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Medicare rules for CPAP: Nonadherence begets more nonadherence for low-income patients
The relationship between adherence and benefit for those prescribed continuous positive airway pressure (CPAP) devices is clear. However, a Medicare-reimbursement rule that demands adherence blind to circumstances appears to be denying access to many low-income patients, according to an analysis delivered at the annual health policy and advocacy conference sponsored by the American College of Chest Physicians.
Over the past several years, adherence to CPAP has improved substantially following a series of studies that demonstrated the device must be used at least 4 hours per night to achieve improved outcomes. Medicare defines adherence as using the device more than 4 hours per night for 70% of nights (21 nights) during a consecutive 30-day period any time in the first 3 months of initial usage.
However, the studies that show improved adherence show a lag among those in the lowest income quartile, according to Sairam Parthasarathy, MD, director of the Center for Sleep and Circadian Sciences at the University of Arizona, Tucson.
When patients are followed for a year after being prescribed CPAP, the lag for the low-income patients is not seen immediately. Rather, adherence studies show a steady climb in adherence in all income groups initially, but ”right at 90 days there is a marked change,” said Dr. Parthasarathy.
This change happens to coincide with Medicare policy that denies reimbursement for CPAP after 90 days if patients are not using CPAP at least 4 hours per night, which is the threshold associated with benefit.
The correlation between this policy and income disparity is “observational” rather than proven, but Dr. Parthasarathy is confident it is valid. He believes it is a prime example of a health inequity driven by poorly conceived policy.
“The 90-day rule needs to go,” he said, calling the choice of threshold “man-made.” He added: “This is the only disease condition for which a therapy is withheld if it is not used according to some magical threshold. I cannot think of a more draconian policy.”
In an effort to illustrate the problem, he likened this policy to withholding insulin in a diabetes patient judged nonadherent because of a persistently elevated Hb1Ac.
At 90 days, adherence rates remain at a relatively early point in their upwards trajectory in all income groups. One year later, adherence rates are more than twice as high in the highest income relative to the lowest quartile and approaching twofold greater in quartiles 2 and 3.
“It takes time to get used to these devices,” Dr. Parthasarathy explained. Given studies demonstrating that “more is better” with CPAP, whether measured by sleep scales or quality of life, Dr. Parthasarathy advocates strategies to improve adherence, but he questioned an approach that penalizes low-income patients for a definition of nonadherence at an arbitrary point in time. He suggested it is just one example of health policies that ultimately penalize individuals with lower incomes.
“There are millions of dollars spent every year on understanding the genetics of disease, but the biggest influence on how long you live is the ZIP code of where you live,” said Dr. Parthasarathy, referring to ZIP codes as a surrogate for socioeconomic status.
This is not to imply, however, that genetics are irrelevant, Dr. Parthasarathy said. He pointed to data linking genetic traits that determine melanin levels and circadian rhythms. He noted one genotype associated with later bedtimes that is more commonly found in African-Americans and Hispanics. This has relevance to a variety of sleep disorders and other health conditions, but it might serve as a fundamental disadvantage for children with this genotype, Dr. Parthasarathy maintained. He cited a study conducted at his center that found Hispanic children sleep on average 30 minutes less than White children (Sleep Med 2016;18:61-6). The reason was simple. Hispanic children went to bed 30 minutes later but rose at the same time.
The later bedtimes and reduced sleep could potentially be one obstacle among many, such as the need for lower-income patients to hold several jobs, that prevent these patients from becoming accustomed to CPAP at the same speed as wealthier patients, according to Dr. Parthasarathy.
The current Medicare policy that withholds CPAP on the basis of a single definition of nonadherence appears to lead directly to an inequity in treatment of sleep apnea, he maintained. Dr. Parthasarathy, who was a coauthor of a recently published paper on addressing disparities in sleep health (Chest 2021;159:1232-40), described this issue as part of a larger problem of the failure to deliver health care that is sensitive to the cultural and racial differences underlying these inequities.
Kathleen Sarmiento, MD, FCCP, director, VISN 21 Sleep Clinical Resource Hub for the San Francisco VA Health Care System, agreed. “This type of issue is exactly what our committee would like to address,” said Dr. Sarmiento, a member of the CHEST Health Policy and Advocacy Committee and the moderator of the session in which Dr. Parthasarathy presented his data.
The association between the 90-day Medicare rule for CPAP reimbursement and reduced access to this therapy among patients of lower economic status is compelling, she indicated. Within the goal of advocacy for health policies that will reduce inequities, Dr. Sarmiento explained that the committee is attempting to identify and reverse the source of these types of disparity.
“Specific rules or regulations are actionable targets to effect broader change in health care access and health care delivery,” said Dr. Sarmiento, alluding to the mission of the Health Policy and Advocacy Committee.
Dr. Parthasarathy and Dr. Sarmiento report no relevant conflicts of interest.
The relationship between adherence and benefit for those prescribed continuous positive airway pressure (CPAP) devices is clear. However, a Medicare-reimbursement rule that demands adherence blind to circumstances appears to be denying access to many low-income patients, according to an analysis delivered at the annual health policy and advocacy conference sponsored by the American College of Chest Physicians.
Over the past several years, adherence to CPAP has improved substantially following a series of studies that demonstrated the device must be used at least 4 hours per night to achieve improved outcomes. Medicare defines adherence as using the device more than 4 hours per night for 70% of nights (21 nights) during a consecutive 30-day period any time in the first 3 months of initial usage.
However, the studies that show improved adherence show a lag among those in the lowest income quartile, according to Sairam Parthasarathy, MD, director of the Center for Sleep and Circadian Sciences at the University of Arizona, Tucson.
When patients are followed for a year after being prescribed CPAP, the lag for the low-income patients is not seen immediately. Rather, adherence studies show a steady climb in adherence in all income groups initially, but ”right at 90 days there is a marked change,” said Dr. Parthasarathy.
This change happens to coincide with Medicare policy that denies reimbursement for CPAP after 90 days if patients are not using CPAP at least 4 hours per night, which is the threshold associated with benefit.
The correlation between this policy and income disparity is “observational” rather than proven, but Dr. Parthasarathy is confident it is valid. He believes it is a prime example of a health inequity driven by poorly conceived policy.
“The 90-day rule needs to go,” he said, calling the choice of threshold “man-made.” He added: “This is the only disease condition for which a therapy is withheld if it is not used according to some magical threshold. I cannot think of a more draconian policy.”
In an effort to illustrate the problem, he likened this policy to withholding insulin in a diabetes patient judged nonadherent because of a persistently elevated Hb1Ac.
At 90 days, adherence rates remain at a relatively early point in their upwards trajectory in all income groups. One year later, adherence rates are more than twice as high in the highest income relative to the lowest quartile and approaching twofold greater in quartiles 2 and 3.
“It takes time to get used to these devices,” Dr. Parthasarathy explained. Given studies demonstrating that “more is better” with CPAP, whether measured by sleep scales or quality of life, Dr. Parthasarathy advocates strategies to improve adherence, but he questioned an approach that penalizes low-income patients for a definition of nonadherence at an arbitrary point in time. He suggested it is just one example of health policies that ultimately penalize individuals with lower incomes.
“There are millions of dollars spent every year on understanding the genetics of disease, but the biggest influence on how long you live is the ZIP code of where you live,” said Dr. Parthasarathy, referring to ZIP codes as a surrogate for socioeconomic status.
This is not to imply, however, that genetics are irrelevant, Dr. Parthasarathy said. He pointed to data linking genetic traits that determine melanin levels and circadian rhythms. He noted one genotype associated with later bedtimes that is more commonly found in African-Americans and Hispanics. This has relevance to a variety of sleep disorders and other health conditions, but it might serve as a fundamental disadvantage for children with this genotype, Dr. Parthasarathy maintained. He cited a study conducted at his center that found Hispanic children sleep on average 30 minutes less than White children (Sleep Med 2016;18:61-6). The reason was simple. Hispanic children went to bed 30 minutes later but rose at the same time.
The later bedtimes and reduced sleep could potentially be one obstacle among many, such as the need for lower-income patients to hold several jobs, that prevent these patients from becoming accustomed to CPAP at the same speed as wealthier patients, according to Dr. Parthasarathy.
The current Medicare policy that withholds CPAP on the basis of a single definition of nonadherence appears to lead directly to an inequity in treatment of sleep apnea, he maintained. Dr. Parthasarathy, who was a coauthor of a recently published paper on addressing disparities in sleep health (Chest 2021;159:1232-40), described this issue as part of a larger problem of the failure to deliver health care that is sensitive to the cultural and racial differences underlying these inequities.
Kathleen Sarmiento, MD, FCCP, director, VISN 21 Sleep Clinical Resource Hub for the San Francisco VA Health Care System, agreed. “This type of issue is exactly what our committee would like to address,” said Dr. Sarmiento, a member of the CHEST Health Policy and Advocacy Committee and the moderator of the session in which Dr. Parthasarathy presented his data.
The association between the 90-day Medicare rule for CPAP reimbursement and reduced access to this therapy among patients of lower economic status is compelling, she indicated. Within the goal of advocacy for health policies that will reduce inequities, Dr. Sarmiento explained that the committee is attempting to identify and reverse the source of these types of disparity.
“Specific rules or regulations are actionable targets to effect broader change in health care access and health care delivery,” said Dr. Sarmiento, alluding to the mission of the Health Policy and Advocacy Committee.
Dr. Parthasarathy and Dr. Sarmiento report no relevant conflicts of interest.
The relationship between adherence and benefit for those prescribed continuous positive airway pressure (CPAP) devices is clear. However, a Medicare-reimbursement rule that demands adherence blind to circumstances appears to be denying access to many low-income patients, according to an analysis delivered at the annual health policy and advocacy conference sponsored by the American College of Chest Physicians.
Over the past several years, adherence to CPAP has improved substantially following a series of studies that demonstrated the device must be used at least 4 hours per night to achieve improved outcomes. Medicare defines adherence as using the device more than 4 hours per night for 70% of nights (21 nights) during a consecutive 30-day period any time in the first 3 months of initial usage.
However, the studies that show improved adherence show a lag among those in the lowest income quartile, according to Sairam Parthasarathy, MD, director of the Center for Sleep and Circadian Sciences at the University of Arizona, Tucson.
When patients are followed for a year after being prescribed CPAP, the lag for the low-income patients is not seen immediately. Rather, adherence studies show a steady climb in adherence in all income groups initially, but ”right at 90 days there is a marked change,” said Dr. Parthasarathy.
This change happens to coincide with Medicare policy that denies reimbursement for CPAP after 90 days if patients are not using CPAP at least 4 hours per night, which is the threshold associated with benefit.
The correlation between this policy and income disparity is “observational” rather than proven, but Dr. Parthasarathy is confident it is valid. He believes it is a prime example of a health inequity driven by poorly conceived policy.
“The 90-day rule needs to go,” he said, calling the choice of threshold “man-made.” He added: “This is the only disease condition for which a therapy is withheld if it is not used according to some magical threshold. I cannot think of a more draconian policy.”
In an effort to illustrate the problem, he likened this policy to withholding insulin in a diabetes patient judged nonadherent because of a persistently elevated Hb1Ac.
At 90 days, adherence rates remain at a relatively early point in their upwards trajectory in all income groups. One year later, adherence rates are more than twice as high in the highest income relative to the lowest quartile and approaching twofold greater in quartiles 2 and 3.
“It takes time to get used to these devices,” Dr. Parthasarathy explained. Given studies demonstrating that “more is better” with CPAP, whether measured by sleep scales or quality of life, Dr. Parthasarathy advocates strategies to improve adherence, but he questioned an approach that penalizes low-income patients for a definition of nonadherence at an arbitrary point in time. He suggested it is just one example of health policies that ultimately penalize individuals with lower incomes.
“There are millions of dollars spent every year on understanding the genetics of disease, but the biggest influence on how long you live is the ZIP code of where you live,” said Dr. Parthasarathy, referring to ZIP codes as a surrogate for socioeconomic status.
This is not to imply, however, that genetics are irrelevant, Dr. Parthasarathy said. He pointed to data linking genetic traits that determine melanin levels and circadian rhythms. He noted one genotype associated with later bedtimes that is more commonly found in African-Americans and Hispanics. This has relevance to a variety of sleep disorders and other health conditions, but it might serve as a fundamental disadvantage for children with this genotype, Dr. Parthasarathy maintained. He cited a study conducted at his center that found Hispanic children sleep on average 30 minutes less than White children (Sleep Med 2016;18:61-6). The reason was simple. Hispanic children went to bed 30 minutes later but rose at the same time.
The later bedtimes and reduced sleep could potentially be one obstacle among many, such as the need for lower-income patients to hold several jobs, that prevent these patients from becoming accustomed to CPAP at the same speed as wealthier patients, according to Dr. Parthasarathy.
The current Medicare policy that withholds CPAP on the basis of a single definition of nonadherence appears to lead directly to an inequity in treatment of sleep apnea, he maintained. Dr. Parthasarathy, who was a coauthor of a recently published paper on addressing disparities in sleep health (Chest 2021;159:1232-40), described this issue as part of a larger problem of the failure to deliver health care that is sensitive to the cultural and racial differences underlying these inequities.
Kathleen Sarmiento, MD, FCCP, director, VISN 21 Sleep Clinical Resource Hub for the San Francisco VA Health Care System, agreed. “This type of issue is exactly what our committee would like to address,” said Dr. Sarmiento, a member of the CHEST Health Policy and Advocacy Committee and the moderator of the session in which Dr. Parthasarathy presented his data.
The association between the 90-day Medicare rule for CPAP reimbursement and reduced access to this therapy among patients of lower economic status is compelling, she indicated. Within the goal of advocacy for health policies that will reduce inequities, Dr. Sarmiento explained that the committee is attempting to identify and reverse the source of these types of disparity.
“Specific rules or regulations are actionable targets to effect broader change in health care access and health care delivery,” said Dr. Sarmiento, alluding to the mission of the Health Policy and Advocacy Committee.
Dr. Parthasarathy and Dr. Sarmiento report no relevant conflicts of interest.
FROM A HEALTH POLICY AND ADVOCACY CONFERENCE
The pandemic changed smokers, but farming didn’t change humans
Pandemic smoking: More or less?
The COVID-19 pandemic has changed a lot of habits in people, for better or worse. Some people may have turned to food and alcohol for comfort, while others started on health kicks to emerge from the ordeal as new people. Well, the same can be said about smokers.
New evidence comes from a survey conducted from May to July 2020 of 694 current and former smokers with an average age of 53 years. All had been hospitalized prior to the pandemic and had previously participated in clinical trials to for smoking cessation in Boston, Nashville, and Pittsburgh hospitals.
Researchers found that 32% of participants smoked more, 37% smoked less, and 31% made no change in their smoking habits. By the time of the survey, 28% of former smokers had relapsed. Although 68% of the participants believed smoking increased the risk of getting COVID-19, that still didn’t stop some people from smoking more. Why?
Respondents “might have increased their smoking due to stress and boredom. On the other hand, the fear of catching COVID might have led them to cut down or quit smoking,” said lead author Nancy A. Rigotti, MD. “Even before the pandemic, tobacco smoking was the leading preventable cause of death in the United States. COVID-19 has given smokers yet another good reason to stop smoking.”
This creates an opportunity for physicians to preach the gospel to smokers about their vulnerability to respiratory disease in hopes of getting them to quit for good. We just wish the same could be said for all of our excessive pandemic online shopping.
3,000 years and just one pair of genomes to wear
Men and women are different. We’ll give you a moment to pick your jaw off the ground.
It makes sense though, the sexes being different, especially when you look at the broader animal kingdom. The males and females of many species are slightly different when it comes to size and shape, but there’s a big question that literally only anthropologists have asked: Were human males and females more different in the past than they are today?
To be more specific, some scientists believe that males and females grew more similar when humans shifted from a hunter-gatherer lifestyle to a farming-based lifestyle, as agriculture encouraged a more equitable division of labor. Others believe that the differences come down to random chance.
Researchers from Penn State University analyzed genomic data from over 350,000 males and females stored in the UK Biobank and looked at the recent (within the last ~3,000 years; post-agriculture adoption in Britain) evolutionary histories of these loci. Height, body mass, hip circumference, body fat percentage, and waist circumference were analyzed, and while there were thousands of differences in the genomes, only one trait occurred more frequently during that time period: Females gained a significantly higher body fat content than males.
It’s a sad day then for the millions of people who were big fans of the “farming caused men and women to become more similar” theory. Count the LOTME crew among them. Be honest: Wouldn’t life be so much simpler if men and women were exactly the same? Just think about it, no more arguments about leaving the toilet seat up. It’d be worth it just for that.
