonymized them so that people would not recognize themselves necessarily, but they’re all real. They’re things that really happened to women in the group.

We first describe the vignette — what happened. Then we explain, for those who need the explanation, what’s wrong with it. Why is it wrong to tell somebody to smile, for example. What could you do differently? What could somebody who sees this happen do, the so-called bystander or upstander? If you witness something like that, can you help the person toward whom this problematic behavior is directed? We came up with some examples. The all-purpose thing is to say, “What did you just say?” Make them repeat it, which often helps people to realize how inappropriate it is.

This got published as an article. It became quite the subject of attention on X [formerly Twitter] and elsewhere. I guess the term going viral would apply to this. It included a large amount of real-world advice. The thing I really loved about it was that it was written by the women in the group who had experienced these things. I would characterize it as having been somewhat therapeutic. We got many messages from women in other disciplines, outside medicine, saying that this happens in oceanography, for example. I think what we described really resonated beyond the field of headache medicine and neurology.
 

Institutional Sexism

Dr. LaFaver: Looking beyond the individual person, do you have any recommendations for medical institutions to share in order to do better and maybe create an environment that is less sexist?

Dr. Loder: Yes. I think many institutions try to deal with the problem of lack of diversity, whether it›s women or other underrepresented groups, by hiring. That’s one way to go about it, but I think retention strategies are also very important, and they need to pay attention to the work environment.

Every institution now has guidelines about harassment, bullying, sexism, racism, and so on. In general though — and I’m not speaking about any particular institution — these policies and procedures are often crafted with an eye toward protecting the institution. I would advise institutions to be a bit more genuine about this, and not to think so quickly about what can we do to prevent the institution from facing a charge of sexism, or what can we do to deny or dismiss these allegations, toward thinking, what can we do to really and truly be helpful to these women? In other words, approach it from the point of view of trying to help the people involved instead of trying to help the institution. That will make a very big difference.

I also think that citizenship activities, serving on committees, doing thankless tasks behind the scenes, and clinical work, seeing patients ... Women are overrepresented among clinicians. Of course, we know that research and bringing in big grants is often prioritized over clinical care, despite what institutions may say about that in public. I think those activities should be valued more highly, both in terms of pay and in terms of academic recognition.

In regard to the issue of salary, I would encourage institutions to publish salaries or at least make them easily findable by people within the institution. I think there should be objective criteria for salary determinations. The most important thing is that I do not think that women should be expected to negotiate their salaries. Women are judged differently than men when they attempt to negotiate salaries. It often backfires for them. It also is something that many women do not feel comfortable doing.

Waiting until somebody tries to negotiate a higher salary really guarantees, embeds, and operationalizes sex differences in salaries. We need to move away from the idea that you have to be a go-getter and that you have to ask for this raise. There should be objective criteria, salaries should be revisited on a regular basis, and the kinds of activities that women do that are undervalued should be more recognized in terms of money and advancement within academia.

Dr. LaFaver: I couldn’t agree more. One of the other topics discussed at the Women in Neurology conference was mid-career development, retention, and career paths. I think it’s known that many women leave academic medicine mid-career. I think these are excellent suggestions and hopefully will help to make careers successful for men and women, without needing to worry about being treated differently or unfairly.

Thank you so much. This was a wonderful overview of this topic.

Dr. Loder: You’re welcome, Dr. LaFaver. Thank you so much for asking me to speak on this topic. I really appreciate it.

Dr. LaFaver: Thanks, everyone.

 

Dr. LaFaver is a neurologist at Saratoga Hospital Medical Group, Saratoga Springs, New York. Dr. LaFaver and Dr. Loder disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

This interview was recorded Dec. 8, 2023. The transcript has been edited for clarity.

Kathrin LaFaver, MD: I have the pleasure of talking with Dr. Elizabeth Loder today. Dr. Loder is the vice chair of academic affairs in the department of neurology and a staff physician at Graham Headache Center at Brigham and Women’s Hospital in Boston. She’s also a professor of neurology at Harvard Medical School and has been a mentor to many headache specialists in the field.

We’ll be talking about the topic of sexism in medicine.

Elizabeth W. Loder, MD, MPH: Thank you so much, Dr. LaFaver. I’m very pleased to be here to talk about something that I think is very important.

Dr. LaFaver: Dr. Loder, you were a speaker at our Women in Neurology third annual conference in Florida, giving a talk on this very topic, sexism in medicine. It was very helpful, especially for many younger women entering the field of neurology, to hear that some of the experiences they’re having are not unique to them, but unfortunately remain a more systemic issue.

To get us started, could you define sexism in medicine for us, and how you got interested in this topic?
 

Sexism Can Be Subtle

Dr. Loder: You’re absolutely right. Sexism is still there. It might be a bit more subtle than it used to be at the beginning of my career, but it’s definitely still there. It’s nice for women, particularly those entering the field, to know that they’re not alone.

What is sexism? Well, it’s generally considered to be prejudice or discrimination against someone based on their sex or gender. One thing that’s important to remember is it’s not always extremely obvious. It’s not always intentional. I think most of us, I’d include myself in that, have sexist views. We may not always be aware of them. This is part of the unconscious bias that many of us have been trained to think.

As one example, we’re socialized — or I certainly was — to think of doctors as male. When a patient says, “I saw a cardiologist,” in my mind, I think that that person might have been male. Sometimes, I will ask, “What did he say?” That’s an example of sexism.

Sexism can be internalized. It can come from any source. We’re all implicated in it. I think that’s very important to remember. This is not a case of them doing something to us. This is something that is much more widespread and engendered in the society that we live in.

Dr. LaFaver: I think that’s really important to realize. Could you mention some other examples, specifically in the field of neurology, that you have encountered?

Dr. Loder: Certainly, looking over my own career — and I’m at a point now where I can look at early, mid, and late career — things were, of course, very different when I began. I would say that sexism was much more overt.

Very early in my career, I experienced a large amount of hostility from a boss. I ended up having to leave. This was, I believe, based on my sex. It turned out that leaving was a good thing for me, but it was a very unpleasant experience.

I also became a leader in my professional society. During my path to leadership and seeing other women attempt to make progress within the organization, I certainly saw behavior that I would characterize as rooted in sexism. To its credit, though, the professional society to which I belong, I think, has become one of the most progressive societies out there. The women within have been able to affect quite a bit of change in that professional organization.

I dealt with a case of sexual harassment in my own division when I was a division chief, which gave me insight into institutional policies and procedures meant to deal with situations like that, which, I think, leave something to be desired. That’s changing.

Now, I work in academic affairs, and I see how likely or unlikely people, based on their sex, are to put themselves forward for promotion, how likely they are to believe in their own capabilities. I also work as a medical journal editor, and I see generally that women are more hesitant to proclaim themselves experts and to accept invitations to provide or write editorial commentary. Sometimes, they do not perceive themselves as being expert enough to do so. I have seen many of these things over my career.

