Sleep Medicine

Recent research suggests that some pediatric patients who develop neuropsychiatric symptoms from COVID-19 may have intrathecal antineural SARS-CoV-2 autoantibodies, which may hint at central nervous system (CNS) autoimmunity in these patients.

“Overall, these findings indicate that severe neuropsychiatric symptoms can occur in the setting of pediatric COVID-19, including patients who lack many of the cardinal systemic features,” Christopher M. Bartley, MD, PhD, of the Weill Institute for Neurosciences at the University of California, San Francisco, and colleagues wrote in their study. “These data highlight the possibility of SARS-CoV-2 neuroinvasion and/or CNS autoimmunity in pediatric patients with COVID-19 and neuropsychiatric symptoms.”

In a case series published Oct. 25 in JAMA Neurology (doi: 10.1001/jamaneurol.2021.3821), Dr. Bartley and colleagues examined three pediatric patients who were infected with SARS-CoV-2 and, over a period of 5 months in 2020, were admitted to the hospital – where they received a neurology consultation for “subacute, functionally impairing behavioral changes.”

Patient 1 had a history of unspecified anxiety and depression, and was admitted for erratic behavior, paranoia-like fears, social withdrawal, and insomnia. The patient did not respond to treatment with risperidone and gabapentin, and was readmitted soon after discharge, then treated with olanzapine followed by a transition to valproate and lorazepam. It was found the patient had cerebrospinal fluid (CSF) abnormalities in the form of elevated protein levels, and an elevated IgG index, and was given intravenous immunoglobulin followed by IV methylprednisolone. While symptoms such as paranoia improved and the patient was able to better organize thoughts after 5 days, other symptoms such as delusions and hyperreflexia persisted for at least 1 month before resolving, and some symptoms, such as lability, did not resolve before discharge.

Patient 2 had a history of motor tics and anxiety, but showed signs of insomnia, mood lability, impaired concentration, difficulty finding words, and problems completing homework following a SARS-CoV-2 infection. The patient’s father previously had been diagnosed with COVID-19 and the patient developed respiratory symptoms and fever; an IgG serology test later confirmed a SARS-CoV-2 infection. The patient went on to experience internal preoccupation, aggression, and suicidal ideation. The patients was treated with aripiprazole and risperidone, but did not respond, and was admitted to the hospital. As with patient 1, patient 2 had CSF abnormalities in the form of elevated protein levels, and responded to IV methylprednisolone, with working memory and bradyphrenia improving. However, the patient developed insomnia, extreme anxiety, suicidal ideation, aggression, and sadness after discharge, and was readmitted. The patient was treated with IV immunoglobulin, and discharged with quetiapine and lithium.

“Six months later, although improved from initial presentation, the patient required academic accommodations and continued to endorse forgetfulness and attention difficulties. The patient’s chronic tics and anxiety were unchanged,” Dr. Bartley and colleagues wrote.

Patient 3 had no psychiatric history but started to demonstrate “odd behavior, including repetitive behaviors, anorexia, and insomnia” following a SARS-CoV-2 infection. After being hospitalized, the patient showed signs of “ideomotor apraxia, abulia, disorganized behavior, agitation, and diffusely brisk reflexes” and had a high white blood cell count, creatine kinase level, and C-reactive protein level. CSF was also abnormal for this patient, with three unique oligoclonal bands identified. The patient was treated with lorazepam and olanzapine, did not receive immunotherapy, and was discharged without psychiatric medications after 4 days.

When the researchers performed testing on each of the three patients, they found intrathecal anti–SARS-CoV-2 IgG and immunostained mouse brain tissue, and “a diverse set of candidate autoantigens by human phage immunoprecipitation sequencing” in patient 1 and patient 2. In comparison, patient 3 “neither appreciably immunostained nor enriched candidates by human phage immunoprecipitation sequencing,” the researchers said.

“These data motivate a systematic study of humoral immunity in the CSF of pediatric patients with COVID-19 and neuropsychiatric involvement and the potential for immunotherapy in some,” Dr. Bartley and colleagues concluded.
 

Potential of CNS autoimmunity

Evan J. Kyzar, MD, PhD, a resident physician in psychiatry at New York State Psychiatric Institute in New York Presbyterian–Columbia Campus, said in an interview that the results of the case series show some pediatric patients with neuropsychiatric symptoms can have anti-SARS-CoV-2 antibodies after viral clearance.

“Interestingly, some of the patients in this study also had antibodies in the CSF that targeted native proteins, demonstrating that COVID-19 may lead to autoimmunity directed at the brain,” he said. “This study increases our knowledge of how COVID-19 interacts with the nervous system and how autoimmune mechanisms might be contributing to at least a portion of patients with neuropsychiatric symptoms during acute infection, and possibly even after viral clearance.”

Dr. Kyzar noted that the immunological methods in the study were “cutting-edge” and the validation exploring the immune responses was detailed, but was limited because of the small sample size.

“[T]he researchers are using similar techniques to explore psychiatric disorders such as depression and schizophrenia to determine if some patients diagnosed with these conditions may have CNS-targeting autoantibodies that contribute to their symptoms and clinical presentation,” Dr. Kyzar said. “This work has the potential to discover novel neuroimmune mechanisms contributing to neuropsychiatric disease and offer possible pathways for the discovery of new treatments.”

The authors reported financial relationships with Allen & Company, the Chan Zuckerberg Initiative, National Institutes of Health, Novartis, Public Health Company, Roche/Genentech, Sandler Foundation, and Takeda in the form of grants and personal fees. They reported funding and/or support from the Brain Research Foundation, Hanna H. Gray Fellowship, Howard Hughes Medical Institute, John A. Watson Scholar Program, Latinx Center of Excellence, the National Institute of Mental Health, the National Institute of Neurological Disorders and Stroke, President’s Postdoctoral Fellowship Program, and Shared Instrumentation grant. Dr. Kyzar reported no relevant financial disclosures.

Recent research suggests that some pediatric patients who develop neuropsychiatric symptoms from COVID-19 may have intrathecal antineural SARS-CoV-2 autoantibodies, which may hint at central nervous system (CNS) autoimmunity in these patients.

“Overall, these findings indicate that severe neuropsychiatric symptoms can occur in the setting of pediatric COVID-19, including patients who lack many of the cardinal systemic features,” Christopher M. Bartley, MD, PhD, of the Weill Institute for Neurosciences at the University of California, San Francisco, and colleagues wrote in their study. “These data highlight the possibility of SARS-CoV-2 neuroinvasion and/or CNS autoimmunity in pediatric patients with COVID-19 and neuropsychiatric symptoms.”

In a case series published Oct. 25 in JAMA Neurology (doi: 10.1001/jamaneurol.2021.3821), Dr. Bartley and colleagues examined three pediatric patients who were infected with SARS-CoV-2 and, over a period of 5 months in 2020, were admitted to the hospital – where they received a neurology consultation for “subacute, functionally impairing behavioral changes.”

Patient 1 had a history of unspecified anxiety and depression, and was admitted for erratic behavior, paranoia-like fears, social withdrawal, and insomnia. The patient did not respond to treatment with risperidone and gabapentin, and was readmitted soon after discharge, then treated with olanzapine followed by a transition to valproate and lorazepam. It was found the patient had cerebrospinal fluid (CSF) abnormalities in the form of elevated protein levels, and an elevated IgG index, and was given intravenous immunoglobulin followed by IV methylprednisolone. While symptoms such as paranoia improved and the patient was able to better organize thoughts after 5 days, other symptoms such as delusions and hyperreflexia persisted for at least 1 month before resolving, and some symptoms, such as lability, did not resolve before discharge.

Patient 2 had a history of motor tics and anxiety, but showed signs of insomnia, mood lability, impaired concentration, difficulty finding words, and problems completing homework following a SARS-CoV-2 infection. The patient’s father previously had been diagnosed with COVID-19 and the patient developed respiratory symptoms and fever; an IgG serology test later confirmed a SARS-CoV-2 infection. The patient went on to experience internal preoccupation, aggression, and suicidal ideation. The patients was treated with aripiprazole and risperidone, but did not respond, and was admitted to the hospital. As with patient 1, patient 2 had CSF abnormalities in the form of elevated protein levels, and responded to IV methylprednisolone, with working memory and bradyphrenia improving. However, the patient developed insomnia, extreme anxiety, suicidal ideation, aggression, and sadness after discharge, and was readmitted. The patient was treated with IV immunoglobulin, and discharged with quetiapine and lithium.

“Six months later, although improved from initial presentation, the patient required academic accommodations and continued to endorse forgetfulness and attention difficulties. The patient’s chronic tics and anxiety were unchanged,” Dr. Bartley and colleagues wrote.

Patient 3 had no psychiatric history but started to demonstrate “odd behavior, including repetitive behaviors, anorexia, and insomnia” following a SARS-CoV-2 infection. After being hospitalized, the patient showed signs of “ideomotor apraxia, abulia, disorganized behavior, agitation, and diffusely brisk reflexes” and had a high white blood cell count, creatine kinase level, and C-reactive protein level. CSF was also abnormal for this patient, with three unique oligoclonal bands identified. The patient was treated with lorazepam and olanzapine, did not receive immunotherapy, and was discharged without psychiatric medications after 4 days.

When the researchers performed testing on each of the three patients, they found intrathecal anti–SARS-CoV-2 IgG and immunostained mouse brain tissue, and “a diverse set of candidate autoantigens by human phage immunoprecipitation sequencing” in patient 1 and patient 2. In comparison, patient 3 “neither appreciably immunostained nor enriched candidates by human phage immunoprecipitation sequencing,” the researchers said.

“These data motivate a systematic study of humoral immunity in the CSF of pediatric patients with COVID-19 and neuropsychiatric involvement and the potential for immunotherapy in some,” Dr. Bartley and colleagues concluded.
 

Potential of CNS autoimmunity

Evan J. Kyzar, MD, PhD, a resident physician in psychiatry at New York State Psychiatric Institute in New York Presbyterian–Columbia Campus, said in an interview that the results of the case series show some pediatric patients with neuropsychiatric symptoms can have anti-SARS-CoV-2 antibodies after viral clearance.

“Interestingly, some of the patients in this study also had antibodies in the CSF that targeted native proteins, demonstrating that COVID-19 may lead to autoimmunity directed at the brain,” he said. “This study increases our knowledge of how COVID-19 interacts with the nervous system and how autoimmune mechanisms might be contributing to at least a portion of patients with neuropsychiatric symptoms during acute infection, and possibly even after viral clearance.”

Dr. Kyzar noted that the immunological methods in the study were “cutting-edge” and the validation exploring the immune responses was detailed, but was limited because of the small sample size.

“[T]he researchers are using similar techniques to explore psychiatric disorders such as depression and schizophrenia to determine if some patients diagnosed with these conditions may have CNS-targeting autoantibodies that contribute to their symptoms and clinical presentation,” Dr. Kyzar said. “This work has the potential to discover novel neuroimmune mechanisms contributing to neuropsychiatric disease and offer possible pathways for the discovery of new treatments.”

The authors reported financial relationships with Allen & Company, the Chan Zuckerberg Initiative, National Institutes of Health, Novartis, Public Health Company, Roche/Genentech, Sandler Foundation, and Takeda in the form of grants and personal fees. They reported funding and/or support from the Brain Research Foundation, Hanna H. Gray Fellowship, Howard Hughes Medical Institute, John A. Watson Scholar Program, Latinx Center of Excellence, the National Institute of Mental Health, the National Institute of Neurological Disorders and Stroke, President’s Postdoctoral Fellowship Program, and Shared Instrumentation grant. Dr. Kyzar reported no relevant financial disclosures.

Recent research suggests that some pediatric patients who develop neuropsychiatric symptoms from COVID-19 may have intrathecal antineural SARS-CoV-2 autoantibodies, which may hint at central nervous system (CNS) autoimmunity in these patients.

“Overall, these findings indicate that severe neuropsychiatric symptoms can occur in the setting of pediatric COVID-19, including patients who lack many of the cardinal systemic features,” Christopher M. Bartley, MD, PhD, of the Weill Institute for Neurosciences at the University of California, San Francisco, and colleagues wrote in their study. “These data highlight the possibility of SARS-CoV-2 neuroinvasion and/or CNS autoimmunity in pediatric patients with COVID-19 and neuropsychiatric symptoms.”

In a case series published Oct. 25 in JAMA Neurology (doi: 10.1001/jamaneurol.2021.3821), Dr. Bartley and colleagues examined three pediatric patients who were infected with SARS-CoV-2 and, over a period of 5 months in 2020, were admitted to the hospital – where they received a neurology consultation for “subacute, functionally impairing behavioral changes.”

Patient 1 had a history of unspecified anxiety and depression, and was admitted for erratic behavior, paranoia-like fears, social withdrawal, and insomnia. The patient did not respond to treatment with risperidone and gabapentin, and was readmitted soon after discharge, then treated with olanzapine followed by a transition to valproate and lorazepam. It was found the patient had cerebrospinal fluid (CSF) abnormalities in the form of elevated protein levels, and an elevated IgG index, and was given intravenous immunoglobulin followed by IV methylprednisolone. While symptoms such as paranoia improved and the patient was able to better organize thoughts after 5 days, other symptoms such as delusions and hyperreflexia persisted for at least 1 month before resolving, and some symptoms, such as lability, did not resolve before discharge.

Patient 2 had a history of motor tics and anxiety, but showed signs of insomnia, mood lability, impaired concentration, difficulty finding words, and problems completing homework following a SARS-CoV-2 infection. The patient’s father previously had been diagnosed with COVID-19 and the patient developed respiratory symptoms and fever; an IgG serology test later confirmed a SARS-CoV-2 infection. The patient went on to experience internal preoccupation, aggression, and suicidal ideation. The patients was treated with aripiprazole and risperidone, but did not respond, and was admitted to the hospital. As with patient 1, patient 2 had CSF abnormalities in the form of elevated protein levels, and responded to IV methylprednisolone, with working memory and bradyphrenia improving. However, the patient developed insomnia, extreme anxiety, suicidal ideation, aggression, and sadness after discharge, and was readmitted. The patient was treated with IV immunoglobulin, and discharged with quetiapine and lithium.

“Six months later, although improved from initial presentation, the patient required academic accommodations and continued to endorse forgetfulness and attention difficulties. The patient’s chronic tics and anxiety were unchanged,” Dr. Bartley and colleagues wrote.

Patient 3 had no psychiatric history but started to demonstrate “odd behavior, including repetitive behaviors, anorexia, and insomnia” following a SARS-CoV-2 infection. After being hospitalized, the patient showed signs of “ideomotor apraxia, abulia, disorganized behavior, agitation, and diffusely brisk reflexes” and had a high white blood cell count, creatine kinase level, and C-reactive protein level. CSF was also abnormal for this patient, with three unique oligoclonal bands identified. The patient was treated with lorazepam and olanzapine, did not receive immunotherapy, and was discharged without psychiatric medications after 4 days.

When the researchers performed testing on each of the three patients, they found intrathecal anti–SARS-CoV-2 IgG and immunostained mouse brain tissue, and “a diverse set of candidate autoantigens by human phage immunoprecipitation sequencing” in patient 1 and patient 2. In comparison, patient 3 “neither appreciably immunostained nor enriched candidates by human phage immunoprecipitation sequencing,” the researchers said.

“These data motivate a systematic study of humoral immunity in the CSF of pediatric patients with COVID-19 and neuropsychiatric involvement and the potential for immunotherapy in some,” Dr. Bartley and colleagues concluded.
 

Potential of CNS autoimmunity

Evan J. Kyzar, MD, PhD, a resident physician in psychiatry at New York State Psychiatric Institute in New York Presbyterian–Columbia Campus, said in an interview that the results of the case series show some pediatric patients with neuropsychiatric symptoms can have anti-SARS-CoV-2 antibodies after viral clearance.

“Interestingly, some of the patients in this study also had antibodies in the CSF that targeted native proteins, demonstrating that COVID-19 may lead to autoimmunity directed at the brain,” he said. “This study increases our knowledge of how COVID-19 interacts with the nervous system and how autoimmune mechanisms might be contributing to at least a portion of patients with neuropsychiatric symptoms during acute infection, and possibly even after viral clearance.”

Dr. Kyzar noted that the immunological methods in the study were “cutting-edge” and the validation exploring the immune responses was detailed, but was limited because of the small sample size.

“[T]he researchers are using similar techniques to explore psychiatric disorders such as depression and schizophrenia to determine if some patients diagnosed with these conditions may have CNS-targeting autoantibodies that contribute to their symptoms and clinical presentation,” Dr. Kyzar said. “This work has the potential to discover novel neuroimmune mechanisms contributing to neuropsychiatric disease and offer possible pathways for the discovery of new treatments.”

The authors reported financial relationships with Allen & Company, the Chan Zuckerberg Initiative, National Institutes of Health, Novartis, Public Health Company, Roche/Genentech, Sandler Foundation, and Takeda in the form of grants and personal fees. They reported funding and/or support from the Brain Research Foundation, Hanna H. Gray Fellowship, Howard Hughes Medical Institute, John A. Watson Scholar Program, Latinx Center of Excellence, the National Institute of Mental Health, the National Institute of Neurological Disorders and Stroke, President’s Postdoctoral Fellowship Program, and Shared Instrumentation grant. Dr. Kyzar reported no relevant financial disclosures.

The greatest autopsy on Earth?

The LOTME staff would like to apologize in advance. The following item contains historical facts.

P.T. Barnum is a rather controversial figure in American history. The greatest show on Earth was certainly popular in its day. However, Barnum got his start in 1835 by leasing a slave named Joyce Heth, an elderly Black woman who told vivid stories of caring for a young George Washington. He toured her around the country, advertising her as a 160-year-old woman who served as George Washington’s nanny. When Ms. Heth died the next year, Barnum sold tickets to the autopsy, charging the equivalent of $30 in today’s money.

fstop123/E+

When a doctor announced that Ms. Heth was actually 75-80 when she died, it caused great controversy in the press and ruined Barnum’s career. Wait, no, that’s not right. The opposite, actually. He weathered the storm, built his famous circus, and never again committed a hoax.

It’s difficult to quantify how wrong publicly dissecting a person and charging people to see said dissection is, but that was almost 200 years ago. At the very least, we can say that such terrible behavior is firmly in the distant past.

Oh wait.

David Saunders, a 98-year-old veteran of World War II and the Korean War, donated his body to science. His body, however, was purchased by DeathScience.org from a medical lab – with the buyer supposedly misleading the medical lab about its intentions, which was for use at the traveling Oddities and Curiosities Expo. Tickets went for up to $500 each to witness the public autopsy of Mr. Saunders’ body, which took place at a Marriott in Portland, Ore. It promised to be an exciting, all-day event from 9 a.m. to 4 p.m., with a break for lunch, of course. You can’t have an autopsy without a catered lunch.

Another public autopsy event was scheduled in Seattle but canceled after news of the first event broke. Oh, and for that extra little kick, Mr. Saunders died from COVID-19, meaning that all those paying customers were exposed.

P.T. Barnum is probably rolling over in his grave right now. His autopsy tickets were a bargain.
 

Go ahead, have that soda before math

We should all know by now that sugary drinks are bad, even artificially sweetened ones. It might not always stop us from drinking them, but we know the deal. But what if sugary drinks like soda could be helpful for girls in school?

©sjlocke/istock.com

You read that right. We said girls. A soda before class might have boys bouncing off the walls, but not girls. A recent study showed that not only was girls’ behavior unaffected by having a sugary drink, their math skills even improved.

Researchers analyzed the behavior of 4- to 6-year-old children before and after having a sugary drink. The sugar rush was actually calming for girls and helped them perform better with numerical skills, but the opposite was true for boys. “Our study is the first to provide large-scale experimental evidence on the impact of sugary drinks on preschool children. The results clearly indicate a causal impact of sugary drinks on children’s behavior and test scores,” Fritz Schiltz, PhD, said in a written statement.