Proteins don’t lie
Research published in Open Biology shows that the human brain contains 14,315 different proteins. The team conducting that study wanted to find out which organ was the most similar to the old brain box, so they did protein counts for the 32 other major tissue types, including heart, salivary gland, lung, spleen, and endometrium.
The tissue with the most proteins in common with the center of human intelligence? You’re thinking it has to be colon at this point, right? We were sure it was going to be colon, but it’s not.
The winner, with 13,442 shared proteins, is the testes. The testes have 15,687 proteins, of which 85.7% are shared with the brain. The researchers, sadly, did not provide protein counts for the other tissue types, but we bet colon was a close second.
Dreaming about COVID?
We thought we were the only ones who have been having crazy dreams lately. Each one seems crazier and more vivid than the one before. Have you been having weird dreams lately?
This is likely your brain’s coping mechanism to handle your pandemic stress, according to Dr. Erik Hoel of Tufts University. Dreams that are crazy and scary might make real life seem lighter and simpler. He calls it the “overfitted brain hypothesis.”
“It is their very strangeness that gives them their biological function,” Dr. Hoel said. It literally makes you feel like COVID-19 and lockdowns aren’t as scary as they seem.
We always knew our minds were powerful things. Apparently, your brain gets tired of everyday familiarity just like you do, and it creates crazy dreams to keep things interesting.
Just remember: That recurring dream that you’re back in college and missing 10 assignments is there to help you, not scare you! Even though it is pretty scary.
Pandemic smoking: More or less?
The COVID-19 pandemic has changed a lot of habits in people, for better or worse. Some people may have turned to food and alcohol for comfort, while others started on health kicks to emerge from the ordeal as new people. Well, the same can be said about smokers.
New evidence comes from a survey conducted from May to July 2020 of 694 current and former smokers with an average age of 53 years. All had been hospitalized prior to the pandemic and had previously participated in clinical trials to for smoking cessation in Boston, Nashville, and Pittsburgh hospitals.
Researchers found that 32% of participants smoked more, 37% smoked less, and 31% made no change in their smoking habits. By the time of the survey, 28% of former smokers had relapsed. Although 68% of the participants believed smoking increased the risk of getting COVID-19, that still didn’t stop some people from smoking more. Why?
Respondents “might have increased their smoking due to stress and boredom. On the other hand, the fear of catching COVID might have led them to cut down or quit smoking,” said lead author Nancy A. Rigotti, MD. “Even before the pandemic, tobacco smoking was the leading preventable cause of death in the United States. COVID-19 has given smokers yet another good reason to stop smoking.”
This creates an opportunity for physicians to preach the gospel to smokers about their vulnerability to respiratory disease in hopes of getting them to quit for good. We just wish the same could be said for all of our excessive pandemic online shopping.
3,000 years and just one pair of genomes to wear
Men and women are different. We’ll give you a moment to pick your jaw off the ground.
It makes sense though, the sexes being different, especially when you look at the broader animal kingdom. The males and females of many species are slightly different when it comes to size and shape, but there’s a big question that literally only anthropologists have asked: Were human males and females more different in the past than they are today?
To be more specific, some scientists believe that males and females grew more similar when humans shifted from a hunter-gatherer lifestyle to a farming-based lifestyle, as agriculture encouraged a more equitable division of labor. Others believe that the differences come down to random chance.
Researchers from Penn State University analyzed genomic data from over 350,000 males and females stored in the UK Biobank and looked at the recent (within the last ~3,000 years; post-agriculture adoption in Britain) evolutionary histories of these loci. Height, body mass, hip circumference, body fat percentage, and waist circumference were analyzed, and while there were thousands of differences in the genomes, only one trait occurred more frequently during that time period: Females gained a significantly higher body fat content than males.
It’s a sad day then for the millions of people who were big fans of the “farming caused men and women to become more similar” theory. Count the LOTME crew among them. Be honest: Wouldn’t life be so much simpler if men and women were exactly the same? Just think about it, no more arguments about leaving the toilet seat up. It’d be worth it just for that.
Proteins don’t lie
Research published in Open Biology shows that the human brain contains 14,315 different proteins. The team conducting that study wanted to find out which organ was the most similar to the old brain box, so they did protein counts for the 32 other major tissue types, including heart, salivary gland, lung, spleen, and endometrium.
The tissue with the most proteins in common with the center of human intelligence? You’re thinking it has to be colon at this point, right? We were sure it was going to be colon, but it’s not.
The winner, with 13,442 shared proteins, is the testes. The testes have 15,687 proteins, of which 85.7% are shared with the brain. The researchers, sadly, did not provide protein counts for the other tissue types, but we bet colon was a close second.
Dreaming about COVID?
We thought we were the only ones who have been having crazy dreams lately. Each one seems crazier and more vivid than the one before. Have you been having weird dreams lately?
This is likely your brain’s coping mechanism to handle your pandemic stress, according to Dr. Erik Hoel of Tufts University. Dreams that are crazy and scary might make real life seem lighter and simpler. He calls it the “overfitted brain hypothesis.”
“It is their very strangeness that gives them their biological function,” Dr. Hoel said. It literally makes you feel like COVID-19 and lockdowns aren’t as scary as they seem.
We always knew our minds were powerful things. Apparently, your brain gets tired of everyday familiarity just like you do, and it creates crazy dreams to keep things interesting.
Just remember: That recurring dream that you’re back in college and missing 10 assignments is there to help you, not scare you! Even though it is pretty scary.
Pandemic smoking: More or less?
The COVID-19 pandemic has changed a lot of habits in people, for better or worse. Some people may have turned to food and alcohol for comfort, while others started on health kicks to emerge from the ordeal as new people. Well, the same can be said about smokers.
New evidence comes from a survey conducted from May to July 2020 of 694 current and former smokers with an average age of 53 years. All had been hospitalized prior to the pandemic and had previously participated in clinical trials to for smoking cessation in Boston, Nashville, and Pittsburgh hospitals.
Researchers found that 32% of participants smoked more, 37% smoked less, and 31% made no change in their smoking habits. By the time of the survey, 28% of former smokers had relapsed. Although 68% of the participants believed smoking increased the risk of getting COVID-19, that still didn’t stop some people from smoking more. Why?
Respondents “might have increased their smoking due to stress and boredom. On the other hand, the fear of catching COVID might have led them to cut down or quit smoking,” said lead author Nancy A. Rigotti, MD. “Even before the pandemic, tobacco smoking was the leading preventable cause of death in the United States. COVID-19 has given smokers yet another good reason to stop smoking.”
This creates an opportunity for physicians to preach the gospel to smokers about their vulnerability to respiratory disease in hopes of getting them to quit for good. We just wish the same could be said for all of our excessive pandemic online shopping.
3,000 years and just one pair of genomes to wear
Men and women are different. We’ll give you a moment to pick your jaw off the ground.
It makes sense though, the sexes being different, especially when you look at the broader animal kingdom. The males and females of many species are slightly different when it comes to size and shape, but there’s a big question that literally only anthropologists have asked: Were human males and females more different in the past than they are today?
To be more specific, some scientists believe that males and females grew more similar when humans shifted from a hunter-gatherer lifestyle to a farming-based lifestyle, as agriculture encouraged a more equitable division of labor. Others believe that the differences come down to random chance.
Researchers from Penn State University analyzed genomic data from over 350,000 males and females stored in the UK Biobank and looked at the recent (within the last ~3,000 years; post-agriculture adoption in Britain) evolutionary histories of these loci. Height, body mass, hip circumference, body fat percentage, and waist circumference were analyzed, and while there were thousands of differences in the genomes, only one trait occurred more frequently during that time period: Females gained a significantly higher body fat content than males.
It’s a sad day then for the millions of people who were big fans of the “farming caused men and women to become more similar” theory. Count the LOTME crew among them. Be honest: Wouldn’t life be so much simpler if men and women were exactly the same? Just think about it, no more arguments about leaving the toilet seat up. It’d be worth it just for that.
Proteins don’t lie
Research published in Open Biology shows that the human brain contains 14,315 different proteins. The team conducting that study wanted to find out which organ was the most similar to the old brain box, so they did protein counts for the 32 other major tissue types, including heart, salivary gland, lung, spleen, and endometrium.
The tissue with the most proteins in common with the center of human intelligence? You’re thinking it has to be colon at this point, right? We were sure it was going to be colon, but it’s not.
The winner, with 13,442 shared proteins, is the testes. The testes have 15,687 proteins, of which 85.7% are shared with the brain. The researchers, sadly, did not provide protein counts for the other tissue types, but we bet colon was a close second.
Dreaming about COVID?
We thought we were the only ones who have been having crazy dreams lately. Each one seems crazier and more vivid than the one before. Have you been having weird dreams lately?
This is likely your brain’s coping mechanism to handle your pandemic stress, according to Dr. Erik Hoel of Tufts University. Dreams that are crazy and scary might make real life seem lighter and simpler. He calls it the “overfitted brain hypothesis.”
“It is their very strangeness that gives them their biological function,” Dr. Hoel said. It literally makes you feel like COVID-19 and lockdowns aren’t as scary as they seem.
We always knew our minds were powerful things. Apparently, your brain gets tired of everyday familiarity just like you do, and it creates crazy dreams to keep things interesting.
Just remember: That recurring dream that you’re back in college and missing 10 assignments is there to help you, not scare you! Even though it is pretty scary.
Schizophrenia meds a key contributor to cognitive impairment
Anticholinergic medication burden from antipsychotics, antidepressants, and other psychotropics has a cumulative effect of worsening cognitive function in patients with schizophrenia, new research indicates.
“The link between long-term use of anticholinergic medications and cognitive impairment is well-known and growing,” lead researcher Yash Joshi, MD, department of psychiatry, University of California, San Diego, said in an interview.
“While this association is relevant for everyone, it is particularly important for those living with schizophrenia, who often struggle with cognitive difficulties conferred by the illness itself,” said Dr. Joshi.
“Brain health in schizophrenia is a game of inches, and even small negative effects on cognitive functioning through anticholinergic medication burden may have large impacts on patients’ lives,” he added.
The study was published online May 14 in the American Journal of Psychiatry.
‘Striking’ results
Dr. Joshi and colleagues set out to comprehensively characterize how the cumulative anticholinergic burden from different classes of medications affect cognition in patients with schizophrenia.
They assessed medical records, including all prescribed medications, for 1,120 adults with a diagnosis of schizophrenia or schizoaffective disorder.
For each participant, prescribed medications were rated and summed using a modified anticholinergic cognitive burden (ACB) scale. Cognitive functioning was assessed by performance on domains of the Penn Computerized Neurocognitive Battery (PCNB).
The investigators found that 63% of participants had an ACB score of at least 3, which is “striking,” said Dr. Joshi, given that previous studies have shown that an ACB score of 3 in a healthy, older adult is associated with cognitive dysfunction and a 50% increased risk of developing dementia.
About one-quarter of participants had an ACB score of 6 or higher.
Yet, these high ACB scores are not hard to achieve in routine psychiatric care, the researchers note.
For example, a patient taking olanzapine daily to ease symptoms of psychosis would have an ACB score of 3; if hydroxyzine was added for anxiety or insomnia, the patient’s ACB score would rise to 6, they point out.
Lightening the load
Antipsychotics contributed more than half of the anticholinergic burden, while traditional anticholinergics, antidepressants, mood stabilizers, and benzodiazepines accounted for the remainder.
“It is easy even for well-meaning clinicians to inadvertently contribute to anticholinergic medication burden through routine and appropriate care. The unique finding here is that this burden comes from medications we don’t usually think of as typical anticholinergic agents,” senior author Gregory Light, PhD, with University of California, San Diego, said in a news release.
Anticholinergic medication burden was significantly associated with generalized impairments in cognitive functioning across all cognitive domains on the PCNB with comparable magnitude and after controlling for multiple proxies of functioning or disease severity.
Higher anticholinergic medication burden was associated with worse cognitive performance. The PCNB global cognitive averages for none, low, average, high, and very high anticholinergic burdens were, respectively (in z values), -0.51, -0.70, -0.85, -0.96, and -1.15.
The results suggest “total cumulative anticholinergic burden – rather than anticholinergic burden attributable to a specific antipsychotic or psychotropic medication class – is a key contributor to cognitive impairment in schizophrenia,” the researchers write.
“The results imply that if it is clinically safe and practical,” said Dr. Joshi.
“This may be accomplished by reducing overall polypharmacy or transitioning to equivalent medications with lower overall anticholinergic burden. While ‘traditional’ anticholinergic medications should always be scrutinized, all medications should be carefully evaluated to understand whether they contribute to cumulative anticholinergic medication burden,” he added.
Confirmatory findings
Commenting on the study for this news organization, Jessica Gannon, MD, assistant professor of psychiatry, University of Pittsburgh, said the author’s findings “aren’t surprising, but the work that they did was pretty comprehensive [and] further fleshed out some of our concerns about the impact of anticholinergics on cognitive function in patients with schizophrenia.”
“We certainly have to use some of these medications for patients, like antipsychotics that do have some anticholinergic burden associated with them. We don’t really have other options,” Dr. Gannon said.
“But certainly I think this calls us to be better stewards of medication in general. And when we prescribe for comorbid conditions, like depression and anxiety, we should be careful in our prescribing practices, try not to prescribe an anticholinergic medication, and, if they have been prescribed, to deprescribe them,” Dr. Gannon added.
The study was supported by grants from the National Institute of Mental Health; the Sidney R. Baer, Jr. Foundation; the Brain and Behavior Research Foundation; the VISN-22 Mental Illness Research, Education, and Clinical Center; and the Department of Veterans Affairs. Dr. Joshi and Dr. Gannon have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Anticholinergic medication burden from antipsychotics, antidepressants, and other psychotropics has a cumulative effect of worsening cognitive function in patients with schizophrenia, new research indicates.
“The link between long-term use of anticholinergic medications and cognitive impairment is well-known and growing,” lead researcher Yash Joshi, MD, department of psychiatry, University of California, San Diego, said in an interview.
“While this association is relevant for everyone, it is particularly important for those living with schizophrenia, who often struggle with cognitive difficulties conferred by the illness itself,” said Dr. Joshi.
“Brain health in schizophrenia is a game of inches, and even small negative effects on cognitive functioning through anticholinergic medication burden may have large impacts on patients’ lives,” he added.
The study was published online May 14 in the American Journal of Psychiatry.
‘Striking’ results
Dr. Joshi and colleagues set out to comprehensively characterize how the cumulative anticholinergic burden from different classes of medications affect cognition in patients with schizophrenia.
They assessed medical records, including all prescribed medications, for 1,120 adults with a diagnosis of schizophrenia or schizoaffective disorder.
For each participant, prescribed medications were rated and summed using a modified anticholinergic cognitive burden (ACB) scale. Cognitive functioning was assessed by performance on domains of the Penn Computerized Neurocognitive Battery (PCNB).
The investigators found that 63% of participants had an ACB score of at least 3, which is “striking,” said Dr. Joshi, given that previous studies have shown that an ACB score of 3 in a healthy, older adult is associated with cognitive dysfunction and a 50% increased risk of developing dementia.
About one-quarter of participants had an ACB score of 6 or higher.
Yet, these high ACB scores are not hard to achieve in routine psychiatric care, the researchers note.
For example, a patient taking olanzapine daily to ease symptoms of psychosis would have an ACB score of 3; if hydroxyzine was added for anxiety or insomnia, the patient’s ACB score would rise to 6, they point out.
Lightening the load
Antipsychotics contributed more than half of the anticholinergic burden, while traditional anticholinergics, antidepressants, mood stabilizers, and benzodiazepines accounted for the remainder.
“It is easy even for well-meaning clinicians to inadvertently contribute to anticholinergic medication burden through routine and appropriate care. The unique finding here is that this burden comes from medications we don’t usually think of as typical anticholinergic agents,” senior author Gregory Light, PhD, with University of California, San Diego, said in a news release.
Anticholinergic medication burden was significantly associated with generalized impairments in cognitive functioning across all cognitive domains on the PCNB with comparable magnitude and after controlling for multiple proxies of functioning or disease severity.
Higher anticholinergic medication burden was associated with worse cognitive performance. The PCNB global cognitive averages for none, low, average, high, and very high anticholinergic burdens were, respectively (in z values), -0.51, -0.70, -0.85, -0.96, and -1.15.
The results suggest “total cumulative anticholinergic burden – rather than anticholinergic burden attributable to a specific antipsychotic or psychotropic medication class – is a key contributor to cognitive impairment in schizophrenia,” the researchers write.