Dr. LaFaver: Thank you for sharing. I think it’s important to realize that it›s not just unidirectional but sometimes affects women and kind of goes both ways.

As you mentioned, these issues are not always overt. In recent years, microaggressions has become more of a term that has been used. Could you talk a bit about that? What are the microaggressions and how do they affect women?
 

Microaggressions and Migraine Mavens

Dr. Loder: The term microaggression has become very popular, and I think many people find it somewhat irritating. That, to me, is inherent in what a microaggression is. Microaggressions, by definition, are small things. It’s hard to prove that they were rooted in sexism. Sometimes, there’s a large amount of ambiguity about it. It can be as simple as inviting a pregnant woman to sit down because you perceive that she needs to sit, commenting on somebody’s shoes, or things like that.

Often, they’re unintentional. Sometimes, they come from a place of what we might term benevolent sexism, people trying to be helpful to a woman because they perceive that she’s weaker or she might not be able to do something, or maybe she has family responsibilities. They think that they’re being helpful. These things happen when we perceive people to be different in some way, as women are perceived to be different in terms of their responsibilities in the home or different in terms of what we expect from them in the workplace.

The problem with microaggressions is because they’re small, each one of them, I think the temptation is often to say, “Oh you know, they didn’t mean it. It’s not that big a deal. It was just a comment on your shoes.” If a woman brings that up, she’s often made to feel, sometimes by other women, that she should just chill out. This isn’t a big deal.

The problem is that they may not be a big deal in and of themselves, but when they are repeated over a long period of time, they can really sap somebody’s confidence in herself, make her question her own competence, and can have a cumulative effect that is very negative.

Although I think many people are skeptical about microaggressions as an important contribution to how women do in the workplace and in other settings, they are, in my opinion, important. I’ll just emphasize again that they come from everywhere, including other women and colleagues who mean to be helpful.

Dr. LaFaver: I know you have led a team of headache specialists and wrote a fantastic article about navigating sexism at work and what not to say to your female colleagues. Could you share some tips for them to navigate sexism at work and, specifically, as it applies to our careers in medicine.

Dr. Loder: Thank you for calling out that article. It actually grew organically out of a Facebook group that I started called Migraine Mavens. I’ve worked in the headache field throughout my career, and I experienced something that, to me, was kind of discouraging that I felt was sexist within our field. I just thought, What can I do? I thought, Well, maybe there’s some strength to be had in sharing this with other women, and maybe we should have our own social media community, so I formed this group.

After I gave a talk at the American Headache Society about sexism in the headache field, one of the members sent me a message saying, “Your talk was very timely. Immediately after you gave this talk, somebody stopped me in the hall and said, ‘Congratulations on your leadership position in the society, but are you really sure you can do this because you’ve got young children at home?’ Your talk was very needed.”

People started just discussing within the group, “Oh, this happened to me,” “That happened to me.” We began to brainstorm what we could have done differently. When these things happen, people are not necessarily prepared for them, and later on, you lie awake thinking of what you could have said.

We decided to write a paper. It ended up being published in The Journal of Head and Face Pain, and it was based on real vignettes from people in the group. We anonymized them so that people would not recognize themselves necessarily, but they’re all real. They’re things that really happened to women in the group.

We first describe the vignette — what happened. Then we explain, for those who need the explanation, what’s wrong with it. Why is it wrong to tell somebody to smile, for example. What could you do differently? What could somebody who sees this happen do, the so-called bystander or upstander? If you witness something like that, can you help the person toward whom this problematic behavior is directed? We came up with some examples. The all-purpose thing is to say, “What did you just say?” Make them repeat it, which often helps people to realize how inappropriate it is.

This got published as an article. It became quite the subject of attention on X [formerly Twitter] and elsewhere. I guess the term going viral would apply to this. It included a large amount of real-world advice. The thing I really loved about it was that it was written by the women in the group who had experienced these things. I would characterize it as having been somewhat therapeutic. We got many messages from women in other disciplines, outside medicine, saying that this happens in oceanography, for example. I think what we described really resonated beyond the field of headache medicine and neurology.
 

Institutional Sexism

Dr. LaFaver: Looking beyond the individual person, do you have any recommendations for medical institutions to share in order to do better and maybe create an environment that is less sexist?

Dr. Loder: Yes. I think many institutions try to deal with the problem of lack of diversity, whether it›s women or other underrepresented groups, by hiring. That’s one way to go about it, but I think retention strategies are also very important, and they need to pay attention to the work environment.

Every institution now has guidelines about harassment, bullying, sexism, racism, and so on. In general though — and I’m not speaking about any particular institution — these policies and procedures are often crafted with an eye toward protecting the institution. I would advise institutions to be a bit more genuine about this, and not to think so quickly about what can we do to prevent the institution from facing a charge of sexism, or what can we do to deny or dismiss these allegations, toward thinking, what can we do to really and truly be helpful to these women? In other words, approach it from the point of view of trying to help the people involved instead of trying to help the institution. That will make a very big difference.

I also think that citizenship activities, serving on committees, doing thankless tasks behind the scenes, and clinical work, seeing patients ... Women are overrepresented among clinicians. Of course, we know that research and bringing in big grants is often prioritized over clinical care, despite what institutions may say about that in public. I think those activities should be valued more highly, both in terms of pay and in terms of academic recognition.

In regard to the issue of salary, I would encourage institutions to publish salaries or at least make them easily findable by people within the institution. I think there should be objective criteria for salary determinations. The most important thing is that I do not think that women should be expected to negotiate their salaries. Women are judged differently than men when they attempt to negotiate salaries. It often backfires for them. It also is something that many women do not feel comfortable doing.

Waiting until somebody tries to negotiate a higher salary really guarantees, embeds, and operationalizes sex differences in salaries. We need to move away from the idea that you have to be a go-getter and that you have to ask for this raise. There should be objective criteria, salaries should be revisited on a regular basis, and the kinds of activities that women do that are undervalued should be more recognized in terms of money and advancement within academia.

Dr. LaFaver: I couldn’t agree more. One of the other topics discussed at the Women in Neurology conference was mid-career development, retention, and career paths. I think it’s known that many women leave academic medicine mid-career. I think these are excellent suggestions and hopefully will help to make careers successful for men and women, without needing to worry about being treated differently or unfairly.

Thank you so much. This was a wonderful overview of this topic.

Dr. Loder: You’re welcome, Dr. LaFaver. Thank you so much for asking me to speak on this topic. I really appreciate it.

Dr. LaFaver: Thanks, everyone.

