Sleep Medicine

Severe maternal sleep-disordered breathing (SDB) is a known risk factor for gestational diabetes, which is commonly diagnosed in the second or third trimester of pregnancy.

Now, a new study suggests that increases in insulin resistance, a precursor for gestational diabetes, may take place as early as the first trimester of pregnancy in women with risk factors for obstructive sleep apnea (OSA), such as overweight and habitual snoring.

This finding could potentially provide physicians with a window of opportunity to improve outcomes by screening at-risk women early in pregnancy or even prior to conception, Laura Sanapo, MD, assistant professor of medicine (research) at Brown University, Providence, R.I., and colleagues wrote in Sleep.

“Further studies are needed to investigate the association and its impact on the development of gestational diabetes, and to establish whether early-gestation or pregestational treatment of SDB would improve glucose metabolic outcomes in pregnancy,” they wrote.

”What this paper demonstrates is that the changes that predate gestational diabetes are seen much earlier in pregnancy,” senior study author Ghada Bourjeily, MD, professor of medicine at Brown University, said in an interview. Women should be screened for SDB rather than insulin resistance in early pregnancy since continuous positive airway pressure therapy (CPAP) is a highly effective intervention.

Waiting until midpregnancy to screen for OSA “is too late to make significant changes in the care of these women,” said Dr. Bourjeily, who is also director of research and training at the Women’s Medicine Collaborative at The Miriam Hospital in Providence, R.I. “By the time you diagnose gestational diabetes, the cat is out of the bag.”

For the study, women with early singleton pregnancies and risk factors for OSA such as habitual snoring and a median body mass index (BMI) of at least 27 kg/m² were recruited from two prospective clinical trial studies enriched for OSA positivity. Women with a history of pregestational diabetes and those using CPAP or receiving chronic steroid therapy were excluded from the current study.

A total of 192 study participants underwent in-home sleep study (HSAT) and homeostatic model assessment (HOMA) between 11 and 15 gestational weeks, respectively. The association between continuous measures of SDB as a respiratory-event index as well as oxygen-desaturation index and glucose metabolism parameters such as insulin resistance (HOMA-IR) were analyzed after adjusting for gestational age, maternal age, BMI, ethnicity, race, and parity.

In all, 61 women (32%) were diagnosed with OSA based on respiratory event index values greater than or equal to five events per hour. These participants were more likely to be older, to have a high BMI, and to be multipara, compared with women who didn’t have a diagnosis of OSA. Women with a diagnosis of OSA exhibited higher glucose and C-peptide values and a higher degree of insulin resistance, compared with women without OSA, the researchers found. An increase of 0.3 in HOMA-IR related to maternal SDB in early pregnancy may significantly affect glucose metabolism.

Although the findings of the current study cannot be extrapolated to women who don’t have overweight or obesity, some women with normal-range BMI (18.5-24.9) are also at increased risk of glucose metabolism changes, Dr. Bourjeily pointed out. This includes those of Southeast Asian descent. “We found that the association of SDB parameters with insulin resistance was actually happening independently of BMI and other factors.”

Ideally, screening for SDB would begin prior to pregnancy, Dr. Bourjeily said. A BMI greater than 25 should be taken into account and patients asked if they snore and if so, whether it’s loud enough to wake their partner. They should also be asked about experiencing daytime sleepiness.

“Based on these answers, especially in women screened prior to pregnancy, there will be time to make the diagnosis of sleep apnea and get the patient on CPAP,” Dr. Bourjeily said.

“This is an interesting study and one of the rare ones looking at early pregnancy and some of the mechanisms that could possibly be contributing to gestational diabetes,” commented Grenye O’Malley, MD, assistant professor in the division of endocrinology, diabetes, and bone disease at the Icahn School of Medicine at Mount Sinai, New York. Dr. O’Malley was not involved in the study.

“It confirms our suspicions that there’s probably a lot of things happening earlier in pregnancy before a diagnosis of gestational diabetes. It also confirms that some of the mechanisms are probably very similar to those involved in the association between disordered sleep and the development of type 2 diabetes.”

However, it’s too early to determine whether screening for SDB and the use of CPAP will prevent glycemic changes, Dr. O’Malley said in an interview. “Whenever we screen, we ask whether we have an intervention that changes outcomes and we don’t know that yet.”