“The results imply that if it is clinically safe and practical,” said Dr. Joshi.
“This may be accomplished by reducing overall polypharmacy or transitioning to equivalent medications with lower overall anticholinergic burden. While ‘traditional’ anticholinergic medications should always be scrutinized, all medications should be carefully evaluated to understand whether they contribute to cumulative anticholinergic medication burden,” he added.
Confirmatory findings
Commenting on the study for this news organization, Jessica Gannon, MD, assistant professor of psychiatry, University of Pittsburgh, said the author’s findings “aren’t surprising, but the work that they did was pretty comprehensive [and] further fleshed out some of our concerns about the impact of anticholinergics on cognitive function in patients with schizophrenia.”
“We certainly have to use some of these medications for patients, like antipsychotics that do have some anticholinergic burden associated with them. We don’t really have other options,” Dr. Gannon said.
“But certainly I think this calls us to be better stewards of medication in general. And when we prescribe for comorbid conditions, like depression and anxiety, we should be careful in our prescribing practices, try not to prescribe an anticholinergic medication, and, if they have been prescribed, to deprescribe them,” Dr. Gannon added.
The study was supported by grants from the National Institute of Mental Health; the Sidney R. Baer, Jr. Foundation; the Brain and Behavior Research Foundation; the VISN-22 Mental Illness Research, Education, and Clinical Center; and the Department of Veterans Affairs. Dr. Joshi and Dr. Gannon have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Anticholinergic medication burden from antipsychotics, antidepressants, and other psychotropics has a cumulative effect of worsening cognitive function in patients with schizophrenia, new research indicates.
“The link between long-term use of anticholinergic medications and cognitive impairment is well-known and growing,” lead researcher Yash Joshi, MD, department of psychiatry, University of California, San Diego, said in an interview.
“While this association is relevant for everyone, it is particularly important for those living with schizophrenia, who often struggle with cognitive difficulties conferred by the illness itself,” said Dr. Joshi.
“Brain health in schizophrenia is a game of inches, and even small negative effects on cognitive functioning through anticholinergic medication burden may have large impacts on patients’ lives,” he added.
The study was published online May 14 in the American Journal of Psychiatry.
‘Striking’ results
Dr. Joshi and colleagues set out to comprehensively characterize how the cumulative anticholinergic burden from different classes of medications affect cognition in patients with schizophrenia.
They assessed medical records, including all prescribed medications, for 1,120 adults with a diagnosis of schizophrenia or schizoaffective disorder.
For each participant, prescribed medications were rated and summed using a modified anticholinergic cognitive burden (ACB) scale. Cognitive functioning was assessed by performance on domains of the Penn Computerized Neurocognitive Battery (PCNB).
The investigators found that 63% of participants had an ACB score of at least 3, which is “striking,” said Dr. Joshi, given that previous studies have shown that an ACB score of 3 in a healthy, older adult is associated with cognitive dysfunction and a 50% increased risk of developing dementia.
About one-quarter of participants had an ACB score of 6 or higher.
Yet, these high ACB scores are not hard to achieve in routine psychiatric care, the researchers note.
For example, a patient taking olanzapine daily to ease symptoms of psychosis would have an ACB score of 3; if hydroxyzine was added for anxiety or insomnia, the patient’s ACB score would rise to 6, they point out.
Lightening the load
Antipsychotics contributed more than half of the anticholinergic burden, while traditional anticholinergics, antidepressants, mood stabilizers, and benzodiazepines accounted for the remainder.
“It is easy even for well-meaning clinicians to inadvertently contribute to anticholinergic medication burden through routine and appropriate care. The unique finding here is that this burden comes from medications we don’t usually think of as typical anticholinergic agents,” senior author Gregory Light, PhD, with University of California, San Diego, said in a news release.
Anticholinergic medication burden was significantly associated with generalized impairments in cognitive functioning across all cognitive domains on the PCNB with comparable magnitude and after controlling for multiple proxies of functioning or disease severity.
Higher anticholinergic medication burden was associated with worse cognitive performance. The PCNB global cognitive averages for none, low, average, high, and very high anticholinergic burdens were, respectively (in z values), -0.51, -0.70, -0.85, -0.96, and -1.15.
The results suggest “total cumulative anticholinergic burden – rather than anticholinergic burden attributable to a specific antipsychotic or psychotropic medication class – is a key contributor to cognitive impairment in schizophrenia,” the researchers write.
“The results imply that if it is clinically safe and practical,” said Dr. Joshi.
“This may be accomplished by reducing overall polypharmacy or transitioning to equivalent medications with lower overall anticholinergic burden. While ‘traditional’ anticholinergic medications should always be scrutinized, all medications should be carefully evaluated to understand whether they contribute to cumulative anticholinergic medication burden,” he added.
Confirmatory findings
Commenting on the study for this news organization, Jessica Gannon, MD, assistant professor of psychiatry, University of Pittsburgh, said the author’s findings “aren’t surprising, but the work that they did was pretty comprehensive [and] further fleshed out some of our concerns about the impact of anticholinergics on cognitive function in patients with schizophrenia.”
“We certainly have to use some of these medications for patients, like antipsychotics that do have some anticholinergic burden associated with them. We don’t really have other options,” Dr. Gannon said.
“But certainly I think this calls us to be better stewards of medication in general. And when we prescribe for comorbid conditions, like depression and anxiety, we should be careful in our prescribing practices, try not to prescribe an anticholinergic medication, and, if they have been prescribed, to deprescribe them,” Dr. Gannon added.
The study was supported by grants from the National Institute of Mental Health; the Sidney R. Baer, Jr. Foundation; the Brain and Behavior Research Foundation; the VISN-22 Mental Illness Research, Education, and Clinical Center; and the Department of Veterans Affairs. Dr. Joshi and Dr. Gannon have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Sleep Medicine A Special Report
Sleep Medicine A Special Report
- MOBILE PHONE RELIANCE
How it’s linked to young adults’ sleep problems in two studies - OBSTRUCTIVE SLEEP APNEA
New research validates phenotypes in Latinos - DEMENTIA
Papers show associations between disease and sleep therapies
Sleep Medicine A Special Report
- MOBILE PHONE RELIANCE
How it’s linked to young adults’ sleep problems in two studies - OBSTRUCTIVE SLEEP APNEA
New research validates phenotypes in Latinos - DEMENTIA
Papers show associations between disease and sleep therapies
Sleep Medicine A Special Report
- MOBILE PHONE RELIANCE
How it’s linked to young adults’ sleep problems in two studies - OBSTRUCTIVE SLEEP APNEA
New research validates phenotypes in Latinos - DEMENTIA
Papers show associations between disease and sleep therapies
Psychiatric fallout from long-COVID: How to prepare
As mounting evidence points to a significant psychiatric component of COVID-19, experts are concerned about an influx of survivors presenting with persistent mental health problems and how best to prepare.
Clinicians should be aware that patients who have had COVID frequently develop psychiatric symptoms, Silvia S. Martins, MD, PhD, associate professor of epidemiology, Columbia University, New York, said in an interview.
“There should be more screening of all patients recovering from a COVID infection for anxiety, posttraumatic stress disorder, and depression, as well as referral to services, including psychotherapy, and medication as needed,” said Dr. Martins, who, along with colleagues, uncovered a high rate of these symptoms in patients who had the disease.
The COVID-19 pandemic has taken an enormous social, emotional, and public health toll. It has disrupted lives and caused stress, fear, and uncertainty about loss of health and income, not to mention forced isolation.
In addition, a significant number of patients who contract COVID-19 continue to have symptoms after the acute phase of the illness. This post-COVID, or “long-haul,” syndrome isn’t well defined; experts cite a range of symptoms that persist for weeks or months.
These ongoing symptoms can include cough, fatigue, and chronic pain, as well as psychiatric complaints. As reported by this news organization, an observational study of more than 230,000 U.S. patient health records revealed that one in three COVID-19 survivors received a psychiatric or neurologic diagnosis within 6 months of contracting the virus.
The most common psychiatric diagnoses were anxiety disorders, mood disorders, substance misuse disorders, and insomnia.
Significant symptoms even in mild cases
Another study showed that even those with mild COVID-19 may experience psychiatric symptoms independently of previous psychiatric diagnoses. Results revealed that 26% of the sample of almost 900 patients reported depression, 22% reported anxiety, and 17% reported symptoms of posttraumatic stress 2 months after testing positive for the virus. This finding is important because the majority of individuals who contract COVID-19 have a mild case.
“We saw very high levels of clinically significant depression, anxiety, and posttraumatic stress symptoms in people who had mild disease,” study investigator João Mauricio Castaldelli-Maia, MD, PhD, postdoctoral fellow, department of epidemiology, Columbia University, said in an interview.
He attributed these symptoms in part to long periods of isolation, even from relatives in the same household, in cramped spaces typical of large cities such as São Paulo.
Social isolation can have a huge impact on persons who depend on social connections and relationships, Vivian Pender, MD, president of the American Psychiatric Association and clinical professor of psychiatry, Weill Cornell Medical Center, New York, said in an interview.
“The fact that we have not been able to see our colleagues, our friends, our family, and in the case of psychiatrists, even our patients has taken a toll on everyone, and that leads to more stress, more anxiety,” she said.
National surveys show that psychiatric symptoms occur after acute COVID. One survey revealed that over 50% of 3,900 respondents who had COVID reported having at least moderate symptoms of major depression.
Unique depression subtype?
Another survey, slated for publication later this year, shows that lead investigator Roy Perlis, MD, professor of psychiatry, Harvard Medical School, Boston, said in an interview.
This might suggest a neurobiological element. Researchers are speculating as to whether lingering psychiatric problems that occur after having COVID are linked to the psychosocial impact of the disease or to pathological processes, such as inflammation, that affect the brain.
Although rates of post-COVID psychiatric symptoms vary from study to study, “they seem to be pretty enduring,” noted Faith Gunning, PhD, vice chair of research, department of psychology, Weill Cornell Medicine, who specializes in clinical neuropsychology.
“So they’re not just a brief response” to getting sick, a fact that points to the possible need for treatment, she told this news organization. “In some of the work that’s starting to emerge, it does appear that the symptoms persist, at least for a relatively large subset of individuals.”
Although depression typically affects twice as many women as men, these new surveys show that, after COVID, “that difference is not so distinct,” said Dr. Gunning.
It’s unclear why this is, but it could be cause by financial stresses that may affect men to a greater extent, she added. “There is so much we’re still learning.”
Increased suicide risk?
Other researchers, including Leo Sher, MD, professor of psychiatry, Icahn School of Medicine at Mount Sinai, and director of inpatient psychiatry, James J. Peters Veterans Affairs Medical Center, both in New York, are concerned that higher rates of psychiatric symptoms among patients with long-haul COVID raise the risk for suicidal ideation and behavior.
Studies of suicidality in COVID-19 survivors “are urgently needed,” said Dr. Sher in an article published in the Monthly Journal of the Association of Physicians.
“We need to study what factors may increase suicide risk among the COVID-19 survivors during and after the recovery. We also need to investigate whether there is a long-term increased suicide risk among COVID-19 survivors,” Dr. Sher said.
COVID-19 is not unique among viral respiratory diseases in being associated with long-term mental health problems. Research shows that survivors of the 2003 outbreak of severe acute respiratory syndrome experienced increased psychological distress that persisted for at least a year, as did patients who in 2015 had Middle East respiratory syndrome coronavirus (MERS-CoV).
Some experts believe clinicians should screen patients for mental health symptoms after the acute phase of COVID and offer early and prolonged care.
“Early mental health intervention such as psychotherapy and supportive groups could play an important role in preventing incident mental health problems for post-COVID sufferers,” said Dr. Castaldelli-Maia.
A version of this article first appeared on Medscape.com.
As mounting evidence points to a significant psychiatric component of COVID-19, experts are concerned about an influx of survivors presenting with persistent mental health problems and how best to prepare.
Clinicians should be aware that patients who have had COVID frequently develop psychiatric symptoms, Silvia S. Martins, MD, PhD, associate professor of epidemiology, Columbia University, New York, said in an interview.
“There should be more screening of all patients recovering from a COVID infection for anxiety, posttraumatic stress disorder, and depression, as well as referral to services, including psychotherapy, and medication as needed,” said Dr. Martins, who, along with colleagues, uncovered a high rate of these symptoms in patients who had the disease.
The COVID-19 pandemic has taken an enormous social, emotional, and public health toll. It has disrupted lives and caused stress, fear, and uncertainty about loss of health and income, not to mention forced isolation.
In addition, a significant number of patients who contract COVID-19 continue to have symptoms after the acute phase of the illness. This post-COVID, or “long-haul,” syndrome isn’t well defined; experts cite a range of symptoms that persist for weeks or months.
These ongoing symptoms can include cough, fatigue, and chronic pain, as well as psychiatric complaints. As reported by this news organization, an observational study of more than 230,000 U.S. patient health records revealed that one in three COVID-19 survivors received a psychiatric or neurologic diagnosis within 6 months of contracting the virus.
The most common psychiatric diagnoses were anxiety disorders, mood disorders, substance misuse disorders, and insomnia.
Significant symptoms even in mild cases
Another study showed that even those with mild COVID-19 may experience psychiatric symptoms independently of previous psychiatric diagnoses. Results revealed that 26% of the sample of almost 900 patients reported depression, 22% reported anxiety, and 17% reported symptoms of posttraumatic stress 2 months after testing positive for the virus. This finding is important because the majority of individuals who contract COVID-19 have a mild case.
“We saw very high levels of clinically significant depression, anxiety, and posttraumatic stress symptoms in people who had mild disease,” study investigator João Mauricio Castaldelli-Maia, MD, PhD, postdoctoral fellow, department of epidemiology, Columbia University, said in an interview.
He attributed these symptoms in part to long periods of isolation, even from relatives in the same household, in cramped spaces typical of large cities such as São Paulo.
Social isolation can have a huge impact on persons who depend on social connections and relationships, Vivian Pender, MD, president of the American Psychiatric Association and clinical professor of psychiatry, Weill Cornell Medical Center, New York, said in an interview.
“The fact that we have not been able to see our colleagues, our friends, our family, and in the case of psychiatrists, even our patients has taken a toll on everyone, and that leads to more stress, more anxiety,” she said.
National surveys show that psychiatric symptoms occur after acute COVID. One survey revealed that over 50% of 3,900 respondents who had COVID reported having at least moderate symptoms of major depression.
Unique depression subtype?
Another survey, slated for publication later this year, shows that lead investigator Roy Perlis, MD, professor of psychiatry, Harvard Medical School, Boston, said in an interview.
This might suggest a neurobiological element. Researchers are speculating as to whether lingering psychiatric problems that occur after having COVID are linked to the psychosocial impact of the disease or to pathological processes, such as inflammation, that affect the brain.
Although rates of post-COVID psychiatric symptoms vary from study to study, “they seem to be pretty enduring,” noted Faith Gunning, PhD, vice chair of research, department of psychology, Weill Cornell Medicine, who specializes in clinical neuropsychology.
“So they’re not just a brief response” to getting sick, a fact that points to the possible need for treatment, she told this news organization. “In some of the work that’s starting to emerge, it does appear that the symptoms persist, at least for a relatively large subset of individuals.”
Although depression typically affects twice as many women as men, these new surveys show that, after COVID, “that difference is not so distinct,” said Dr. Gunning.
It’s unclear why this is, but it could be cause by financial stresses that may affect men to a greater extent, she added. “There is so much we’re still learning.”
Increased suicide risk?
Other researchers, including Leo Sher, MD, professor of psychiatry, Icahn School of Medicine at Mount Sinai, and director of inpatient psychiatry, James J. Peters Veterans Affairs Medical Center, both in New York, are concerned that higher rates of psychiatric symptoms among patients with long-haul COVID raise the risk for suicidal ideation and behavior.
Studies of suicidality in COVID-19 survivors “are urgently needed,” said Dr. Sher in an article published in the Monthly Journal of the Association of Physicians.
“We need to study what factors may increase suicide risk among the COVID-19 survivors during and after the recovery. We also need to investigate whether there is a long-term increased suicide risk among COVID-19 survivors,” Dr. Sher said.
COVID-19 is not unique among viral respiratory diseases in being associated with long-term mental health problems. Research shows that survivors of the 2003 outbreak of severe acute respiratory syndrome experienced increased psychological distress that persisted for at least a year, as did patients who in 2015 had Middle East respiratory syndrome coronavirus (MERS-CoV).