 

Dr. LaFaver is a neurologist at Saratoga Hospital Medical Group, Saratoga Springs, New York. Dr. LaFaver and Dr. Loder disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Using an advanced microscopic technique, American researchers have detected 100,000 nanoplastic molecules per liter of water in plastic bottles. Because of their small size, these particles can enter the bloodstream, cells, and the brain, thus posing potential health risks. The study, recently published in the Proceedings of the National Academy of Sciences, raises concerns about the impact of these nanoparticles.

An Unknown Realm

In recent years, the global presence of tiny particles known as microplastics has raised concerns. The particles are found in polar ice, soil, drinking water, and food. Formed as plastics break down into increasingly small pieces, these particles are consumed by humans and other organisms, with unknown effects on health and ecosystems. Whereas macroplastics have been found in various organs, including the lungs and liver, the study marks a unique exploration into the world of nanoplastics.

Concerns about nanoplastic presence in humans intensified when a 2018 study revealed contamination signs in 93% of 259 examined bottles from nine countries.

The novelty of this research lies in its focus, using a refined spectrometry method, on the poorly understood world of nanoplastics, which derive from the decomposition of microplastics. For the first time, American researchers, including biophysicists and chemists, counted and identified these tiny particles in bottled water. On average, they found around 240,000 detectable plastic fragments per liter, which is 10-100 times more than previous estimates based on larger sizes.

Microplastics are defined as fragments ranging from 5 mm to 1 µm, whereas nanoplastics, particles < 1 µm, are measured in billionths of a meter.

In contrast to microplastics, nanoplastics are so small that they can traverse the intestines and lungs and move directly into the bloodstream, reaching organs such as the heart or brain or even the fetus via the placenta.

“This was previously an obscure, unexplored area. Toxicity studies could only speculate about what was in there,” said Beizhan Yan, PhD, coauthor of the study and environmental chemist at the Lamont–Doherty Earth Observatory of Columbia University, New York. “This study opens a window for us to observe a world we were not exposed to before.”
 

90% Nanoplastics Found

The new study employed a technique called stimulated Raman scattering microscopy, which was invented by study coauthor Wei Min, a biophysicist at Columbia. This method involves probing samples simultaneously with two lasers tuned to resonate specific molecules.

Researchers tested three bottled water brands that are popular in the United States, analyzing plastic particles up to 100 nm in size. They identified 110,000-370,000 plastic particles per liter. About 90% were nanoplastics — which are invisible by standard imaging techniques — and the rest were microplastics. The study also identified the seven plastics involved.

The most common is polyamide, a type of nylon, likely from plastic filters purportedly used to purify water before bottling. Next is polyethylene terephthalate, which is commonly used for water bottles and other food containers. Researchers also found other common plastics, including polystyrene, polyvinyl chloride, and methyl methacrylate, used in various industrial processes.
 

Not Size But Quantity

What’s more concerning is that the seven types of plastics accounted for only about 10% of all nanoparticles found in the samples. Researchers have no idea about the composition of the remaining 90%. If these are all nanoparticles, their number could reach tens of millions per liter, representing the complex composition of seemingly simple water samples, as noted by the authors.

Researchers now plan to expand beyond bottled water, exploring the vast realm of nanoplastics. They emphasize that, in terms of mass, nanoplastics are far smaller than microplastics, but “it’s not about size. It’s about the numbers as smaller things can easily penetrate us.”

The team aims to study tap water, which also contains microplastics but in much smaller proportions than bottled water.

This article was translated from the Medscape French edition. 

Using an advanced microscopic technique, American researchers have detected 100,000 nanoplastic molecules per liter of water in plastic bottles. Because of their small size, these particles can enter the bloodstream, cells, and the brain, thus posing potential health risks. The study, recently published in the Proceedings of the National Academy of Sciences, raises concerns about the impact of these nanoparticles.

An Unknown Realm

In recent years, the global presence of tiny particles known as microplastics has raised concerns. The particles are found in polar ice, soil, drinking water, and food. Formed as plastics break down into increasingly small pieces, these particles are consumed by humans and other organisms, with unknown effects on health and ecosystems. Whereas macroplastics have been found in various organs, including the lungs and liver, the study marks a unique exploration into the world of nanoplastics.

Concerns about nanoplastic presence in humans intensified when a 2018 study revealed contamination signs in 93% of 259 examined bottles from nine countries.

The novelty of this research lies in its focus, using a refined spectrometry method, on the poorly understood world of nanoplastics, which derive from the decomposition of microplastics. For the first time, American researchers, including biophysicists and chemists, counted and identified these tiny particles in bottled water. On average, they found around 240,000 detectable plastic fragments per liter, which is 10-100 times more than previous estimates based on larger sizes.

Microplastics are defined as fragments ranging from 5 mm to 1 µm, whereas nanoplastics, particles < 1 µm, are measured in billionths of a meter.

In contrast to microplastics, nanoplastics are so small that they can traverse the intestines and lungs and move directly into the bloodstream, reaching organs such as the heart or brain or even the fetus via the placenta.

“This was previously an obscure, unexplored area. Toxicity studies could only speculate about what was in there,” said Beizhan Yan, PhD, coauthor of the study and environmental chemist at the Lamont–Doherty Earth Observatory of Columbia University, New York. “This study opens a window for us to observe a world we were not exposed to before.”
 

90% Nanoplastics Found

The new study employed a technique called stimulated Raman scattering microscopy, which was invented by study coauthor Wei Min, a biophysicist at Columbia. This method involves probing samples simultaneously with two lasers tuned to resonate specific molecules.

Researchers tested three bottled water brands that are popular in the United States, analyzing plastic particles up to 100 nm in size. They identified 110,000-370,000 plastic particles per liter. About 90% were nanoplastics — which are invisible by standard imaging techniques — and the rest were microplastics. The study also identified the seven plastics involved.

The most common is polyamide, a type of nylon, likely from plastic filters purportedly used to purify water before bottling. Next is polyethylene terephthalate, which is commonly used for water bottles and other food containers. Researchers also found other common plastics, including polystyrene, polyvinyl chloride, and methyl methacrylate, used in various industrial processes.
 

Not Size But Quantity

What’s more concerning is that the seven types of plastics accounted for only about 10% of all nanoparticles found in the samples. Researchers have no idea about the composition of the remaining 90%. If these are all nanoparticles, their number could reach tens of millions per liter, representing the complex composition of seemingly simple water samples, as noted by the authors.

Researchers now plan to expand beyond bottled water, exploring the vast realm of nanoplastics. They emphasize that, in terms of mass, nanoplastics are far smaller than microplastics, but “it’s not about size. It’s about the numbers as smaller things can easily penetrate us.”

The team aims to study tap water, which also contains microplastics but in much smaller proportions than bottled water.

This article was translated from the Medscape French edition. 