Some of the symptoms of SDB are also common in early pregnancy, such as a BMI greater than 25 and daytime sleepiness, Dr. O’Malley pointed out. It was unclear whether the study participants had a propensity to develop type 2 diabetes or whether they were at risk of gestational diabetes.

This study was funded by the National Heart, Lung, and Blood Institute; the National Institute for Child Health; and the National Institute of General Medical Sciences. Dr. Bourjeily and colleagues, as well as Dr. O’Malley, reported having no potential financial conflicts of interest.

Severe maternal sleep-disordered breathing (SDB) is a known risk factor for gestational diabetes, which is commonly diagnosed in the second or third trimester of pregnancy.

Now, a new study suggests that increases in insulin resistance, a precursor for gestational diabetes, may take place as early as the first trimester of pregnancy in women with risk factors for obstructive sleep apnea (OSA), such as overweight and habitual snoring.

This finding could potentially provide physicians with a window of opportunity to improve outcomes by screening at-risk women early in pregnancy or even prior to conception, Laura Sanapo, MD, assistant professor of medicine (research) at Brown University, Providence, R.I., and colleagues wrote in Sleep.

“Further studies are needed to investigate the association and its impact on the development of gestational diabetes, and to establish whether early-gestation or pregestational treatment of SDB would improve glucose metabolic outcomes in pregnancy,” they wrote.

”What this paper demonstrates is that the changes that predate gestational diabetes are seen much earlier in pregnancy,” senior study author Ghada Bourjeily, MD, professor of medicine at Brown University, said in an interview. Women should be screened for SDB rather than insulin resistance in early pregnancy since continuous positive airway pressure therapy (CPAP) is a highly effective intervention.

Waiting until midpregnancy to screen for OSA “is too late to make significant changes in the care of these women,” said Dr. Bourjeily, who is also director of research and training at the Women’s Medicine Collaborative at The Miriam Hospital in Providence, R.I. “By the time you diagnose gestational diabetes, the cat is out of the bag.”

For the study, women with early singleton pregnancies and risk factors for OSA such as habitual snoring and a median body mass index (BMI) of at least 27 kg/m² were recruited from two prospective clinical trial studies enriched for OSA positivity. Women with a history of pregestational diabetes and those using CPAP or receiving chronic steroid therapy were excluded from the current study.

A total of 192 study participants underwent in-home sleep study (HSAT) and homeostatic model assessment (HOMA) between 11 and 15 gestational weeks, respectively. The association between continuous measures of SDB as a respiratory-event index as well as oxygen-desaturation index and glucose metabolism parameters such as insulin resistance (HOMA-IR) were analyzed after adjusting for gestational age, maternal age, BMI, ethnicity, race, and parity.

In all, 61 women (32%) were diagnosed with OSA based on respiratory event index values greater than or equal to five events per hour. These participants were more likely to be older, to have a high BMI, and to be multipara, compared with women who didn’t have a diagnosis of OSA. Women with a diagnosis of OSA exhibited higher glucose and C-peptide values and a higher degree of insulin resistance, compared with women without OSA, the researchers found. An increase of 0.3 in HOMA-IR related to maternal SDB in early pregnancy may significantly affect glucose metabolism.

Although the findings of the current study cannot be extrapolated to women who don’t have overweight or obesity, some women with normal-range BMI (18.5-24.9) are also at increased risk of glucose metabolism changes, Dr. Bourjeily pointed out. This includes those of Southeast Asian descent. “We found that the association of SDB parameters with insulin resistance was actually happening independently of BMI and other factors.”

Ideally, screening for SDB would begin prior to pregnancy, Dr. Bourjeily said. A BMI greater than 25 should be taken into account and patients asked if they snore and if so, whether it’s loud enough to wake their partner. They should also be asked about experiencing daytime sleepiness.

“Based on these answers, especially in women screened prior to pregnancy, there will be time to make the diagnosis of sleep apnea and get the patient on CPAP,” Dr. Bourjeily said.

“This is an interesting study and one of the rare ones looking at early pregnancy and some of the mechanisms that could possibly be contributing to gestational diabetes,” commented Grenye O’Malley, MD, assistant professor in the division of endocrinology, diabetes, and bone disease at the Icahn School of Medicine at Mount Sinai, New York. Dr. O’Malley was not involved in the study.