Some experts believe clinicians should screen patients for mental health symptoms after the acute phase of COVID and offer early and prolonged care.
“Early mental health intervention such as psychotherapy and supportive groups could play an important role in preventing incident mental health problems for post-COVID sufferers,” said Dr. Castaldelli-Maia.
A version of this article first appeared on Medscape.com.
As mounting evidence points to a significant psychiatric component of COVID-19, experts are concerned about an influx of survivors presenting with persistent mental health problems and how best to prepare.
Clinicians should be aware that patients who have had COVID frequently develop psychiatric symptoms, Silvia S. Martins, MD, PhD, associate professor of epidemiology, Columbia University, New York, said in an interview.
“There should be more screening of all patients recovering from a COVID infection for anxiety, posttraumatic stress disorder, and depression, as well as referral to services, including psychotherapy, and medication as needed,” said Dr. Martins, who, along with colleagues, uncovered a high rate of these symptoms in patients who had the disease.
The COVID-19 pandemic has taken an enormous social, emotional, and public health toll. It has disrupted lives and caused stress, fear, and uncertainty about loss of health and income, not to mention forced isolation.
In addition, a significant number of patients who contract COVID-19 continue to have symptoms after the acute phase of the illness. This post-COVID, or “long-haul,” syndrome isn’t well defined; experts cite a range of symptoms that persist for weeks or months.
These ongoing symptoms can include cough, fatigue, and chronic pain, as well as psychiatric complaints. As reported by this news organization, an observational study of more than 230,000 U.S. patient health records revealed that one in three COVID-19 survivors received a psychiatric or neurologic diagnosis within 6 months of contracting the virus.
The most common psychiatric diagnoses were anxiety disorders, mood disorders, substance misuse disorders, and insomnia.
Significant symptoms even in mild cases
Another study showed that even those with mild COVID-19 may experience psychiatric symptoms independently of previous psychiatric diagnoses. Results revealed that 26% of the sample of almost 900 patients reported depression, 22% reported anxiety, and 17% reported symptoms of posttraumatic stress 2 months after testing positive for the virus. This finding is important because the majority of individuals who contract COVID-19 have a mild case.
“We saw very high levels of clinically significant depression, anxiety, and posttraumatic stress symptoms in people who had mild disease,” study investigator João Mauricio Castaldelli-Maia, MD, PhD, postdoctoral fellow, department of epidemiology, Columbia University, said in an interview.
He attributed these symptoms in part to long periods of isolation, even from relatives in the same household, in cramped spaces typical of large cities such as São Paulo.
Social isolation can have a huge impact on persons who depend on social connections and relationships, Vivian Pender, MD, president of the American Psychiatric Association and clinical professor of psychiatry, Weill Cornell Medical Center, New York, said in an interview.
“The fact that we have not been able to see our colleagues, our friends, our family, and in the case of psychiatrists, even our patients has taken a toll on everyone, and that leads to more stress, more anxiety,” she said.
National surveys show that psychiatric symptoms occur after acute COVID. One survey revealed that over 50% of 3,900 respondents who had COVID reported having at least moderate symptoms of major depression.
Unique depression subtype?
Another survey, slated for publication later this year, shows that lead investigator Roy Perlis, MD, professor of psychiatry, Harvard Medical School, Boston, said in an interview.
This might suggest a neurobiological element. Researchers are speculating as to whether lingering psychiatric problems that occur after having COVID are linked to the psychosocial impact of the disease or to pathological processes, such as inflammation, that affect the brain.
Although rates of post-COVID psychiatric symptoms vary from study to study, “they seem to be pretty enduring,” noted Faith Gunning, PhD, vice chair of research, department of psychology, Weill Cornell Medicine, who specializes in clinical neuropsychology.
“So they’re not just a brief response” to getting sick, a fact that points to the possible need for treatment, she told this news organization. “In some of the work that’s starting to emerge, it does appear that the symptoms persist, at least for a relatively large subset of individuals.”
Although depression typically affects twice as many women as men, these new surveys show that, after COVID, “that difference is not so distinct,” said Dr. Gunning.
It’s unclear why this is, but it could be cause by financial stresses that may affect men to a greater extent, she added. “There is so much we’re still learning.”
Increased suicide risk?
Other researchers, including Leo Sher, MD, professor of psychiatry, Icahn School of Medicine at Mount Sinai, and director of inpatient psychiatry, James J. Peters Veterans Affairs Medical Center, both in New York, are concerned that higher rates of psychiatric symptoms among patients with long-haul COVID raise the risk for suicidal ideation and behavior.
Studies of suicidality in COVID-19 survivors “are urgently needed,” said Dr. Sher in an article published in the Monthly Journal of the Association of Physicians.
“We need to study what factors may increase suicide risk among the COVID-19 survivors during and after the recovery. We also need to investigate whether there is a long-term increased suicide risk among COVID-19 survivors,” Dr. Sher said.
COVID-19 is not unique among viral respiratory diseases in being associated with long-term mental health problems. Research shows that survivors of the 2003 outbreak of severe acute respiratory syndrome experienced increased psychological distress that persisted for at least a year, as did patients who in 2015 had Middle East respiratory syndrome coronavirus (MERS-CoV).
Some experts believe clinicians should screen patients for mental health symptoms after the acute phase of COVID and offer early and prolonged care.
“Early mental health intervention such as psychotherapy and supportive groups could play an important role in preventing incident mental health problems for post-COVID sufferers,” said Dr. Castaldelli-Maia.
A version of this article first appeared on Medscape.com.
Obstructive sleep apnea linked to COVID-19 risk
Greater severity of obstructive sleep apnea (OSA) is associated with a higher risk of contracting COVID-19, and positive airway pressure (PAP) treatment may counter that risk, according to a retrospective analysis from the records of Kaiser Permanente Southern California.
OSA patients often worry that PAP therapy might increase risk of severe COVID-19, said Dennis Hwang, MD, who presented the study at the American Thoracic Society’s virtual international conference (Abstract A1108). But the findings should be reassuring. “If you have obstructive sleep apnea, and you’re supposed to be using PAP, we recommend that you continue using PAP. It’s good for your overall wellness and reducing the risk of cardiovascular disease, but as it relates to COVID-19, it’s possible that it could protect. And there doesn’t appear to be any risk of increased severity of illness (with use of PAP),” Dr. Hwang said in an interview. He is medical director of sleep medicine for Kaiser Permanente San Bernardino County and cochair of sleep medicine for Kaiser Southern California.
He noted that the retrospective nature of the study makes it difficult to pin down whether PAP therapy is truly protective, “but I think there’s enough that we’ve been able conceptually to understand, to suggest that a direct causative relationship is possible,” said Dr. Hwang.
The results may imply that OSA patients should pay special attention to their OSA when there’s concern about exposure to an infectious agent like SARS-CoV-2. “The intermittent hypoxia at night, which can linger over to the day as increased sympathetic activity, increased heart rate. All of these are stresses to the body. So if you’re going to get infected, you want to start at a healthier level. You want to eliminate your sleep apnea to help reduce your risk of morbidity,” said Esra Tasali, MD, who was asked to comment on the study. Dr. Tasali is associate professor of medicine at the University of Chicago, and director of the Sleep Research Center there.
During the Q&A session after the talk, audience members asked about the timing of PAP use during COVID-19 infection, for example how often it was used during the asymptomatic phase of infection and if PAP has a positive effect. The data were not available, but “I think that the way to go is to understand this chronology,” said Dr. Tasali.
The researchers examined records between 2015 and 2020, using sleep study data, remotely collected daily PAP data, and electronic health records, all from Kaiser Permanente Southern California. Included subjects were adults who had enrolled before Feb. 1, 2020, and had sleep diagnostic or PAP data on record by March 1, 2020. The researchers analyzed PAP adherence between March 1, 2020, and the time of COVID-19 diagnosis, or until the study ended on July 31, 2020.
Patients were defined as being untreated (< 2 hours/night PAP), moderately treated (2-3.9 hours/night), or well treated (4 or more hours/night). Apnea hypopnea index (AHI) was used to determine severity. The analysis included 81,932 patients (39.8% were women, mean age was 54.0 years, 9.9% were Black, and 34.5% were Hispanic). A total of 1.7% of subjects without OSA experienced COVID-19 infection, compared to 1.8% with OSA; 0.3% with OSA were hospitalized and 0.07% underwent intensive care or died.
There were some differences between the two groups. The non-USA population was younger (mean age 47.0 vs. 54.5 years), was less likely to be men (44% vs. 60.3%), had a lower mean body mass index (30.4 vs. 34.3), had fewer comorbidities according to the Charleston Comorbidity Index (1.3 vs. 2.0), and were less likely to have hypertension (5.6% vs. 12.4%; P < .0001 for all).
Infection rates were higher in patients with more severe OSA. The rates in untreated mild, moderate, and severe OSA were 2%, 2%, and 2.4% respectively. The rate among all treated patients was 1.4% (P < .0001). Infection rates also dropped among patients with better treatment: untreated, 2.1%; moderately treated, 1.7%; and well treated, 1.3% (P < .0001).
Not having OSA was associated with a lower infection risk than was having OSA (odds ratio [OR], 0.82; 95% confidence interval, 0.70-0.96). Compared to untreated patients, there was lower infection risk in the moderately treated (OR, 0.82; 95% CI, 0.65-1.03) and well treated (OR, 0.68; 95% CI, 0.59-0.79) groups. Higher infection rates were associated with obesity, higher Charlson Comorbidity score (> 2; OR, 1.29; 95% CI, 1.09-1.53), Black (OR, 1.51; 95% CI, 1.24-1.84) and Hispanic ethnicities (OR, 2.23; 95% CI, 1.96-2.54), and Medicaid enrollment. Increasing age was associated with lower risk of infection, with each 5-year increment linked to reduced risk (OR, 0.88; 95% CI, 0.86-0.90). Dr. Hwang suggested that the age association may be because older individuals were more likely to follow social distancing and other precautions.
A multivariate analysis found that OSA was associated with infection risk according to OSA severity, including mild (OR, 1.21; 95% CI, 1.01-1.44), and moderate to severe (OR, 1.27; 95% CI, 1.07-1.51). There was no association between hospitalization rate or ICU admission/death and presence of OSA or PAP adherence in the data presented, but Dr. Hwang said that an updated analysis suggests that OSA may be associated with a risk of greater COVID-19 severity.
The control group was composed of individuals who had undergone sleep testing, but found to not have OSA. Still, they aren’t necessarily representative of the general population, since symptoms likely drove them to testing. A high percentage were also obese, and the average BMI was 30. “It’s certainly not a ‘normal population,’ but the advantage of what we did in terms of using this control group is that they underwent sleep testing, so they were proven to have no obstructive sleep apnea, whereas if we used a general population, we just don’t know,” said Dr. Hwang.
The study received technical and data support from Somnoware, and was funded by Kaiser Permanente. Dr. Tasali has no relevant financial disclosures.
Greater severity of obstructive sleep apnea (OSA) is associated with a higher risk of contracting COVID-19, and positive airway pressure (PAP) treatment may counter that risk, according to a retrospective analysis from the records of Kaiser Permanente Southern California.
OSA patients often worry that PAP therapy might increase risk of severe COVID-19, said Dennis Hwang, MD, who presented the study at the American Thoracic Society’s virtual international conference (Abstract A1108). But the findings should be reassuring. “If you have obstructive sleep apnea, and you’re supposed to be using PAP, we recommend that you continue using PAP. It’s good for your overall wellness and reducing the risk of cardiovascular disease, but as it relates to COVID-19, it’s possible that it could protect. And there doesn’t appear to be any risk of increased severity of illness (with use of PAP),” Dr. Hwang said in an interview. He is medical director of sleep medicine for Kaiser Permanente San Bernardino County and cochair of sleep medicine for Kaiser Southern California.
He noted that the retrospective nature of the study makes it difficult to pin down whether PAP therapy is truly protective, “but I think there’s enough that we’ve been able conceptually to understand, to suggest that a direct causative relationship is possible,” said Dr. Hwang.
The results may imply that OSA patients should pay special attention to their OSA when there’s concern about exposure to an infectious agent like SARS-CoV-2. “The intermittent hypoxia at night, which can linger over to the day as increased sympathetic activity, increased heart rate. All of these are stresses to the body. So if you’re going to get infected, you want to start at a healthier level. You want to eliminate your sleep apnea to help reduce your risk of morbidity,” said Esra Tasali, MD, who was asked to comment on the study. Dr. Tasali is associate professor of medicine at the University of Chicago, and director of the Sleep Research Center there.
During the Q&A session after the talk, audience members asked about the timing of PAP use during COVID-19 infection, for example how often it was used during the asymptomatic phase of infection and if PAP has a positive effect. The data were not available, but “I think that the way to go is to understand this chronology,” said Dr. Tasali.
The researchers examined records between 2015 and 2020, using sleep study data, remotely collected daily PAP data, and electronic health records, all from Kaiser Permanente Southern California. Included subjects were adults who had enrolled before Feb. 1, 2020, and had sleep diagnostic or PAP data on record by March 1, 2020. The researchers analyzed PAP adherence between March 1, 2020, and the time of COVID-19 diagnosis, or until the study ended on July 31, 2020.
Patients were defined as being untreated (< 2 hours/night PAP), moderately treated (2-3.9 hours/night), or well treated (4 or more hours/night). Apnea hypopnea index (AHI) was used to determine severity. The analysis included 81,932 patients (39.8% were women, mean age was 54.0 years, 9.9% were Black, and 34.5% were Hispanic). A total of 1.7% of subjects without OSA experienced COVID-19 infection, compared to 1.8% with OSA; 0.3% with OSA were hospitalized and 0.07% underwent intensive care or died.
There were some differences between the two groups. The non-USA population was younger (mean age 47.0 vs. 54.5 years), was less likely to be men (44% vs. 60.3%), had a lower mean body mass index (30.4 vs. 34.3), had fewer comorbidities according to the Charleston Comorbidity Index (1.3 vs. 2.0), and were less likely to have hypertension (5.6% vs. 12.4%; P < .0001 for all).
Infection rates were higher in patients with more severe OSA. The rates in untreated mild, moderate, and severe OSA were 2%, 2%, and 2.4% respectively. The rate among all treated patients was 1.4% (P < .0001). Infection rates also dropped among patients with better treatment: untreated, 2.1%; moderately treated, 1.7%; and well treated, 1.3% (P < .0001).
Not having OSA was associated with a lower infection risk than was having OSA (odds ratio [OR], 0.82; 95% confidence interval, 0.70-0.96). Compared to untreated patients, there was lower infection risk in the moderately treated (OR, 0.82; 95% CI, 0.65-1.03) and well treated (OR, 0.68; 95% CI, 0.59-0.79) groups. Higher infection rates were associated with obesity, higher Charlson Comorbidity score (> 2; OR, 1.29; 95% CI, 1.09-1.53), Black (OR, 1.51; 95% CI, 1.24-1.84) and Hispanic ethnicities (OR, 2.23; 95% CI, 1.96-2.54), and Medicaid enrollment. Increasing age was associated with lower risk of infection, with each 5-year increment linked to reduced risk (OR, 0.88; 95% CI, 0.86-0.90). Dr. Hwang suggested that the age association may be because older individuals were more likely to follow social distancing and other precautions.
A multivariate analysis found that OSA was associated with infection risk according to OSA severity, including mild (OR, 1.21; 95% CI, 1.01-1.44), and moderate to severe (OR, 1.27; 95% CI, 1.07-1.51). There was no association between hospitalization rate or ICU admission/death and presence of OSA or PAP adherence in the data presented, but Dr. Hwang said that an updated analysis suggests that OSA may be associated with a risk of greater COVID-19 severity.
The control group was composed of individuals who had undergone sleep testing, but found to not have OSA. Still, they aren’t necessarily representative of the general population, since symptoms likely drove them to testing. A high percentage were also obese, and the average BMI was 30. “It’s certainly not a ‘normal population,’ but the advantage of what we did in terms of using this control group is that they underwent sleep testing, so they were proven to have no obstructive sleep apnea, whereas if we used a general population, we just don’t know,” said Dr. Hwang.
The study received technical and data support from Somnoware, and was funded by Kaiser Permanente. Dr. Tasali has no relevant financial disclosures.
Greater severity of obstructive sleep apnea (OSA) is associated with a higher risk of contracting COVID-19, and positive airway pressure (PAP) treatment may counter that risk, according to a retrospective analysis from the records of Kaiser Permanente Southern California.