Using an advanced microscopic technique, American researchers have detected 100,000 nanoplastic molecules per liter of water in plastic bottles. Because of their small size, these particles can enter the bloodstream, cells, and the brain, thus posing potential health risks. The study, recently published in the Proceedings of the National Academy of Sciences, raises concerns about the impact of these nanoparticles.

An Unknown Realm

In recent years, the global presence of tiny particles known as microplastics has raised concerns. The particles are found in polar ice, soil, drinking water, and food. Formed as plastics break down into increasingly small pieces, these particles are consumed by humans and other organisms, with unknown effects on health and ecosystems. Whereas macroplastics have been found in various organs, including the lungs and liver, the study marks a unique exploration into the world of nanoplastics.

Concerns about nanoplastic presence in humans intensified when a 2018 study revealed contamination signs in 93% of 259 examined bottles from nine countries.

The novelty of this research lies in its focus, using a refined spectrometry method, on the poorly understood world of nanoplastics, which derive from the decomposition of microplastics. For the first time, American researchers, including biophysicists and chemists, counted and identified these tiny particles in bottled water. On average, they found around 240,000 detectable plastic fragments per liter, which is 10-100 times more than previous estimates based on larger sizes.

Microplastics are defined as fragments ranging from 5 mm to 1 µm, whereas nanoplastics, particles < 1 µm, are measured in billionths of a meter.

In contrast to microplastics, nanoplastics are so small that they can traverse the intestines and lungs and move directly into the bloodstream, reaching organs such as the heart or brain or even the fetus via the placenta.

“This was previously an obscure, unexplored area. Toxicity studies could only speculate about what was in there,” said Beizhan Yan, PhD, coauthor of the study and environmental chemist at the Lamont–Doherty Earth Observatory of Columbia University, New York. “This study opens a window for us to observe a world we were not exposed to before.”
 

90% Nanoplastics Found

The new study employed a technique called stimulated Raman scattering microscopy, which was invented by study coauthor Wei Min, a biophysicist at Columbia. This method involves probing samples simultaneously with two lasers tuned to resonate specific molecules.

Researchers tested three bottled water brands that are popular in the United States, analyzing plastic particles up to 100 nm in size. They identified 110,000-370,000 plastic particles per liter. About 90% were nanoplastics — which are invisible by standard imaging techniques — and the rest were microplastics. The study also identified the seven plastics involved.

The most common is polyamide, a type of nylon, likely from plastic filters purportedly used to purify water before bottling. Next is polyethylene terephthalate, which is commonly used for water bottles and other food containers. Researchers also found other common plastics, including polystyrene, polyvinyl chloride, and methyl methacrylate, used in various industrial processes.
 

Not Size But Quantity

What’s more concerning is that the seven types of plastics accounted for only about 10% of all nanoparticles found in the samples. Researchers have no idea about the composition of the remaining 90%. If these are all nanoparticles, their number could reach tens of millions per liter, representing the complex composition of seemingly simple water samples, as noted by the authors.

Researchers now plan to expand beyond bottled water, exploring the vast realm of nanoplastics. They emphasize that, in terms of mass, nanoplastics are far smaller than microplastics, but “it’s not about size. It’s about the numbers as smaller things can easily penetrate us.”

The team aims to study tap water, which also contains microplastics but in much smaller proportions than bottled water.

This article was translated from the Medscape French edition. 

New data from the Cocoa Supplement and Multivitamin Outcomes Study (COSMOS) suggest that a daily multivitamin may help protect the aging brain. However, at least one expert has concerns about the study’s methodology and, as a result, the interpretation of its findings. 

The meta-analysis of three separate cognition studies provides “strong and consistent evidence that taking a daily multivitamin, containing more than 20 essential micronutrients, can help prevent memory loss and slow down cognitive aging,” study investigator Chirag Vyas, MBBS, MPH, with Massachusetts General Hospital and Harvard Medical School, Boston, told this news organization. 

“We are not now recommending multivitamin use, but the evidence is compelling that supports the promise of multivitamins to help prevent cognitive decline,” Dr. Vyas said. 

The new data, from the cognitive substudies of COSMOS, were published online in the American Journal of Clinical Nutrition.
 

Clinically Meaningful Benefit?

To recap, COSMOS was a 2 x 2 factorial trial of coca extract (500 mg/d flavanols) and/or a daily commercial multivitamin-mineral (MVM) supplement for cardiovascular disease and cancer prevention among more than 21,000 US adults aged 60 years or older. 

Neither the cocoa extract nor the MVM supplement had a significant impact on cancer or cardiovascular disease events.

COMOS-Mind was a substudy of 2262 participants aged 65 or older without dementia who completed telephone-based cognitive assessments at baseline and annually for 3 years. 

As previously reported by this news organization in COSMOS-Mind, there was no cognitive benefit of daily cocoa extract, but daily MVM supplementation was associated with improved global cognition, episodic memory, and executive function. However, the difference in global cognitive function between MVM and placebo was small, with a mean 0.07-point improvement on the z-score at 3 years. 

COSMOS-Web was a substudy of 3562 original participants who were evaluated annually for 3 years using an internet-based battery of neuropsychological tests. 

In this analysis, those taking the MVM supplement performed better on a test for immediate memory recall (remembering a list of 20 words); they were able to remember an additional 0.71 word on average compared with 0.44 word in the placebo group. However, they did not improve on tests of memory retention, executive function, or novel object recognition.

The new data are from COSMOS-Clinic, an analysis of 573 participants who completed in-person cognitive assessments. 

COSMOS-Clinic showed a modest benefit of MVM, compared with placebo, on global cognition over 2 years (mean difference, 0.06 SD units [SU]), with a significantly more favorable change in episodic memory (mean difference, 0.12 SU) but not in executive function/attention (mean difference, 0.04 SU), the researchers reported. 

They also conducted a meta-analysis based on the three separate cognitive substudies, with 5200 nonoverlapping COSMOS participants. 

The results showed “clear evidence” of MVM benefits on global cognition (mean difference, 0.07 SU; P = .0009) and episodic memory (mean difference, 0.06 SU; P =.0007), they reported, with the magnitude of effect on global cognition equivalent to reducing cognitive aging by 2 years.

In a statement, JoAnn Manson, MD, DrPH, chief of the Division of Preventive Medicine at Brigham and Women’s Hospital, who led the overall COSMOS trial, said that “the finding that a daily multivitamin improved memory and slowed cognitive aging in three separate placebo-controlled studies in COSMOS is exciting and further supports the promise of multivitamins as a safe, accessible, and affordable approach to protecting cognitive health in older adults.”
 

Not a Meta-analysis?

In an interview with this news organization, Christopher Labos, MD CM, MSc, a cardiologist and epidemiologist based in Montreal, Canada, who wasn’t involved in COSMOS, cautioned that the evidence to date on multivitamins for memory and brain health are “not all that impressive.”