This probably isn’t the green light to have as many sugary drinks as you want, but it might be interesting to see how your work is affected after a soda.
 

Chicken nuggets and the meat paradox

Two young children are fighting over the last chicken nugget when an adult comes in to see what’s going on.

Liam: Vegetable!

Olivia: Meat!

Liam: Chicken nuggets are vegetables!

Olivia: No, dorkface! They’re meat.

Caregiver: Good news, kids. You’re both right.

Olivia: How can we both be right?

At this point, a woman enters the room. She’s wearing a white lab coat, so she must be a scientist.

Dr. Scientist: You can’t both be right, Olivia. You are being fed a serving of the meat paradox. That’s why Liam here doesn’t know that chicken nuggets are made of chicken, which is a form of meat. Sadly, he’s not the only one.

pxfuel

In a recent study, scientists from Furman University in Greenville, S.C., found that 38% of 176 children aged 4-7 years thought that chicken nuggets were vegetables and more than 46% identified French fries as animal based.

Olivia: Did our caregiver lie to us, Dr. Scientist?

Dr. Scientist: Yes, Olivia. The researchers I mentioned explained that “many people experience unease while eating meat. Omnivores eat foods that entail animal suffering and death while at the same time endorsing the compassionate treatment of animals.” That’s the meat paradox.

Liam: What else did they say, Dr. Scientist?

Dr. Scientist: Over 70% of those children said that cows and pigs were not edible and 5% thought that cats and horses were. The investigators wrote “that children and youth should be viewed as agents of environmental change” in the future, but suggested that parents need to bring honesty to the table.

Caregiver: How did you get in here anyway? And how do you know their names?

Dr. Scientist: I’ve been rooting through your garbage for years. All in the name of science, of course.

Bedtimes aren’t just for children

There are multiple ways to prevent heart disease, but what if it could be as easy as switching your bedtime? A recent study in European Heart Journal–Digital Health suggests that there’s a sweet spot when it comes to sleep timing.

Tumisu/Pixabay

Through smartwatch-like devices, researchers measured the sleep-onset and wake-up times for 7 days in 88,026 participants aged 43-79 years. After 5.7 years of follow-up to see if anyone had a heart attack, stroke, or any other cardiovascular event, 3.6% developed some kind of cardiovascular disease.

Those who went to bed between 10 p.m. and 11 p.m. had a lower risk of developing heart disease. The risk was 25% higher for subjects who went to bed at midnight or later, 24% higher for bedtimes before 10 p.m., and 12% higher for bedtimes between 11 p.m. and midnight.

So, why can you go to bed before “The Tonight Show” and lower your cardiovascular risk but not before the nightly news? Well, it has something to do with your body’s natural clock.

“The optimum time to go to sleep is at a specific point in the body’s 24-hour cycle and deviations may be detrimental to health. The riskiest time was after midnight, potentially because it may reduce the likelihood of seeing morning light, which resets the body clock,” said study author Dr. David Plans of the University of Exeter, England.

Although a sleep schedule is preferred, it isn’t realistic all the time for those in certain occupations who might have to resort to other methods to keep their circadian clocks ticking optimally for their health. But if all it takes is prescribing a sleep time to reduce heart disease on a massive scale it would make a great “low-cost public health target.”

So bedtimes aren’t just for children.

The greatest autopsy on Earth?

The LOTME staff would like to apologize in advance. The following item contains historical facts.

P.T. Barnum is a rather controversial figure in American history. The greatest show on Earth was certainly popular in its day. However, Barnum got his start in 1835 by leasing a slave named Joyce Heth, an elderly Black woman who told vivid stories of caring for a young George Washington. He toured her around the country, advertising her as a 160-year-old woman who served as George Washington’s nanny. When Ms. Heth died the next year, Barnum sold tickets to the autopsy, charging the equivalent of $30 in today’s money.

fstop123/E+

When a doctor announced that Ms. Heth was actually 75-80 when she died, it caused great controversy in the press and ruined Barnum’s career. Wait, no, that’s not right. The opposite, actually. He weathered the storm, built his famous circus, and never again committed a hoax.

It’s difficult to quantify how wrong publicly dissecting a person and charging people to see said dissection is, but that was almost 200 years ago. At the very least, we can say that such terrible behavior is firmly in the distant past.

Oh wait.

David Saunders, a 98-year-old veteran of World War II and the Korean War, donated his body to science. His body, however, was purchased by DeathScience.org from a medical lab – with the buyer supposedly misleading the medical lab about its intentions, which was for use at the traveling Oddities and Curiosities Expo. Tickets went for up to $500 each to witness the public autopsy of Mr. Saunders’ body, which took place at a Marriott in Portland, Ore. It promised to be an exciting, all-day event from 9 a.m. to 4 p.m., with a break for lunch, of course. You can’t have an autopsy without a catered lunch.

Another public autopsy event was scheduled in Seattle but canceled after news of the first event broke. Oh, and for that extra little kick, Mr. Saunders died from COVID-19, meaning that all those paying customers were exposed.

P.T. Barnum is probably rolling over in his grave right now. His autopsy tickets were a bargain.
 

Go ahead, have that soda before math

We should all know by now that sugary drinks are bad, even artificially sweetened ones. It might not always stop us from drinking them, but we know the deal. But what if sugary drinks like soda could be helpful for girls in school?

©sjlocke/istock.com

You read that right. We said girls. A soda before class might have boys bouncing off the walls, but not girls. A recent study showed that not only was girls’ behavior unaffected by having a sugary drink, their math skills even improved.

Researchers analyzed the behavior of 4- to 6-year-old children before and after having a sugary drink. The sugar rush was actually calming for girls and helped them perform better with numerical skills, but the opposite was true for boys. “Our study is the first to provide large-scale experimental evidence on the impact of sugary drinks on preschool children. The results clearly indicate a causal impact of sugary drinks on children’s behavior and test scores,” Fritz Schiltz, PhD, said in a written statement.

This probably isn’t the green light to have as many sugary drinks as you want, but it might be interesting to see how your work is affected after a soda.
 

Chicken nuggets and the meat paradox

Two young children are fighting over the last chicken nugget when an adult comes in to see what’s going on.

Liam: Vegetable!

Olivia: Meat!

Liam: Chicken nuggets are vegetables!

Olivia: No, dorkface! They’re meat.

Caregiver: Good news, kids. You’re both right.

Olivia: How can we both be right?

At this point, a woman enters the room. She’s wearing a white lab coat, so she must be a scientist.

Dr. Scientist: You can’t both be right, Olivia. You are being fed a serving of the meat paradox. That’s why Liam here doesn’t know that chicken nuggets are made of chicken, which is a form of meat. Sadly, he’s not the only one.

pxfuel

In a recent study, scientists from Furman University in Greenville, S.C., found that 38% of 176 children aged 4-7 years thought that chicken nuggets were vegetables and more than 46% identified French fries as animal based.

Olivia: Did our caregiver lie to us, Dr. Scientist?

Dr. Scientist: Yes, Olivia. The researchers I mentioned explained that “many people experience unease while eating meat. Omnivores eat foods that entail animal suffering and death while at the same time endorsing the compassionate treatment of animals.” That’s the meat paradox.

Liam: What else did they say, Dr. Scientist?

Dr. Scientist: Over 70% of those children said that cows and pigs were not edible and 5% thought that cats and horses were. The investigators wrote “that children and youth should be viewed as agents of environmental change” in the future, but suggested that parents need to bring honesty to the table.

Caregiver: How did you get in here anyway? And how do you know their names?

Dr. Scientist: I’ve been rooting through your garbage for years. All in the name of science, of course.

Bedtimes aren’t just for children

There are multiple ways to prevent heart disease, but what if it could be as easy as switching your bedtime? A recent study in European Heart Journal–Digital Health suggests that there’s a sweet spot when it comes to sleep timing.

Tumisu/Pixabay

Through smartwatch-like devices, researchers measured the sleep-onset and wake-up times for 7 days in 88,026 participants aged 43-79 years. After 5.7 years of follow-up to see if anyone had a heart attack, stroke, or any other cardiovascular event, 3.6% developed some kind of cardiovascular disease.

Those who went to bed between 10 p.m. and 11 p.m. had a lower risk of developing heart disease. The risk was 25% higher for subjects who went to bed at midnight or later, 24% higher for bedtimes before 10 p.m., and 12% higher for bedtimes between 11 p.m. and midnight.

So, why can you go to bed before “The Tonight Show” and lower your cardiovascular risk but not before the nightly news? Well, it has something to do with your body’s natural clock.

“The optimum time to go to sleep is at a specific point in the body’s 24-hour cycle and deviations may be detrimental to health. The riskiest time was after midnight, potentially because it may reduce the likelihood of seeing morning light, which resets the body clock,” said study author Dr. David Plans of the University of Exeter, England.

Although a sleep schedule is preferred, it isn’t realistic all the time for those in certain occupations who might have to resort to other methods to keep their circadian clocks ticking optimally for their health. But if all it takes is prescribing a sleep time to reduce heart disease on a massive scale it would make a great “low-cost public health target.”

So bedtimes aren’t just for children.

The greatest autopsy on Earth?

The LOTME staff would like to apologize in advance. The following item contains historical facts.

P.T. Barnum is a rather controversial figure in American history. The greatest show on Earth was certainly popular in its day. However, Barnum got his start in 1835 by leasing a slave named Joyce Heth, an elderly Black woman who told vivid stories of caring for a young George Washington. He toured her around the country, advertising her as a 160-year-old woman who served as George Washington’s nanny. When Ms. Heth died the next year, Barnum sold tickets to the autopsy, charging the equivalent of $30 in today’s money.

fstop123/E+

When a doctor announced that Ms. Heth was actually 75-80 when she died, it caused great controversy in the press and ruined Barnum’s career. Wait, no, that’s not right. The opposite, actually. He weathered the storm, built his famous circus, and never again committed a hoax.

It’s difficult to quantify how wrong publicly dissecting a person and charging people to see said dissection is, but that was almost 200 years ago. At the very least, we can say that such terrible behavior is firmly in the distant past.

Oh wait.

David Saunders, a 98-year-old veteran of World War II and the Korean War, donated his body to science. His body, however, was purchased by DeathScience.org from a medical lab – with the buyer supposedly misleading the medical lab about its intentions, which was for use at the traveling Oddities and Curiosities Expo. Tickets went for up to $500 each to witness the public autopsy of Mr. Saunders’ body, which took place at a Marriott in Portland, Ore. It promised to be an exciting, all-day event from 9 a.m. to 4 p.m., with a break for lunch, of course. You can’t have an autopsy without a catered lunch.

Another public autopsy event was scheduled in Seattle but canceled after news of the first event broke. Oh, and for that extra little kick, Mr. Saunders died from COVID-19, meaning that all those paying customers were exposed.

P.T. Barnum is probably rolling over in his grave right now. His autopsy tickets were a bargain.
 

Go ahead, have that soda before math

We should all know by now that sugary drinks are bad, even artificially sweetened ones. It might not always stop us from drinking them, but we know the deal. But what if sugary drinks like soda could be helpful for girls in school?

©sjlocke/istock.com

You read that right. We said girls. A soda before class might have boys bouncing off the walls, but not girls. A recent study showed that not only was girls’ behavior unaffected by having a sugary drink, their math skills even improved.

Researchers analyzed the behavior of 4- to 6-year-old children before and after having a sugary drink. The sugar rush was actually calming for girls and helped them perform better with numerical skills, but the opposite was true for boys. “Our study is the first to provide large-scale experimental evidence on the impact of sugary drinks on preschool children. The results clearly indicate a causal impact of sugary drinks on children’s behavior and test scores,” Fritz Schiltz, PhD, said in a written statement.

This probably isn’t the green light to have as many sugary drinks as you want, but it might be interesting to see how your work is affected after a soda.
 

Chicken nuggets and the meat paradox

Two young children are fighting over the last chicken nugget when an adult comes in to see what’s going on.

Liam: Vegetable!

Olivia: Meat!

Liam: Chicken nuggets are vegetables!

Olivia: No, dorkface! They’re meat.

Caregiver: Good news, kids. You’re both right.

Olivia: How can we both be right?

At this point, a woman enters the room. She’s wearing a white lab coat, so she must be a scientist.

Dr. Scientist: You can’t both be right, Olivia. You are being fed a serving of the meat paradox. That’s why Liam here doesn’t know that chicken nuggets are made of chicken, which is a form of meat. Sadly, he’s not the only one.

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In a recent study, scientists from Furman University in Greenville, S.C., found that 38% of 176 children aged 4-7 years thought that chicken nuggets were vegetables and more than 46% identified French fries as animal based.

Olivia: Did our caregiver lie to us, Dr. Scientist?

Dr. Scientist: Yes, Olivia. The researchers I mentioned explained that “many people experience unease while eating meat. Omnivores eat foods that entail animal suffering and death while at the same time endorsing the compassionate treatment of animals.” That’s the meat paradox.

Liam: What else did they say, Dr. Scientist?

Dr. Scientist: Over 70% of those children said that cows and pigs were not edible and 5% thought that cats and horses were. The investigators wrote “that children and youth should be viewed as agents of environmental change” in the future, but suggested that parents need to bring honesty to the table.

Caregiver: How did you get in here anyway? And how do you know their names?

Dr. Scientist: I’ve been rooting through your garbage for years. All in the name of science, of course.

Bedtimes aren’t just for children

There are multiple ways to prevent heart disease, but what if it could be as easy as switching your bedtime? A recent study in European Heart Journal–Digital Health suggests that there’s a sweet spot when it comes to sleep timing.

Tumisu/Pixabay

Through smartwatch-like devices, researchers measured the sleep-onset and wake-up times for 7 days in 88,026 participants aged 43-79 years. After 5.7 years of follow-up to see if anyone had a heart attack, stroke, or any other cardiovascular event, 3.6% developed some kind of cardiovascular disease.

Those who went to bed between 10 p.m. and 11 p.m. had a lower risk of developing heart disease. The risk was 25% higher for subjects who went to bed at midnight or later, 24% higher for bedtimes before 10 p.m., and 12% higher for bedtimes between 11 p.m. and midnight.

So, why can you go to bed before “The Tonight Show” and lower your cardiovascular risk but not before the nightly news? Well, it has something to do with your body’s natural clock.

“The optimum time to go to sleep is at a specific point in the body’s 24-hour cycle and deviations may be detrimental to health. The riskiest time was after midnight, potentially because it may reduce the likelihood of seeing morning light, which resets the body clock,” said study author Dr. David Plans of the University of Exeter, England.

Although a sleep schedule is preferred, it isn’t realistic all the time for those in certain occupations who might have to resort to other methods to keep their circadian clocks ticking optimally for their health. But if all it takes is prescribing a sleep time to reduce heart disease on a massive scale it would make a great “low-cost public health target.”

So bedtimes aren’t just for children.

While working as a registered nurse on inpatient Stroke and Generalized Rehabilitation unit, she pursued for a degree in Adult and Gerontology Primary Care degree. She currently practices at UW Medicine/Harborview Medical Center for Sleep Medicine treating a variety of sleep disorders. She strives to provide quality and safe care to her patients.

1. According to the American Academy of Sleep Medicine, even in normal times, 30 to 35 % of the US population contends with acute, or short-term insomnia. As a board-certified nurse practitioner focusing on treating sleep disorders among older adults, can you discuss whether that percentage has increased during the coronavirus (COVID-19) pandemic, and if so, what would you say are the underlying reasons or causes?

As a sleep medicine nurse practitioner at UW (University of Washington) Medicine, I have seen quite a few patients with sleep disorders including acute and chronic insomnia. Since the start of  the COVID-19 pandemic there has been a noticeable increase in poor-sleep complaints -- the data indicate a 37% increase in the rate of clinical insomnia since the pandemic started.

Stress can worsen insomnia, and the pandemic has negatively affected most if not everyone’s life. It has changed lifestyles through social distancing, mask mandates, and stay-at-home orders. Many have been forced to balance working from home with household duties; parents are supervising their children’s schooling. This disruption in the workday environment and workload can be hard to manage. The uncertainty of the pandemic has increased worries – health related and financially related. Ready access to media can also increase stress. Moreover, the lack of structure in a person’s day can cause many problems. Working from home, quarantining, living a more sedentary lifestyle, losing a job, losing socialization, including attending events, all can cause a disruption in a person’s daily routine and induce later bed- and wake-up times. This disruption to the body’s biological or circadian rhythm can reduce sleep quality and INCREASE phase-delay insomnia. Moreover, the pandemic has been especially hard on people’s mental health.  One CDC study showed that 40% of adults are struggling with adverse mental health and substance-use issues due to COVID. Also, 13.3% of adults have responded to surveys saying they’ve started or increased their use of substances. As the pandemic continues, acute insomnia will likely turn into chronic insomnia.  

2. How can increased stress and lack of exercise cause insomnia? What risk factors contribute to lack of sleep and impact our overall health?

The incidence of anxiety disorder and depressive disorder has increased significantly as compared to pre-pandemic rates. Psychological stress, especially at bedtime, increases psychophysiological arousal. The hypothalamic- pituitary- adrenal (HPA) axis responds to stress by releasing cortisol. HPA activation is associated with poorer sleep quality – it increases sleep latency, frequency of awakening, decreases in slow-wave sleep, and degrades overall sleep efficiency. The result of poor quality and fragmented sleep can further activate the HPA axis, causing a positive feedback loop.

A deterrent to poor sleep is physical activity. It greatly improves sleep by improving sleep efficiency, decreasing light sleep, increasing REM sleep, and regulating circadian rhythm. Lack of physical activity has been  associated with increased sleep problems such as daytime sleepiness, an insufficient amount of sleep, snoring, sleep apnea symptoms, and restless sleep. And poor sleep further reduces physical activity which perpetuates the problem. The pandemic’s effect on physical activity is significant. It has caused people to stay home more often and therefore decreases in levels of exercise. and increased sedentary lifestyle. More than half of the adults in this country do not meet federal guidelines for aerobic physical activity.

Sleep deprivation can be dangerous, as sleepiness increases the likelihood of major occupational and road traffic accidents. Being awake for at least 18 hours is equivalent to having a blood alcohol content of 0.05% to 0.10% for 24 hours. Chronic sleep deprivation, defined as getting, on average, fewer than 7 hours per night negatively affects all systems of the body. Sleep deprivation therefore reduces quality of life and can reduce life expectancy.

Cardiovascular – Sleep deprivation can increase excessive heart age and reduce heart rate recovery after exercise. It is also linked to increases in heart rate, blood pressure, and death from cardiovascular issues.

Respiratory – Even one night of sleep deprivation can increase respiratory load. Studies have shown an association between sleep apnea and sleep deprivation. Sleep deprivation and respiratory disorders can perpetuate each other.

Neurologic – Sleep is crucial in brain development. Lack of sleep is associated with low grade neuroinflammation, memory and cognitive function decline, and acceleration of Alzheimer’s disease. Sleep deprivation can increase pain sensitivity, the risk of stroke, aggressive behavior, cognitive instability, hyperactivity, and socialization problems.

Endocrine – Sleep deprivation increases appetite stimulation causing excessive food intake and weight gain. It can also impair metabolism, which leads to obesity and insulin resistance.

Reproductive – Studies on sleep deprivation and the human reproduction system are limited. A study in male rats shows a relation between less sleep and overall lower reproductive health such as alteration of spermatic function, “decreased sexual behavior, lower testosterone level, and lower sperm viability level”. Studies also show renal dysfunction and high blood pressure in the offspring of sleep deprived rats in the last week of pregnancy.

3. Please discuss coronasomnia and its symptoms. Also, will you discuss your thoughts on the diagnosis and provide examples of the types of stressors associated with coronasomnia.