“It confirms our suspicions that there’s probably a lot of things happening earlier in pregnancy before a diagnosis of gestational diabetes. It also confirms that some of the mechanisms are probably very similar to those involved in the association between disordered sleep and the development of type 2 diabetes.”

However, it’s too early to determine whether screening for SDB and the use of CPAP will prevent glycemic changes, Dr. O’Malley said in an interview. “Whenever we screen, we ask whether we have an intervention that changes outcomes and we don’t know that yet.”

Some of the symptoms of SDB are also common in early pregnancy, such as a BMI greater than 25 and daytime sleepiness, Dr. O’Malley pointed out. It was unclear whether the study participants had a propensity to develop type 2 diabetes or whether they were at risk of gestational diabetes.

This study was funded by the National Heart, Lung, and Blood Institute; the National Institute for Child Health; and the National Institute of General Medical Sciences. Dr. Bourjeily and colleagues, as well as Dr. O’Malley, reported having no potential financial conflicts of interest.

Severe maternal sleep-disordered breathing (SDB) is a known risk factor for gestational diabetes, which is commonly diagnosed in the second or third trimester of pregnancy.

Now, a new study suggests that increases in insulin resistance, a precursor for gestational diabetes, may take place as early as the first trimester of pregnancy in women with risk factors for obstructive sleep apnea (OSA), such as overweight and habitual snoring.

This finding could potentially provide physicians with a window of opportunity to improve outcomes by screening at-risk women early in pregnancy or even prior to conception, Laura Sanapo, MD, assistant professor of medicine (research) at Brown University, Providence, R.I., and colleagues wrote in Sleep.

“Further studies are needed to investigate the association and its impact on the development of gestational diabetes, and to establish whether early-gestation or pregestational treatment of SDB would improve glucose metabolic outcomes in pregnancy,” they wrote.

”What this paper demonstrates is that the changes that predate gestational diabetes are seen much earlier in pregnancy,” senior study author Ghada Bourjeily, MD, professor of medicine at Brown University, said in an interview. Women should be screened for SDB rather than insulin resistance in early pregnancy since continuous positive airway pressure therapy (CPAP) is a highly effective intervention.

Waiting until midpregnancy to screen for OSA “is too late to make significant changes in the care of these women,” said Dr. Bourjeily, who is also director of research and training at the Women’s Medicine Collaborative at The Miriam Hospital in Providence, R.I. “By the time you diagnose gestational diabetes, the cat is out of the bag.”

For the study, women with early singleton pregnancies and risk factors for OSA such as habitual snoring and a median body mass index (BMI) of at least 27 kg/m² were recruited from two prospective clinical trial studies enriched for OSA positivity. Women with a history of pregestational diabetes and those using CPAP or receiving chronic steroid therapy were excluded from the current study.

A total of 192 study participants underwent in-home sleep study (HSAT) and homeostatic model assessment (HOMA) between 11 and 15 gestational weeks, respectively. The association between continuous measures of SDB as a respiratory-event index as well as oxygen-desaturation index and glucose metabolism parameters such as insulin resistance (HOMA-IR) were analyzed after adjusting for gestational age, maternal age, BMI, ethnicity, race, and parity.

In all, 61 women (32%) were diagnosed with OSA based on respiratory event index values greater than or equal to five events per hour. These participants were more likely to be older, to have a high BMI, and to be multipara, compared with women who didn’t have a diagnosis of OSA. Women with a diagnosis of OSA exhibited higher glucose and C-peptide values and a higher degree of insulin resistance, compared with women without OSA, the researchers found. An increase of 0.3 in HOMA-IR related to maternal SDB in early pregnancy may significantly affect glucose metabolism.

Although the findings of the current study cannot be extrapolated to women who don’t have overweight or obesity, some women with normal-range BMI (18.5-24.9) are also at increased risk of glucose metabolism changes, Dr. Bourjeily pointed out. This includes those of Southeast Asian descent. “We found that the association of SDB parameters with insulin resistance was actually happening independently of BMI and other factors.”

Ideally, screening for SDB would begin prior to pregnancy, Dr. Bourjeily said. A BMI greater than 25 should be taken into account and patients asked if they snore and if so, whether it’s loud enough to wake their partner. They should also be asked about experiencing daytime sleepiness.

“Based on these answers, especially in women screened prior to pregnancy, there will be time to make the diagnosis of sleep apnea and get the patient on CPAP,” Dr. Bourjeily said.