OSA patients often worry that PAP therapy might increase risk of severe COVID-19, said Dennis Hwang, MD, who presented the study at the American Thoracic Society’s virtual international conference (Abstract A1108). But the findings should be reassuring. “If you have obstructive sleep apnea, and you’re supposed to be using PAP, we recommend that you continue using PAP. It’s good for your overall wellness and reducing the risk of cardiovascular disease, but as it relates to COVID-19, it’s possible that it could protect. And there doesn’t appear to be any risk of increased severity of illness (with use of PAP),” Dr. Hwang said in an interview. He is medical director of sleep medicine for Kaiser Permanente San Bernardino County and cochair of sleep medicine for Kaiser Southern California.
He noted that the retrospective nature of the study makes it difficult to pin down whether PAP therapy is truly protective, “but I think there’s enough that we’ve been able conceptually to understand, to suggest that a direct causative relationship is possible,” said Dr. Hwang.
The results may imply that OSA patients should pay special attention to their OSA when there’s concern about exposure to an infectious agent like SARS-CoV-2. “The intermittent hypoxia at night, which can linger over to the day as increased sympathetic activity, increased heart rate. All of these are stresses to the body. So if you’re going to get infected, you want to start at a healthier level. You want to eliminate your sleep apnea to help reduce your risk of morbidity,” said Esra Tasali, MD, who was asked to comment on the study. Dr. Tasali is associate professor of medicine at the University of Chicago, and director of the Sleep Research Center there.
During the Q&A session after the talk, audience members asked about the timing of PAP use during COVID-19 infection, for example how often it was used during the asymptomatic phase of infection and if PAP has a positive effect. The data were not available, but “I think that the way to go is to understand this chronology,” said Dr. Tasali.
The researchers examined records between 2015 and 2020, using sleep study data, remotely collected daily PAP data, and electronic health records, all from Kaiser Permanente Southern California. Included subjects were adults who had enrolled before Feb. 1, 2020, and had sleep diagnostic or PAP data on record by March 1, 2020. The researchers analyzed PAP adherence between March 1, 2020, and the time of COVID-19 diagnosis, or until the study ended on July 31, 2020.
Patients were defined as being untreated (< 2 hours/night PAP), moderately treated (2-3.9 hours/night), or well treated (4 or more hours/night). Apnea hypopnea index (AHI) was used to determine severity. The analysis included 81,932 patients (39.8% were women, mean age was 54.0 years, 9.9% were Black, and 34.5% were Hispanic). A total of 1.7% of subjects without OSA experienced COVID-19 infection, compared to 1.8% with OSA; 0.3% with OSA were hospitalized and 0.07% underwent intensive care or died.
There were some differences between the two groups. The non-USA population was younger (mean age 47.0 vs. 54.5 years), was less likely to be men (44% vs. 60.3%), had a lower mean body mass index (30.4 vs. 34.3), had fewer comorbidities according to the Charleston Comorbidity Index (1.3 vs. 2.0), and were less likely to have hypertension (5.6% vs. 12.4%; P < .0001 for all).
Infection rates were higher in patients with more severe OSA. The rates in untreated mild, moderate, and severe OSA were 2%, 2%, and 2.4% respectively. The rate among all treated patients was 1.4% (P < .0001). Infection rates also dropped among patients with better treatment: untreated, 2.1%; moderately treated, 1.7%; and well treated, 1.3% (P < .0001).
Not having OSA was associated with a lower infection risk than was having OSA (odds ratio [OR], 0.82; 95% confidence interval, 0.70-0.96). Compared to untreated patients, there was lower infection risk in the moderately treated (OR, 0.82; 95% CI, 0.65-1.03) and well treated (OR, 0.68; 95% CI, 0.59-0.79) groups. Higher infection rates were associated with obesity, higher Charlson Comorbidity score (> 2; OR, 1.29; 95% CI, 1.09-1.53), Black (OR, 1.51; 95% CI, 1.24-1.84) and Hispanic ethnicities (OR, 2.23; 95% CI, 1.96-2.54), and Medicaid enrollment. Increasing age was associated with lower risk of infection, with each 5-year increment linked to reduced risk (OR, 0.88; 95% CI, 0.86-0.90). Dr. Hwang suggested that the age association may be because older individuals were more likely to follow social distancing and other precautions.
A multivariate analysis found that OSA was associated with infection risk according to OSA severity, including mild (OR, 1.21; 95% CI, 1.01-1.44), and moderate to severe (OR, 1.27; 95% CI, 1.07-1.51). There was no association between hospitalization rate or ICU admission/death and presence of OSA or PAP adherence in the data presented, but Dr. Hwang said that an updated analysis suggests that OSA may be associated with a risk of greater COVID-19 severity.
The control group was composed of individuals who had undergone sleep testing, but found to not have OSA. Still, they aren’t necessarily representative of the general population, since symptoms likely drove them to testing. A high percentage were also obese, and the average BMI was 30. “It’s certainly not a ‘normal population,’ but the advantage of what we did in terms of using this control group is that they underwent sleep testing, so they were proven to have no obstructive sleep apnea, whereas if we used a general population, we just don’t know,” said Dr. Hwang.
The study received technical and data support from Somnoware, and was funded by Kaiser Permanente. Dr. Tasali has no relevant financial disclosures.
FROM ATS 2021
APA, AMA, others move to stop insurer from overturning mental health claims ruling
The American Psychiatric Association has joined with the American Medical Association and other medical societies to oppose United Behavioral Health’s (UBH) request that a court throw out a ruling that found the insurer unfairly denied tens of thousands of claims for mental health and substance use disorder services.
Wit v. United Behavioral Health, in litigation since 2014, is being closely watched by clinicians, patients, providers, and attorneys.
Reena Kapoor, MD, chair of the APA’s Committee on Judicial Action, said in an interview that the APA is hopeful that “whatever the court says about UBH should be applicable to all insurance companies that are providing employer-sponsored health benefits.”
In a friend of the court (amicus curiae) brief, the APA, AMA, the California Medical Association, Southern California Psychiatric Society, Northern California Psychiatric Society, Orange County Psychiatric Society, Central California Psychiatric Society, and San Diego Psychiatric Society argue that “despite the availability of professionally developed, evidence-based guidelines embodying generally accepted standards of care for mental health and substance use disorders, managed care organizations commonly base coverage decisions on internally developed ‘level of care guidelines’ that are inappropriately restrictive.”
The guidelines “may lead to denial of coverage for treatment that is recommended by a patient’s physician and even cut off coverage when treatment is already being delivered,” said the groups.
The U.S. Department of Labor also filed a brief in support of the plaintiffs who are suing UBH. Those individuals suffered injury when they were denied coverage, said the federal agency, which regulates employer-sponsored insurance plans.
California Attorney General Rob Bonta also made an amicus filing supporting the plaintiffs.
“When insurers limit access to this critical care, they leave Californians who need it feeling as if they have no other option than to try to cope alone,” said Mr. Bonta in a statement.
‘Discrimination must end’
Mr. Bonta said he agreed with a 2019 ruling by the U.S. District Court for the Northern District of California that UBH had violated its fiduciary duties by wrongfully using its internally developed coverage determination guidelines and level of care guidelines to deny care.
The court also found that UBH’s medically necessary criteria meant that only “acute” episodes would be covered. Instead, said the court last November, chronic and comorbid conditions should always be treated, according to Maureen Gammon and Kathleen Rosenow of Willis Towers Watson, a risk advisor.
In November, the same Northern California District Court ruled on the remedies it would require of United, including that the insurer reprocess more than 67,000 claims. UBH was also barred indefinitely from using any of its guidelines to make coverage determinations. Instead, it was ordered to make determinations “consistent with generally accepted standards of care,” and consistent with state laws.
The District Court denied a request by UBH to put a hold on the claims reprocessing until it appealed the overall case. But the Ninth Circuit Court of Appeals in February granted that request.
Then, in March, United appealed the District Court’s overall ruling, claiming that the plaintiffs had not proven harm.
The U.S. Chamber of Commerce has filed a brief in support of United, agreeing with its arguments.
However, the APA and other clinician groups said there is no question of harm.
“Failure to provide appropriate levels of care for treatment of mental illness and substance use disorders leads to relapse, overdose, transmission of infectious diseases, and death,” said APA CEO and Medical Director Saul Levin, MD, MPA, in a statement.
APA President Vivian Pender, MD, said guidelines that “are overly focused on stabilizing acute symptoms of mental health and substance use disorders” are not treating the underlying disease. “When the injury is physical, insurers treat the underlying disease and not just the symptoms. Discrimination against patients with mental illness must end,” she said.
No court has ever recognized the type of claims reprocessing ordered by the District Court judge, said attorneys Nathaniel Cohen and Joseph Laska of Manatt, Phelps & Phillips, in an analysis of the case.
Mr. Cohen and Mr. Laska write. “Practitioners, health plans, and health insurers would be wise to track UBH’s long-awaited appeal to the Ninth Circuit.”
This article first appeared on Medscape.com.
The American Psychiatric Association has joined with the American Medical Association and other medical societies to oppose United Behavioral Health’s (UBH) request that a court throw out a ruling that found the insurer unfairly denied tens of thousands of claims for mental health and substance use disorder services.
Wit v. United Behavioral Health, in litigation since 2014, is being closely watched by clinicians, patients, providers, and attorneys.
Reena Kapoor, MD, chair of the APA’s Committee on Judicial Action, said in an interview that the APA is hopeful that “whatever the court says about UBH should be applicable to all insurance companies that are providing employer-sponsored health benefits.”
In a friend of the court (amicus curiae) brief, the APA, AMA, the California Medical Association, Southern California Psychiatric Society, Northern California Psychiatric Society, Orange County Psychiatric Society, Central California Psychiatric Society, and San Diego Psychiatric Society argue that “despite the availability of professionally developed, evidence-based guidelines embodying generally accepted standards of care for mental health and substance use disorders, managed care organizations commonly base coverage decisions on internally developed ‘level of care guidelines’ that are inappropriately restrictive.”
The guidelines “may lead to denial of coverage for treatment that is recommended by a patient’s physician and even cut off coverage when treatment is already being delivered,” said the groups.
The U.S. Department of Labor also filed a brief in support of the plaintiffs who are suing UBH. Those individuals suffered injury when they were denied coverage, said the federal agency, which regulates employer-sponsored insurance plans.
California Attorney General Rob Bonta also made an amicus filing supporting the plaintiffs.
“When insurers limit access to this critical care, they leave Californians who need it feeling as if they have no other option than to try to cope alone,” said Mr. Bonta in a statement.
‘Discrimination must end’
Mr. Bonta said he agreed with a 2019 ruling by the U.S. District Court for the Northern District of California that UBH had violated its fiduciary duties by wrongfully using its internally developed coverage determination guidelines and level of care guidelines to deny care.
The court also found that UBH’s medically necessary criteria meant that only “acute” episodes would be covered. Instead, said the court last November, chronic and comorbid conditions should always be treated, according to Maureen Gammon and Kathleen Rosenow of Willis Towers Watson, a risk advisor.
In November, the same Northern California District Court ruled on the remedies it would require of United, including that the insurer reprocess more than 67,000 claims. UBH was also barred indefinitely from using any of its guidelines to make coverage determinations. Instead, it was ordered to make determinations “consistent with generally accepted standards of care,” and consistent with state laws.
The District Court denied a request by UBH to put a hold on the claims reprocessing until it appealed the overall case. But the Ninth Circuit Court of Appeals in February granted that request.
Then, in March, United appealed the District Court’s overall ruling, claiming that the plaintiffs had not proven harm.
The U.S. Chamber of Commerce has filed a brief in support of United, agreeing with its arguments.
However, the APA and other clinician groups said there is no question of harm.
“Failure to provide appropriate levels of care for treatment of mental illness and substance use disorders leads to relapse, overdose, transmission of infectious diseases, and death,” said APA CEO and Medical Director Saul Levin, MD, MPA, in a statement.
APA President Vivian Pender, MD, said guidelines that “are overly focused on stabilizing acute symptoms of mental health and substance use disorders” are not treating the underlying disease. “When the injury is physical, insurers treat the underlying disease and not just the symptoms. Discrimination against patients with mental illness must end,” she said.
No court has ever recognized the type of claims reprocessing ordered by the District Court judge, said attorneys Nathaniel Cohen and Joseph Laska of Manatt, Phelps & Phillips, in an analysis of the case.
Mr. Cohen and Mr. Laska write. “Practitioners, health plans, and health insurers would be wise to track UBH’s long-awaited appeal to the Ninth Circuit.”
This article first appeared on Medscape.com.
The American Psychiatric Association has joined with the American Medical Association and other medical societies to oppose United Behavioral Health’s (UBH) request that a court throw out a ruling that found the insurer unfairly denied tens of thousands of claims for mental health and substance use disorder services.
Wit v. United Behavioral Health, in litigation since 2014, is being closely watched by clinicians, patients, providers, and attorneys.
Reena Kapoor, MD, chair of the APA’s Committee on Judicial Action, said in an interview that the APA is hopeful that “whatever the court says about UBH should be applicable to all insurance companies that are providing employer-sponsored health benefits.”
In a friend of the court (amicus curiae) brief, the APA, AMA, the California Medical Association, Southern California Psychiatric Society, Northern California Psychiatric Society, Orange County Psychiatric Society, Central California Psychiatric Society, and San Diego Psychiatric Society argue that “despite the availability of professionally developed, evidence-based guidelines embodying generally accepted standards of care for mental health and substance use disorders, managed care organizations commonly base coverage decisions on internally developed ‘level of care guidelines’ that are inappropriately restrictive.”
The guidelines “may lead to denial of coverage for treatment that is recommended by a patient’s physician and even cut off coverage when treatment is already being delivered,” said the groups.
The U.S. Department of Labor also filed a brief in support of the plaintiffs who are suing UBH. Those individuals suffered injury when they were denied coverage, said the federal agency, which regulates employer-sponsored insurance plans.
California Attorney General Rob Bonta also made an amicus filing supporting the plaintiffs.
“When insurers limit access to this critical care, they leave Californians who need it feeling as if they have no other option than to try to cope alone,” said Mr. Bonta in a statement.
‘Discrimination must end’
Mr. Bonta said he agreed with a 2019 ruling by the U.S. District Court for the Northern District of California that UBH had violated its fiduciary duties by wrongfully using its internally developed coverage determination guidelines and level of care guidelines to deny care.
The court also found that UBH’s medically necessary criteria meant that only “acute” episodes would be covered. Instead, said the court last November, chronic and comorbid conditions should always be treated, according to Maureen Gammon and Kathleen Rosenow of Willis Towers Watson, a risk advisor.
In November, the same Northern California District Court ruled on the remedies it would require of United, including that the insurer reprocess more than 67,000 claims. UBH was also barred indefinitely from using any of its guidelines to make coverage determinations. Instead, it was ordered to make determinations “consistent with generally accepted standards of care,” and consistent with state laws.
The District Court denied a request by UBH to put a hold on the claims reprocessing until it appealed the overall case. But the Ninth Circuit Court of Appeals in February granted that request.
Then, in March, United appealed the District Court’s overall ruling, claiming that the plaintiffs had not proven harm.
The U.S. Chamber of Commerce has filed a brief in support of United, agreeing with its arguments.
However, the APA and other clinician groups said there is no question of harm.
“Failure to provide appropriate levels of care for treatment of mental illness and substance use disorders leads to relapse, overdose, transmission of infectious diseases, and death,” said APA CEO and Medical Director Saul Levin, MD, MPA, in a statement.
APA President Vivian Pender, MD, said guidelines that “are overly focused on stabilizing acute symptoms of mental health and substance use disorders” are not treating the underlying disease. “When the injury is physical, insurers treat the underlying disease and not just the symptoms. Discrimination against patients with mental illness must end,” she said.
No court has ever recognized the type of claims reprocessing ordered by the District Court judge, said attorneys Nathaniel Cohen and Joseph Laska of Manatt, Phelps & Phillips, in an analysis of the case.
Mr. Cohen and Mr. Laska write. “Practitioners, health plans, and health insurers would be wise to track UBH’s long-awaited appeal to the Ninth Circuit.”
This article first appeared on Medscape.com.
OSA: Heart rate change may signal CPAP benefit
Some nonsleepy patients with coronary artery disease and obstructive sleep apnea (OSA) may receive cardiovascular benefit from continuous positive airway pressure (CPAP) therapy, according to a post hoc analysis of the RICCADSA clinical trial. That study found no benefit among patients overall, but the new analysis found that patients whose heart rate increases (delta heart rate, or dHR) more than average during apnea or hypopnea experienced fewer cardiovascular or cerebrovascular events during apnea or hypopnea when treated with CPAP.