Coronasomnia is the term used to describe the increase in sleep problems associated with the COVID-19 pandemic. Coronasomnia is associated with increased sleep onset, maintenance insomnia, delayed sleep schedule, nocturnal awakening, sleep deprivation, and worsened pre-existing sleep issues. The worst insomnia and psychological symptoms are among those who are in the center of the pandemic, such as frontline workers and people living in areas more impacted by COVID-19.

During the pandemic, anxiety, depression, stress, and poor sleep have significantly increased. Anxiety and depression can be accompanied by intrusive thoughts which interfere with falling asleep. Patients with depression have a twofold risk of sleep disruption. Lack of daily routine may be associated with an increase in poor dental hygiene, such as lower rates of flossing and brushing.There’s also an increased rate in snacking (weight gain) and avoidance of visits to the dentists.

More time at home leads to more time spent on TV or social media. Increased screen time and media use at night, especially close to bedtime, are linked to poorer sleep. Blue light emitted by electronic devices can suppress the release of melatonin, making it more difficult to fall asleep. In addition, viewing or listening to content that is distressing or exciting right before bedtime negatively affects sleep quality. Following pandemic news for more than 3 hours a day has been found to be associated with increased levels of anxiety.

Health care providers are especially susceptible to coronasomnia. Those who work directly with COVID -19 patients are twice as likely to report disrupted sleep, anxiety, and depression. An increased work and patient load, the shortage of both fellow providers and supplies, all contribute to increased anxiety and disrupted sleep. Poor sleep, especially coupled with longer work hours and shift work, are associated with a worsened immune system and poor work performance. 

4. In looking at the overall challenges pertaining to pandemic-induced sleep problems, what are your guideline recommendations to help ensure we sleep well during this outbreak?

Poor sleep can be detrimental to physical and mental health, and poor sleep hygiene practices can significantly impact sleep quality. Below are some general sleep-hygiene recommendations.

Caffeine – Caffeine consumed  close to bedtime can disrupt sleep. Caffeine should be avoided 6 hours prior to bedtime. Everyone’s tolerance to caffeine is different so timing and caffeine dosage may need to be individually tailored.

Alcohol – Alcohol consumed  close to bedtime can decrease sleep latency. However, it increases arousal during the second half of the night. It can also worsen snoring and sleep apnea. The effect can be alcohol level dependent.

Exercise – Regular exercise, as already discussed, is linked to better sleep quality. It is typically recommended to exercise earlier in the day; research has shown conflicting results on nighttime exercise. One study of  patients with insomnia who exercised at night showed that aerobic exercise of moderate intensity improved polysomnography patient-reported sleep latency, and total sleep time.

Routine – An irregular sleep schedule is associated with poor sleep and daytime sleepiness. Following a consistent sleep schedule promotes stable circadian rhythm. A familiar relaxing routine should be established before bedtime.

Stress – To lower stress, patients should be advised to schedule brief meditation sessions so they can reflect on stressful situations. Patients also should limit the amount of exposure to pandemic news. Writing down and talking about stress, relaxation, and mindfulness techniques may reduce stress. However, stress and anxiety significantly differ case by case and interventions from health care providers may be needed.

Time in bed – Limit the amount of time in bed only for sleep and sex. Limit the use of electronics before bed and avoid use of electronics in bed. Turning off devices or silencing notifications can all help in reducing sleep disruption. 

Cognitive behavioral therapy for insomnia (CBT-I) should be considered for patients with chronic insomnia. This therapy often includes sleep hygiene education, sleep restriction therapy, and relaxation training.  Benefits of CBT-I treatment are long-term and reduce the need for additional pharmacologic therapies.

While many patients are experiencing insomnia these days, other underlying sleep disorders also should be  considered. Patients should be evaluated to see if a sleep specialist is needed to diagnose and treat their sleep disorders.

While working as a registered nurse on inpatient Stroke and Generalized Rehabilitation unit, she pursued for a degree in Adult and Gerontology Primary Care degree. She currently practices at UW Medicine/Harborview Medical Center for Sleep Medicine treating a variety of sleep disorders. She strives to provide quality and safe care to her patients.

1. According to the American Academy of Sleep Medicine, even in normal times, 30 to 35 % of the US population contends with acute, or short-term insomnia. As a board-certified nurse practitioner focusing on treating sleep disorders among older adults, can you discuss whether that percentage has increased during the coronavirus (COVID-19) pandemic, and if so, what would you say are the underlying reasons or causes?

As a sleep medicine nurse practitioner at UW (University of Washington) Medicine, I have seen quite a few patients with sleep disorders including acute and chronic insomnia. Since the start of  the COVID-19 pandemic there has been a noticeable increase in poor-sleep complaints -- the data indicate a 37% increase in the rate of clinical insomnia since the pandemic started.

Stress can worsen insomnia, and the pandemic has negatively affected most if not everyone’s life. It has changed lifestyles through social distancing, mask mandates, and stay-at-home orders. Many have been forced to balance working from home with household duties; parents are supervising their children’s schooling. This disruption in the workday environment and workload can be hard to manage. The uncertainty of the pandemic has increased worries – health related and financially related. Ready access to media can also increase stress. Moreover, the lack of structure in a person’s day can cause many problems. Working from home, quarantining, living a more sedentary lifestyle, losing a job, losing socialization, including attending events, all can cause a disruption in a person’s daily routine and induce later bed- and wake-up times. This disruption to the body’s biological or circadian rhythm can reduce sleep quality and INCREASE phase-delay insomnia. Moreover, the pandemic has been especially hard on people’s mental health.  One CDC study showed that 40% of adults are struggling with adverse mental health and substance-use issues due to COVID. Also, 13.3% of adults have responded to surveys saying they’ve started or increased their use of substances. As the pandemic continues, acute insomnia will likely turn into chronic insomnia.  

2. How can increased stress and lack of exercise cause insomnia? What risk factors contribute to lack of sleep and impact our overall health?

The incidence of anxiety disorder and depressive disorder has increased significantly as compared to pre-pandemic rates. Psychological stress, especially at bedtime, increases psychophysiological arousal. The hypothalamic- pituitary- adrenal (HPA) axis responds to stress by releasing cortisol. HPA activation is associated with poorer sleep quality – it increases sleep latency, frequency of awakening, decreases in slow-wave sleep, and degrades overall sleep efficiency. The result of poor quality and fragmented sleep can further activate the HPA axis, causing a positive feedback loop.

A deterrent to poor sleep is physical activity. It greatly improves sleep by improving sleep efficiency, decreasing light sleep, increasing REM sleep, and regulating circadian rhythm. Lack of physical activity has been  associated with increased sleep problems such as daytime sleepiness, an insufficient amount of sleep, snoring, sleep apnea symptoms, and restless sleep. And poor sleep further reduces physical activity which perpetuates the problem. The pandemic’s effect on physical activity is significant. It has caused people to stay home more often and therefore decreases in levels of exercise. and increased sedentary lifestyle. More than half of the adults in this country do not meet federal guidelines for aerobic physical activity.

Sleep deprivation can be dangerous, as sleepiness increases the likelihood of major occupational and road traffic accidents. Being awake for at least 18 hours is equivalent to having a blood alcohol content of 0.05% to 0.10% for 24 hours. Chronic sleep deprivation, defined as getting, on average, fewer than 7 hours per night negatively affects all systems of the body. Sleep deprivation therefore reduces quality of life and can reduce life expectancy.

Cardiovascular – Sleep deprivation can increase excessive heart age and reduce heart rate recovery after exercise. It is also linked to increases in heart rate, blood pressure, and death from cardiovascular issues.

Respiratory – Even one night of sleep deprivation can increase respiratory load. Studies have shown an association between sleep apnea and sleep deprivation. Sleep deprivation and respiratory disorders can perpetuate each other.

Neurologic – Sleep is crucial in brain development. Lack of sleep is associated with low grade neuroinflammation, memory and cognitive function decline, and acceleration of Alzheimer’s disease. Sleep deprivation can increase pain sensitivity, the risk of stroke, aggressive behavior, cognitive instability, hyperactivity, and socialization problems.

Endocrine – Sleep deprivation increases appetite stimulation causing excessive food intake and weight gain. It can also impair metabolism, which leads to obesity and insulin resistance.

Reproductive – Studies on sleep deprivation and the human reproduction system are limited. A study in male rats shows a relation between less sleep and overall lower reproductive health such as alteration of spermatic function, “decreased sexual behavior, lower testosterone level, and lower sperm viability level”. Studies also show renal dysfunction and high blood pressure in the offspring of sleep deprived rats in the last week of pregnancy.

3. Please discuss coronasomnia and its symptoms. Also, will you discuss your thoughts on the diagnosis and provide examples of the types of stressors associated with coronasomnia.

Coronasomnia is the term used to describe the increase in sleep problems associated with the COVID-19 pandemic. Coronasomnia is associated with increased sleep onset, maintenance insomnia, delayed sleep schedule, nocturnal awakening, sleep deprivation, and worsened pre-existing sleep issues. The worst insomnia and psychological symptoms are among those who are in the center of the pandemic, such as frontline workers and people living in areas more impacted by COVID-19.

During the pandemic, anxiety, depression, stress, and poor sleep have significantly increased. Anxiety and depression can be accompanied by intrusive thoughts which interfere with falling asleep. Patients with depression have a twofold risk of sleep disruption. Lack of daily routine may be associated with an increase in poor dental hygiene, such as lower rates of flossing and brushing.There’s also an increased rate in snacking (weight gain) and avoidance of visits to the dentists.

More time at home leads to more time spent on TV or social media. Increased screen time and media use at night, especially close to bedtime, are linked to poorer sleep. Blue light emitted by electronic devices can suppress the release of melatonin, making it more difficult to fall asleep. In addition, viewing or listening to content that is distressing or exciting right before bedtime negatively affects sleep quality. Following pandemic news for more than 3 hours a day has been found to be associated with increased levels of anxiety.

Health care providers are especially susceptible to coronasomnia. Those who work directly with COVID -19 patients are twice as likely to report disrupted sleep, anxiety, and depression. An increased work and patient load, the shortage of both fellow providers and supplies, all contribute to increased anxiety and disrupted sleep. Poor sleep, especially coupled with longer work hours and shift work, are associated with a worsened immune system and poor work performance. 

4. In looking at the overall challenges pertaining to pandemic-induced sleep problems, what are your guideline recommendations to help ensure we sleep well during this outbreak?

Poor sleep can be detrimental to physical and mental health, and poor sleep hygiene practices can significantly impact sleep quality. Below are some general sleep-hygiene recommendations.

Caffeine – Caffeine consumed  close to bedtime can disrupt sleep. Caffeine should be avoided 6 hours prior to bedtime. Everyone’s tolerance to caffeine is different so timing and caffeine dosage may need to be individually tailored.

Alcohol – Alcohol consumed  close to bedtime can decrease sleep latency. However, it increases arousal during the second half of the night. It can also worsen snoring and sleep apnea. The effect can be alcohol level dependent.

Exercise – Regular exercise, as already discussed, is linked to better sleep quality. It is typically recommended to exercise earlier in the day; research has shown conflicting results on nighttime exercise. One study of  patients with insomnia who exercised at night showed that aerobic exercise of moderate intensity improved polysomnography patient-reported sleep latency, and total sleep time.

Routine – An irregular sleep schedule is associated with poor sleep and daytime sleepiness. Following a consistent sleep schedule promotes stable circadian rhythm. A familiar relaxing routine should be established before bedtime.

Stress – To lower stress, patients should be advised to schedule brief meditation sessions so they can reflect on stressful situations. Patients also should limit the amount of exposure to pandemic news. Writing down and talking about stress, relaxation, and mindfulness techniques may reduce stress. However, stress and anxiety significantly differ case by case and interventions from health care providers may be needed.

Time in bed – Limit the amount of time in bed only for sleep and sex. Limit the use of electronics before bed and avoid use of electronics in bed. Turning off devices or silencing notifications can all help in reducing sleep disruption. 

Cognitive behavioral therapy for insomnia (CBT-I) should be considered for patients with chronic insomnia. This therapy often includes sleep hygiene education, sleep restriction therapy, and relaxation training.  Benefits of CBT-I treatment are long-term and reduce the need for additional pharmacologic therapies.

While many patients are experiencing insomnia these days, other underlying sleep disorders also should be  considered. Patients should be evaluated to see if a sleep specialist is needed to diagnose and treat their sleep disorders.

While working as a registered nurse on inpatient Stroke and Generalized Rehabilitation unit, she pursued for a degree in Adult and Gerontology Primary Care degree. She currently practices at UW Medicine/Harborview Medical Center for Sleep Medicine treating a variety of sleep disorders. She strives to provide quality and safe care to her patients.

1. According to the American Academy of Sleep Medicine, even in normal times, 30 to 35 % of the US population contends with acute, or short-term insomnia. As a board-certified nurse practitioner focusing on treating sleep disorders among older adults, can you discuss whether that percentage has increased during the coronavirus (COVID-19) pandemic, and if so, what would you say are the underlying reasons or causes?

As a sleep medicine nurse practitioner at UW (University of Washington) Medicine, I have seen quite a few patients with sleep disorders including acute and chronic insomnia. Since the start of  the COVID-19 pandemic there has been a noticeable increase in poor-sleep complaints -- the data indicate a 37% increase in the rate of clinical insomnia since the pandemic started.

Stress can worsen insomnia, and the pandemic has negatively affected most if not everyone’s life. It has changed lifestyles through social distancing, mask mandates, and stay-at-home orders. Many have been forced to balance working from home with household duties; parents are supervising their children’s schooling. This disruption in the workday environment and workload can be hard to manage. The uncertainty of the pandemic has increased worries – health related and financially related. Ready access to media can also increase stress. Moreover, the lack of structure in a person’s day can cause many problems. Working from home, quarantining, living a more sedentary lifestyle, losing a job, losing socialization, including attending events, all can cause a disruption in a person’s daily routine and induce later bed- and wake-up times. This disruption to the body’s biological or circadian rhythm can reduce sleep quality and INCREASE phase-delay insomnia. Moreover, the pandemic has been especially hard on people’s mental health.  One CDC study showed that 40% of adults are struggling with adverse mental health and substance-use issues due to COVID. Also, 13.3% of adults have responded to surveys saying they’ve started or increased their use of substances. As the pandemic continues, acute insomnia will likely turn into chronic insomnia.  

2. How can increased stress and lack of exercise cause insomnia? What risk factors contribute to lack of sleep and impact our overall health?

The incidence of anxiety disorder and depressive disorder has increased significantly as compared to pre-pandemic rates. Psychological stress, especially at bedtime, increases psychophysiological arousal. The hypothalamic- pituitary- adrenal (HPA) axis responds to stress by releasing cortisol. HPA activation is associated with poorer sleep quality – it increases sleep latency, frequency of awakening, decreases in slow-wave sleep, and degrades overall sleep efficiency. The result of poor quality and fragmented sleep can further activate the HPA axis, causing a positive feedback loop.

A deterrent to poor sleep is physical activity. It greatly improves sleep by improving sleep efficiency, decreasing light sleep, increasing REM sleep, and regulating circadian rhythm. Lack of physical activity has been  associated with increased sleep problems such as daytime sleepiness, an insufficient amount of sleep, snoring, sleep apnea symptoms, and restless sleep. And poor sleep further reduces physical activity which perpetuates the problem. The pandemic’s effect on physical activity is significant. It has caused people to stay home more often and therefore decreases in levels of exercise. and increased sedentary lifestyle. More than half of the adults in this country do not meet federal guidelines for aerobic physical activity.

Sleep deprivation can be dangerous, as sleepiness increases the likelihood of major occupational and road traffic accidents. Being awake for at least 18 hours is equivalent to having a blood alcohol content of 0.05% to 0.10% for 24 hours. Chronic sleep deprivation, defined as getting, on average, fewer than 7 hours per night negatively affects all systems of the body. Sleep deprivation therefore reduces quality of life and can reduce life expectancy.

Cardiovascular – Sleep deprivation can increase excessive heart age and reduce heart rate recovery after exercise. It is also linked to increases in heart rate, blood pressure, and death from cardiovascular issues.

Respiratory – Even one night of sleep deprivation can increase respiratory load. Studies have shown an association between sleep apnea and sleep deprivation. Sleep deprivation and respiratory disorders can perpetuate each other.

Neurologic – Sleep is crucial in brain development. Lack of sleep is associated with low grade neuroinflammation, memory and cognitive function decline, and acceleration of Alzheimer’s disease. Sleep deprivation can increase pain sensitivity, the risk of stroke, aggressive behavior, cognitive instability, hyperactivity, and socialization problems.

Endocrine – Sleep deprivation increases appetite stimulation causing excessive food intake and weight gain. It can also impair metabolism, which leads to obesity and insulin resistance.

Reproductive – Studies on sleep deprivation and the human reproduction system are limited. A study in male rats shows a relation between less sleep and overall lower reproductive health such as alteration of spermatic function, “decreased sexual behavior, lower testosterone level, and lower sperm viability level”. Studies also show renal dysfunction and high blood pressure in the offspring of sleep deprived rats in the last week of pregnancy.

3. Please discuss coronasomnia and its symptoms. Also, will you discuss your thoughts on the diagnosis and provide examples of the types of stressors associated with coronasomnia.

Coronasomnia is the term used to describe the increase in sleep problems associated with the COVID-19 pandemic. Coronasomnia is associated with increased sleep onset, maintenance insomnia, delayed sleep schedule, nocturnal awakening, sleep deprivation, and worsened pre-existing sleep issues. The worst insomnia and psychological symptoms are among those who are in the center of the pandemic, such as frontline workers and people living in areas more impacted by COVID-19.

During the pandemic, anxiety, depression, stress, and poor sleep have significantly increased. Anxiety and depression can be accompanied by intrusive thoughts which interfere with falling asleep. Patients with depression have a twofold risk of sleep disruption. Lack of daily routine may be associated with an increase in poor dental hygiene, such as lower rates of flossing and brushing.There’s also an increased rate in snacking (weight gain) and avoidance of visits to the dentists.

More time at home leads to more time spent on TV or social media. Increased screen time and media use at night, especially close to bedtime, are linked to poorer sleep. Blue light emitted by electronic devices can suppress the release of melatonin, making it more difficult to fall asleep. In addition, viewing or listening to content that is distressing or exciting right before bedtime negatively affects sleep quality. Following pandemic news for more than 3 hours a day has been found to be associated with increased levels of anxiety.

Health care providers are especially susceptible to coronasomnia. Those who work directly with COVID -19 patients are twice as likely to report disrupted sleep, anxiety, and depression. An increased work and patient load, the shortage of both fellow providers and supplies, all contribute to increased anxiety and disrupted sleep. Poor sleep, especially coupled with longer work hours and shift work, are associated with a worsened immune system and poor work performance. 

4. In looking at the overall challenges pertaining to pandemic-induced sleep problems, what are your guideline recommendations to help ensure we sleep well during this outbreak?

Poor sleep can be detrimental to physical and mental health, and poor sleep hygiene practices can significantly impact sleep quality. Below are some general sleep-hygiene recommendations.

Caffeine – Caffeine consumed  close to bedtime can disrupt sleep. Caffeine should be avoided 6 hours prior to bedtime. Everyone’s tolerance to caffeine is different so timing and caffeine dosage may need to be individually tailored.

Alcohol – Alcohol consumed  close to bedtime can decrease sleep latency. However, it increases arousal during the second half of the night. It can also worsen snoring and sleep apnea. The effect can be alcohol level dependent.

Exercise – Regular exercise, as already discussed, is linked to better sleep quality. It is typically recommended to exercise earlier in the day; research has shown conflicting results on nighttime exercise. One study of  patients with insomnia who exercised at night showed that aerobic exercise of moderate intensity improved polysomnography patient-reported sleep latency, and total sleep time.