“This is an interesting study and one of the rare ones looking at early pregnancy and some of the mechanisms that could possibly be contributing to gestational diabetes,” commented Grenye O’Malley, MD, assistant professor in the division of endocrinology, diabetes, and bone disease at the Icahn School of Medicine at Mount Sinai, New York. Dr. O’Malley was not involved in the study.

“It confirms our suspicions that there’s probably a lot of things happening earlier in pregnancy before a diagnosis of gestational diabetes. It also confirms that some of the mechanisms are probably very similar to those involved in the association between disordered sleep and the development of type 2 diabetes.”

However, it’s too early to determine whether screening for SDB and the use of CPAP will prevent glycemic changes, Dr. O’Malley said in an interview. “Whenever we screen, we ask whether we have an intervention that changes outcomes and we don’t know that yet.”

Some of the symptoms of SDB are also common in early pregnancy, such as a BMI greater than 25 and daytime sleepiness, Dr. O’Malley pointed out. It was unclear whether the study participants had a propensity to develop type 2 diabetes or whether they were at risk of gestational diabetes.

This study was funded by the National Heart, Lung, and Blood Institute; the National Institute for Child Health; and the National Institute of General Medical Sciences. Dr. Bourjeily and colleagues, as well as Dr. O’Malley, reported having no potential financial conflicts of interest.

The Food and Drug Administration has approved the dual orexin receptor antagonist daridorexant (Quviviq) for the treatment of insomnia in adults, the drug’s manufacturer, Idorsia, has announced.

The FDA’s decision was based partly on a phase 3 trial of adults with moderate to severe insomnia who were randomly assigned to receive 25 or 50 mg of daridorexant or matching placebo. Daridorexant was associated with dose-dependent improvements in wake after sleep onset, total sleep time, and latency to persistent sleep.

Whereas the overall results are very positive, the improvements in daytime functioning are especially “exciting,” Thomas Roth, PhD, director of the Sleep Disorders and Research Center at Henry Ford Hospital in Detroit, said in an interview.

“That’s sort of a big deal. For me, that’s the biggest deal there is,” said Dr. Roth, who was a consultant on the design of the phase 3 trial and on the interpretation of the data.

The drug will be available in doses of 25 mg and 50 mg, and the FDA has recommended that it be classified as a controlled substance. After it is scheduled by the Drug Enforcement Administration, daridorexant is expected to be made available in May.
 

Favorable safety profile

Insomnia is a common disorder characterized by difficulty falling asleep or staying asleep and by early-morning awakenings. Patients with insomnia often report fatigue, irritability, and difficulty with concentration. The condition can also result in significant problems with work and social activities, thus contributing to anxiety or depression.

As with other dual orexin receptor antagonists, daridorexant competitively binds with both orexin receptors in the lateral hypothalamus to block the activity of orexin in a reversible way. This approach decreases the downstream action of the wake-promoting neurotransmitters that are overactive in patients with insomnia.

The phase 3 trial measured daytime functioning using the new Insomnia Daytime Symptoms and Impacts Questionnaire (IDSIQ), a patient-reported outcome instrument. Daridorexant was associated with significant improvements in daytime function, particularly in sleepiness and mood.

Previous trials of other dual orexin receptor antagonists did not use the IDSIQ as an outcome, so it is not possible to compare daridorexant with those drugs in this respect, Dr. Roth noted. Researchers also have not conducted head-to-head trials of the drug with other dual orexin receptor antagonists.

Daridorexant also had a favorable safety profile and was not associated with rebound insomnia or withdrawal effects. The most common adverse events were headache and somnolence or fatigue.

“They had no effect on sleep stage distribution [and] they had no significant effects on sleep and breathing in people with mild to moderate sleep apnea,” said Dr. Roth, who presented the phase 3 findings at SLEEP 2020. 

In addition to serving as a consultant for Idorsia on the trial design and interpretation of results, Dr. Roth has also served as a consultant for other companies that develop sleep agents.

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

The Food and Drug Administration has approved the dual orexin receptor antagonist daridorexant (Quviviq) for the treatment of insomnia in adults, the drug’s manufacturer, Idorsia, has announced.

The FDA’s decision was based partly on a phase 3 trial of adults with moderate to severe insomnia who were randomly assigned to receive 25 or 50 mg of daridorexant or matching placebo. Daridorexant was associated with dose-dependent improvements in wake after sleep onset, total sleep time, and latency to persistent sleep.