Although RICCADSA showed no benefit, an analysis of the Multi-Ethnic Study of Atherosclerosis (MESA) and the Sleep Heart Health Study (SHHS) cohorts found that elevated pulse rate response to respiratory events was associated with greater risk of cardiovascular disease (CVD) morbidity and mortality. But the effect was seen only in nonsleepy patients. “We hypothesized that pulse rate response to apneas would predict which patients with OSA may most benefit from CPAP treatment. Now, our study suggests that there is, in fact, a subgroup of nonsleepy patients with OSA for whom CPAP could provide a reduction in risk, specifically those with a higher pulse rate response to their respiratory events,” Ali Azarbarzin, PhD, said in an interview.
Dr. Azarbarzin presented the study at the American Thoracic Society’s virtual international conference (Abstract A1103). He is in the division of sleep and circadian disorders at Brigham and Women’s Hospital, and is assistant professor of medicine at Harvard Medical School, both in Boston.
The study is in line with recent efforts to subgroup OSA patients to determine which are at higher risk of cardiovascular events and other complications, and which are most likely to respond to treatment, according to Esra Tasali, MD, of the University of Chicago, who moderated the session where the study was presented. “The field is really urgently in need of coming up with new methods, and I think this study is getting a handle on that,” said Dr. Tasali in an interview.
“I think that this is really pointing toward a new area that the whole (sleep field) is moving toward, which is better phenotyping of sleep apnea so that we can come up with more personalized treatments,” said Dr. Tasali.
The patients who appeared to gain a cardiovascular benefit from CPAP represented about 16% of trial participants. Dr. Azarbarzin refrained from making clinical recommendations, citing the need for more data. The team next plans to reproduce the findings in additional, larger trials such as the SAVE and ISAACC trials. “Ultimately, our goal is to confirm our findings in a future randomized controlled trial of CPAP by enrolling participants based on their pulse rate response,” said Dr. Azarbarzin.
The RICCADSA study was a single center randomized, controlled trial with 226 patients with coronary artery disease and OSA who were randomized to CPAP or no CPAP treatment. In the overall population, CPAP treatment was not associated with a statistically significant change in repeat revascularization, myocardial infarction, stroke, or cardiovascular mortality (hazard ratio [HR], 0.79; P = .435). That study assumed that the effect of OSA on CVD is similar across all subgroups of dHR.
The mean increase in heart rate was 7.1 beats per minute (BPM; standard deviation, 3.7). Each standard deviation increase in dHR was linked to greater CVD risk (HR, 1.45; P = .029). For each standard deviation decrease in dHR, treatment with CPAP decreased the CVD risk (HR, 0.54; P = .043).
For patients with a low dHR of 4 BPM, the hazard ratio for CVD was 0.8 with no CPAP treatment and 1.2 for CPAP treatment. For those at the mean value of 7 BPM, the HRs were 1.1 and 0.9 respectively. For those with a high dHR, (10 BPM), the hazard ratio was 1.6 without treatment and 0.7 with CPAP.
“We modeled delta heart rate interaction with CPAP, which was significant. What this means is that for someone with a mean delta heart rate of 7 beats per minute, the risk reduction (with CPAP) is similar to what RICCADSA reported. But if you look at those with high delta heart rate, the risk reduction was significantly larger. It was actually a more than 50% reduction of risk with CPAP treatment,” said Dr. Azarbarzin.
Dr. Azarbarzin has consulted for Somnifix and Apnimed and has received grants from Somnifix. Dr. Tasali has no relevant financial disclosures.
Some nonsleepy patients with coronary artery disease and obstructive sleep apnea (OSA) may receive cardiovascular benefit from continuous positive airway pressure (CPAP) therapy, according to a post hoc analysis of the RICCADSA clinical trial. That study found no benefit among patients overall, but the new analysis found that patients whose heart rate increases (delta heart rate, or dHR) more than average during apnea or hypopnea experienced fewer cardiovascular or cerebrovascular events during apnea or hypopnea when treated with CPAP.
Although RICCADSA showed no benefit, an analysis of the Multi-Ethnic Study of Atherosclerosis (MESA) and the Sleep Heart Health Study (SHHS) cohorts found that elevated pulse rate response to respiratory events was associated with greater risk of cardiovascular disease (CVD) morbidity and mortality. But the effect was seen only in nonsleepy patients. “We hypothesized that pulse rate response to apneas would predict which patients with OSA may most benefit from CPAP treatment. Now, our study suggests that there is, in fact, a subgroup of nonsleepy patients with OSA for whom CPAP could provide a reduction in risk, specifically those with a higher pulse rate response to their respiratory events,” Ali Azarbarzin, PhD, said in an interview.
Dr. Azarbarzin presented the study at the American Thoracic Society’s virtual international conference (Abstract A1103). He is in the division of sleep and circadian disorders at Brigham and Women’s Hospital, and is assistant professor of medicine at Harvard Medical School, both in Boston.
The study is in line with recent efforts to subgroup OSA patients to determine which are at higher risk of cardiovascular events and other complications, and which are most likely to respond to treatment, according to Esra Tasali, MD, of the University of Chicago, who moderated the session where the study was presented. “The field is really urgently in need of coming up with new methods, and I think this study is getting a handle on that,” said Dr. Tasali in an interview.
“I think that this is really pointing toward a new area that the whole (sleep field) is moving toward, which is better phenotyping of sleep apnea so that we can come up with more personalized treatments,” said Dr. Tasali.
The patients who appeared to gain a cardiovascular benefit from CPAP represented about 16% of trial participants. Dr. Azarbarzin refrained from making clinical recommendations, citing the need for more data. The team next plans to reproduce the findings in additional, larger trials such as the SAVE and ISAACC trials. “Ultimately, our goal is to confirm our findings in a future randomized controlled trial of CPAP by enrolling participants based on their pulse rate response,” said Dr. Azarbarzin.
The RICCADSA study was a single center randomized, controlled trial with 226 patients with coronary artery disease and OSA who were randomized to CPAP or no CPAP treatment. In the overall population, CPAP treatment was not associated with a statistically significant change in repeat revascularization, myocardial infarction, stroke, or cardiovascular mortality (hazard ratio [HR], 0.79; P = .435). That study assumed that the effect of OSA on CVD is similar across all subgroups of dHR.
The mean increase in heart rate was 7.1 beats per minute (BPM; standard deviation, 3.7). Each standard deviation increase in dHR was linked to greater CVD risk (HR, 1.45; P = .029). For each standard deviation decrease in dHR, treatment with CPAP decreased the CVD risk (HR, 0.54; P = .043).
For patients with a low dHR of 4 BPM, the hazard ratio for CVD was 0.8 with no CPAP treatment and 1.2 for CPAP treatment. For those at the mean value of 7 BPM, the HRs were 1.1 and 0.9 respectively. For those with a high dHR, (10 BPM), the hazard ratio was 1.6 without treatment and 0.7 with CPAP.
“We modeled delta heart rate interaction with CPAP, which was significant. What this means is that for someone with a mean delta heart rate of 7 beats per minute, the risk reduction (with CPAP) is similar to what RICCADSA reported. But if you look at those with high delta heart rate, the risk reduction was significantly larger. It was actually a more than 50% reduction of risk with CPAP treatment,” said Dr. Azarbarzin.
Dr. Azarbarzin has consulted for Somnifix and Apnimed and has received grants from Somnifix. Dr. Tasali has no relevant financial disclosures.
Some nonsleepy patients with coronary artery disease and obstructive sleep apnea (OSA) may receive cardiovascular benefit from continuous positive airway pressure (CPAP) therapy, according to a post hoc analysis of the RICCADSA clinical trial. That study found no benefit among patients overall, but the new analysis found that patients whose heart rate increases (delta heart rate, or dHR) more than average during apnea or hypopnea experienced fewer cardiovascular or cerebrovascular events during apnea or hypopnea when treated with CPAP.
Although RICCADSA showed no benefit, an analysis of the Multi-Ethnic Study of Atherosclerosis (MESA) and the Sleep Heart Health Study (SHHS) cohorts found that elevated pulse rate response to respiratory events was associated with greater risk of cardiovascular disease (CVD) morbidity and mortality. But the effect was seen only in nonsleepy patients. “We hypothesized that pulse rate response to apneas would predict which patients with OSA may most benefit from CPAP treatment. Now, our study suggests that there is, in fact, a subgroup of nonsleepy patients with OSA for whom CPAP could provide a reduction in risk, specifically those with a higher pulse rate response to their respiratory events,” Ali Azarbarzin, PhD, said in an interview.
Dr. Azarbarzin presented the study at the American Thoracic Society’s virtual international conference (Abstract A1103). He is in the division of sleep and circadian disorders at Brigham and Women’s Hospital, and is assistant professor of medicine at Harvard Medical School, both in Boston.
The study is in line with recent efforts to subgroup OSA patients to determine which are at higher risk of cardiovascular events and other complications, and which are most likely to respond to treatment, according to Esra Tasali, MD, of the University of Chicago, who moderated the session where the study was presented. “The field is really urgently in need of coming up with new methods, and I think this study is getting a handle on that,” said Dr. Tasali in an interview.
“I think that this is really pointing toward a new area that the whole (sleep field) is moving toward, which is better phenotyping of sleep apnea so that we can come up with more personalized treatments,” said Dr. Tasali.
The patients who appeared to gain a cardiovascular benefit from CPAP represented about 16% of trial participants. Dr. Azarbarzin refrained from making clinical recommendations, citing the need for more data. The team next plans to reproduce the findings in additional, larger trials such as the SAVE and ISAACC trials. “Ultimately, our goal is to confirm our findings in a future randomized controlled trial of CPAP by enrolling participants based on their pulse rate response,” said Dr. Azarbarzin.
The RICCADSA study was a single center randomized, controlled trial with 226 patients with coronary artery disease and OSA who were randomized to CPAP or no CPAP treatment. In the overall population, CPAP treatment was not associated with a statistically significant change in repeat revascularization, myocardial infarction, stroke, or cardiovascular mortality (hazard ratio [HR], 0.79; P = .435). That study assumed that the effect of OSA on CVD is similar across all subgroups of dHR.
The mean increase in heart rate was 7.1 beats per minute (BPM; standard deviation, 3.7). Each standard deviation increase in dHR was linked to greater CVD risk (HR, 1.45; P = .029). For each standard deviation decrease in dHR, treatment with CPAP decreased the CVD risk (HR, 0.54; P = .043).
For patients with a low dHR of 4 BPM, the hazard ratio for CVD was 0.8 with no CPAP treatment and 1.2 for CPAP treatment. For those at the mean value of 7 BPM, the HRs were 1.1 and 0.9 respectively. For those with a high dHR, (10 BPM), the hazard ratio was 1.6 without treatment and 0.7 with CPAP.
“We modeled delta heart rate interaction with CPAP, which was significant. What this means is that for someone with a mean delta heart rate of 7 beats per minute, the risk reduction (with CPAP) is similar to what RICCADSA reported. But if you look at those with high delta heart rate, the risk reduction was significantly larger. It was actually a more than 50% reduction of risk with CPAP treatment,” said Dr. Azarbarzin.
Dr. Azarbarzin has consulted for Somnifix and Apnimed and has received grants from Somnifix. Dr. Tasali has no relevant financial disclosures.
FROM ATS 2021
Long-term use of prescription sleep meds unsupported by new research
a new study shows.
“While there are good data from [randomized, controlled trials] that these medications improve sleep disturbances in the short term,” few studies have examined whether they provide long-term benefits, stated the authors of the paper, which was published in BMJ Open.
“The current observational study does not support use of sleep medications over the long term, as there were no self-reported differences at 1 or 2 years of follow-up comparing sleep medication users with nonusers,” author Daniel H. Solomon, MD, MPH, from Brigham and Women’s Hospital, Boston, and colleagues wrote.
Women included in the analysis were drawn from the Study of Women’s Health Across the Nation (SWAN), an ongoing multicenter, longitudinal study examining women during the menopausal transition. The average age of the women included in the cohort was 49.5 years and approximately half were White. All women reported a sleep disturbance on at least 3 nights per week during a 2-week interval. At follow up, women were asked to use a Likert scale to rate three aspects of sleep: difficulty initiating sleep, frequent awakening, and waking up early. On the scale, 1 represented having no difficulties on any nights, 3 represented having difficulties 1-2 nights per week, and 5 represented having difficulty 5-7 nights per week.
Women already using prescription sleep medication at their baseline visit were excluded from the study. Medications used included benzodiazepines, selective BZD receptor agonists, and other hypnotics.
Over the 21 years of follow-up in the SWAN study (1995-2016), Dr. Solomon and colleagues identified 238 women using sleep medication and these were compared with a cohort of 447 propensity score–matched non–sleep medication uses. Overall, the 685 women included were similar in characteristics to each other as well as to the other potentially eligible women not included in the analysis.
Sleep disturbance patterns compared
At baseline, sleep disturbance patterns were similar between the two groups. Among medication users, the mean score for difficulty initiating sleep was 2.7 (95% confidence interval, 2.5-2.9), waking frequently 3.8 (95% CI, 3.6-3.9), and waking early 2.9 (95% CI, 2.7-3.1). Among the nonusers, the baseline scores were 2.6 (95% CI, 2.5-2.7), 3.7 (95% CI, 3.6-3.8), and 2.7 (95% CI, 2.5-2.8), respectively. After 1 year, there was no statistically significant difference in scores between the two groups. The average ratings for medication users were 2.6 (95% CI, 2.3-2.8) for difficulty initiating sleep, 3.8 (95% CI, 3.6-4.0) for waking frequently, and 2.8 (95% CI, 2.6-3.0) for waking early.
Average ratings among nonusers were 2.3 (95% CI, 2.2-2.4), 3.5 (95% CI, 3.3-3.6), and 2.5 (95% CI, 2.3-2.6), respectively.
After 2 years, there were still no statistically significant reductions in sleep disturbances among those taking prescription sleep medications, compared with those not taking medication.
The researchers noted that approximately half of the women in this cohort were current or past tobacco users and that 20% were moderate to heavy alcohol users.
More work-up, not more medication, needed
The study authors acknowledged the limitations of an observational study and noted that, since participants only reported medication use and sleep disturbances at annual visits, they did not know whether patients’ medication use was intermittent or of any interim outcomes. Additionally, the authors pointed out that those classified as “nonusers” may have been using over-the-counter medication.
“Investigations should look at detailed-use patterns, on a daily or weekly basis, with frequent outcomes data,” Dr. Solomon said in an interview. “While our data shed new light on chronic use, we only had data collected on an annual basis; daily or weekly data would provide more granular information.”
Regarding clinician prescribing practices, Dr. Solomon said, “short-term, intermittent use can be helpful, but use these agents sparingly” and “educate patients that chronic regular use of medications for sleep is not associated with improvement in sleep disturbances.”
Commenting on the study, Andrea Matsumura, MD, a sleep specialist at the Oregon Clinic in Portland, echoed this sentiment: “When someone says they are having trouble sleeping this is the tip of the iceberg and it warrants an evaluation to determine if someone has a breathing disorder, a circadian disorder, a life situation, or a type of insomnia that is driving the sleeplessness.”
“I think this study supports what we all should know,” Dr. Matsumura concluded. “Sleep aids are not meant to be used long term” and should not be used for longer than 2 weeks without further work-up.
Funding for this study was provided through a grant from the National Institutes of Health. Dr. Solomon has received salary support from research grants to Brigham and Women’s Hospital for unrelated work from AbbVie, Amgen, Corrona, Genentech and Pfizer. The other authors and Dr. Matsumura have reported no relevant financial relationships.
a new study shows.
“While there are good data from [randomized, controlled trials] that these medications improve sleep disturbances in the short term,” few studies have examined whether they provide long-term benefits, stated the authors of the paper, which was published in BMJ Open.
“The current observational study does not support use of sleep medications over the long term, as there were no self-reported differences at 1 or 2 years of follow-up comparing sleep medication users with nonusers,” author Daniel H. Solomon, MD, MPH, from Brigham and Women’s Hospital, Boston, and colleagues wrote.
Women included in the analysis were drawn from the Study of Women’s Health Across the Nation (SWAN), an ongoing multicenter, longitudinal study examining women during the menopausal transition. The average age of the women included in the cohort was 49.5 years and approximately half were White. All women reported a sleep disturbance on at least 3 nights per week during a 2-week interval. At follow up, women were asked to use a Likert scale to rate three aspects of sleep: difficulty initiating sleep, frequent awakening, and waking up early. On the scale, 1 represented having no difficulties on any nights, 3 represented having difficulties 1-2 nights per week, and 5 represented having difficulty 5-7 nights per week.