Routine – An irregular sleep schedule is associated with poor sleep and daytime sleepiness. Following a consistent sleep schedule promotes stable circadian rhythm. A familiar relaxing routine should be established before bedtime.

Stress – To lower stress, patients should be advised to schedule brief meditation sessions so they can reflect on stressful situations. Patients also should limit the amount of exposure to pandemic news. Writing down and talking about stress, relaxation, and mindfulness techniques may reduce stress. However, stress and anxiety significantly differ case by case and interventions from health care providers may be needed.

Time in bed – Limit the amount of time in bed only for sleep and sex. Limit the use of electronics before bed and avoid use of electronics in bed. Turning off devices or silencing notifications can all help in reducing sleep disruption. 

Cognitive behavioral therapy for insomnia (CBT-I) should be considered for patients with chronic insomnia. This therapy often includes sleep hygiene education, sleep restriction therapy, and relaxation training.  Benefits of CBT-I treatment are long-term and reduce the need for additional pharmacologic therapies.

While many patients are experiencing insomnia these days, other underlying sleep disorders also should be  considered. Patients should be evaluated to see if a sleep specialist is needed to diagnose and treat their sleep disorders.

Sleeping too much or too little can lead to cognitive decline over time, but new research suggests there could be a sleep time “sweet spot” that stabilizes cognitive function.

JGI/Tom Grill/Getty Images

In a longitudinal study, investigators found older adults who slept less than 4.5 hours or more than 6.5 hours a night reported significant cognitive decline over time, but cognitive scores for those with sleep duration in between that range remained stable.

“This really suggests that there’s this middle range, a ‘sweet spot,’ where your sleep is really optimal,” lead author Brendan Lucey, MD, MSCI, associate professor of neurology and director of the Washington University Sleep Medicine Center, St. Louis, said in an interview.

The study, published online Oct. 20, 2021, in the journal Brain, is part of a growing body of research that seeks to determine if sleep can be used as a marker of Alzheimer’s disease progression.
 

A complex relationship

Studies suggest a strong relationship between sleep patterns and Alzheimer’s disease, which affects nearly 6 million Americans. The challenge, Dr. Lucey said, is unwinding the complex links between sleep, AD, and cognitive function.

An earlier study by Dr. Lucey and colleagues found that poor sleep quality is associated with early signs of AD, and a report published in September found that elderly people who slept less than 6 hours a night had a greater burden of amyloid-beta, a hallmark sign of AD.

For this new study, researchers monitored sleep-wake activity over 4-6 nights in 100 participants who underwent annual cognitive assessments and clinical studies, including APOE genotyping, as part of a longitudinal study at the Knight Alzheimer Disease Research Center at Washington University.

Participants also provided cerebrospinal fluid (CSF) total tau and amyloid-beta 42 and wore a small EEG device on their forehead while they slept.

The majority of participants had a clinical dementia rating (CDR) score of 0, indicating no cognitive impairment. Twelve individuals had a CDR greater than 0, with most reporting mild cognitive impairment.

As expected, CSF analysis showed greater evidence of AD pathology in those with a baseline CDR greater than 0.

Changes in cognitive function were measured using a Preclinical Alzheimer Cognitive Composite (PACC) score, a composite of results from a neuropsychological testing battery that included the Free and Cued Selective Reminding Test, the Logical Memory Delayed Recall Test from the Wechsler Memory Scale–Revised, the Digit Symbol Substitution Test from the Wechsler Adult Intelligence Scale–Revised, and the Mini-Mental State Examination.

Researchers found an upside-down U-shaped relationship between PACC scores and sleep duration, with dramatic cognitive decline in those who slept less than 4.5 hours or more than 6.5 hours a night (P < .001 for both).

The U-shaped relationship was also found with measures of sleep phases, including time spent in rapid eye movement and in non-REM sleep (P < .001 for both).

The findings persisted even after controlling for confounders that can affect sleep and cognition, such as age, CSF total tau/amyloid-beta ₄₂ ratio, apo E four-allele carrier status, years of education, and sex.

Understanding how sleep changes at different stages of AD could help researchers determine if sleep can be used as a marker of disease progression, Dr. Lucey said. That could lead to interventions to slow that process.

“We’re not at the point yet where we can say that we need to monitor someone’s sleep time and then do an intervention to see if it would improve their risk for cognitive decline,” said Dr. Lucey, who plans to repeat this sleep study with the same cohort to track changes in sleep patterns and cognitive function over time. “But that’s a question I’m very excited to try to answer.”
 

A component of cognitive health

Commenting on the findings for this news organization, Heather Snyder, PhD, vice president of medical and scientific relations for the Alzheimer’s Association, noted that the study adds to a body of evidence linking sleep and cognition, especially how sleep quality can optimize brain function.

“We’ve seen previous research that’s shown poor sleep contributes to dementia risk, as well as research showing sleep duration may play a role in cognition,” she said.

“We also need studies that look at sleep as an intervention for cognitive health,” Dr. Snyder said. “Sleep is an important aspect of our overall health. Clinicians should have conversations with their patients about sleep as part of standard discussions about their health habits and wellness.”

The study was funded by the National Institutes of Health, the American Sleep Medicine Foundation, the Roger and Paula Riney Fund, and the Daniel J. Brennan, MD Fund. Dr. Lucey consults for Merck and Eli Lilly. Dr. Snyder has disclosed no relevant financial relationships.

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

Sleeping too much or too little can lead to cognitive decline over time, but new research suggests there could be a sleep time “sweet spot” that stabilizes cognitive function.

JGI/Tom Grill/Getty Images

In a longitudinal study, investigators found older adults who slept less than 4.5 hours or more than 6.5 hours a night reported significant cognitive decline over time, but cognitive scores for those with sleep duration in between that range remained stable.

“This really suggests that there’s this middle range, a ‘sweet spot,’ where your sleep is really optimal,” lead author Brendan Lucey, MD, MSCI, associate professor of neurology and director of the Washington University Sleep Medicine Center, St. Louis, said in an interview.

The study, published online Oct. 20, 2021, in the journal Brain, is part of a growing body of research that seeks to determine if sleep can be used as a marker of Alzheimer’s disease progression.
 

A complex relationship

Studies suggest a strong relationship between sleep patterns and Alzheimer’s disease, which affects nearly 6 million Americans. The challenge, Dr. Lucey said, is unwinding the complex links between sleep, AD, and cognitive function.

An earlier study by Dr. Lucey and colleagues found that poor sleep quality is associated with early signs of AD, and a report published in September found that elderly people who slept less than 6 hours a night had a greater burden of amyloid-beta, a hallmark sign of AD.

For this new study, researchers monitored sleep-wake activity over 4-6 nights in 100 participants who underwent annual cognitive assessments and clinical studies, including APOE genotyping, as part of a longitudinal study at the Knight Alzheimer Disease Research Center at Washington University.

Participants also provided cerebrospinal fluid (CSF) total tau and amyloid-beta 42 and wore a small EEG device on their forehead while they slept.

The majority of participants had a clinical dementia rating (CDR) score of 0, indicating no cognitive impairment. Twelve individuals had a CDR greater than 0, with most reporting mild cognitive impairment.

As expected, CSF analysis showed greater evidence of AD pathology in those with a baseline CDR greater than 0.

Changes in cognitive function were measured using a Preclinical Alzheimer Cognitive Composite (PACC) score, a composite of results from a neuropsychological testing battery that included the Free and Cued Selective Reminding Test, the Logical Memory Delayed Recall Test from the Wechsler Memory Scale–Revised, the Digit Symbol Substitution Test from the Wechsler Adult Intelligence Scale–Revised, and the Mini-Mental State Examination.

Researchers found an upside-down U-shaped relationship between PACC scores and sleep duration, with dramatic cognitive decline in those who slept less than 4.5 hours or more than 6.5 hours a night (P < .001 for both).

The U-shaped relationship was also found with measures of sleep phases, including time spent in rapid eye movement and in non-REM sleep (P < .001 for both).

The findings persisted even after controlling for confounders that can affect sleep and cognition, such as age, CSF total tau/amyloid-beta ₄₂ ratio, apo E four-allele carrier status, years of education, and sex.

Understanding how sleep changes at different stages of AD could help researchers determine if sleep can be used as a marker of disease progression, Dr. Lucey said. That could lead to interventions to slow that process.

“We’re not at the point yet where we can say that we need to monitor someone’s sleep time and then do an intervention to see if it would improve their risk for cognitive decline,” said Dr. Lucey, who plans to repeat this sleep study with the same cohort to track changes in sleep patterns and cognitive function over time. “But that’s a question I’m very excited to try to answer.”
 

A component of cognitive health

Commenting on the findings for this news organization, Heather Snyder, PhD, vice president of medical and scientific relations for the Alzheimer’s Association, noted that the study adds to a body of evidence linking sleep and cognition, especially how sleep quality can optimize brain function.

“We’ve seen previous research that’s shown poor sleep contributes to dementia risk, as well as research showing sleep duration may play a role in cognition,” she said.

“We also need studies that look at sleep as an intervention for cognitive health,” Dr. Snyder said. “Sleep is an important aspect of our overall health. Clinicians should have conversations with their patients about sleep as part of standard discussions about their health habits and wellness.”

The study was funded by the National Institutes of Health, the American Sleep Medicine Foundation, the Roger and Paula Riney Fund, and the Daniel J. Brennan, MD Fund. Dr. Lucey consults for Merck and Eli Lilly. Dr. Snyder has disclosed no relevant financial relationships.

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

Sleeping too much or too little can lead to cognitive decline over time, but new research suggests there could be a sleep time “sweet spot” that stabilizes cognitive function.

JGI/Tom Grill/Getty Images

In a longitudinal study, investigators found older adults who slept less than 4.5 hours or more than 6.5 hours a night reported significant cognitive decline over time, but cognitive scores for those with sleep duration in between that range remained stable.

“This really suggests that there’s this middle range, a ‘sweet spot,’ where your sleep is really optimal,” lead author Brendan Lucey, MD, MSCI, associate professor of neurology and director of the Washington University Sleep Medicine Center, St. Louis, said in an interview.

The study, published online Oct. 20, 2021, in the journal Brain, is part of a growing body of research that seeks to determine if sleep can be used as a marker of Alzheimer’s disease progression.
 

A complex relationship

Studies suggest a strong relationship between sleep patterns and Alzheimer’s disease, which affects nearly 6 million Americans. The challenge, Dr. Lucey said, is unwinding the complex links between sleep, AD, and cognitive function.

An earlier study by Dr. Lucey and colleagues found that poor sleep quality is associated with early signs of AD, and a report published in September found that elderly people who slept less than 6 hours a night had a greater burden of amyloid-beta, a hallmark sign of AD.

For this new study, researchers monitored sleep-wake activity over 4-6 nights in 100 participants who underwent annual cognitive assessments and clinical studies, including APOE genotyping, as part of a longitudinal study at the Knight Alzheimer Disease Research Center at Washington University.

Participants also provided cerebrospinal fluid (CSF) total tau and amyloid-beta 42 and wore a small EEG device on their forehead while they slept.

The majority of participants had a clinical dementia rating (CDR) score of 0, indicating no cognitive impairment. Twelve individuals had a CDR greater than 0, with most reporting mild cognitive impairment.

As expected, CSF analysis showed greater evidence of AD pathology in those with a baseline CDR greater than 0.

Changes in cognitive function were measured using a Preclinical Alzheimer Cognitive Composite (PACC) score, a composite of results from a neuropsychological testing battery that included the Free and Cued Selective Reminding Test, the Logical Memory Delayed Recall Test from the Wechsler Memory Scale–Revised, the Digit Symbol Substitution Test from the Wechsler Adult Intelligence Scale–Revised, and the Mini-Mental State Examination.

Researchers found an upside-down U-shaped relationship between PACC scores and sleep duration, with dramatic cognitive decline in those who slept less than 4.5 hours or more than 6.5 hours a night (P < .001 for both).

The U-shaped relationship was also found with measures of sleep phases, including time spent in rapid eye movement and in non-REM sleep (P < .001 for both).

The findings persisted even after controlling for confounders that can affect sleep and cognition, such as age, CSF total tau/amyloid-beta ₄₂ ratio, apo E four-allele carrier status, years of education, and sex.

Understanding how sleep changes at different stages of AD could help researchers determine if sleep can be used as a marker of disease progression, Dr. Lucey said. That could lead to interventions to slow that process.

“We’re not at the point yet where we can say that we need to monitor someone’s sleep time and then do an intervention to see if it would improve their risk for cognitive decline,” said Dr. Lucey, who plans to repeat this sleep study with the same cohort to track changes in sleep patterns and cognitive function over time. “But that’s a question I’m very excited to try to answer.”
 

A component of cognitive health

Commenting on the findings for this news organization, Heather Snyder, PhD, vice president of medical and scientific relations for the Alzheimer’s Association, noted that the study adds to a body of evidence linking sleep and cognition, especially how sleep quality can optimize brain function.

“We’ve seen previous research that’s shown poor sleep contributes to dementia risk, as well as research showing sleep duration may play a role in cognition,” she said.

“We also need studies that look at sleep as an intervention for cognitive health,” Dr. Snyder said. “Sleep is an important aspect of our overall health. Clinicians should have conversations with their patients about sleep as part of standard discussions about their health habits and wellness.”

The study was funded by the National Institutes of Health, the American Sleep Medicine Foundation, the Roger and Paula Riney Fund, and the Daniel J. Brennan, MD Fund. Dr. Lucey consults for Merck and Eli Lilly. Dr. Snyder has disclosed no relevant financial relationships.

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

Marijuana use is now a legal activity in many parts of the United States, but those managing patients with psychiatric disorders are in the difficult position of determining whether this use is helpful, harmful, or irrelevant to the underlying illness on the basis of limited and largely incomplete data, according to an overview of this issue presented at the virtual Psychopharmacology Update presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

HighGradeRoots/iStock/Getty Images

While there is clear evidence that cannabis use relative to the general population “is more prevalent among patients with psychiatric disorders,” it is less certain how often this use is risky, said Diana M. Martinez, MD, professor of psychiatry at Columbia University in New York.

Independent of euphoric effects, cannabis can be perceived by individuals with psychiatric diagnosis as self-medication for feelings of stress, social anxiety, and insomnia, among other symptoms. These are the same reasons why many individuals without psychiatric conditions use cannabis-containing products.

The perception that cannabis use is generally benign presumably explains the successful efforts at legalization, but there are risks for those with or without psychiatric illnesses, Dr. Martinez pointed out at the meeting, sponsored by Medscape Live. Not least, about 20% of regular users of cannabis develop cannabis use disorder (CUD), a condition defined in the DSM-5 as the continued use of cannabis despite adverse consequences, such as dependence.
 

Impact of severe CUD ‘incapacitating’

“Of those who meet criteria for CUD, 23% have severe CUD, which is an incapacitating form,” reported Dr. Martinez, citing work led by Deborah Hasin, PhD, professor of clinical epidemiology at Columbia University.

However, relative to otherwise healthy individuals, those with a psychiatric diagnosis might face greater benefits or greater risks from cannabis use, according to Dr. Martinez, who cited a 2017 report from the National Academies of Science, Engineering, and Medicine (NASEM).

This report evaluated the potential risks and benefits on the basis of published studies.

There is limited evidence that regular cannabis increases rather than modifies symptoms of mania and hypomania in patients with bipolar disorder, according to the report. The report also cited limited evidence that cannabis use increases severity of posttraumatic stress disorder (PTSD). There was limited evidence of adverse effects on symptoms of anxiety, although this appeared to depend on daily or nearly daily use.

The report found no data of acceptable quality to draw conclusions about the effect of cannabis use on symptoms of depression.

In patients with attention-deficit/hyperactivity disorder (ADHD), “a recent study showed that daily but not occasional use of cannabis increased impulsivity but not inattention, working memory, or verbal intelligence,” said Dr. Martinez, citing a study published this year.

Some evidence also suggests that patients with a psychiatric disorder might benefit from cannabis use, but, again, this evidence is limited. For one example, it includes a potential reduction in symptoms of obsessive-compulsive disorder, Dr. Martinez said.
 

More support for cannabis in medical disease

Relative to the quality of evidence supporting benefit from cannabis in psychiatric disease, the data appear to be stronger for patients with medical illnesses, such as cancer. For example, Dr. Martinez cited evidence that tetrahydrocannabinol (THC), a major active ingredient in cannabis, improves sleep in the context of a medical illnesses. There is also evidence for anxiolytic effects in patients with a medical illness, although that is weaker.

In patients with or without a psychiatric disorder, marijuana does pose a risk of substance abuse disorder, and it shares the risks of intoxicants, such as inattention leading to increased risk of accidents, including motor vehicle accidents. This pertains to those with or without a psychiatric or medical condition, Dr. Martinez said.

While intermittent light use of cannabis appears to pose no risk or a very low risk of long-term adverse effects on cognition, at least in patients without psychiatric disorders, Dr. Martinez indicated that the risk-benefit ratio for any individual is use dependent. The risk of CUD, for example, increases with the frequency of exposure and the potency of the cannabis. Dr. Martinez indicated that a conservative approach is prudent with the limited evidence available for patients with psychiatric disorders.
 

Empirical evidence for therapeutic role

In published studies, other researchers have expressed interest in a potential therapeutic role of cannabis for psychiatric disorders, but there appears to be a general consensus that the supportive data remain weak. One expert who has written on this topic, Jerome Sarris, PhD, professor of integrative mental health, NICM Health Research Institute, Western Sydney University, Westmead, Australia, said that empirical evidence does support a benefit in selected patients.

“Of course, high THC forms are strongly discouraged in people with schizophrenia or high risk of developing psychotic disorder, or in youths,” Dr. Sarris explained. “However, there is a potential role for use in people with sleep and pain issues, and many find it beneficial to also assist with affective disorder symptoms.”

In a systematic review he led that was published last year, the evidence to support cannabis for psychiatric disorders was characterized as “embryonic.” However, small studies and case reports appear to support benefit for such indications as ADHD if precautions are taken.

“I certainly would not discourage use of prescribed standardized medicinal cannabis therapeutics for all people with psychiatric disorders,” Dr. Sarris said. He suggested that attention should be made to the THC potency and terpene composition of the products that patients with psychiatric disorders are taking.

Marijuana use is now a legal activity in many parts of the United States, but those managing patients with psychiatric disorders are in the difficult position of determining whether this use is helpful, harmful, or irrelevant to the underlying illness on the basis of limited and largely incomplete data, according to an overview of this issue presented at the virtual Psychopharmacology Update presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

HighGradeRoots/iStock/Getty Images

While there is clear evidence that cannabis use relative to the general population “is more prevalent among patients with psychiatric disorders,” it is less certain how often this use is risky, said Diana M. Martinez, MD, professor of psychiatry at Columbia University in New York.

Independent of euphoric effects, cannabis can be perceived by individuals with psychiatric diagnosis as self-medication for feelings of stress, social anxiety, and insomnia, among other symptoms. These are the same reasons why many individuals without psychiatric conditions use cannabis-containing products.

The perception that cannabis use is generally benign presumably explains the successful efforts at legalization, but there are risks for those with or without psychiatric illnesses, Dr. Martinez pointed out at the meeting, sponsored by Medscape Live. Not least, about 20% of regular users of cannabis develop cannabis use disorder (CUD), a condition defined in the DSM-5 as the continued use of cannabis despite adverse consequences, such as dependence.
 

Impact of severe CUD ‘incapacitating’

“Of those who meet criteria for CUD, 23% have severe CUD, which is an incapacitating form,” reported Dr. Martinez, citing work led by Deborah Hasin, PhD, professor of clinical epidemiology at Columbia University.