Whereas the overall results are very positive, the improvements in daytime functioning are especially “exciting,” Thomas Roth, PhD, director of the Sleep Disorders and Research Center at Henry Ford Hospital in Detroit, said in an interview.

“That’s sort of a big deal. For me, that’s the biggest deal there is,” said Dr. Roth, who was a consultant on the design of the phase 3 trial and on the interpretation of the data.

The drug will be available in doses of 25 mg and 50 mg, and the FDA has recommended that it be classified as a controlled substance. After it is scheduled by the Drug Enforcement Administration, daridorexant is expected to be made available in May.
 

Favorable safety profile

Insomnia is a common disorder characterized by difficulty falling asleep or staying asleep and by early-morning awakenings. Patients with insomnia often report fatigue, irritability, and difficulty with concentration. The condition can also result in significant problems with work and social activities, thus contributing to anxiety or depression.

As with other dual orexin receptor antagonists, daridorexant competitively binds with both orexin receptors in the lateral hypothalamus to block the activity of orexin in a reversible way. This approach decreases the downstream action of the wake-promoting neurotransmitters that are overactive in patients with insomnia.

The phase 3 trial measured daytime functioning using the new Insomnia Daytime Symptoms and Impacts Questionnaire (IDSIQ), a patient-reported outcome instrument. Daridorexant was associated with significant improvements in daytime function, particularly in sleepiness and mood.

Previous trials of other dual orexin receptor antagonists did not use the IDSIQ as an outcome, so it is not possible to compare daridorexant with those drugs in this respect, Dr. Roth noted. Researchers also have not conducted head-to-head trials of the drug with other dual orexin receptor antagonists.

Daridorexant also had a favorable safety profile and was not associated with rebound insomnia or withdrawal effects. The most common adverse events were headache and somnolence or fatigue.

“They had no effect on sleep stage distribution [and] they had no significant effects on sleep and breathing in people with mild to moderate sleep apnea,” said Dr. Roth, who presented the phase 3 findings at SLEEP 2020. 

In addition to serving as a consultant for Idorsia on the trial design and interpretation of results, Dr. Roth has also served as a consultant for other companies that develop sleep agents.

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

The Food and Drug Administration has approved the dual orexin receptor antagonist daridorexant (Quviviq) for the treatment of insomnia in adults, the drug’s manufacturer, Idorsia, has announced.

The FDA’s decision was based partly on a phase 3 trial of adults with moderate to severe insomnia who were randomly assigned to receive 25 or 50 mg of daridorexant or matching placebo. Daridorexant was associated with dose-dependent improvements in wake after sleep onset, total sleep time, and latency to persistent sleep.

Whereas the overall results are very positive, the improvements in daytime functioning are especially “exciting,” Thomas Roth, PhD, director of the Sleep Disorders and Research Center at Henry Ford Hospital in Detroit, said in an interview.

“That’s sort of a big deal. For me, that’s the biggest deal there is,” said Dr. Roth, who was a consultant on the design of the phase 3 trial and on the interpretation of the data.

The drug will be available in doses of 25 mg and 50 mg, and the FDA has recommended that it be classified as a controlled substance. After it is scheduled by the Drug Enforcement Administration, daridorexant is expected to be made available in May.
 

Favorable safety profile

Insomnia is a common disorder characterized by difficulty falling asleep or staying asleep and by early-morning awakenings. Patients with insomnia often report fatigue, irritability, and difficulty with concentration. The condition can also result in significant problems with work and social activities, thus contributing to anxiety or depression.

As with other dual orexin receptor antagonists, daridorexant competitively binds with both orexin receptors in the lateral hypothalamus to block the activity of orexin in a reversible way. This approach decreases the downstream action of the wake-promoting neurotransmitters that are overactive in patients with insomnia.

The phase 3 trial measured daytime functioning using the new Insomnia Daytime Symptoms and Impacts Questionnaire (IDSIQ), a patient-reported outcome instrument. Daridorexant was associated with significant improvements in daytime function, particularly in sleepiness and mood.

Previous trials of other dual orexin receptor antagonists did not use the IDSIQ as an outcome, so it is not possible to compare daridorexant with those drugs in this respect, Dr. Roth noted. Researchers also have not conducted head-to-head trials of the drug with other dual orexin receptor antagonists.