Dr. Labos is a columnist for this news organization and previously has written about the COSMOS trial. 

He said it is important to note that this “meta-analysis of COSMOS data, strictly speaking, is not a meta-analysis” because the patients were all from the original COSMOS study without including any additional patients, “so you don’t have any more data than what you started with.

“The fact that the results are consistent with the original trial is not surprising. In fact, it would be concerning if they were not consistent because they’re the same population. They were just assessed differently — by phone, online, or in person,” Dr. Labos explained. 

“It is hard to tell what the benefit with multivitamins actually means in terms of hard clinical endpoints that matter to patients. Scoring a little bit better on a standardized test — I guess that’s a good thing, but does that mean you’re less likely to get dementia? I’m not sure we’re there yet,” he told this news organization. 

The bottom line, said Dr. Labos, is that “at this point, the evidence does not support recommending multivitamins purely for brain health. There is also a cost and potential downside associated with their use.”

Also weighing in on the new analyses from COSMOS, Claire Sexton, DPhil, Alzheimer’s Association senior director of scientific programs and outreach, said while there are now “positive, large-scale, long-term studies that show that multivitamin-mineral supplementation for older adults may slow cognitive aging, the Alzheimer’s Association is not ready to recommend widespread use of a multivitamin supplement to reduce risk of cognitive decline in older adults.

“Independent confirmatory studies are needed in larger, more diverse, and representative study populations. COSMOS-Clinic, for example, had less than 2% non-White in the multivitamin group and 5% non-White in the placebo group. It is critical that future treatments and preventions are effective in all populations,” Dr. Sexton told this news organization.

She noted that multivitamin supplements are “generally easy to find and relatively affordable. With confirmation, these promising findings have the potential to significantly impact public health — improving brain health, lowering healthcare costs, reducing caregiver burden — especially among older adults.”

The Alzheimer’s Association, Dr. Sexton said, “envisions a future where there are multiple treatments available that address the disease in multiple ways — like heart disease and cancer — and that can be combined into powerful combination therapies, in conjunction with brain-healthy guidelines for lifestyle, like diet and physical activity.”

The Alzheimer’s Association is leading a 2-year clinical trial known as US POINTER to evaluate whether lifestyle interventions that target multiple risk factors can protect cognition in older adults at increased risk for cognitive decline.

COSMOS-Clinic and the cognition studies in the meta-analysis were supported by investigator-initiated grants from Mars Edge, a segment of Mars Inc., and the National Institutes of Health. Multivitamin and placebo tablets and packaging were donated by Pfizer, Inc Consumer Healthcare (now Haleon). Disclosures for the COSMOS investigators are available with the original article. Dr. Labos and Dr. Sexton have no relevant disclosures. 

A version of this article appeared on Medscape.com.

New data from the Cocoa Supplement and Multivitamin Outcomes Study (COSMOS) suggest that a daily multivitamin may help protect the aging brain. However, at least one expert has concerns about the study’s methodology and, as a result, the interpretation of its findings. 

The meta-analysis of three separate cognition studies provides “strong and consistent evidence that taking a daily multivitamin, containing more than 20 essential micronutrients, can help prevent memory loss and slow down cognitive aging,” study investigator Chirag Vyas, MBBS, MPH, with Massachusetts General Hospital and Harvard Medical School, Boston, told this news organization. 

“We are not now recommending multivitamin use, but the evidence is compelling that supports the promise of multivitamins to help prevent cognitive decline,” Dr. Vyas said. 

The new data, from the cognitive substudies of COSMOS, were published online in the American Journal of Clinical Nutrition.
 

Clinically Meaningful Benefit?

To recap, COSMOS was a 2 x 2 factorial trial of coca extract (500 mg/d flavanols) and/or a daily commercial multivitamin-mineral (MVM) supplement for cardiovascular disease and cancer prevention among more than 21,000 US adults aged 60 years or older. 

Neither the cocoa extract nor the MVM supplement had a significant impact on cancer or cardiovascular disease events.

COMOS-Mind was a substudy of 2262 participants aged 65 or older without dementia who completed telephone-based cognitive assessments at baseline and annually for 3 years. 

As previously reported by this news organization in COSMOS-Mind, there was no cognitive benefit of daily cocoa extract, but daily MVM supplementation was associated with improved global cognition, episodic memory, and executive function. However, the difference in global cognitive function between MVM and placebo was small, with a mean 0.07-point improvement on the z-score at 3 years. 

COSMOS-Web was a substudy of 3562 original participants who were evaluated annually for 3 years using an internet-based battery of neuropsychological tests. 

In this analysis, those taking the MVM supplement performed better on a test for immediate memory recall (remembering a list of 20 words); they were able to remember an additional 0.71 word on average compared with 0.44 word in the placebo group. However, they did not improve on tests of memory retention, executive function, or novel object recognition.

The new data are from COSMOS-Clinic, an analysis of 573 participants who completed in-person cognitive assessments. 

COSMOS-Clinic showed a modest benefit of MVM, compared with placebo, on global cognition over 2 years (mean difference, 0.06 SD units [SU]), with a significantly more favorable change in episodic memory (mean difference, 0.12 SU) but not in executive function/attention (mean difference, 0.04 SU), the researchers reported. 

They also conducted a meta-analysis based on the three separate cognitive substudies, with 5200 nonoverlapping COSMOS participants. 

The results showed “clear evidence” of MVM benefits on global cognition (mean difference, 0.07 SU; P = .0009) and episodic memory (mean difference, 0.06 SU; P =.0007), they reported, with the magnitude of effect on global cognition equivalent to reducing cognitive aging by 2 years.

In a statement, JoAnn Manson, MD, DrPH, chief of the Division of Preventive Medicine at Brigham and Women’s Hospital, who led the overall COSMOS trial, said that “the finding that a daily multivitamin improved memory and slowed cognitive aging in three separate placebo-controlled studies in COSMOS is exciting and further supports the promise of multivitamins as a safe, accessible, and affordable approach to protecting cognitive health in older adults.”
 

Not a Meta-analysis?

In an interview with this news organization, Christopher Labos, MD CM, MSc, a cardiologist and epidemiologist based in Montreal, Canada, who wasn’t involved in COSMOS, cautioned that the evidence to date on multivitamins for memory and brain health are “not all that impressive.”

Dr. Labos is a columnist for this news organization and previously has written about the COSMOS trial. 

He said it is important to note that this “meta-analysis of COSMOS data, strictly speaking, is not a meta-analysis” because the patients were all from the original COSMOS study without including any additional patients, “so you don’t have any more data than what you started with.

“The fact that the results are consistent with the original trial is not surprising. In fact, it would be concerning if they were not consistent because they’re the same population. They were just assessed differently — by phone, online, or in person,” Dr. Labos explained. 