However, relative to otherwise healthy individuals, those with a psychiatric diagnosis might face greater benefits or greater risks from cannabis use, according to Dr. Martinez, who cited a 2017 report from the National Academies of Science, Engineering, and Medicine (NASEM).

This report evaluated the potential risks and benefits on the basis of published studies.

There is limited evidence that regular cannabis increases rather than modifies symptoms of mania and hypomania in patients with bipolar disorder, according to the report. The report also cited limited evidence that cannabis use increases severity of posttraumatic stress disorder (PTSD). There was limited evidence of adverse effects on symptoms of anxiety, although this appeared to depend on daily or nearly daily use.

The report found no data of acceptable quality to draw conclusions about the effect of cannabis use on symptoms of depression.

In patients with attention-deficit/hyperactivity disorder (ADHD), “a recent study showed that daily but not occasional use of cannabis increased impulsivity but not inattention, working memory, or verbal intelligence,” said Dr. Martinez, citing a study published this year.

Some evidence also suggests that patients with a psychiatric disorder might benefit from cannabis use, but, again, this evidence is limited. For one example, it includes a potential reduction in symptoms of obsessive-compulsive disorder, Dr. Martinez said.
 

More support for cannabis in medical disease

Relative to the quality of evidence supporting benefit from cannabis in psychiatric disease, the data appear to be stronger for patients with medical illnesses, such as cancer. For example, Dr. Martinez cited evidence that tetrahydrocannabinol (THC), a major active ingredient in cannabis, improves sleep in the context of a medical illnesses. There is also evidence for anxiolytic effects in patients with a medical illness, although that is weaker.

In patients with or without a psychiatric disorder, marijuana does pose a risk of substance abuse disorder, and it shares the risks of intoxicants, such as inattention leading to increased risk of accidents, including motor vehicle accidents. This pertains to those with or without a psychiatric or medical condition, Dr. Martinez said.

While intermittent light use of cannabis appears to pose no risk or a very low risk of long-term adverse effects on cognition, at least in patients without psychiatric disorders, Dr. Martinez indicated that the risk-benefit ratio for any individual is use dependent. The risk of CUD, for example, increases with the frequency of exposure and the potency of the cannabis. Dr. Martinez indicated that a conservative approach is prudent with the limited evidence available for patients with psychiatric disorders.
 

Empirical evidence for therapeutic role

In published studies, other researchers have expressed interest in a potential therapeutic role of cannabis for psychiatric disorders, but there appears to be a general consensus that the supportive data remain weak. One expert who has written on this topic, Jerome Sarris, PhD, professor of integrative mental health, NICM Health Research Institute, Western Sydney University, Westmead, Australia, said that empirical evidence does support a benefit in selected patients.

“Of course, high THC forms are strongly discouraged in people with schizophrenia or high risk of developing psychotic disorder, or in youths,” Dr. Sarris explained. “However, there is a potential role for use in people with sleep and pain issues, and many find it beneficial to also assist with affective disorder symptoms.”

In a systematic review he led that was published last year, the evidence to support cannabis for psychiatric disorders was characterized as “embryonic.” However, small studies and case reports appear to support benefit for such indications as ADHD if precautions are taken.

“I certainly would not discourage use of prescribed standardized medicinal cannabis therapeutics for all people with psychiatric disorders,” Dr. Sarris said. He suggested that attention should be made to the THC potency and terpene composition of the products that patients with psychiatric disorders are taking.

Marijuana use is now a legal activity in many parts of the United States, but those managing patients with psychiatric disorders are in the difficult position of determining whether this use is helpful, harmful, or irrelevant to the underlying illness on the basis of limited and largely incomplete data, according to an overview of this issue presented at the virtual Psychopharmacology Update presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

HighGradeRoots/iStock/Getty Images

While there is clear evidence that cannabis use relative to the general population “is more prevalent among patients with psychiatric disorders,” it is less certain how often this use is risky, said Diana M. Martinez, MD, professor of psychiatry at Columbia University in New York.

Independent of euphoric effects, cannabis can be perceived by individuals with psychiatric diagnosis as self-medication for feelings of stress, social anxiety, and insomnia, among other symptoms. These are the same reasons why many individuals without psychiatric conditions use cannabis-containing products.

The perception that cannabis use is generally benign presumably explains the successful efforts at legalization, but there are risks for those with or without psychiatric illnesses, Dr. Martinez pointed out at the meeting, sponsored by Medscape Live. Not least, about 20% of regular users of cannabis develop cannabis use disorder (CUD), a condition defined in the DSM-5 as the continued use of cannabis despite adverse consequences, such as dependence.
 

Impact of severe CUD ‘incapacitating’

“Of those who meet criteria for CUD, 23% have severe CUD, which is an incapacitating form,” reported Dr. Martinez, citing work led by Deborah Hasin, PhD, professor of clinical epidemiology at Columbia University.

However, relative to otherwise healthy individuals, those with a psychiatric diagnosis might face greater benefits or greater risks from cannabis use, according to Dr. Martinez, who cited a 2017 report from the National Academies of Science, Engineering, and Medicine (NASEM).

This report evaluated the potential risks and benefits on the basis of published studies.

There is limited evidence that regular cannabis increases rather than modifies symptoms of mania and hypomania in patients with bipolar disorder, according to the report. The report also cited limited evidence that cannabis use increases severity of posttraumatic stress disorder (PTSD). There was limited evidence of adverse effects on symptoms of anxiety, although this appeared to depend on daily or nearly daily use.

The report found no data of acceptable quality to draw conclusions about the effect of cannabis use on symptoms of depression.

In patients with attention-deficit/hyperactivity disorder (ADHD), “a recent study showed that daily but not occasional use of cannabis increased impulsivity but not inattention, working memory, or verbal intelligence,” said Dr. Martinez, citing a study published this year.

Some evidence also suggests that patients with a psychiatric disorder might benefit from cannabis use, but, again, this evidence is limited. For one example, it includes a potential reduction in symptoms of obsessive-compulsive disorder, Dr. Martinez said.
 

More support for cannabis in medical disease

Relative to the quality of evidence supporting benefit from cannabis in psychiatric disease, the data appear to be stronger for patients with medical illnesses, such as cancer. For example, Dr. Martinez cited evidence that tetrahydrocannabinol (THC), a major active ingredient in cannabis, improves sleep in the context of a medical illnesses. There is also evidence for anxiolytic effects in patients with a medical illness, although that is weaker.

In patients with or without a psychiatric disorder, marijuana does pose a risk of substance abuse disorder, and it shares the risks of intoxicants, such as inattention leading to increased risk of accidents, including motor vehicle accidents. This pertains to those with or without a psychiatric or medical condition, Dr. Martinez said.

While intermittent light use of cannabis appears to pose no risk or a very low risk of long-term adverse effects on cognition, at least in patients without psychiatric disorders, Dr. Martinez indicated that the risk-benefit ratio for any individual is use dependent. The risk of CUD, for example, increases with the frequency of exposure and the potency of the cannabis. Dr. Martinez indicated that a conservative approach is prudent with the limited evidence available for patients with psychiatric disorders.
 

Empirical evidence for therapeutic role

In published studies, other researchers have expressed interest in a potential therapeutic role of cannabis for psychiatric disorders, but there appears to be a general consensus that the supportive data remain weak. One expert who has written on this topic, Jerome Sarris, PhD, professor of integrative mental health, NICM Health Research Institute, Western Sydney University, Westmead, Australia, said that empirical evidence does support a benefit in selected patients.

“Of course, high THC forms are strongly discouraged in people with schizophrenia or high risk of developing psychotic disorder, or in youths,” Dr. Sarris explained. “However, there is a potential role for use in people with sleep and pain issues, and many find it beneficial to also assist with affective disorder symptoms.”

In a systematic review he led that was published last year, the evidence to support cannabis for psychiatric disorders was characterized as “embryonic.” However, small studies and case reports appear to support benefit for such indications as ADHD if precautions are taken.

“I certainly would not discourage use of prescribed standardized medicinal cannabis therapeutics for all people with psychiatric disorders,” Dr. Sarris said. He suggested that attention should be made to the THC potency and terpene composition of the products that patients with psychiatric disorders are taking.

Sleeping too much or too little can lead to cognitive decline over time, but new research suggests there could be a sleep time “sweet spot” that stabilizes cognitive function.

In a longitudinal study, investigators found older adults who slept less than 4.5 hours or more than 6.5 hours a night reported significant cognitive decline over time, but cognitive scores for those with sleep duration in between that range remained stable.

“This really suggests that there’s this middle range, a ‘sweet spot,’ where your sleep is really optimal,” said lead author Brendan Lucey, MD, MSCI, associate professor of neurology and director of the Washington University Sleep Medicine Center, St. Louis.

The study, published online Oct. 20 in Brain, is part of a growing body of research that seeks to determine if sleep can be used as a marker of Alzheimer’s disease progression.
 

A complex relationship

Studies suggest a strong relationship between sleep patterns and Alzheimer’s disease, which affects nearly 6 million Americans. The challenge, Dr. Lucey said, is unwinding the complex links between sleep, Alzheimer’s disease, and cognitive function.

An earlier study by Dr. Lucey and colleagues found that poor sleep quality is associated with early signs of Alzheimer’s disease, and a report published in September found that elderly people who slept less than 6 hours a night had a greater burden of amyloid beta, a hallmark sign of Alzheimer’s disease.

For this new study, researchers monitored sleep-wake activity over 4-6 nights in 100 participants who underwent annual cognitive assessments and clinical studies, including APOE genotyping, as part of a longitudinal study at the Knight Alzheimer Disease Research Center at Washington University. Participants also provided cerebrospinal fluid (CSF) total tau and amyloid-beta42 and wore a small EEG device on their forehead while they slept.

The majority of participants had a clinical dementia rating (CDR) score of 0, indicating no cognitive impairment. Twelve individuals had a CDR >0, with most reporting mild cognitive impairment.

As expected, CSF analysis showed greater evidence of Alzheimer’s disease pathology in those with a baseline CDR greater than 0.

Changes in cognitive function were measured using a Preclinical Alzheimer Cognitive Composite (PACC) score, a composite of results from a neuropsychological testing battery that included the Free and Cued Selective Reminding Test, the Logical Memory Delayed Recall Test from the Wechsler Memory Scale-Revised, the Digit Symbol Substitution Test from the Wechsler Adult Intelligence Scale-Revised, and the Mini-Mental State Examination.

Researchers found an upside-down U-shaped relationship between PACC scores and sleep duration, with dramatic cognitive decline in those who slept less than 4.5 hours or more than 6.5 hours a night (P < .001 for both). The U-shaped relationship was also found with measures of sleep phases, including time spent in rapid eye movement and in non-REM sleep (P < .001 for both).

The findings persisted even after controlling for confounders that can affect sleep and cognition, such as age, CSF total tau/amyloid-beta-42 ratio, APOE ε4 allele carrier status, years of education, and sex.

Understanding how sleep changes at different stages of Alzheimer’s disease could help researchers determine if sleep can be used as a marker of disease progression, Dr. Lucey said. That could lead to interventions to slow that process.

“We’re not at the point yet where we can say that we need to monitor someone’s sleep time and then do an intervention to see if it would improve their risk for cognitive decline,” said Dr. Lucey, who plans to repeat this sleep study with the same cohort to track changes in sleep patterns and cognitive function over time. “But that’s a question I’m very excited to try to answer.”
 

A component of cognitive health

Commenting on the findings, Heather Snyder, PhD, vice president of medical and scientific relations for the Alzheimer’s Association, noted that the study adds to a body of evidence linking sleep and cognition, especially how sleep quality can optimize brain function.

“We’ve seen previous research that’s shown poor sleep contributes to dementia risk, as well as research showing sleep duration may play a role in cognition,” she said.

“We also need studies that look at sleep as an intervention for cognitive health,” Dr. Snyder said. “Sleep is an important aspect of our overall health. Clinicians should have conversations with their patients about sleep as part of standard discussions about their health habits and wellness.”

The study was funded by the National Institutes of Health, the American Sleep Medicine Foundation, the Roger and Paula Riney Fund, and the Daniel J. Brennan, MD Fund. Dr. Lucey consults for Merck and Eli Lilly. Dr. Snyder has disclosed no relevant financial relationships. Full disclosures are included in the original article.

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

Sleeping too much or too little can lead to cognitive decline over time, but new research suggests there could be a sleep time “sweet spot” that stabilizes cognitive function.

In a longitudinal study, investigators found older adults who slept less than 4.5 hours or more than 6.5 hours a night reported significant cognitive decline over time, but cognitive scores for those with sleep duration in between that range remained stable.

“This really suggests that there’s this middle range, a ‘sweet spot,’ where your sleep is really optimal,” said lead author Brendan Lucey, MD, MSCI, associate professor of neurology and director of the Washington University Sleep Medicine Center, St. Louis.

The study, published online Oct. 20 in Brain, is part of a growing body of research that seeks to determine if sleep can be used as a marker of Alzheimer’s disease progression.
 

A complex relationship

Studies suggest a strong relationship between sleep patterns and Alzheimer’s disease, which affects nearly 6 million Americans. The challenge, Dr. Lucey said, is unwinding the complex links between sleep, Alzheimer’s disease, and cognitive function.

An earlier study by Dr. Lucey and colleagues found that poor sleep quality is associated with early signs of Alzheimer’s disease, and a report published in September found that elderly people who slept less than 6 hours a night had a greater burden of amyloid beta, a hallmark sign of Alzheimer’s disease.

For this new study, researchers monitored sleep-wake activity over 4-6 nights in 100 participants who underwent annual cognitive assessments and clinical studies, including APOE genotyping, as part of a longitudinal study at the Knight Alzheimer Disease Research Center at Washington University. Participants also provided cerebrospinal fluid (CSF) total tau and amyloid-beta42 and wore a small EEG device on their forehead while they slept.

The majority of participants had a clinical dementia rating (CDR) score of 0, indicating no cognitive impairment. Twelve individuals had a CDR >0, with most reporting mild cognitive impairment.

As expected, CSF analysis showed greater evidence of Alzheimer’s disease pathology in those with a baseline CDR greater than 0.

Changes in cognitive function were measured using a Preclinical Alzheimer Cognitive Composite (PACC) score, a composite of results from a neuropsychological testing battery that included the Free and Cued Selective Reminding Test, the Logical Memory Delayed Recall Test from the Wechsler Memory Scale-Revised, the Digit Symbol Substitution Test from the Wechsler Adult Intelligence Scale-Revised, and the Mini-Mental State Examination.

Researchers found an upside-down U-shaped relationship between PACC scores and sleep duration, with dramatic cognitive decline in those who slept less than 4.5 hours or more than 6.5 hours a night (P < .001 for both). The U-shaped relationship was also found with measures of sleep phases, including time spent in rapid eye movement and in non-REM sleep (P < .001 for both).

The findings persisted even after controlling for confounders that can affect sleep and cognition, such as age, CSF total tau/amyloid-beta-42 ratio, APOE ε4 allele carrier status, years of education, and sex.

Understanding how sleep changes at different stages of Alzheimer’s disease could help researchers determine if sleep can be used as a marker of disease progression, Dr. Lucey said. That could lead to interventions to slow that process.

“We’re not at the point yet where we can say that we need to monitor someone’s sleep time and then do an intervention to see if it would improve their risk for cognitive decline,” said Dr. Lucey, who plans to repeat this sleep study with the same cohort to track changes in sleep patterns and cognitive function over time. “But that’s a question I’m very excited to try to answer.”
 

A component of cognitive health

Commenting on the findings, Heather Snyder, PhD, vice president of medical and scientific relations for the Alzheimer’s Association, noted that the study adds to a body of evidence linking sleep and cognition, especially how sleep quality can optimize brain function.

“We’ve seen previous research that’s shown poor sleep contributes to dementia risk, as well as research showing sleep duration may play a role in cognition,” she said.

“We also need studies that look at sleep as an intervention for cognitive health,” Dr. Snyder said. “Sleep is an important aspect of our overall health. Clinicians should have conversations with their patients about sleep as part of standard discussions about their health habits and wellness.”

The study was funded by the National Institutes of Health, the American Sleep Medicine Foundation, the Roger and Paula Riney Fund, and the Daniel J. Brennan, MD Fund. Dr. Lucey consults for Merck and Eli Lilly. Dr. Snyder has disclosed no relevant financial relationships. Full disclosures are included in the original article.

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

Sleeping too much or too little can lead to cognitive decline over time, but new research suggests there could be a sleep time “sweet spot” that stabilizes cognitive function.

In a longitudinal study, investigators found older adults who slept less than 4.5 hours or more than 6.5 hours a night reported significant cognitive decline over time, but cognitive scores for those with sleep duration in between that range remained stable.

“This really suggests that there’s this middle range, a ‘sweet spot,’ where your sleep is really optimal,” said lead author Brendan Lucey, MD, MSCI, associate professor of neurology and director of the Washington University Sleep Medicine Center, St. Louis.

The study, published online Oct. 20 in Brain, is part of a growing body of research that seeks to determine if sleep can be used as a marker of Alzheimer’s disease progression.
 

A complex relationship

Studies suggest a strong relationship between sleep patterns and Alzheimer’s disease, which affects nearly 6 million Americans. The challenge, Dr. Lucey said, is unwinding the complex links between sleep, Alzheimer’s disease, and cognitive function.

An earlier study by Dr. Lucey and colleagues found that poor sleep quality is associated with early signs of Alzheimer’s disease, and a report published in September found that elderly people who slept less than 6 hours a night had a greater burden of amyloid beta, a hallmark sign of Alzheimer’s disease.

For this new study, researchers monitored sleep-wake activity over 4-6 nights in 100 participants who underwent annual cognitive assessments and clinical studies, including APOE genotyping, as part of a longitudinal study at the Knight Alzheimer Disease Research Center at Washington University. Participants also provided cerebrospinal fluid (CSF) total tau and amyloid-beta42 and wore a small EEG device on their forehead while they slept.

The majority of participants had a clinical dementia rating (CDR) score of 0, indicating no cognitive impairment. Twelve individuals had a CDR >0, with most reporting mild cognitive impairment.

As expected, CSF analysis showed greater evidence of Alzheimer’s disease pathology in those with a baseline CDR greater than 0.

Changes in cognitive function were measured using a Preclinical Alzheimer Cognitive Composite (PACC) score, a composite of results from a neuropsychological testing battery that included the Free and Cued Selective Reminding Test, the Logical Memory Delayed Recall Test from the Wechsler Memory Scale-Revised, the Digit Symbol Substitution Test from the Wechsler Adult Intelligence Scale-Revised, and the Mini-Mental State Examination.

Researchers found an upside-down U-shaped relationship between PACC scores and sleep duration, with dramatic cognitive decline in those who slept less than 4.5 hours or more than 6.5 hours a night (P < .001 for both). The U-shaped relationship was also found with measures of sleep phases, including time spent in rapid eye movement and in non-REM sleep (P < .001 for both).

The findings persisted even after controlling for confounders that can affect sleep and cognition, such as age, CSF total tau/amyloid-beta-42 ratio, APOE ε4 allele carrier status, years of education, and sex.

Understanding how sleep changes at different stages of Alzheimer’s disease could help researchers determine if sleep can be used as a marker of disease progression, Dr. Lucey said. That could lead to interventions to slow that process.

“We’re not at the point yet where we can say that we need to monitor someone’s sleep time and then do an intervention to see if it would improve their risk for cognitive decline,” said Dr. Lucey, who plans to repeat this sleep study with the same cohort to track changes in sleep patterns and cognitive function over time. “But that’s a question I’m very excited to try to answer.”
 

A component of cognitive health

Commenting on the findings, Heather Snyder, PhD, vice president of medical and scientific relations for the Alzheimer’s Association, noted that the study adds to a body of evidence linking sleep and cognition, especially how sleep quality can optimize brain function.

“We’ve seen previous research that’s shown poor sleep contributes to dementia risk, as well as research showing sleep duration may play a role in cognition,” she said.