Daridorexant also had a favorable safety profile and was not associated with rebound insomnia or withdrawal effects. The most common adverse events were headache and somnolence or fatigue.

“They had no effect on sleep stage distribution [and] they had no significant effects on sleep and breathing in people with mild to moderate sleep apnea,” said Dr. Roth, who presented the phase 3 findings at SLEEP 2020. 

In addition to serving as a consultant for Idorsia on the trial design and interpretation of results, Dr. Roth has also served as a consultant for other companies that develop sleep agents.

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

If you don’t think it’s important to assess for sleep disorders in your patients with atopic dermatitis (AD), think again.

According to Sabra M. Abbott, MD, PhD, professor of neurology at Northwestern University, Chicago, AD is associated with difficulty falling asleep, nighttime awakenings, early morning awakenings, increased daytime sleepiness, decreased sleep efficiency, increased arousals, awakenings, and sleep fragmentation, as well as increased night kicks and nocturnal leg cramps, and a more than twofold increased risk for insomnia.

During the Revolutionizing Atopic Dermatitis symposium, she offered key questions to ask AD patients who present with sleep complaints:

When do you go to bed? “This does not refer to when you get into bed, but when do you actually go to bed with an intention to go to sleep, outside of watching television or answering emails?” Dr. Abbott said.

How long does it take for you to fall asleep?

Do you wake up in the middle of the night, and for how long? What do you do if you wake up?

When do you wake up in the morning? Is it on your own, or with an alarm clock?

Does this schedule change on nonworkdays?

Do you have daytime impairment? Meaning, do your sleep complaints impact how you function during the daytime?

Do you snore? Meaning, is there concern for sleep apnea?

Do you have uncomfortable sensations in your legs? Are they worse in the evening and improve with movement? These are signs of possible restless legs syndrome.

The Epworth Sleepiness Scale is one self-administered questionnaire to consider using for AD patients with sleep complaints. “This provides patients with several examples of typical scenarios they might encounter during the day and queries whether or not they feel that they could deal with any of those scenarios,” Dr. Abbott said. “A score of greater than 10 indicates that they are sleepy; it’s not just an overall sense of fatigue and decreased energy.”

Other brief self-assessment tools she recommended are the Insomnia Severity Index and the STOP-Bang questionnaire.

Dr. Abbott reported having no financial disclosures.

[email protected]

If you don’t think it’s important to assess for sleep disorders in your patients with atopic dermatitis (AD), think again.

According to Sabra M. Abbott, MD, PhD, professor of neurology at Northwestern University, Chicago, AD is associated with difficulty falling asleep, nighttime awakenings, early morning awakenings, increased daytime sleepiness, decreased sleep efficiency, increased arousals, awakenings, and sleep fragmentation, as well as increased night kicks and nocturnal leg cramps, and a more than twofold increased risk for insomnia.

During the Revolutionizing Atopic Dermatitis symposium, she offered key questions to ask AD patients who present with sleep complaints:

When do you go to bed? “This does not refer to when you get into bed, but when do you actually go to bed with an intention to go to sleep, outside of watching television or answering emails?” Dr. Abbott said.

How long does it take for you to fall asleep?

Do you wake up in the middle of the night, and for how long? What do you do if you wake up?

When do you wake up in the morning? Is it on your own, or with an alarm clock?

Does this schedule change on nonworkdays?

Do you have daytime impairment? Meaning, do your sleep complaints impact how you function during the daytime?

Do you snore? Meaning, is there concern for sleep apnea?

Do you have uncomfortable sensations in your legs? Are they worse in the evening and improve with movement? These are signs of possible restless legs syndrome.

The Epworth Sleepiness Scale is one self-administered questionnaire to consider using for AD patients with sleep complaints. “This provides patients with several examples of typical scenarios they might encounter during the day and queries whether or not they feel that they could deal with any of those scenarios,” Dr. Abbott said. “A score of greater than 10 indicates that they are sleepy; it’s not just an overall sense of fatigue and decreased energy.”

Other brief self-assessment tools she recommended are the Insomnia Severity Index and the STOP-Bang questionnaire.

Dr. Abbott reported having no financial disclosures.

[email protected]

If you don’t think it’s important to assess for sleep disorders in your patients with atopic dermatitis (AD), think again.