“It is hard to tell what the benefit with multivitamins actually means in terms of hard clinical endpoints that matter to patients. Scoring a little bit better on a standardized test — I guess that’s a good thing, but does that mean you’re less likely to get dementia? I’m not sure we’re there yet,” he told this news organization. 

The bottom line, said Dr. Labos, is that “at this point, the evidence does not support recommending multivitamins purely for brain health. There is also a cost and potential downside associated with their use.”

Also weighing in on the new analyses from COSMOS, Claire Sexton, DPhil, Alzheimer’s Association senior director of scientific programs and outreach, said while there are now “positive, large-scale, long-term studies that show that multivitamin-mineral supplementation for older adults may slow cognitive aging, the Alzheimer’s Association is not ready to recommend widespread use of a multivitamin supplement to reduce risk of cognitive decline in older adults.

“Independent confirmatory studies are needed in larger, more diverse, and representative study populations. COSMOS-Clinic, for example, had less than 2% non-White in the multivitamin group and 5% non-White in the placebo group. It is critical that future treatments and preventions are effective in all populations,” Dr. Sexton told this news organization.

She noted that multivitamin supplements are “generally easy to find and relatively affordable. With confirmation, these promising findings have the potential to significantly impact public health — improving brain health, lowering healthcare costs, reducing caregiver burden — especially among older adults.”

The Alzheimer’s Association, Dr. Sexton said, “envisions a future where there are multiple treatments available that address the disease in multiple ways — like heart disease and cancer — and that can be combined into powerful combination therapies, in conjunction with brain-healthy guidelines for lifestyle, like diet and physical activity.”

The Alzheimer’s Association is leading a 2-year clinical trial known as US POINTER to evaluate whether lifestyle interventions that target multiple risk factors can protect cognition in older adults at increased risk for cognitive decline.

COSMOS-Clinic and the cognition studies in the meta-analysis were supported by investigator-initiated grants from Mars Edge, a segment of Mars Inc., and the National Institutes of Health. Multivitamin and placebo tablets and packaging were donated by Pfizer, Inc Consumer Healthcare (now Haleon). Disclosures for the COSMOS investigators are available with the original article. Dr. Labos and Dr. Sexton have no relevant disclosures. 

A version of this article appeared on Medscape.com.

New data from the Cocoa Supplement and Multivitamin Outcomes Study (COSMOS) suggest that a daily multivitamin may help protect the aging brain. However, at least one expert has concerns about the study’s methodology and, as a result, the interpretation of its findings. 

The meta-analysis of three separate cognition studies provides “strong and consistent evidence that taking a daily multivitamin, containing more than 20 essential micronutrients, can help prevent memory loss and slow down cognitive aging,” study investigator Chirag Vyas, MBBS, MPH, with Massachusetts General Hospital and Harvard Medical School, Boston, told this news organization. 

“We are not now recommending multivitamin use, but the evidence is compelling that supports the promise of multivitamins to help prevent cognitive decline,” Dr. Vyas said. 

The new data, from the cognitive substudies of COSMOS, were published online in the American Journal of Clinical Nutrition.
 

Clinically Meaningful Benefit?

To recap, COSMOS was a 2 x 2 factorial trial of coca extract (500 mg/d flavanols) and/or a daily commercial multivitamin-mineral (MVM) supplement for cardiovascular disease and cancer prevention among more than 21,000 US adults aged 60 years or older. 

Neither the cocoa extract nor the MVM supplement had a significant impact on cancer or cardiovascular disease events.

COMOS-Mind was a substudy of 2262 participants aged 65 or older without dementia who completed telephone-based cognitive assessments at baseline and annually for 3 years. 

As previously reported by this news organization in COSMOS-Mind, there was no cognitive benefit of daily cocoa extract, but daily MVM supplementation was associated with improved global cognition, episodic memory, and executive function. However, the difference in global cognitive function between MVM and placebo was small, with a mean 0.07-point improvement on the z-score at 3 years. 

COSMOS-Web was a substudy of 3562 original participants who were evaluated annually for 3 years using an internet-based battery of neuropsychological tests. 

In this analysis, those taking the MVM supplement performed better on a test for immediate memory recall (remembering a list of 20 words); they were able to remember an additional 0.71 word on average compared with 0.44 word in the placebo group. However, they did not improve on tests of memory retention, executive function, or novel object recognition.

The new data are from COSMOS-Clinic, an analysis of 573 participants who completed in-person cognitive assessments. 

COSMOS-Clinic showed a modest benefit of MVM, compared with placebo, on global cognition over 2 years (mean difference, 0.06 SD units [SU]), with a significantly more favorable change in episodic memory (mean difference, 0.12 SU) but not in executive function/attention (mean difference, 0.04 SU), the researchers reported. 

They also conducted a meta-analysis based on the three separate cognitive substudies, with 5200 nonoverlapping COSMOS participants. 

The results showed “clear evidence” of MVM benefits on global cognition (mean difference, 0.07 SU; P = .0009) and episodic memory (mean difference, 0.06 SU; P =.0007), they reported, with the magnitude of effect on global cognition equivalent to reducing cognitive aging by 2 years.

In a statement, JoAnn Manson, MD, DrPH, chief of the Division of Preventive Medicine at Brigham and Women’s Hospital, who led the overall COSMOS trial, said that “the finding that a daily multivitamin improved memory and slowed cognitive aging in three separate placebo-controlled studies in COSMOS is exciting and further supports the promise of multivitamins as a safe, accessible, and affordable approach to protecting cognitive health in older adults.”
 

Not a Meta-analysis?

In an interview with this news organization, Christopher Labos, MD CM, MSc, a cardiologist and epidemiologist based in Montreal, Canada, who wasn’t involved in COSMOS, cautioned that the evidence to date on multivitamins for memory and brain health are “not all that impressive.”

Dr. Labos is a columnist for this news organization and previously has written about the COSMOS trial. 

He said it is important to note that this “meta-analysis of COSMOS data, strictly speaking, is not a meta-analysis” because the patients were all from the original COSMOS study without including any additional patients, “so you don’t have any more data than what you started with.

“The fact that the results are consistent with the original trial is not surprising. In fact, it would be concerning if they were not consistent because they’re the same population. They were just assessed differently — by phone, online, or in person,” Dr. Labos explained. 

“It is hard to tell what the benefit with multivitamins actually means in terms of hard clinical endpoints that matter to patients. Scoring a little bit better on a standardized test — I guess that’s a good thing, but does that mean you’re less likely to get dementia? I’m not sure we’re there yet,” he told this news organization. 

The bottom line, said Dr. Labos, is that “at this point, the evidence does not support recommending multivitamins purely for brain health. There is also a cost and potential downside associated with their use.”