“We also need studies that look at sleep as an intervention for cognitive health,” Dr. Snyder said. “Sleep is an important aspect of our overall health. Clinicians should have conversations with their patients about sleep as part of standard discussions about their health habits and wellness.”

The study was funded by the National Institutes of Health, the American Sleep Medicine Foundation, the Roger and Paula Riney Fund, and the Daniel J. Brennan, MD Fund. Dr. Lucey consults for Merck and Eli Lilly. Dr. Snyder has disclosed no relevant financial relationships. Full disclosures are included in the original article.

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

I recently saw a 62-year-old patient who had been struggling in her job at a law firm. She had been one of the top paralegals for over a decade, but recently had received a poor job performance. She told me she was forgetting things and was worried she might be developing dementia. Fortunately her problem stemmed from sleep apnea, and resolved with continuous positive airway pressure (CPAP) therapy.

Wallace and Bucks performed a meta analysis of 42 studies of memory in patients with sleep apnea and found sleep apnea patients were impaired when compared to healthy controls on verbal episodic memory (immediate recall, delayed recall, learning, and recognition) and visuospatial episodic memory (immediate and delayed recall).¹ A meta-analysis by Olaithe and associates found an improvement in executive function in patients with sleep apnea who were treated with CPAP.² I think this is worth considering especially in your patients who have subjective memory disturbances and do not appear to have a mild cognitive impairment or dementia.

About 15 years ago I saw a 74-year-old man for nocturia. He had seen two urologists and had a transurethral resection of the prostate (TURP) without any real change in his nocturia. I trialed him on all sorts of medications, and he seemed to improve temporarily a little on trazodone (went from seven episodes a night to four).

Eventually, after several years, I sent him for a sleep study. He had severe sleep apnea (Apnea Hypopnea Index, 65; O₂ saturations as low as 60%). With treatment, his nocturia resolved. He went from seven episodes to two each night.

Zhou and colleagues performed a meta-analysis of 13 studies looking at the association of sleep apnea with nocturia.³ They found that men with sleep apnea have a high incidence of nocturia.

Miyazato and colleagues looked at the effect of CPAP treatment on nighttime urine production in patients with obstructive sleep apnea.⁴ In this small study of 40 patients, mean nighttime voiding episodes decreased from 2.1 to 1.2 (P < .01).

I have seen several patients with night sweats who ended up having sleep apnea. These patients have had a resolution of their night sweats with sleep apnea treatment.

Arnardottir and colleagues found that obstructive sleep apnea was associated with frequent nocturnal sweating.⁵ They found that 31% of men and 33% of women with OSA had nocturnal sweating, compared with about 10% of the general population.

When the OSA patients were treated with positive airway pressure, the prevalence of nocturnal sweating decreased to 11.5%, which is similar to general population numbers. Given how common both sleep apnea and night sweats are, this is an important consideration as you evaluate night sweats.

I have seen many patients who have had atrial fibrillation and sleep apnea. Shapira-Daniels and colleagues did a prospective study of 188 patients with atrial fibrillation without a history of sleep apnea who were referred for ablation.⁶ All patients had home sleep studies, and testing was consistent with sleep apnea in 82% of patients.

Kanagala and associates found that patients with untreated sleep apnea had a greater chance of recurrent atrial fibrillation after cardioversion.⁷ Recurrence of atrial fibrillation at 12 months was 82% in untreated OSA patients, higher than the 42% recurrence in the treated OSA group (P = .013) and the 53% recurrence in control patients.

I think sleep apnea evaluation should be strongly considered in patients with atrial fibrillation and should be done before referral for ablations.

Pearl: Consider sleep apnea as a possible cause of or contributing factor to the common primary care problems of cognitive concerns, nocturia, night sweats, and atrial fibrillation.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as 3rd-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].

References

1. Wallace A and Bucks RS. Memory and obstructive sleep apnea: a meta-analysis. Sleep. 2013;36(2):203. Epub 2013 Feb 1.

2. Olaithe M and Bucks RS. Executive dysfunction in OSA before and after treatment: a meta-analysis. Sleep. 2013;36(9):1297. Epub 2013 Sep 1.

3. Zhou J et al. Association between obstructive sleep apnea syndrome and nocturia: a meta-analysis. Sleep Breath. 2020 Dec;24(4):1293-8.

4. Miyauchi Y et al. Effect of the continuous positive airway pressure on the nocturnal urine volume or night-time frequency in patients with obstructive sleep apnea syndrome. Urology 2015;85:333.

5. Arnardottir ES et al. Nocturnal sweating–a common symptom of obstructive sleep apnoea: the Icelandic sleep apnoea cohort. BMJ Open. 2013 May 14;3(5):e002795. BMJ Open 2013;3:e002795

6. Shapira-Daniels A et al. Prevalence of undiagnosed sleep apnea in patients with atrial fibrillation and its impact on therapy. JACC Clin Electrophysiol. 2020;6(12):1499. Epub 2020 Aug 12.

7. Kanagala R et al. Obstructive sleep apnea and the recurrence of atrial fibrillation. Circulation. 2003;107(20):2589. Epub 2003 May 12.

I recently saw a 62-year-old patient who had been struggling in her job at a law firm. She had been one of the top paralegals for over a decade, but recently had received a poor job performance. She told me she was forgetting things and was worried she might be developing dementia. Fortunately her problem stemmed from sleep apnea, and resolved with continuous positive airway pressure (CPAP) therapy.

Wallace and Bucks performed a meta analysis of 42 studies of memory in patients with sleep apnea and found sleep apnea patients were impaired when compared to healthy controls on verbal episodic memory (immediate recall, delayed recall, learning, and recognition) and visuospatial episodic memory (immediate and delayed recall).¹ A meta-analysis by Olaithe and associates found an improvement in executive function in patients with sleep apnea who were treated with CPAP.² I think this is worth considering especially in your patients who have subjective memory disturbances and do not appear to have a mild cognitive impairment or dementia.

About 15 years ago I saw a 74-year-old man for nocturia. He had seen two urologists and had a transurethral resection of the prostate (TURP) without any real change in his nocturia. I trialed him on all sorts of medications, and he seemed to improve temporarily a little on trazodone (went from seven episodes a night to four).

Eventually, after several years, I sent him for a sleep study. He had severe sleep apnea (Apnea Hypopnea Index, 65; O₂ saturations as low as 60%). With treatment, his nocturia resolved. He went from seven episodes to two each night.

Zhou and colleagues performed a meta-analysis of 13 studies looking at the association of sleep apnea with nocturia.³ They found that men with sleep apnea have a high incidence of nocturia.

Miyazato and colleagues looked at the effect of CPAP treatment on nighttime urine production in patients with obstructive sleep apnea.⁴ In this small study of 40 patients, mean nighttime voiding episodes decreased from 2.1 to 1.2 (P < .01).

I have seen several patients with night sweats who ended up having sleep apnea. These patients have had a resolution of their night sweats with sleep apnea treatment.

Arnardottir and colleagues found that obstructive sleep apnea was associated with frequent nocturnal sweating.⁵ They found that 31% of men and 33% of women with OSA had nocturnal sweating, compared with about 10% of the general population.

When the OSA patients were treated with positive airway pressure, the prevalence of nocturnal sweating decreased to 11.5%, which is similar to general population numbers. Given how common both sleep apnea and night sweats are, this is an important consideration as you evaluate night sweats.

I have seen many patients who have had atrial fibrillation and sleep apnea. Shapira-Daniels and colleagues did a prospective study of 188 patients with atrial fibrillation without a history of sleep apnea who were referred for ablation.⁶ All patients had home sleep studies, and testing was consistent with sleep apnea in 82% of patients.

Kanagala and associates found that patients with untreated sleep apnea had a greater chance of recurrent atrial fibrillation after cardioversion.⁷ Recurrence of atrial fibrillation at 12 months was 82% in untreated OSA patients, higher than the 42% recurrence in the treated OSA group (P = .013) and the 53% recurrence in control patients.

I think sleep apnea evaluation should be strongly considered in patients with atrial fibrillation and should be done before referral for ablations.

Pearl: Consider sleep apnea as a possible cause of or contributing factor to the common primary care problems of cognitive concerns, nocturia, night sweats, and atrial fibrillation.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as 3rd-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].

References

1. Wallace A and Bucks RS. Memory and obstructive sleep apnea: a meta-analysis. Sleep. 2013;36(2):203. Epub 2013 Feb 1.

2. Olaithe M and Bucks RS. Executive dysfunction in OSA before and after treatment: a meta-analysis. Sleep. 2013;36(9):1297. Epub 2013 Sep 1.

3. Zhou J et al. Association between obstructive sleep apnea syndrome and nocturia: a meta-analysis. Sleep Breath. 2020 Dec;24(4):1293-8.

4. Miyauchi Y et al. Effect of the continuous positive airway pressure on the nocturnal urine volume or night-time frequency in patients with obstructive sleep apnea syndrome. Urology 2015;85:333.

5. Arnardottir ES et al. Nocturnal sweating–a common symptom of obstructive sleep apnoea: the Icelandic sleep apnoea cohort. BMJ Open. 2013 May 14;3(5):e002795. BMJ Open 2013;3:e002795

6. Shapira-Daniels A et al. Prevalence of undiagnosed sleep apnea in patients with atrial fibrillation and its impact on therapy. JACC Clin Electrophysiol. 2020;6(12):1499. Epub 2020 Aug 12.

7. Kanagala R et al. Obstructive sleep apnea and the recurrence of atrial fibrillation. Circulation. 2003;107(20):2589. Epub 2003 May 12.

I recently saw a 62-year-old patient who had been struggling in her job at a law firm. She had been one of the top paralegals for over a decade, but recently had received a poor job performance. She told me she was forgetting things and was worried she might be developing dementia. Fortunately her problem stemmed from sleep apnea, and resolved with continuous positive airway pressure (CPAP) therapy.

Wallace and Bucks performed a meta analysis of 42 studies of memory in patients with sleep apnea and found sleep apnea patients were impaired when compared to healthy controls on verbal episodic memory (immediate recall, delayed recall, learning, and recognition) and visuospatial episodic memory (immediate and delayed recall).¹ A meta-analysis by Olaithe and associates found an improvement in executive function in patients with sleep apnea who were treated with CPAP.² I think this is worth considering especially in your patients who have subjective memory disturbances and do not appear to have a mild cognitive impairment or dementia.

About 15 years ago I saw a 74-year-old man for nocturia. He had seen two urologists and had a transurethral resection of the prostate (TURP) without any real change in his nocturia. I trialed him on all sorts of medications, and he seemed to improve temporarily a little on trazodone (went from seven episodes a night to four).

Eventually, after several years, I sent him for a sleep study. He had severe sleep apnea (Apnea Hypopnea Index, 65; O₂ saturations as low as 60%). With treatment, his nocturia resolved. He went from seven episodes to two each night.

Zhou and colleagues performed a meta-analysis of 13 studies looking at the association of sleep apnea with nocturia.³ They found that men with sleep apnea have a high incidence of nocturia.

Miyazato and colleagues looked at the effect of CPAP treatment on nighttime urine production in patients with obstructive sleep apnea.⁴ In this small study of 40 patients, mean nighttime voiding episodes decreased from 2.1 to 1.2 (P < .01).

I have seen several patients with night sweats who ended up having sleep apnea. These patients have had a resolution of their night sweats with sleep apnea treatment.

Arnardottir and colleagues found that obstructive sleep apnea was associated with frequent nocturnal sweating.⁵ They found that 31% of men and 33% of women with OSA had nocturnal sweating, compared with about 10% of the general population.

When the OSA patients were treated with positive airway pressure, the prevalence of nocturnal sweating decreased to 11.5%, which is similar to general population numbers. Given how common both sleep apnea and night sweats are, this is an important consideration as you evaluate night sweats.

I have seen many patients who have had atrial fibrillation and sleep apnea. Shapira-Daniels and colleagues did a prospective study of 188 patients with atrial fibrillation without a history of sleep apnea who were referred for ablation.⁶ All patients had home sleep studies, and testing was consistent with sleep apnea in 82% of patients.

Kanagala and associates found that patients with untreated sleep apnea had a greater chance of recurrent atrial fibrillation after cardioversion.⁷ Recurrence of atrial fibrillation at 12 months was 82% in untreated OSA patients, higher than the 42% recurrence in the treated OSA group (P = .013) and the 53% recurrence in control patients.

I think sleep apnea evaluation should be strongly considered in patients with atrial fibrillation and should be done before referral for ablations.

Pearl: Consider sleep apnea as a possible cause of or contributing factor to the common primary care problems of cognitive concerns, nocturia, night sweats, and atrial fibrillation.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as 3rd-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].

References

1. Wallace A and Bucks RS. Memory and obstructive sleep apnea: a meta-analysis. Sleep. 2013;36(2):203. Epub 2013 Feb 1.

2. Olaithe M and Bucks RS. Executive dysfunction in OSA before and after treatment: a meta-analysis. Sleep. 2013;36(9):1297. Epub 2013 Sep 1.

3. Zhou J et al. Association between obstructive sleep apnea syndrome and nocturia: a meta-analysis. Sleep Breath. 2020 Dec;24(4):1293-8.

4. Miyauchi Y et al. Effect of the continuous positive airway pressure on the nocturnal urine volume or night-time frequency in patients with obstructive sleep apnea syndrome. Urology 2015;85:333.

5. Arnardottir ES et al. Nocturnal sweating–a common symptom of obstructive sleep apnoea: the Icelandic sleep apnoea cohort. BMJ Open. 2013 May 14;3(5):e002795. BMJ Open 2013;3:e002795

6. Shapira-Daniels A et al. Prevalence of undiagnosed sleep apnea in patients with atrial fibrillation and its impact on therapy. JACC Clin Electrophysiol. 2020;6(12):1499. Epub 2020 Aug 12.

7. Kanagala R et al. Obstructive sleep apnea and the recurrence of atrial fibrillation. Circulation. 2003;107(20):2589. Epub 2003 May 12.

An inpatient psychiatric diagnosis at some point over a lifetime is significantly associated with a range of sleep problems, results from the largest study of its kind show.

A prior diagnosis of major depression, schizophrenia, anxiety, or bipolar disorder was associated with a later bedtime, earlier waking time, and significantly poorer sleep quality that included frequent awakenings during the night and shorter sleep bouts.

“We were struck by the pervasiveness of sleep problems across all the diagnoses of mental illness and sleep parameters we looked at,” study investigator Michael Wainberg, PhD, a postdoctoral fellow at the Krembil Centre for Neuroinformatics at the Center for Addiction and Mental Health (CAMH), Toronto, told this news organization. “This suggests there may need to be even more of an emphasis on sleep in these patients than there already is.”

The study, which includes data from nearly 90,000 adults in the United Kingdom, was published online October 12 in PLoS Medicine.

Wavebreak Media/Thinkstockphotos

Trove of data

Data for the analysis comes from the UK Biobank, a large-scale biomedical database launched in 2006 that has collected biological and medical data on more than 500,000 individuals who consented to provide blood, urine, and saliva samples and detailed lifestyle information that is matched to their medical records.

Between 2013 and 2015, more than 103,000 of these participants agreed to wear accelerometers on their wrists for 24 hours a day for 7 days, collecting a trove of data for researchers to mine.

“This allows us to get at objectively derived sleep measures and to measure them in greater numbers of people who have experienced mental illness,” said senior author Shreejoy Tripathy, PhD, assistant professor at the University of Toronto and independent scientist for CAMH. “You can study multiple disorders at once and the influence of other variables that might not be possible in the context of other studies.”

The research is the first known large-scale transdiagnostic study of objectively measured sleep and mental health. Insomnia and other sleep disorders are common among people with mental illness, as shown in prior research, including at least one study that used the same dataset the team employed for this project.

The new findings add to that body of work, Dr. Wainberg said, and look beyond just how long a person sleeps to the quality of the sleep they get.

“We found that the metrics of sleep quality seem to be affected more than mere sleep duration,” he said.
 

Unexpected finding

After excluding participants with faulty accelerometers and those who didn’t wear them for the entire 7-day study period, data from 89,205 participants (aged 43-79, 56% female, 97% self-reported White) was included. Lifetime inpatient psychiatric diagnoses were reported in 2.5% of the entire cohort.

Researchers looked at 10 sleep measures: bedtime, wake-up time, sleep duration, wake after sleep onset, sleep efficiency, number of awakenings, duration of longest sleep bout, number of naps, and variability in bedtime and sleep duration.

Although the effect sizes were small, having any psychiatric diagnosis was associated with significantly lower scores on every sleep measure except sleep duration.

Compared with those with no inpatient psychiatric diagnosis, those with any psychiatric diagnosis were significantly more likely to:

• have a later bedtime (beta = 0.07; 95% confidence interval, 0.06-0.09)
• have later wake-up time (beta = 0.10; 95% CI, 0.09-0.11)
• wake after sleep onset (beta = 0.10; 95% CI, 0.09-0.12)
• have poorer sleep efficiency (beta = –0.12; 95% CI, −0.14 to −0.11)
• have more awakenings (beta = 0.10; 95% CI, 0.09-0.11)
• have shorter duration of their longest sleep bout (beta = –0.09; 95% CI, −0.11 to −0.08)
• take more naps (beta = 0.11; 95% CI, 0.09-0.12)
• have greater variability in their bedtime (beta = 0.08; 95% CI, 0.06-0.09)
• have greater variability in their sleep duration (beta = 0.10; 95% CI, 0.09-0.12)

The only significant differences in sleep duration were found in those with lifetime major depressive disorder, who slept significantly less (beta = −0.02; P = .003), and in those with lifetime schizophrenia, who slept significantly longer (beta = 0.02; P = .0008).

Researchers found similar results when they examined patient-reported sleep measures collected when participants enrolled in the biobank, long before they agreed to wear an accelerometer.

“Everyone with a lifetime mental illness diagnosis trended toward worse sleep quality, regardless of their diagnosis,” Dr. Tripathy said. “We didn’t expect to see that.”

Limitations of the biobank data prohibited analysis by age and past or current use of psychiatric medications. In addition, investigators were unable to determine whether mental illness was active or controlled at the time of the study. Information on these, and other factors, is needed to truly begin to understand the real-world status of sleep patterns in people with mental illness, the researchers note.

However, the biobank data demonstrates how this type of information can be collected, helping Dr. Tripathy and others to design a new study that will launch next year with patients at CAMH. This effort is part of the BrainHealth Databank, a project that aims to develop a patient data bank similar to the one in the UK that was used for this study.

“We’ve shown that you can use wearable devices to measure correlates of sleep and derive insights about the objective measurements of sleep and associate them with mental illness diagnosis,” Dr. Tripathy said.

The study received no outside funding. Dr. Wainberg and Dr. Tripathy report receiving funding from Kavli Foundation, Krembil Foundation, CAMH Discovery Fund, the McLaughlin Foundation, NSERC, and CIHR. Disclosures for other authors are fully listed in the original article.

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

An inpatient psychiatric diagnosis at some point over a lifetime is significantly associated with a range of sleep problems, results from the largest study of its kind show.

A prior diagnosis of major depression, schizophrenia, anxiety, or bipolar disorder was associated with a later bedtime, earlier waking time, and significantly poorer sleep quality that included frequent awakenings during the night and shorter sleep bouts.

“We were struck by the pervasiveness of sleep problems across all the diagnoses of mental illness and sleep parameters we looked at,” study investigator Michael Wainberg, PhD, a postdoctoral fellow at the Krembil Centre for Neuroinformatics at the Center for Addiction and Mental Health (CAMH), Toronto, told this news organization. “This suggests there may need to be even more of an emphasis on sleep in these patients than there already is.”

The study, which includes data from nearly 90,000 adults in the United Kingdom, was published online October 12 in PLoS Medicine.