According to Sabra M. Abbott, MD, PhD, professor of neurology at Northwestern University, Chicago, AD is associated with difficulty falling asleep, nighttime awakenings, early morning awakenings, increased daytime sleepiness, decreased sleep efficiency, increased arousals, awakenings, and sleep fragmentation, as well as increased night kicks and nocturnal leg cramps, and a more than twofold increased risk for insomnia.

During the Revolutionizing Atopic Dermatitis symposium, she offered key questions to ask AD patients who present with sleep complaints:

When do you go to bed? “This does not refer to when you get into bed, but when do you actually go to bed with an intention to go to sleep, outside of watching television or answering emails?” Dr. Abbott said.

How long does it take for you to fall asleep?

Do you wake up in the middle of the night, and for how long? What do you do if you wake up?

When do you wake up in the morning? Is it on your own, or with an alarm clock?

Does this schedule change on nonworkdays?

Do you have daytime impairment? Meaning, do your sleep complaints impact how you function during the daytime?

Do you snore? Meaning, is there concern for sleep apnea?

Do you have uncomfortable sensations in your legs? Are they worse in the evening and improve with movement? These are signs of possible restless legs syndrome.

The Epworth Sleepiness Scale is one self-administered questionnaire to consider using for AD patients with sleep complaints. “This provides patients with several examples of typical scenarios they might encounter during the day and queries whether or not they feel that they could deal with any of those scenarios,” Dr. Abbott said. “A score of greater than 10 indicates that they are sleepy; it’s not just an overall sense of fatigue and decreased energy.”

Other brief self-assessment tools she recommended are the Insomnia Severity Index and the STOP-Bang questionnaire.

Dr. Abbott reported having no financial disclosures.

[email protected]

Children and adolescents who do not receive sufficient sleep can experience worsening inattention, daytime fatigue, and cognitive and behavioral difficulties. Assessment and treatment of insomnia and other sleep difficulties in young patients is critical as poor sleep increases their risk for depression, self-harm, and suicide.

In Part 1 of this article (Pediatric insomnia: Assessment and diagnosis, Current Psychiatry, December 2021, p. 9-13,24-25), we described sleep architecture, sleep in healthy youth and in those with certain psychiatric disorders, and how to assess sleep in pediatric patients. In Part 2, we focus on psychotherapeutic and psychopharmacologic interventions for youth with insomnia, and describe an effective approach to consultation with pediatric behavioral sleep medicine specialists.

Psychotherapeutic interventions

Regardless of the source of a child’s insomnia or co-occurring disorders, healthy sleep practices are the first line behavioral treatment, including for youth with attention-deficit/hyperactivity disorder (ADHD), anxiety disorders, obsessive-compulsive disorder, and depressive disorders.

Healthy sleep practices/sleep hygiene

Developmentally appropriate bedtimes and routines (Table). Helping children establish a regular, consistent bedtime is key in promoting healthy sleep. Ideally, the bedtime routine involves 3 to 4 activities each night in the same order, and these activities should be relaxing and soothing (eg, taking a bath, putting on pajamas, reading books). Setting age-appropriate bedtimes also is important. If an older child is asked to go to bed at 8 pm but cannot fall asleep for an hour, they may not have insomnia but instead a developmentally inappropriate bedtime. Several studies found that children younger than age 10 should go to bed no later than 9 pm. Bedtimes later than 9 pm for young children are correlated with shorter sleep duration.¹

Consistent sleep schedules. Another important aspect of healthy sleep is working with parents to enforce a consistent bedtime and wake-up time, including weekdays and weekends. Ideally, bedtime on weekdays and weekends should not vary by more than 1 hour. Helping children wake up at the same time each day helps to set and regulate their circadian rhythm. Keeping these schedules consistent on vacations and school holidays also is helpful. For adolescents, the weekday/weekend bedtimes can vary by up to 2 hours because adolescents have a delayed circadian rhythm and wake-up times for high school can be early.

Environmental factors. An important piece of parental education is stimulus control and the ingredients of healthy sleep. Healthy sleep ingredients include a dark, quiet, consistent, and cool bedroom; a comfortable bed, the child feeling safe, and limited environmental stimuli.

Continue to: Cognitive-behavioral therapy for insomnia...