Also weighing in on the new analyses from COSMOS, Claire Sexton, DPhil, Alzheimer’s Association senior director of scientific programs and outreach, said while there are now “positive, large-scale, long-term studies that show that multivitamin-mineral supplementation for older adults may slow cognitive aging, the Alzheimer’s Association is not ready to recommend widespread use of a multivitamin supplement to reduce risk of cognitive decline in older adults.

“Independent confirmatory studies are needed in larger, more diverse, and representative study populations. COSMOS-Clinic, for example, had less than 2% non-White in the multivitamin group and 5% non-White in the placebo group. It is critical that future treatments and preventions are effective in all populations,” Dr. Sexton told this news organization.

She noted that multivitamin supplements are “generally easy to find and relatively affordable. With confirmation, these promising findings have the potential to significantly impact public health — improving brain health, lowering healthcare costs, reducing caregiver burden — especially among older adults.”

The Alzheimer’s Association, Dr. Sexton said, “envisions a future where there are multiple treatments available that address the disease in multiple ways — like heart disease and cancer — and that can be combined into powerful combination therapies, in conjunction with brain-healthy guidelines for lifestyle, like diet and physical activity.”

The Alzheimer’s Association is leading a 2-year clinical trial known as US POINTER to evaluate whether lifestyle interventions that target multiple risk factors can protect cognition in older adults at increased risk for cognitive decline.

COSMOS-Clinic and the cognition studies in the meta-analysis were supported by investigator-initiated grants from Mars Edge, a segment of Mars Inc., and the National Institutes of Health. Multivitamin and placebo tablets and packaging were donated by Pfizer, Inc Consumer Healthcare (now Haleon). Disclosures for the COSMOS investigators are available with the original article. Dr. Labos and Dr. Sexton have no relevant disclosures. 

A version of this article appeared on Medscape.com.

I began practicing medicine on July 1, 1981. In the 43-plus years since then, I have not missed a single day in the office because of illness. Does that mean I have never been sick? Of course not. I have simply never felt that I was sick enough to warrant staying home.

There are several reasons, both good and bad, why this is so: (1) like most physicians, I am a terrible patient; (2) as a solo practitioner, there was (until recently — I’ll get to that in a minute) no one else to see an office full of patients who had waited significant amounts of time for their appointments and in many cases had taken off work themselves to keep them; and (3) there is an unspoken rule against it. Taking sick days is highly frowned upon in the medical world. As a medical student, intern, and resident I was told in so many words not to call in sick, no matter how serious the illness might be.

Apparently, I was not the only doctor-in-training to receive that message. In a survey reported in JAMA Pediatrics several years ago, 95% of the physicians and advanced practice clinicians (APCs) surveyed believed that working while sick put patients at risk — yet 83% reported working sick at least one time over the prior year. They understood the risks, but did it anyway.

There is no question that this practice does put patients’ health at risk. The JAMA study linked numerous reports of outbreaks traceable to symptomatic healthcare workers. Some outbreaks of flu, staph infections, norovirus, and pertussis were shown to originate from a sick physician or supporting staff member. These associations have led to increased morbidity and mortality, as well as excess costs. Those of us who treat immunocompromised patients on a regular basis risk inducing a life-threatening illness by unnecessarily exposing them to pathogens.

The JAMA survey results also confirmed my own observation that many physicians feel boxed in by their institutions or practice situations. “The study illustrates the complex social and logistic factors that cause this behavior,” the authors wrote. “These results may inform efforts to design systems at our hospital to provide support for attending physicians and APCs and help them make the right choice to keep their patients and colleagues safe while caring for themselves.” 

What might those efforts look like? For one thing, we can take the obvious and necessary steps to avoid getting sick in the first place, such as staying fit and hydrated, and eating well. We can keep up with routine health visits and measures such as colorectal screening, pap smears, and mammograms, and stay up to date with flu shots and all other essential immunizations.

Next, we can minimize the risk of spreading any illnesses we encounter in the course of our work by practicing the basic infectious disease prevention measures driven home so forcefully by the recent COVID-19 pandemic — washing our hands, using hand sanitizers, and, when appropriate, wearing gloves and masks.

Finally, we can work to overcome this institutional taboo against staying home when we do get sick. Work out a system of mutual coverage for such situations. Two years ago, I merged my solo practice with a local, larger group. I did it for a variety of reasons, but a principal one was to assure that a partner could cover for me if I became ill. Practitioners who choose to remain solo or in small groups should contact colleagues and work out a coverage agreement.

Now, during flu season, it is especially important to resist the temptation to work while sick. The CDC has guidelines for employees specific for the flu, which notes that “persons with the flu are most contagious during the first 3 days of their illness,” and should remain at home until at least 24 hours after their fever subsides (without the use of fever-reducing medications) or after symptoms have improved (at least 4-5 days after they started) — or, if they do not have a fever, after symptoms improve “for at least 4-5 days after the onset of symptoms.”

Of course, we need to remember that COVID-19 is still with us. With the constant evolution of new strains, it is especially important to avoid exposing patients and colleagues to the disease should you become infected. The most recent advice from the CDC includes the recommendation that those who are mildly ill and not moderately or severely immunocompromised should isolate after SARS-CoV-2 infection for at least 5 days after symptom onset (day 0 is the day symptoms appeared, and day 1 is the next full day thereafter) if fever has resolved for at least 24 hours (without taking fever-reducing medications) and other symptoms are improving. In addition, “a high-quality mask should be worn around others at home and in public through day 10.”

We should also extend these rules to our support staff, starting with providing them with adequate sick leave and encouraging them to use it when necessary. Research has found a direct correlation between preventative health care and the number of paid sick leave days a worker gets. In a study of over 3000 US workers, those with 10 paid sick days or more annually accessed preventative care more frequently than those without paid sick days.

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

I began practicing medicine on July 1, 1981. In the 43-plus years since then, I have not missed a single day in the office because of illness. Does that mean I have never been sick? Of course not. I have simply never felt that I was sick enough to warrant staying home.

There are several reasons, both good and bad, why this is so: (1) like most physicians, I am a terrible patient; (2) as a solo practitioner, there was (until recently — I’ll get to that in a minute) no one else to see an office full of patients who had waited significant amounts of time for their appointments and in many cases had taken off work themselves to keep them; and (3) there is an unspoken rule against it. Taking sick days is highly frowned upon in the medical world. As a medical student, intern, and resident I was told in so many words not to call in sick, no matter how serious the illness might be.

Apparently, I was not the only doctor-in-training to receive that message. In a survey reported in JAMA Pediatrics several years ago, 95% of the physicians and advanced practice clinicians (APCs) surveyed believed that working while sick put patients at risk — yet 83% reported working sick at least one time over the prior year. They understood the risks, but did it anyway.