Wavebreak Media/Thinkstockphotos

Trove of data

Data for the analysis comes from the UK Biobank, a large-scale biomedical database launched in 2006 that has collected biological and medical data on more than 500,000 individuals who consented to provide blood, urine, and saliva samples and detailed lifestyle information that is matched to their medical records.

Between 2013 and 2015, more than 103,000 of these participants agreed to wear accelerometers on their wrists for 24 hours a day for 7 days, collecting a trove of data for researchers to mine.

“This allows us to get at objectively derived sleep measures and to measure them in greater numbers of people who have experienced mental illness,” said senior author Shreejoy Tripathy, PhD, assistant professor at the University of Toronto and independent scientist for CAMH. “You can study multiple disorders at once and the influence of other variables that might not be possible in the context of other studies.”

The research is the first known large-scale transdiagnostic study of objectively measured sleep and mental health. Insomnia and other sleep disorders are common among people with mental illness, as shown in prior research, including at least one study that used the same dataset the team employed for this project.

The new findings add to that body of work, Dr. Wainberg said, and look beyond just how long a person sleeps to the quality of the sleep they get.

“We found that the metrics of sleep quality seem to be affected more than mere sleep duration,” he said.
 

Unexpected finding

After excluding participants with faulty accelerometers and those who didn’t wear them for the entire 7-day study period, data from 89,205 participants (aged 43-79, 56% female, 97% self-reported White) was included. Lifetime inpatient psychiatric diagnoses were reported in 2.5% of the entire cohort.

Researchers looked at 10 sleep measures: bedtime, wake-up time, sleep duration, wake after sleep onset, sleep efficiency, number of awakenings, duration of longest sleep bout, number of naps, and variability in bedtime and sleep duration.

Although the effect sizes were small, having any psychiatric diagnosis was associated with significantly lower scores on every sleep measure except sleep duration.

Compared with those with no inpatient psychiatric diagnosis, those with any psychiatric diagnosis were significantly more likely to:

• have a later bedtime (beta = 0.07; 95% confidence interval, 0.06-0.09)
• have later wake-up time (beta = 0.10; 95% CI, 0.09-0.11)
• wake after sleep onset (beta = 0.10; 95% CI, 0.09-0.12)
• have poorer sleep efficiency (beta = –0.12; 95% CI, −0.14 to −0.11)
• have more awakenings (beta = 0.10; 95% CI, 0.09-0.11)
• have shorter duration of their longest sleep bout (beta = –0.09; 95% CI, −0.11 to −0.08)
• take more naps (beta = 0.11; 95% CI, 0.09-0.12)
• have greater variability in their bedtime (beta = 0.08; 95% CI, 0.06-0.09)
• have greater variability in their sleep duration (beta = 0.10; 95% CI, 0.09-0.12)

The only significant differences in sleep duration were found in those with lifetime major depressive disorder, who slept significantly less (beta = −0.02; P = .003), and in those with lifetime schizophrenia, who slept significantly longer (beta = 0.02; P = .0008).

Researchers found similar results when they examined patient-reported sleep measures collected when participants enrolled in the biobank, long before they agreed to wear an accelerometer.

“Everyone with a lifetime mental illness diagnosis trended toward worse sleep quality, regardless of their diagnosis,” Dr. Tripathy said. “We didn’t expect to see that.”

Limitations of the biobank data prohibited analysis by age and past or current use of psychiatric medications. In addition, investigators were unable to determine whether mental illness was active or controlled at the time of the study. Information on these, and other factors, is needed to truly begin to understand the real-world status of sleep patterns in people with mental illness, the researchers note.

However, the biobank data demonstrates how this type of information can be collected, helping Dr. Tripathy and others to design a new study that will launch next year with patients at CAMH. This effort is part of the BrainHealth Databank, a project that aims to develop a patient data bank similar to the one in the UK that was used for this study.

“We’ve shown that you can use wearable devices to measure correlates of sleep and derive insights about the objective measurements of sleep and associate them with mental illness diagnosis,” Dr. Tripathy said.

The study received no outside funding. Dr. Wainberg and Dr. Tripathy report receiving funding from Kavli Foundation, Krembil Foundation, CAMH Discovery Fund, the McLaughlin Foundation, NSERC, and CIHR. Disclosures for other authors are fully listed in the original article.

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

An inpatient psychiatric diagnosis at some point over a lifetime is significantly associated with a range of sleep problems, results from the largest study of its kind show.

A prior diagnosis of major depression, schizophrenia, anxiety, or bipolar disorder was associated with a later bedtime, earlier waking time, and significantly poorer sleep quality that included frequent awakenings during the night and shorter sleep bouts.

“We were struck by the pervasiveness of sleep problems across all the diagnoses of mental illness and sleep parameters we looked at,” study investigator Michael Wainberg, PhD, a postdoctoral fellow at the Krembil Centre for Neuroinformatics at the Center for Addiction and Mental Health (CAMH), Toronto, told this news organization. “This suggests there may need to be even more of an emphasis on sleep in these patients than there already is.”

The study, which includes data from nearly 90,000 adults in the United Kingdom, was published online October 12 in PLoS Medicine.

Wavebreak Media/Thinkstockphotos

Trove of data

Data for the analysis comes from the UK Biobank, a large-scale biomedical database launched in 2006 that has collected biological and medical data on more than 500,000 individuals who consented to provide blood, urine, and saliva samples and detailed lifestyle information that is matched to their medical records.

Between 2013 and 2015, more than 103,000 of these participants agreed to wear accelerometers on their wrists for 24 hours a day for 7 days, collecting a trove of data for researchers to mine.

“This allows us to get at objectively derived sleep measures and to measure them in greater numbers of people who have experienced mental illness,” said senior author Shreejoy Tripathy, PhD, assistant professor at the University of Toronto and independent scientist for CAMH. “You can study multiple disorders at once and the influence of other variables that might not be possible in the context of other studies.”

The research is the first known large-scale transdiagnostic study of objectively measured sleep and mental health. Insomnia and other sleep disorders are common among people with mental illness, as shown in prior research, including at least one study that used the same dataset the team employed for this project.

The new findings add to that body of work, Dr. Wainberg said, and look beyond just how long a person sleeps to the quality of the sleep they get.

“We found that the metrics of sleep quality seem to be affected more than mere sleep duration,” he said.
 

Unexpected finding

After excluding participants with faulty accelerometers and those who didn’t wear them for the entire 7-day study period, data from 89,205 participants (aged 43-79, 56% female, 97% self-reported White) was included. Lifetime inpatient psychiatric diagnoses were reported in 2.5% of the entire cohort.

Researchers looked at 10 sleep measures: bedtime, wake-up time, sleep duration, wake after sleep onset, sleep efficiency, number of awakenings, duration of longest sleep bout, number of naps, and variability in bedtime and sleep duration.

Although the effect sizes were small, having any psychiatric diagnosis was associated with significantly lower scores on every sleep measure except sleep duration.

Compared with those with no inpatient psychiatric diagnosis, those with any psychiatric diagnosis were significantly more likely to:

• have a later bedtime (beta = 0.07; 95% confidence interval, 0.06-0.09)
• have later wake-up time (beta = 0.10; 95% CI, 0.09-0.11)
• wake after sleep onset (beta = 0.10; 95% CI, 0.09-0.12)
• have poorer sleep efficiency (beta = –0.12; 95% CI, −0.14 to −0.11)
• have more awakenings (beta = 0.10; 95% CI, 0.09-0.11)
• have shorter duration of their longest sleep bout (beta = –0.09; 95% CI, −0.11 to −0.08)
• take more naps (beta = 0.11; 95% CI, 0.09-0.12)
• have greater variability in their bedtime (beta = 0.08; 95% CI, 0.06-0.09)
• have greater variability in their sleep duration (beta = 0.10; 95% CI, 0.09-0.12)

The only significant differences in sleep duration were found in those with lifetime major depressive disorder, who slept significantly less (beta = −0.02; P = .003), and in those with lifetime schizophrenia, who slept significantly longer (beta = 0.02; P = .0008).

Researchers found similar results when they examined patient-reported sleep measures collected when participants enrolled in the biobank, long before they agreed to wear an accelerometer.

“Everyone with a lifetime mental illness diagnosis trended toward worse sleep quality, regardless of their diagnosis,” Dr. Tripathy said. “We didn’t expect to see that.”

Limitations of the biobank data prohibited analysis by age and past or current use of psychiatric medications. In addition, investigators were unable to determine whether mental illness was active or controlled at the time of the study. Information on these, and other factors, is needed to truly begin to understand the real-world status of sleep patterns in people with mental illness, the researchers note.

However, the biobank data demonstrates how this type of information can be collected, helping Dr. Tripathy and others to design a new study that will launch next year with patients at CAMH. This effort is part of the BrainHealth Databank, a project that aims to develop a patient data bank similar to the one in the UK that was used for this study.

“We’ve shown that you can use wearable devices to measure correlates of sleep and derive insights about the objective measurements of sleep and associate them with mental illness diagnosis,” Dr. Tripathy said.

The study received no outside funding. Dr. Wainberg and Dr. Tripathy report receiving funding from Kavli Foundation, Krembil Foundation, CAMH Discovery Fund, the McLaughlin Foundation, NSERC, and CIHR. Disclosures for other authors are fully listed in the original article.

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

American children gained a lot of weight in the last year, setting a dangerous trajectory towards metabolic disease that requires urgent policy change, according to a new report from the Robert Wood Johnson Foundation.

“Our nation’s safety net is fragile, outdated, and out of reach for millions of eligible kids and caregivers,” said Jamie Bussel, senior program officer at the RWJF, and senior author of the report. She added that the pandemic further fractured an already broken system that disproportionately overlooks “children of color and those who live farthest from economic opportunity”.
 

It’s time to think ‘bigger and better’

Ms. Bussel said, during a press conference, that congress responded to the pandemic with “an array of policy solutions,” but it’s now time to think ‘bigger and better.’

“There have been huge flexibilities deployed across the safety net program and these have been really important reliefs, but the fact is many of them are temporary emergency relief measures,” she explained.

For the past 3 years, the RWJF’s annual State of Childhood Obesity report has drawn national and state obesity data from large surveys including the National Survey of Children’s Health, the Youth Risk Behavior Surveillance System, the WIC Participant and Program Characteristics Survey, and the National Health and Nutrition Examination Survey.

Similar to in past years, this year’s data show that rates of obesity and overweight have remained relatively steady and have been highest among minority and low-income populations. For example, data from the 2019-2020 National Survey of Children’s Health, along with an analysis conducted by the Health Resources and Services Administration’s Maternal and Child Health Bureau, show that one in six – or 16.2% – of youth aged 10-17 years have obesity.

While non-Hispanic Asian children had the lowest obesity rate (8.1%), followed by non-Hispanic White children (12.1%), rates were significantly higher for Hispanic (21.4%), non-Hispanic Black (23.8%), and non-Hispanic American Indian/Alaska Native (28.7%) children, according to the report.

“Additional years of data are needed to assess whether obesity rates changed after the onset of the pandemic,” explained Ms. Bussel.
 

Digging deeper

Other studies included in this year’s report were specifically designed to measure the impact of the pandemic, and show a distinct rise in overweight and obesity, especially in younger children. For example, a retrospective cohort study using data from Kaiser Permanente Southern California showed the rate of overweight and obesity in children aged 5-11 years rose to 45.7% between March 2020 and January 2021, up from 36.2% before the pandemic.

Another of these studies, which was based on national electronic health records of more than 430,000 children, showed the obesity rate crept from 19.3% to 22.4% between August 2019 and August 2020.

“The lid we had been trying desperately to put on the obesity epidemic has come off again,” said Sandra G Hassink, MD, MSc, who is medical director of the American Academy of Pediatrics Institute for Healthy Childhood Weight.

“In the absence of COVID we had been seeing slow upticks in the numbers – and in some groups we’d been thinking maybe we were headed toward stabilization – but these numbers blow that out of the water ... COVID has escalated the rates,” she said in an interview.

“Unfortunately, these two crises – the COVID pandemic, the childhood obesity epidemic – in so many ways have exacerbated one another,” said Ms. Bussel. “It’s not a huge surprise that we’re seeing an increase in childhood obesity rates given the complete and utter disruption of every single system that circumscribes our lives.”
 

The systems that feed obesity

Addressing childhood obesity requires targeting far beyond healthy eating and physical activity, Ms. Bussel said.

“As important is whether that child has a safe place to call home. Does mom or dad or their care provider have a stable income? Is there reliable transportation? Is their access to health insurance? Is there access to high-quality health care? ... All of those factors influence the child and the family’s opportunities to live well, be healthy, and be at a healthy weight,” she noted.

The report includes a list of five main policy recommendations.

• Making free, universal school meal programs permanent.
• Extending eligibility for WIC, the Special Supplemental Nutrition Program for Women, Infants, and Children, to postpartum mothers and to children through age 6.
• Extending and expanding other programs, such as the Child Tax Credit.
• Closing the Medicaid coverage gap.
• Developing a consistent approach to collecting obesity data organized by race, ethnicity, and income level.

“Collectively, over at least the course of the last generation or two, our policy approach to obesity prevention has not been sufficient. But that doesn’t mean all of our policy approaches have been failures,” Ms. Bussel said during an interview. “Policy change does not always need to be dramatic to have a real impact on families.”

Fighting complacency

For Dr. Hassink, one of the barriers to change is society’s level of acceptance. She said an identifiable explanation for pandemic weight gain doesn’t mean society should simply shrug it off.

“If we regarded childhood obesity as the population level catastrophe that it is for chronic disease maybe people would be activated around these policy changes,” she said.

“We’re accepting a disease process that wreaks havoc on people,” noted Dr. Hassink, who was not involved in the new report. “I think it’s hard for people to realize the magnitude of the disease burden that we’re seeing. If you’re in a weight management clinic or any pediatrician’s office you would see it – you would see kids coming in with liver disease, 9-year-olds on [continuous positive airway pressure] for sleep apnea, kids needing their hips pinned because they had a hip fracture because of obesity.

“So, those of us that see the disease burden see what’s behind those numbers. The sadness of what we’re talking about is we know a lot about what could push the dial and help reduce this epidemic and we’re not doing what we already know,” added Dr. Hassink.

Ms. Bussel and Dr. Hassink reported no conflicts.

American children gained a lot of weight in the last year, setting a dangerous trajectory towards metabolic disease that requires urgent policy change, according to a new report from the Robert Wood Johnson Foundation.

“Our nation’s safety net is fragile, outdated, and out of reach for millions of eligible kids and caregivers,” said Jamie Bussel, senior program officer at the RWJF, and senior author of the report. She added that the pandemic further fractured an already broken system that disproportionately overlooks “children of color and those who live farthest from economic opportunity”.
 

It’s time to think ‘bigger and better’

Ms. Bussel said, during a press conference, that congress responded to the pandemic with “an array of policy solutions,” but it’s now time to think ‘bigger and better.’

“There have been huge flexibilities deployed across the safety net program and these have been really important reliefs, but the fact is many of them are temporary emergency relief measures,” she explained.

For the past 3 years, the RWJF’s annual State of Childhood Obesity report has drawn national and state obesity data from large surveys including the National Survey of Children’s Health, the Youth Risk Behavior Surveillance System, the WIC Participant and Program Characteristics Survey, and the National Health and Nutrition Examination Survey.

Similar to in past years, this year’s data show that rates of obesity and overweight have remained relatively steady and have been highest among minority and low-income populations. For example, data from the 2019-2020 National Survey of Children’s Health, along with an analysis conducted by the Health Resources and Services Administration’s Maternal and Child Health Bureau, show that one in six – or 16.2% – of youth aged 10-17 years have obesity.

While non-Hispanic Asian children had the lowest obesity rate (8.1%), followed by non-Hispanic White children (12.1%), rates were significantly higher for Hispanic (21.4%), non-Hispanic Black (23.8%), and non-Hispanic American Indian/Alaska Native (28.7%) children, according to the report.

“Additional years of data are needed to assess whether obesity rates changed after the onset of the pandemic,” explained Ms. Bussel.
 

Digging deeper

Other studies included in this year’s report were specifically designed to measure the impact of the pandemic, and show a distinct rise in overweight and obesity, especially in younger children. For example, a retrospective cohort study using data from Kaiser Permanente Southern California showed the rate of overweight and obesity in children aged 5-11 years rose to 45.7% between March 2020 and January 2021, up from 36.2% before the pandemic.

Another of these studies, which was based on national electronic health records of more than 430,000 children, showed the obesity rate crept from 19.3% to 22.4% between August 2019 and August 2020.

“The lid we had been trying desperately to put on the obesity epidemic has come off again,” said Sandra G Hassink, MD, MSc, who is medical director of the American Academy of Pediatrics Institute for Healthy Childhood Weight.

“In the absence of COVID we had been seeing slow upticks in the numbers – and in some groups we’d been thinking maybe we were headed toward stabilization – but these numbers blow that out of the water ... COVID has escalated the rates,” she said in an interview.

“Unfortunately, these two crises – the COVID pandemic, the childhood obesity epidemic – in so many ways have exacerbated one another,” said Ms. Bussel. “It’s not a huge surprise that we’re seeing an increase in childhood obesity rates given the complete and utter disruption of every single system that circumscribes our lives.”
 

The systems that feed obesity

Addressing childhood obesity requires targeting far beyond healthy eating and physical activity, Ms. Bussel said.

“As important is whether that child has a safe place to call home. Does mom or dad or their care provider have a stable income? Is there reliable transportation? Is their access to health insurance? Is there access to high-quality health care? ... All of those factors influence the child and the family’s opportunities to live well, be healthy, and be at a healthy weight,” she noted.

The report includes a list of five main policy recommendations.

• Making free, universal school meal programs permanent.
• Extending eligibility for WIC, the Special Supplemental Nutrition Program for Women, Infants, and Children, to postpartum mothers and to children through age 6.
• Extending and expanding other programs, such as the Child Tax Credit.
• Closing the Medicaid coverage gap.
• Developing a consistent approach to collecting obesity data organized by race, ethnicity, and income level.

“Collectively, over at least the course of the last generation or two, our policy approach to obesity prevention has not been sufficient. But that doesn’t mean all of our policy approaches have been failures,” Ms. Bussel said during an interview. “Policy change does not always need to be dramatic to have a real impact on families.”

Fighting complacency

For Dr. Hassink, one of the barriers to change is society’s level of acceptance. She said an identifiable explanation for pandemic weight gain doesn’t mean society should simply shrug it off.

“If we regarded childhood obesity as the population level catastrophe that it is for chronic disease maybe people would be activated around these policy changes,” she said.

“We’re accepting a disease process that wreaks havoc on people,” noted Dr. Hassink, who was not involved in the new report. “I think it’s hard for people to realize the magnitude of the disease burden that we’re seeing. If you’re in a weight management clinic or any pediatrician’s office you would see it – you would see kids coming in with liver disease, 9-year-olds on [continuous positive airway pressure] for sleep apnea, kids needing their hips pinned because they had a hip fracture because of obesity.

“So, those of us that see the disease burden see what’s behind those numbers. The sadness of what we’re talking about is we know a lot about what could push the dial and help reduce this epidemic and we’re not doing what we already know,” added Dr. Hassink.

Ms. Bussel and Dr. Hassink reported no conflicts.

American children gained a lot of weight in the last year, setting a dangerous trajectory towards metabolic disease that requires urgent policy change, according to a new report from the Robert Wood Johnson Foundation.

“Our nation’s safety net is fragile, outdated, and out of reach for millions of eligible kids and caregivers,” said Jamie Bussel, senior program officer at the RWJF, and senior author of the report. She added that the pandemic further fractured an already broken system that disproportionately overlooks “children of color and those who live farthest from economic opportunity”.
 