Women already using prescription sleep medication at their baseline visit were excluded from the study. Medications used included benzodiazepines, selective BZD receptor agonists, and other hypnotics.
Over the 21 years of follow-up in the SWAN study (1995-2016), Dr. Solomon and colleagues identified 238 women using sleep medication and these were compared with a cohort of 447 propensity score–matched non–sleep medication uses. Overall, the 685 women included were similar in characteristics to each other as well as to the other potentially eligible women not included in the analysis.
Sleep disturbance patterns compared
At baseline, sleep disturbance patterns were similar between the two groups. Among medication users, the mean score for difficulty initiating sleep was 2.7 (95% confidence interval, 2.5-2.9), waking frequently 3.8 (95% CI, 3.6-3.9), and waking early 2.9 (95% CI, 2.7-3.1). Among the nonusers, the baseline scores were 2.6 (95% CI, 2.5-2.7), 3.7 (95% CI, 3.6-3.8), and 2.7 (95% CI, 2.5-2.8), respectively. After 1 year, there was no statistically significant difference in scores between the two groups. The average ratings for medication users were 2.6 (95% CI, 2.3-2.8) for difficulty initiating sleep, 3.8 (95% CI, 3.6-4.0) for waking frequently, and 2.8 (95% CI, 2.6-3.0) for waking early.
Average ratings among nonusers were 2.3 (95% CI, 2.2-2.4), 3.5 (95% CI, 3.3-3.6), and 2.5 (95% CI, 2.3-2.6), respectively.
After 2 years, there were still no statistically significant reductions in sleep disturbances among those taking prescription sleep medications, compared with those not taking medication.
The researchers noted that approximately half of the women in this cohort were current or past tobacco users and that 20% were moderate to heavy alcohol users.
More work-up, not more medication, needed
The study authors acknowledged the limitations of an observational study and noted that, since participants only reported medication use and sleep disturbances at annual visits, they did not know whether patients’ medication use was intermittent or of any interim outcomes. Additionally, the authors pointed out that those classified as “nonusers” may have been using over-the-counter medication.
“Investigations should look at detailed-use patterns, on a daily or weekly basis, with frequent outcomes data,” Dr. Solomon said in an interview. “While our data shed new light on chronic use, we only had data collected on an annual basis; daily or weekly data would provide more granular information.”
Regarding clinician prescribing practices, Dr. Solomon said, “short-term, intermittent use can be helpful, but use these agents sparingly” and “educate patients that chronic regular use of medications for sleep is not associated with improvement in sleep disturbances.”
Commenting on the study, Andrea Matsumura, MD, a sleep specialist at the Oregon Clinic in Portland, echoed this sentiment: “When someone says they are having trouble sleeping this is the tip of the iceberg and it warrants an evaluation to determine if someone has a breathing disorder, a circadian disorder, a life situation, or a type of insomnia that is driving the sleeplessness.”
“I think this study supports what we all should know,” Dr. Matsumura concluded. “Sleep aids are not meant to be used long term” and should not be used for longer than 2 weeks without further work-up.
Funding for this study was provided through a grant from the National Institutes of Health. Dr. Solomon has received salary support from research grants to Brigham and Women’s Hospital for unrelated work from AbbVie, Amgen, Corrona, Genentech and Pfizer. The other authors and Dr. Matsumura have reported no relevant financial relationships.
a new study shows.
“While there are good data from [randomized, controlled trials] that these medications improve sleep disturbances in the short term,” few studies have examined whether they provide long-term benefits, stated the authors of the paper, which was published in BMJ Open.
“The current observational study does not support use of sleep medications over the long term, as there were no self-reported differences at 1 or 2 years of follow-up comparing sleep medication users with nonusers,” author Daniel H. Solomon, MD, MPH, from Brigham and Women’s Hospital, Boston, and colleagues wrote.
Women included in the analysis were drawn from the Study of Women’s Health Across the Nation (SWAN), an ongoing multicenter, longitudinal study examining women during the menopausal transition. The average age of the women included in the cohort was 49.5 years and approximately half were White. All women reported a sleep disturbance on at least 3 nights per week during a 2-week interval. At follow up, women were asked to use a Likert scale to rate three aspects of sleep: difficulty initiating sleep, frequent awakening, and waking up early. On the scale, 1 represented having no difficulties on any nights, 3 represented having difficulties 1-2 nights per week, and 5 represented having difficulty 5-7 nights per week.
Women already using prescription sleep medication at their baseline visit were excluded from the study. Medications used included benzodiazepines, selective BZD receptor agonists, and other hypnotics.
Over the 21 years of follow-up in the SWAN study (1995-2016), Dr. Solomon and colleagues identified 238 women using sleep medication and these were compared with a cohort of 447 propensity score–matched non–sleep medication uses. Overall, the 685 women included were similar in characteristics to each other as well as to the other potentially eligible women not included in the analysis.
Sleep disturbance patterns compared
At baseline, sleep disturbance patterns were similar between the two groups. Among medication users, the mean score for difficulty initiating sleep was 2.7 (95% confidence interval, 2.5-2.9), waking frequently 3.8 (95% CI, 3.6-3.9), and waking early 2.9 (95% CI, 2.7-3.1). Among the nonusers, the baseline scores were 2.6 (95% CI, 2.5-2.7), 3.7 (95% CI, 3.6-3.8), and 2.7 (95% CI, 2.5-2.8), respectively. After 1 year, there was no statistically significant difference in scores between the two groups. The average ratings for medication users were 2.6 (95% CI, 2.3-2.8) for difficulty initiating sleep, 3.8 (95% CI, 3.6-4.0) for waking frequently, and 2.8 (95% CI, 2.6-3.0) for waking early.
Average ratings among nonusers were 2.3 (95% CI, 2.2-2.4), 3.5 (95% CI, 3.3-3.6), and 2.5 (95% CI, 2.3-2.6), respectively.
After 2 years, there were still no statistically significant reductions in sleep disturbances among those taking prescription sleep medications, compared with those not taking medication.
The researchers noted that approximately half of the women in this cohort were current or past tobacco users and that 20% were moderate to heavy alcohol users.
More work-up, not more medication, needed
The study authors acknowledged the limitations of an observational study and noted that, since participants only reported medication use and sleep disturbances at annual visits, they did not know whether patients’ medication use was intermittent or of any interim outcomes. Additionally, the authors pointed out that those classified as “nonusers” may have been using over-the-counter medication.
“Investigations should look at detailed-use patterns, on a daily or weekly basis, with frequent outcomes data,” Dr. Solomon said in an interview. “While our data shed new light on chronic use, we only had data collected on an annual basis; daily or weekly data would provide more granular information.”
Regarding clinician prescribing practices, Dr. Solomon said, “short-term, intermittent use can be helpful, but use these agents sparingly” and “educate patients that chronic regular use of medications for sleep is not associated with improvement in sleep disturbances.”
Commenting on the study, Andrea Matsumura, MD, a sleep specialist at the Oregon Clinic in Portland, echoed this sentiment: “When someone says they are having trouble sleeping this is the tip of the iceberg and it warrants an evaluation to determine if someone has a breathing disorder, a circadian disorder, a life situation, or a type of insomnia that is driving the sleeplessness.”
“I think this study supports what we all should know,” Dr. Matsumura concluded. “Sleep aids are not meant to be used long term” and should not be used for longer than 2 weeks without further work-up.
Funding for this study was provided through a grant from the National Institutes of Health. Dr. Solomon has received salary support from research grants to Brigham and Women’s Hospital for unrelated work from AbbVie, Amgen, Corrona, Genentech and Pfizer. The other authors and Dr. Matsumura have reported no relevant financial relationships.
FROM BMJ OPEN
Obstructive sleep apnea and COVID-19
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused by the novel coronavirus of the year 2019 (COVID-19) has had a major impact on global health and economy. United States reported a total caseload of 28,998,834 patients and total mortality of 525,031 as of March 2021 (NPR.org; worldometer. Accessed March 8, 2021). The beginning of 2021 ushered positivity with the development of multiple highly effective SARS-CoV-2 vaccines. Although the medical world has gained much knowledge about this deadly disease, there are many unknowns and still much to be learned.
Two early landmark studies from Italy (Lombardy) and United States (New York City area) provided initial insight on comorbid conditions associated with increased risk of severe COVID-19 infection (Richardson S, et al. JAMA. 2020;323[20]:2052; Grasselli G, et al. JAMA Intern Med. 2020;180[10]:1345). In the United States cohort, hypertension (HTN), obesity, and diabetes (DM) were independent risk factors for severe disease, while in the Italy cohort, older age, male, COPD, hypercholesterolemia, and diabetes were independent risk factors for increased mortality. Obstructive sleep apnea (OSA) was not mentioned as a comorbid risk factor.
There is much speculation regarding OSA as an independent risk factor for severe COVID-19 infection. OSA is a common sleep-related breathing disorder with increased prevalence in men, older age, and higher body mass index (BMI); and OSA is associated with hypertension, obesity, and diabetes, all of which are risk factors for severe COVID-19. Because of the shared similarities in pathophysiology between OSA and COVID-19 (Tufik S, et al. J Clin Sleep Med. 2020;16[8]:1425), and shared comorbid conditions associated with increased risk of severe COVID-19 disease, OSA has been suggested as an independent risk factor for unfavorable COVID-19-related outcomes.
SARS-CoV-2 triggers a severe inflammatory response involving type-II pneumocytes and angiotensin-converting enzyme 2 pathway. OSA is characterized by intermittent hypoxia and sleep fragmentation, leading to a cascade of systemic inflammatory response involving oxidative stress, pro-inflammatory cytokines, endothelial dysfunction, and consequent cardiovascular injury (Jose RJ, et al. Lancet Respir Med. 2020;8[6]:e46; Saxena K, et al. Sleep Medicine. 2021;79:223). In this regard, OSA may contribute to COVID-19 “cytokine storm” by causing or exacerbating endothelial dysfunction, inflammation, and oxidative stress.
Multiple studies have recently been published on the impact of OSA on COVID-19 outcomes. The Coronavirus SARS-CoV-2 and Diabetes Outcomes (CORONADO) study was one of the initial studies that analyzed the relationship between OSA and COVID-19-related outcomes. This was a multicenter observational study involving diabetic patients hospitalized with COVID-19. The primary outcome was mechanical ventilation and/or death within 7 days of admission. Multivariate adjustment showed that age, BMI, and OSA, among other factors, were independently associated with risk of death on day 7 (Cariou B, et al. Diabetologia. 2020;63[8]:1500). Strausz and colleagues also evaluated OSA as an independent risk factor for severe COVID-19 in a large registry of hospital discharge patients (FinnGen study). The authors reported that although the risk of contracting COVID-19 was the same for patients with or without OSA, after adjusting for age, sex, and BMI, OSA was associated with higher risk of hospitalization (Strausz S, et al. BMJ Open Resp Res. 2021;8:e000845). Similar findings were confirmed by the Maas et al. study, which utilized a large socioeconomically diverse database composed of 10 hospital systems. Diagnoses and outcomes were identified by ICD-10 coding and medical record data. After adjustments for diabetes, HTN, and BMI, OSA conferred an eight-fold risk for COVID-19 infection, was associated with increased risk of hospitalization, and doubled the risk of developing respiratory failure (Maas MB, et al. Sleep Breath. 2020 Sep; 29:1-3. doi: 10.1007/s11325-020-02203-0).
Peker and colleagues conducted a prospective multicenter observational study comparing clinical outcomes of severe COVID-19 infection in patients with low vs high pretest probability of having OSA based on the Berlin questionnaire. The authors reported a clinically significant risk of poorer clinical outcomes in the high pretest probability OSA group after adjustments for age, sex, and comorbidities (Peker Y, et al. Ann Am Thorac Soc. 2021. Feb 17. doi: 10.1513/AnnalsATS.202011-1409OC). A timely meta-analysis including 21 studies (19 with retrospective design) with 54,276 COVID-19 patients and 4,640 OSA patients concluded poor composite outcomes including severe COVID-19, intensive care unit admission, mechanical ventilatory support, and death in association with OSA (OR – 1.72 95% CI 1.55-1.91, P< .00001). In patients with obesity, OSA is a highly prevalent co-morbid condition. BMI, however, was not adjusted in this model (Hariyanto TI, et al. Sleep Med. 2021. doi: 10.1016/j.sleep.2021.03.029).
Other studies have concluded the opposite with OSA not being an independent risk factor for severe COVID-19 infection. Cade and colleagues conducted a retrospective analysis from a comprehensive electronic health dataset using ICD codes to identify OSA patients with severe COVID-19 infection. A significant association between OSA and COVID-19 death was noted after adjustment for demographics (ethnicity, age, sex). However, when fully adjusted for demographics, BMI, asthma, COPD, HTN, or DM, OSA was not an independent risk factor for COVID-19-related mortality and hospitalization (Cade BE, et al. Am J Respir Crit Care Med. 2020;202[10]:1462). The FinnGen study (Strausz et al.) was part of a meta-analysis examining the association between OSA and severe COVID-19 with and without adjustments for BMI. This meta-analysis consisted of 15,835 COVID-19 patients including 1,294 with OSA. The authors found that OSA was a risk factor with a two-fold increased risk of severe COVID-19 infection (OR = 2.37, P = .021). However, after adjustments were made for BMI, this finding lost statistical significance (OR=1.55, P=.13) (Strausz S, et al. BMJ Open Resp Res. 2021;8:e000845).
It is worth noting that a majority of studies identified OSA by indirect and imperfect methods through chart review, ICD codes, and databases. Confirmed OSA based on formal testing with a sleep study in COVID-19 patients remains a challenge. Perhaps well performed screening questionnaires, such as STOP-Bang, Berlin, or NoSAS, can be utilized as was the case in one study. It is also unclear if outcomes of COVID-19 infection differ in patients with treated or untreated OSA, as raised by the CORONADO study. A recent cross-sectional telephone interview survey of patients with confirmed OSA in Iran alluded to higher prevalence of COVID-19 in patients with severe OSA with suggestion of lower prevalence in patients who were currently receiving OSA treatment with positive airway pressure (PAP) therapy (Najafi A, et al. Sleep Health. 2021 Feb;7[1]:14). This is a crucial question as PAP therapy is considered an aerosol-generating procedure (Lance CG. Cleve Clin J Med. 2020 May 5. doi: 10.3949/ccjm.87a.ccc003). Studies have suggested continued use of PAP therapy with additional measures to mitigate the spread of virus, since failure to use PAP could be deleterious to the patient’s quality of life. Interestingly, PAP adherence seemed to have improved during the pandemic as evidenced by a telephonic survey done in New York City that showed 88% of patients with OSA used a PAP device consistently (Attias D, et al. Eur Respir J. 2020 Jul 30;56[1]:2001607. doi: 10.1183/13993003.01607-2020).
In summary, the jury is still out on whether OSA is a facilitator for viral replication, or an independent risk factor for poor prognosis related to COVID-19 infection, or has no clinical relevance to COVID-19. COVID-19 and OSA share comorbidities and pathways leading to a systemic inflammatory cascade. Theoretically, it would make sense that OSA is a risk factor for severe COVID-19 infection; however, it remains to be proven. The recent studies are limited by retrospective and observational nature, imprecise OSA classification/diagnostic criteria, and confounded by difficult to control variables. Further research is needed to expand our understanding of OSA -induced intermittent hypoxemia, inflammation, and endothelial dysfunction that may play a role in COVID-19 morbidity and mortality. Until we have more clarity, close monitoring of OSA patients infected with COVID-19 is recommended along with implementation of safe protocols for continuation of PAP usage during the infectious phase. Identifying underlying comorbid conditions that contribute to worsening of a COVID-19 infectious course is a crucial step in improving clinical outcomes.
Dr. Sahni is Assistant Professor of Clinical Medicine, Division of Pulmonary, Critical Care, Sleep and Allergy, Department of Medicine, University of Illinois at Chicago. Dr. Cao is Clinical Associate Professor, Division of Sleep Medicine and Division of Neuromuscular Medicine, Department of Psychiatry and Department of Neurology, Stanford (Calif.) University.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused by the novel coronavirus of the year 2019 (COVID-19) has had a major impact on global health and economy. United States reported a total caseload of 28,998,834 patients and total mortality of 525,031 as of March 2021 (NPR.org; worldometer. Accessed March 8, 2021). The beginning of 2021 ushered positivity with the development of multiple highly effective SARS-CoV-2 vaccines. Although the medical world has gained much knowledge about this deadly disease, there are many unknowns and still much to be learned.