There is no question that this practice does put patients’ health at risk. The JAMA study linked numerous reports of outbreaks traceable to symptomatic healthcare workers. Some outbreaks of flu, staph infections, norovirus, and pertussis were shown to originate from a sick physician or supporting staff member. These associations have led to increased morbidity and mortality, as well as excess costs. Those of us who treat immunocompromised patients on a regular basis risk inducing a life-threatening illness by unnecessarily exposing them to pathogens.

The JAMA survey results also confirmed my own observation that many physicians feel boxed in by their institutions or practice situations. “The study illustrates the complex social and logistic factors that cause this behavior,” the authors wrote. “These results may inform efforts to design systems at our hospital to provide support for attending physicians and APCs and help them make the right choice to keep their patients and colleagues safe while caring for themselves.” 

What might those efforts look like? For one thing, we can take the obvious and necessary steps to avoid getting sick in the first place, such as staying fit and hydrated, and eating well. We can keep up with routine health visits and measures such as colorectal screening, pap smears, and mammograms, and stay up to date with flu shots and all other essential immunizations.

Next, we can minimize the risk of spreading any illnesses we encounter in the course of our work by practicing the basic infectious disease prevention measures driven home so forcefully by the recent COVID-19 pandemic — washing our hands, using hand sanitizers, and, when appropriate, wearing gloves and masks.

Finally, we can work to overcome this institutional taboo against staying home when we do get sick. Work out a system of mutual coverage for such situations. Two years ago, I merged my solo practice with a local, larger group. I did it for a variety of reasons, but a principal one was to assure that a partner could cover for me if I became ill. Practitioners who choose to remain solo or in small groups should contact colleagues and work out a coverage agreement.

Now, during flu season, it is especially important to resist the temptation to work while sick. The CDC has guidelines for employees specific for the flu, which notes that “persons with the flu are most contagious during the first 3 days of their illness,” and should remain at home until at least 24 hours after their fever subsides (without the use of fever-reducing medications) or after symptoms have improved (at least 4-5 days after they started) — or, if they do not have a fever, after symptoms improve “for at least 4-5 days after the onset of symptoms.”

Of course, we need to remember that COVID-19 is still with us. With the constant evolution of new strains, it is especially important to avoid exposing patients and colleagues to the disease should you become infected. The most recent advice from the CDC includes the recommendation that those who are mildly ill and not moderately or severely immunocompromised should isolate after SARS-CoV-2 infection for at least 5 days after symptom onset (day 0 is the day symptoms appeared, and day 1 is the next full day thereafter) if fever has resolved for at least 24 hours (without taking fever-reducing medications) and other symptoms are improving. In addition, “a high-quality mask should be worn around others at home and in public through day 10.”

We should also extend these rules to our support staff, starting with providing them with adequate sick leave and encouraging them to use it when necessary. Research has found a direct correlation between preventative health care and the number of paid sick leave days a worker gets. In a study of over 3000 US workers, those with 10 paid sick days or more annually accessed preventative care more frequently than those without paid sick days.

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

I began practicing medicine on July 1, 1981. In the 43-plus years since then, I have not missed a single day in the office because of illness. Does that mean I have never been sick? Of course not. I have simply never felt that I was sick enough to warrant staying home.

There are several reasons, both good and bad, why this is so: (1) like most physicians, I am a terrible patient; (2) as a solo practitioner, there was (until recently — I’ll get to that in a minute) no one else to see an office full of patients who had waited significant amounts of time for their appointments and in many cases had taken off work themselves to keep them; and (3) there is an unspoken rule against it. Taking sick days is highly frowned upon in the medical world. As a medical student, intern, and resident I was told in so many words not to call in sick, no matter how serious the illness might be.

Apparently, I was not the only doctor-in-training to receive that message. In a survey reported in JAMA Pediatrics several years ago, 95% of the physicians and advanced practice clinicians (APCs) surveyed believed that working while sick put patients at risk — yet 83% reported working sick at least one time over the prior year. They understood the risks, but did it anyway.

There is no question that this practice does put patients’ health at risk. The JAMA study linked numerous reports of outbreaks traceable to symptomatic healthcare workers. Some outbreaks of flu, staph infections, norovirus, and pertussis were shown to originate from a sick physician or supporting staff member. These associations have led to increased morbidity and mortality, as well as excess costs. Those of us who treat immunocompromised patients on a regular basis risk inducing a life-threatening illness by unnecessarily exposing them to pathogens.

The JAMA survey results also confirmed my own observation that many physicians feel boxed in by their institutions or practice situations. “The study illustrates the complex social and logistic factors that cause this behavior,” the authors wrote. “These results may inform efforts to design systems at our hospital to provide support for attending physicians and APCs and help them make the right choice to keep their patients and colleagues safe while caring for themselves.” 

What might those efforts look like? For one thing, we can take the obvious and necessary steps to avoid getting sick in the first place, such as staying fit and hydrated, and eating well. We can keep up with routine health visits and measures such as colorectal screening, pap smears, and mammograms, and stay up to date with flu shots and all other essential immunizations.

Next, we can minimize the risk of spreading any illnesses we encounter in the course of our work by practicing the basic infectious disease prevention measures driven home so forcefully by the recent COVID-19 pandemic — washing our hands, using hand sanitizers, and, when appropriate, wearing gloves and masks.

Finally, we can work to overcome this institutional taboo against staying home when we do get sick. Work out a system of mutual coverage for such situations. Two years ago, I merged my solo practice with a local, larger group. I did it for a variety of reasons, but a principal one was to assure that a partner could cover for me if I became ill. Practitioners who choose to remain solo or in small groups should contact colleagues and work out a coverage agreement.

Now, during flu season, it is especially important to resist the temptation to work while sick. The CDC has guidelines for employees specific for the flu, which notes that “persons with the flu are most contagious during the first 3 days of their illness,” and should remain at home until at least 24 hours after their fever subsides (without the use of fever-reducing medications) or after symptoms have improved (at least 4-5 days after they started) — or, if they do not have a fever, after symptoms improve “for at least 4-5 days after the onset of symptoms.”

Of course, we need to remember that COVID-19 is still with us. With the constant evolution of new strains, it is especially important to avoid exposing patients and colleagues to the disease should you become infected. The most recent advice from the CDC includes the recommendation that those who are mildly ill and not moderately or severely immunocompromised should isolate after SARS-CoV-2 infection for at least 5 days after symptom onset (day 0 is the day symptoms appeared, and day 1 is the next full day thereafter) if fever has resolved for at least 24 hours (without taking fever-reducing medications) and other symptoms are improving. In addition, “a high-quality mask should be worn around others at home and in public through day 10.”

We should also extend these rules to our support staff, starting with providing them with adequate sick leave and encouraging them to use it when necessary. Research has found a direct correlation between preventative health care and the number of paid sick leave days a worker gets. In a study of over 3000 US workers, those with 10 paid sick days or more annually accessed preventative care more frequently than those without paid sick days.

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