It’s time to think ‘bigger and better’

Ms. Bussel said, during a press conference, that congress responded to the pandemic with “an array of policy solutions,” but it’s now time to think ‘bigger and better.’

“There have been huge flexibilities deployed across the safety net program and these have been really important reliefs, but the fact is many of them are temporary emergency relief measures,” she explained.

For the past 3 years, the RWJF’s annual State of Childhood Obesity report has drawn national and state obesity data from large surveys including the National Survey of Children’s Health, the Youth Risk Behavior Surveillance System, the WIC Participant and Program Characteristics Survey, and the National Health and Nutrition Examination Survey.

Similar to in past years, this year’s data show that rates of obesity and overweight have remained relatively steady and have been highest among minority and low-income populations. For example, data from the 2019-2020 National Survey of Children’s Health, along with an analysis conducted by the Health Resources and Services Administration’s Maternal and Child Health Bureau, show that one in six – or 16.2% – of youth aged 10-17 years have obesity.

While non-Hispanic Asian children had the lowest obesity rate (8.1%), followed by non-Hispanic White children (12.1%), rates were significantly higher for Hispanic (21.4%), non-Hispanic Black (23.8%), and non-Hispanic American Indian/Alaska Native (28.7%) children, according to the report.

“Additional years of data are needed to assess whether obesity rates changed after the onset of the pandemic,” explained Ms. Bussel.
 

Digging deeper

Other studies included in this year’s report were specifically designed to measure the impact of the pandemic, and show a distinct rise in overweight and obesity, especially in younger children. For example, a retrospective cohort study using data from Kaiser Permanente Southern California showed the rate of overweight and obesity in children aged 5-11 years rose to 45.7% between March 2020 and January 2021, up from 36.2% before the pandemic.

Another of these studies, which was based on national electronic health records of more than 430,000 children, showed the obesity rate crept from 19.3% to 22.4% between August 2019 and August 2020.

“The lid we had been trying desperately to put on the obesity epidemic has come off again,” said Sandra G Hassink, MD, MSc, who is medical director of the American Academy of Pediatrics Institute for Healthy Childhood Weight.

“In the absence of COVID we had been seeing slow upticks in the numbers – and in some groups we’d been thinking maybe we were headed toward stabilization – but these numbers blow that out of the water ... COVID has escalated the rates,” she said in an interview.

“Unfortunately, these two crises – the COVID pandemic, the childhood obesity epidemic – in so many ways have exacerbated one another,” said Ms. Bussel. “It’s not a huge surprise that we’re seeing an increase in childhood obesity rates given the complete and utter disruption of every single system that circumscribes our lives.”
 

The systems that feed obesity

Addressing childhood obesity requires targeting far beyond healthy eating and physical activity, Ms. Bussel said.

“As important is whether that child has a safe place to call home. Does mom or dad or their care provider have a stable income? Is there reliable transportation? Is their access to health insurance? Is there access to high-quality health care? ... All of those factors influence the child and the family’s opportunities to live well, be healthy, and be at a healthy weight,” she noted.

The report includes a list of five main policy recommendations.

• Making free, universal school meal programs permanent.
• Extending eligibility for WIC, the Special Supplemental Nutrition Program for Women, Infants, and Children, to postpartum mothers and to children through age 6.
• Extending and expanding other programs, such as the Child Tax Credit.
• Closing the Medicaid coverage gap.
• Developing a consistent approach to collecting obesity data organized by race, ethnicity, and income level.

“Collectively, over at least the course of the last generation or two, our policy approach to obesity prevention has not been sufficient. But that doesn’t mean all of our policy approaches have been failures,” Ms. Bussel said during an interview. “Policy change does not always need to be dramatic to have a real impact on families.”

Fighting complacency

For Dr. Hassink, one of the barriers to change is society’s level of acceptance. She said an identifiable explanation for pandemic weight gain doesn’t mean society should simply shrug it off.

“If we regarded childhood obesity as the population level catastrophe that it is for chronic disease maybe people would be activated around these policy changes,” she said.

“We’re accepting a disease process that wreaks havoc on people,” noted Dr. Hassink, who was not involved in the new report. “I think it’s hard for people to realize the magnitude of the disease burden that we’re seeing. If you’re in a weight management clinic or any pediatrician’s office you would see it – you would see kids coming in with liver disease, 9-year-olds on [continuous positive airway pressure] for sleep apnea, kids needing their hips pinned because they had a hip fracture because of obesity.

“So, those of us that see the disease burden see what’s behind those numbers. The sadness of what we’re talking about is we know a lot about what could push the dial and help reduce this epidemic and we’re not doing what we already know,” added Dr. Hassink.

Ms. Bussel and Dr. Hassink reported no conflicts.

Sixteen-year-old Ana and is sitting on the bench with her science teacher, Ms. Tehrani, waiting for the bus to take them back to their village after school. Ana wants to hear her science teacher’s opinion about her grandmother.

Do you respect your grandmother?

Why yes, of course, why to do you ask?

So you think my grandmother is wise when she tells me old wife tales?

Like what?

Well, she says not to take my medicine because it will have bad effects and that I should take her remedies instead.

What else does she tell you?

Well, she says that people are born how they are and that they belong to either God or the Devil, not to their parents.

What else?

She thinks I am a fay child; she has always said that about me.

What does that mean?

It means that I have my own ways, fairy ways, and that I should go out in the forest and listen.

Do you?

Yes.

What do you hear?

I hear about my destiny.

What do you hear?

I hear that I must wash in witch hazel. My grandmother taught me how to find it and how to prepare it. She said I should sit in the forest and wait for a sign.

What sign?

I don’t know.

Well, what do you think about your grandmother?

I love her but …

But what?

I think she might be wrong about all of this, you know, science and all that.

But you do it, anyway?

Yes.

Why?

Aren’t we supposed to respect our elders, and aren’t they supposed to be wise?



Ms. Tehrani is in a bind. What to say? She has no ready answer, feeling caught between two beliefs: the unscientific basis of ineffective old wives’ treatments and the purported wisdom of our elders. She knows Ana’s family and that there are women in that family going back generations who are identified as medicine women or women with the special powers of the forest.

Ana wants to study science but she is being groomed as the family wise mother. Ana is caught between the ways of the past and the ways of the future. She sees that to go with the future is to devalue her family tradition. If she chooses to study medicine, can she keep the balance between magical ways and the ways of science?

Ms. Tehrani decides to expose her class to Indigenous and preindustrial cultural practices and what science has to say. She describes how knowledge is passed down through the generations, and how some of this knowledge has now been proved correct by science, such as the use of opium for pain management and how some knowledge has been corrected by science. She asks the class: What myths have been passed down in your family that science has shown to be effective or ineffective? What does science have to say about how we live our lives?

After a baby in the village dies, Ms. Tehrani asks the local health center to think about implementing a teaching course on caring for babies, a course that will discuss tradition and science. She is well aware of the fact that Black mothers tend not to follow the advice of the pediatricians who now recommend that parents put babies to sleep on their backs. Black women trust the advice of their paternal and maternal grandmothers more than the advice of health care providers, research by Deborah Stiffler, PhD, RN, CNM, shows (J Spec Pediatr Nurs. 2018 Apr;23[2]:e12213). While new Black mothers feel that they have limited knowledge and are eager to learn about safe sleep practices, their grandmothers were skeptical – and the grandmothers often won that argument. Black mothers believed that their own mothers knew best, based on their experience raising infants.

In Dr. Stiffler’s study, one grandmother commented: “Girls today need a mother to help them take care of their babies. They don’t know how to do anything. When I was growing up, our moms helped us.”

One new mother said: I “listen more to the elderly people because like the social workers and stuff some of them don’t have kids. They just go by the book … so I feel like I listen more to like my grandparents.”
 

Integrating traditions

When Ana enters medical school she is faced with the task of integration of traditional practice and Western medicine. Ana looks to the National Center for Complementary and Integrative Health (NCCIH), the U.S. government’s lead agency for scientific research on complementary and integrative health approaches for support in her task. The NCCIH was established in 1998 with the mission of determining the usefulness and safety of complementary and integrative health approaches, and their roles in improving health and health care.

The NCCIH notes that more than 30% of adults use health care approaches that are not part of conventional medical care or that have origins outside of usual Western practice, and 17.7% of American adults had used a dietary supplement other than vitamins and minerals in the past year, most commonly fish oil. This agency notes that large rigorous research studies extend to only a few dietary supplements, with results showing that the products didn’t work for the conditions studied. The work of the NCCIH is mirrored worldwide.

The 2008 Beijing Declaration called on World Health Organization member states and other stakeholders to integrate traditional medicine and complementary alternative medicines into national health care systems. The WHO Congress on Traditional Medicine recognizes that traditional medicine (TM) may be more affordable and accessible than Western medicine, and that it plays an important role in meeting the demands of primary health care in many developing countries. From 70% to 80% of the population in India and Ethiopia depend on TM for primary health care, and 70% of the population in Canada and 80% in Germany are reported to have used TM as complementary and/or alternative medical treatment.

After graduation and residency, Ana returns to her village and helps her science teacher consider how best to shape the intergenerational transmission of knowledge, so that it is both honored by the elders and also shaped by the science of medicine.

Every village, regardless of where it is in the world, has to contend with finding the balance between the traditional medical knowledge that is passed down through the family and the discoveries of science. When it comes to practicing medicine and psychiatry, a respect for family tradition must be weighed against the application of science: this is a long conversation that is well worth its time.
 

Dr. Heru is professor of psychiatry at the University of Colorado at Denver, Aurora. She is editor of “Working With Families in Medical Settings: A Multidisciplinary Guide for Psychiatrists and Other Health Professionals” (New York: Routledge, 2013). Dr. Heru has no conflicts of interest. Contact Dr. Heru at [email protected].

Sixteen-year-old Ana and is sitting on the bench with her science teacher, Ms. Tehrani, waiting for the bus to take them back to their village after school. Ana wants to hear her science teacher’s opinion about her grandmother.

Do you respect your grandmother?

Why yes, of course, why to do you ask?

So you think my grandmother is wise when she tells me old wife tales?

Like what?

Well, she says not to take my medicine because it will have bad effects and that I should take her remedies instead.

What else does she tell you?

Well, she says that people are born how they are and that they belong to either God or the Devil, not to their parents.

What else?

She thinks I am a fay child; she has always said that about me.

What does that mean?

It means that I have my own ways, fairy ways, and that I should go out in the forest and listen.

Do you?

Yes.

What do you hear?

I hear about my destiny.

What do you hear?

I hear that I must wash in witch hazel. My grandmother taught me how to find it and how to prepare it. She said I should sit in the forest and wait for a sign.

What sign?

I don’t know.

Well, what do you think about your grandmother?

I love her but …

But what?

I think she might be wrong about all of this, you know, science and all that.

But you do it, anyway?

Yes.

Why?

Aren’t we supposed to respect our elders, and aren’t they supposed to be wise?



Ms. Tehrani is in a bind. What to say? She has no ready answer, feeling caught between two beliefs: the unscientific basis of ineffective old wives’ treatments and the purported wisdom of our elders. She knows Ana’s family and that there are women in that family going back generations who are identified as medicine women or women with the special powers of the forest.

Ana wants to study science but she is being groomed as the family wise mother. Ana is caught between the ways of the past and the ways of the future. She sees that to go with the future is to devalue her family tradition. If she chooses to study medicine, can she keep the balance between magical ways and the ways of science?

Ms. Tehrani decides to expose her class to Indigenous and preindustrial cultural practices and what science has to say. She describes how knowledge is passed down through the generations, and how some of this knowledge has now been proved correct by science, such as the use of opium for pain management and how some knowledge has been corrected by science. She asks the class: What myths have been passed down in your family that science has shown to be effective or ineffective? What does science have to say about how we live our lives?

After a baby in the village dies, Ms. Tehrani asks the local health center to think about implementing a teaching course on caring for babies, a course that will discuss tradition and science. She is well aware of the fact that Black mothers tend not to follow the advice of the pediatricians who now recommend that parents put babies to sleep on their backs. Black women trust the advice of their paternal and maternal grandmothers more than the advice of health care providers, research by Deborah Stiffler, PhD, RN, CNM, shows (J Spec Pediatr Nurs. 2018 Apr;23[2]:e12213). While new Black mothers feel that they have limited knowledge and are eager to learn about safe sleep practices, their grandmothers were skeptical – and the grandmothers often won that argument. Black mothers believed that their own mothers knew best, based on their experience raising infants.

In Dr. Stiffler’s study, one grandmother commented: “Girls today need a mother to help them take care of their babies. They don’t know how to do anything. When I was growing up, our moms helped us.”

One new mother said: I “listen more to the elderly people because like the social workers and stuff some of them don’t have kids. They just go by the book … so I feel like I listen more to like my grandparents.”
 

Integrating traditions

When Ana enters medical school she is faced with the task of integration of traditional practice and Western medicine. Ana looks to the National Center for Complementary and Integrative Health (NCCIH), the U.S. government’s lead agency for scientific research on complementary and integrative health approaches for support in her task. The NCCIH was established in 1998 with the mission of determining the usefulness and safety of complementary and integrative health approaches, and their roles in improving health and health care.

The NCCIH notes that more than 30% of adults use health care approaches that are not part of conventional medical care or that have origins outside of usual Western practice, and 17.7% of American adults had used a dietary supplement other than vitamins and minerals in the past year, most commonly fish oil. This agency notes that large rigorous research studies extend to only a few dietary supplements, with results showing that the products didn’t work for the conditions studied. The work of the NCCIH is mirrored worldwide.

The 2008 Beijing Declaration called on World Health Organization member states and other stakeholders to integrate traditional medicine and complementary alternative medicines into national health care systems. The WHO Congress on Traditional Medicine recognizes that traditional medicine (TM) may be more affordable and accessible than Western medicine, and that it plays an important role in meeting the demands of primary health care in many developing countries. From 70% to 80% of the population in India and Ethiopia depend on TM for primary health care, and 70% of the population in Canada and 80% in Germany are reported to have used TM as complementary and/or alternative medical treatment.

After graduation and residency, Ana returns to her village and helps her science teacher consider how best to shape the intergenerational transmission of knowledge, so that it is both honored by the elders and also shaped by the science of medicine.

Every village, regardless of where it is in the world, has to contend with finding the balance between the traditional medical knowledge that is passed down through the family and the discoveries of science. When it comes to practicing medicine and psychiatry, a respect for family tradition must be weighed against the application of science: this is a long conversation that is well worth its time.
 

Dr. Heru is professor of psychiatry at the University of Colorado at Denver, Aurora. She is editor of “Working With Families in Medical Settings: A Multidisciplinary Guide for Psychiatrists and Other Health Professionals” (New York: Routledge, 2013). Dr. Heru has no conflicts of interest. Contact Dr. Heru at [email protected].

Sixteen-year-old Ana and is sitting on the bench with her science teacher, Ms. Tehrani, waiting for the bus to take them back to their village after school. Ana wants to hear her science teacher’s opinion about her grandmother.

Do you respect your grandmother?

Why yes, of course, why to do you ask?

So you think my grandmother is wise when she tells me old wife tales?

Like what?

Well, she says not to take my medicine because it will have bad effects and that I should take her remedies instead.

What else does she tell you?

Well, she says that people are born how they are and that they belong to either God or the Devil, not to their parents.

What else?

She thinks I am a fay child; she has always said that about me.

What does that mean?

It means that I have my own ways, fairy ways, and that I should go out in the forest and listen.

Do you?

Yes.

What do you hear?

I hear about my destiny.

What do you hear?

I hear that I must wash in witch hazel. My grandmother taught me how to find it and how to prepare it. She said I should sit in the forest and wait for a sign.

What sign?

I don’t know.

Well, what do you think about your grandmother?

I love her but …

But what?

I think she might be wrong about all of this, you know, science and all that.

But you do it, anyway?

Yes.

Why?

Aren’t we supposed to respect our elders, and aren’t they supposed to be wise?



Ms. Tehrani is in a bind. What to say? She has no ready answer, feeling caught between two beliefs: the unscientific basis of ineffective old wives’ treatments and the purported wisdom of our elders. She knows Ana’s family and that there are women in that family going back generations who are identified as medicine women or women with the special powers of the forest.

Ana wants to study science but she is being groomed as the family wise mother. Ana is caught between the ways of the past and the ways of the future. She sees that to go with the future is to devalue her family tradition. If she chooses to study medicine, can she keep the balance between magical ways and the ways of science?

Ms. Tehrani decides to expose her class to Indigenous and preindustrial cultural practices and what science has to say. She describes how knowledge is passed down through the generations, and how some of this knowledge has now been proved correct by science, such as the use of opium for pain management and how some knowledge has been corrected by science. She asks the class: What myths have been passed down in your family that science has shown to be effective or ineffective? What does science have to say about how we live our lives?

After a baby in the village dies, Ms. Tehrani asks the local health center to think about implementing a teaching course on caring for babies, a course that will discuss tradition and science. She is well aware of the fact that Black mothers tend not to follow the advice of the pediatricians who now recommend that parents put babies to sleep on their backs. Black women trust the advice of their paternal and maternal grandmothers more than the advice of health care providers, research by Deborah Stiffler, PhD, RN, CNM, shows (J Spec Pediatr Nurs. 2018 Apr;23[2]:e12213). While new Black mothers feel that they have limited knowledge and are eager to learn about safe sleep practices, their grandmothers were skeptical – and the grandmothers often won that argument. Black mothers believed that their own mothers knew best, based on their experience raising infants.

In Dr. Stiffler’s study, one grandmother commented: “Girls today need a mother to help them take care of their babies. They don’t know how to do anything. When I was growing up, our moms helped us.”

One new mother said: I “listen more to the elderly people because like the social workers and stuff some of them don’t have kids. They just go by the book … so I feel like I listen more to like my grandparents.”
 

Integrating traditions

When Ana enters medical school she is faced with the task of integration of traditional practice and Western medicine. Ana looks to the National Center for Complementary and Integrative Health (NCCIH), the U.S. government’s lead agency for scientific research on complementary and integrative health approaches for support in her task. The NCCIH was established in 1998 with the mission of determining the usefulness and safety of complementary and integrative health approaches, and their roles in improving health and health care.

The NCCIH notes that more than 30% of adults use health care approaches that are not part of conventional medical care or that have origins outside of usual Western practice, and 17.7% of American adults had used a dietary supplement other than vitamins and minerals in the past year, most commonly fish oil. This agency notes that large rigorous research studies extend to only a few dietary supplements, with results showing that the products didn’t work for the conditions studied. The work of the NCCIH is mirrored worldwide.

The 2008 Beijing Declaration called on World Health Organization member states and other stakeholders to integrate traditional medicine and complementary alternative medicines into national health care systems. The WHO Congress on Traditional Medicine recognizes that traditional medicine (TM) may be more affordable and accessible than Western medicine, and that it plays an important role in meeting the demands of primary health care in many developing countries. From 70% to 80% of the population in India and Ethiopia depend on TM for primary health care, and 70% of the population in Canada and 80% in Germany are reported to have used TM as complementary and/or alternative medical treatment.

After graduation and residency, Ana returns to her village and helps her science teacher consider how best to shape the intergenerational transmission of knowledge, so that it is both honored by the elders and also shaped by the science of medicine.

Every village, regardless of where it is in the world, has to contend with finding the balance between the traditional medical knowledge that is passed down through the family and the discoveries of science. When it comes to practicing medicine and psychiatry, a respect for family tradition must be weighed against the application of science: this is a long conversation that is well worth its time.
 

Dr. Heru is professor of psychiatry at the University of Colorado at Denver, Aurora. She is editor of “Working With Families in Medical Settings: A Multidisciplinary Guide for Psychiatrists and Other Health Professionals” (New York: Routledge, 2013). Dr. Heru has no conflicts of interest. Contact Dr. Heru at [email protected].