Two early landmark studies from Italy (Lombardy) and United States (New York City area) provided initial insight on comorbid conditions associated with increased risk of severe COVID-19 infection (Richardson S, et al. JAMA. 2020;323[20]:2052; Grasselli G, et al. JAMA Intern Med. 2020;180[10]:1345). In the United States cohort, hypertension (HTN), obesity, and diabetes (DM) were independent risk factors for severe disease, while in the Italy cohort, older age, male, COPD, hypercholesterolemia, and diabetes were independent risk factors for increased mortality. Obstructive sleep apnea (OSA) was not mentioned as a comorbid risk factor.
There is much speculation regarding OSA as an independent risk factor for severe COVID-19 infection. OSA is a common sleep-related breathing disorder with increased prevalence in men, older age, and higher body mass index (BMI); and OSA is associated with hypertension, obesity, and diabetes, all of which are risk factors for severe COVID-19. Because of the shared similarities in pathophysiology between OSA and COVID-19 (Tufik S, et al. J Clin Sleep Med. 2020;16[8]:1425), and shared comorbid conditions associated with increased risk of severe COVID-19 disease, OSA has been suggested as an independent risk factor for unfavorable COVID-19-related outcomes.
SARS-CoV-2 triggers a severe inflammatory response involving type-II pneumocytes and angiotensin-converting enzyme 2 pathway. OSA is characterized by intermittent hypoxia and sleep fragmentation, leading to a cascade of systemic inflammatory response involving oxidative stress, pro-inflammatory cytokines, endothelial dysfunction, and consequent cardiovascular injury (Jose RJ, et al. Lancet Respir Med. 2020;8[6]:e46; Saxena K, et al. Sleep Medicine. 2021;79:223). In this regard, OSA may contribute to COVID-19 “cytokine storm” by causing or exacerbating endothelial dysfunction, inflammation, and oxidative stress.
Multiple studies have recently been published on the impact of OSA on COVID-19 outcomes. The Coronavirus SARS-CoV-2 and Diabetes Outcomes (CORONADO) study was one of the initial studies that analyzed the relationship between OSA and COVID-19-related outcomes. This was a multicenter observational study involving diabetic patients hospitalized with COVID-19. The primary outcome was mechanical ventilation and/or death within 7 days of admission. Multivariate adjustment showed that age, BMI, and OSA, among other factors, were independently associated with risk of death on day 7 (Cariou B, et al. Diabetologia. 2020;63[8]:1500). Strausz and colleagues also evaluated OSA as an independent risk factor for severe COVID-19 in a large registry of hospital discharge patients (FinnGen study). The authors reported that although the risk of contracting COVID-19 was the same for patients with or without OSA, after adjusting for age, sex, and BMI, OSA was associated with higher risk of hospitalization (Strausz S, et al. BMJ Open Resp Res. 2021;8:e000845). Similar findings were confirmed by the Maas et al. study, which utilized a large socioeconomically diverse database composed of 10 hospital systems. Diagnoses and outcomes were identified by ICD-10 coding and medical record data. After adjustments for diabetes, HTN, and BMI, OSA conferred an eight-fold risk for COVID-19 infection, was associated with increased risk of hospitalization, and doubled the risk of developing respiratory failure (Maas MB, et al. Sleep Breath. 2020 Sep; 29:1-3. doi: 10.1007/s11325-020-02203-0).
Peker and colleagues conducted a prospective multicenter observational study comparing clinical outcomes of severe COVID-19 infection in patients with low vs high pretest probability of having OSA based on the Berlin questionnaire. The authors reported a clinically significant risk of poorer clinical outcomes in the high pretest probability OSA group after adjustments for age, sex, and comorbidities (Peker Y, et al. Ann Am Thorac Soc. 2021. Feb 17. doi: 10.1513/AnnalsATS.202011-1409OC). A timely meta-analysis including 21 studies (19 with retrospective design) with 54,276 COVID-19 patients and 4,640 OSA patients concluded poor composite outcomes including severe COVID-19, intensive care unit admission, mechanical ventilatory support, and death in association with OSA (OR – 1.72 95% CI 1.55-1.91, P< .00001). In patients with obesity, OSA is a highly prevalent co-morbid condition. BMI, however, was not adjusted in this model (Hariyanto TI, et al. Sleep Med. 2021. doi: 10.1016/j.sleep.2021.03.029).
Other studies have concluded the opposite with OSA not being an independent risk factor for severe COVID-19 infection. Cade and colleagues conducted a retrospective analysis from a comprehensive electronic health dataset using ICD codes to identify OSA patients with severe COVID-19 infection. A significant association between OSA and COVID-19 death was noted after adjustment for demographics (ethnicity, age, sex). However, when fully adjusted for demographics, BMI, asthma, COPD, HTN, or DM, OSA was not an independent risk factor for COVID-19-related mortality and hospitalization (Cade BE, et al. Am J Respir Crit Care Med. 2020;202[10]:1462). The FinnGen study (Strausz et al.) was part of a meta-analysis examining the association between OSA and severe COVID-19 with and without adjustments for BMI. This meta-analysis consisted of 15,835 COVID-19 patients including 1,294 with OSA. The authors found that OSA was a risk factor with a two-fold increased risk of severe COVID-19 infection (OR = 2.37, P = .021). However, after adjustments were made for BMI, this finding lost statistical significance (OR=1.55, P=.13) (Strausz S, et al. BMJ Open Resp Res. 2021;8:e000845).
It is worth noting that a majority of studies identified OSA by indirect and imperfect methods through chart review, ICD codes, and databases. Confirmed OSA based on formal testing with a sleep study in COVID-19 patients remains a challenge. Perhaps well performed screening questionnaires, such as STOP-Bang, Berlin, or NoSAS, can be utilized as was the case in one study. It is also unclear if outcomes of COVID-19 infection differ in patients with treated or untreated OSA, as raised by the CORONADO study. A recent cross-sectional telephone interview survey of patients with confirmed OSA in Iran alluded to higher prevalence of COVID-19 in patients with severe OSA with suggestion of lower prevalence in patients who were currently receiving OSA treatment with positive airway pressure (PAP) therapy (Najafi A, et al. Sleep Health. 2021 Feb;7[1]:14). This is a crucial question as PAP therapy is considered an aerosol-generating procedure (Lance CG. Cleve Clin J Med. 2020 May 5. doi: 10.3949/ccjm.87a.ccc003). Studies have suggested continued use of PAP therapy with additional measures to mitigate the spread of virus, since failure to use PAP could be deleterious to the patient’s quality of life. Interestingly, PAP adherence seemed to have improved during the pandemic as evidenced by a telephonic survey done in New York City that showed 88% of patients with OSA used a PAP device consistently (Attias D, et al. Eur Respir J. 2020 Jul 30;56[1]:2001607. doi: 10.1183/13993003.01607-2020).
In summary, the jury is still out on whether OSA is a facilitator for viral replication, or an independent risk factor for poor prognosis related to COVID-19 infection, or has no clinical relevance to COVID-19. COVID-19 and OSA share comorbidities and pathways leading to a systemic inflammatory cascade. Theoretically, it would make sense that OSA is a risk factor for severe COVID-19 infection; however, it remains to be proven. The recent studies are limited by retrospective and observational nature, imprecise OSA classification/diagnostic criteria, and confounded by difficult to control variables. Further research is needed to expand our understanding of OSA -induced intermittent hypoxemia, inflammation, and endothelial dysfunction that may play a role in COVID-19 morbidity and mortality. Until we have more clarity, close monitoring of OSA patients infected with COVID-19 is recommended along with implementation of safe protocols for continuation of PAP usage during the infectious phase. Identifying underlying comorbid conditions that contribute to worsening of a COVID-19 infectious course is a crucial step in improving clinical outcomes.
Dr. Sahni is Assistant Professor of Clinical Medicine, Division of Pulmonary, Critical Care, Sleep and Allergy, Department of Medicine, University of Illinois at Chicago. Dr. Cao is Clinical Associate Professor, Division of Sleep Medicine and Division of Neuromuscular Medicine, Department of Psychiatry and Department of Neurology, Stanford (Calif.) University.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused by the novel coronavirus of the year 2019 (COVID-19) has had a major impact on global health and economy. United States reported a total caseload of 28,998,834 patients and total mortality of 525,031 as of March 2021 (NPR.org; worldometer. Accessed March 8, 2021). The beginning of 2021 ushered positivity with the development of multiple highly effective SARS-CoV-2 vaccines. Although the medical world has gained much knowledge about this deadly disease, there are many unknowns and still much to be learned.
Two early landmark studies from Italy (Lombardy) and United States (New York City area) provided initial insight on comorbid conditions associated with increased risk of severe COVID-19 infection (Richardson S, et al. JAMA. 2020;323[20]:2052; Grasselli G, et al. JAMA Intern Med. 2020;180[10]:1345). In the United States cohort, hypertension (HTN), obesity, and diabetes (DM) were independent risk factors for severe disease, while in the Italy cohort, older age, male, COPD, hypercholesterolemia, and diabetes were independent risk factors for increased mortality. Obstructive sleep apnea (OSA) was not mentioned as a comorbid risk factor.
There is much speculation regarding OSA as an independent risk factor for severe COVID-19 infection. OSA is a common sleep-related breathing disorder with increased prevalence in men, older age, and higher body mass index (BMI); and OSA is associated with hypertension, obesity, and diabetes, all of which are risk factors for severe COVID-19. Because of the shared similarities in pathophysiology between OSA and COVID-19 (Tufik S, et al. J Clin Sleep Med. 2020;16[8]:1425), and shared comorbid conditions associated with increased risk of severe COVID-19 disease, OSA has been suggested as an independent risk factor for unfavorable COVID-19-related outcomes.
SARS-CoV-2 triggers a severe inflammatory response involving type-II pneumocytes and angiotensin-converting enzyme 2 pathway. OSA is characterized by intermittent hypoxia and sleep fragmentation, leading to a cascade of systemic inflammatory response involving oxidative stress, pro-inflammatory cytokines, endothelial dysfunction, and consequent cardiovascular injury (Jose RJ, et al. Lancet Respir Med. 2020;8[6]:e46; Saxena K, et al. Sleep Medicine. 2021;79:223). In this regard, OSA may contribute to COVID-19 “cytokine storm” by causing or exacerbating endothelial dysfunction, inflammation, and oxidative stress.
Multiple studies have recently been published on the impact of OSA on COVID-19 outcomes. The Coronavirus SARS-CoV-2 and Diabetes Outcomes (CORONADO) study was one of the initial studies that analyzed the relationship between OSA and COVID-19-related outcomes. This was a multicenter observational study involving diabetic patients hospitalized with COVID-19. The primary outcome was mechanical ventilation and/or death within 7 days of admission. Multivariate adjustment showed that age, BMI, and OSA, among other factors, were independently associated with risk of death on day 7 (Cariou B, et al. Diabetologia. 2020;63[8]:1500). Strausz and colleagues also evaluated OSA as an independent risk factor for severe COVID-19 in a large registry of hospital discharge patients (FinnGen study). The authors reported that although the risk of contracting COVID-19 was the same for patients with or without OSA, after adjusting for age, sex, and BMI, OSA was associated with higher risk of hospitalization (Strausz S, et al. BMJ Open Resp Res. 2021;8:e000845). Similar findings were confirmed by the Maas et al. study, which utilized a large socioeconomically diverse database composed of 10 hospital systems. Diagnoses and outcomes were identified by ICD-10 coding and medical record data. After adjustments for diabetes, HTN, and BMI, OSA conferred an eight-fold risk for COVID-19 infection, was associated with increased risk of hospitalization, and doubled the risk of developing respiratory failure (Maas MB, et al. Sleep Breath. 2020 Sep; 29:1-3. doi: 10.1007/s11325-020-02203-0).
Peker and colleagues conducted a prospective multicenter observational study comparing clinical outcomes of severe COVID-19 infection in patients with low vs high pretest probability of having OSA based on the Berlin questionnaire. The authors reported a clinically significant risk of poorer clinical outcomes in the high pretest probability OSA group after adjustments for age, sex, and comorbidities (Peker Y, et al. Ann Am Thorac Soc. 2021. Feb 17. doi: 10.1513/AnnalsATS.202011-1409OC). A timely meta-analysis including 21 studies (19 with retrospective design) with 54,276 COVID-19 patients and 4,640 OSA patients concluded poor composite outcomes including severe COVID-19, intensive care unit admission, mechanical ventilatory support, and death in association with OSA (OR – 1.72 95% CI 1.55-1.91, P< .00001). In patients with obesity, OSA is a highly prevalent co-morbid condition. BMI, however, was not adjusted in this model (Hariyanto TI, et al. Sleep Med. 2021. doi: 10.1016/j.sleep.2021.03.029).
Other studies have concluded the opposite with OSA not being an independent risk factor for severe COVID-19 infection. Cade and colleagues conducted a retrospective analysis from a comprehensive electronic health dataset using ICD codes to identify OSA patients with severe COVID-19 infection. A significant association between OSA and COVID-19 death was noted after adjustment for demographics (ethnicity, age, sex). However, when fully adjusted for demographics, BMI, asthma, COPD, HTN, or DM, OSA was not an independent risk factor for COVID-19-related mortality and hospitalization (Cade BE, et al. Am J Respir Crit Care Med. 2020;202[10]:1462). The FinnGen study (Strausz et al.) was part of a meta-analysis examining the association between OSA and severe COVID-19 with and without adjustments for BMI. This meta-analysis consisted of 15,835 COVID-19 patients including 1,294 with OSA. The authors found that OSA was a risk factor with a two-fold increased risk of severe COVID-19 infection (OR = 2.37, P = .021). However, after adjustments were made for BMI, this finding lost statistical significance (OR=1.55, P=.13) (Strausz S, et al. BMJ Open Resp Res. 2021;8:e000845).
It is worth noting that a majority of studies identified OSA by indirect and imperfect methods through chart review, ICD codes, and databases. Confirmed OSA based on formal testing with a sleep study in COVID-19 patients remains a challenge. Perhaps well performed screening questionnaires, such as STOP-Bang, Berlin, or NoSAS, can be utilized as was the case in one study. It is also unclear if outcomes of COVID-19 infection differ in patients with treated or untreated OSA, as raised by the CORONADO study. A recent cross-sectional telephone interview survey of patients with confirmed OSA in Iran alluded to higher prevalence of COVID-19 in patients with severe OSA with suggestion of lower prevalence in patients who were currently receiving OSA treatment with positive airway pressure (PAP) therapy (Najafi A, et al. Sleep Health. 2021 Feb;7[1]:14). This is a crucial question as PAP therapy is considered an aerosol-generating procedure (Lance CG. Cleve Clin J Med. 2020 May 5. doi: 10.3949/ccjm.87a.ccc003). Studies have suggested continued use of PAP therapy with additional measures to mitigate the spread of virus, since failure to use PAP could be deleterious to the patient’s quality of life. Interestingly, PAP adherence seemed to have improved during the pandemic as evidenced by a telephonic survey done in New York City that showed 88% of patients with OSA used a PAP device consistently (Attias D, et al. Eur Respir J. 2020 Jul 30;56[1]:2001607. doi: 10.1183/13993003.01607-2020).
In summary, the jury is still out on whether OSA is a facilitator for viral replication, or an independent risk factor for poor prognosis related to COVID-19 infection, or has no clinical relevance to COVID-19. COVID-19 and OSA share comorbidities and pathways leading to a systemic inflammatory cascade. Theoretically, it would make sense that OSA is a risk factor for severe COVID-19 infection; however, it remains to be proven. The recent studies are limited by retrospective and observational nature, imprecise OSA classification/diagnostic criteria, and confounded by difficult to control variables. Further research is needed to expand our understanding of OSA -induced intermittent hypoxemia, inflammation, and endothelial dysfunction that may play a role in COVID-19 morbidity and mortality. Until we have more clarity, close monitoring of OSA patients infected with COVID-19 is recommended along with implementation of safe protocols for continuation of PAP usage during the infectious phase. Identifying underlying comorbid conditions that contribute to worsening of a COVID-19 infectious course is a crucial step in improving clinical outcomes.
Dr. Sahni is Assistant Professor of Clinical Medicine, Division of Pulmonary, Critical Care, Sleep and Allergy, Department of Medicine, University of Illinois at Chicago. Dr. Cao is Clinical Associate Professor, Division of Sleep Medicine and Division of Neuromuscular Medicine, Department of Psychiatry and Department of Neurology, Stanford (Calif.) University.