Cognitive-behavioral therapy for insomnia

Relaxation. Pediatric patients can be taught relaxation, mindfulness, meditation, and progressive muscle relaxation techniques to help lower overall stress. This can be especially helpful for youth with sleep disorders or anxiety. Guided relaxation apps are popular among children and teens, and various apps offer soothing sounds, deep breathing, progressive muscle relaxation, and guided imagery. This can be taught in psychotherapy sessions and used at home to promote gains in between sessions.

Stimulus control. Stimulus control involves using the bed exclusively for sleep and avoiding nonsleep activities in bed (eg, reading, watching television, using a computer, worrying). These activities promote wakefulness and insomnia. This may mean the child does not get into bed until they cannot keep their eyes open, even if that delays bedtime. If the child is still awake within 15 to 20 minutes, they should be encouraged to get out of bed and engage in a nonstimulating activity such as meditation, reading, or sitting quietly in the dark or low light. This recommendation can run counter to parents’ intuition that children with sleep problems should go to bed earlier. Using the bed only for sleep conditions the child to falling asleep or being asleep when in bed.

Sleep restriction. Sleep restriction involves restricting sleep to a set number of hours in order to increase their sleep efficiency (time slept in bed divided by total time spent in bed x 100). Restricting sleep to 6 to 7 hours increases sleep efficiency, consolidates sleep, and extinguishes the association of being awake in bed. For older adolescents, sleep restriction may help to limit their time in bed to either falling asleep or being asleep. This is intended to be used as a short-term strategy and only after other sleep hygiene measures (bedtime routine, environmental factors, etc) have been put into place for several weeks. While this strategy sounds unappealing to most individuals with insomnia, it can lead to lasting change due to the use of behavioral conditioning in bed. Because sleep restriction can lead to significant daytime sleepiness and impairment during the day, sleep should not be restricted to <6 hours a day for children and adolescents. Once the adolescent is sleeping more consistently and sleep efficiency reaches 85% or higher, time in bed for sleep is increased.²

Cognitive restructuring. Some children and adolescents develop maladaptive thoughts about sleep that further promote insomnia. These thoughts might include “I will never get to sleep,” “I am going to have a terrible day if I cannot fall asleep,” or “I will fail my test tomorrow if I am unable to sleep.” Such maladaptive thoughts are often untrue but promote wakefulness in the early or middle part of the night. Cognitive restructuring involves helping the child identify each problematic thought, challenge how accurate each thought is with evidence, and replace the problematic thought with a more helpful thought. For instance, an adolescent can recognize that even if they have a sleepless night, their catastrophic outcome (eg, “I will not be able to function”) is likely untrue. A psychologist can help review evidence for this, including previous times when the adolescent has not slept well and managed to get through the next day.

When is pharmacologic treatment needed?

Pharmacologic treatment may be indicated if a child does not show significant improvement following behavioral intervention (Figure). However, it is critical to exclude other primary causes of dyssomnia (eg, obstructive sleep apnea, iron deficiency anemia) before pursuing pharmacotherapy, because pharmacotherapy could mask an underlying disorder. Moreover, while there is relatively limited evidence for psychopharmacologic interventions for sleep difficulties in children and adolescents, a large survey of child and adolescent psychiatrists (N = 1,273) suggested that medications were considered for one-quarter of pediatric patients with insomnia.³ Further, patients with specific comorbidities such as neurodevelopmental disorders may be more likely to be prescribed soporifics.⁴

Continue to: What is the evidence for pharmacotherapy?...

What is the evidence for pharmacotherapy?

Antihistamines. Histamine antagonists—which promote sleep by blocking the wakefulness-promoting and circadian-related effects of histamine—are the most commonly used medications to treat pediatric insomnia, despite a dearth of data from prospective trials.^5,6 In 1 small study, Russo et al⁷ found diphenhydramine, 1 mg/kg at bedtime, reduced sleep latency and nighttime awakenings, and increased sleep duration in patients ages 2 to 12; similar effects have been observed in pediatric burn patients.⁸ There are some limited data for other H1 antagonists (eg, hydroxyzine) in pediatric insomnia.^9-11

Alpha-2 agonists increase rapid eye movement sleep via dose-dependent downregulation of noradrenergic signaling¹² and thus have been commonly prescribed for insomnia in children and adolescents. In fact, the nonselective alpha-2 agonist clonidine is among the most prescribed medications for youth with insomnia, and may be efficacious in youth with neurodevelopmental disorders and ADHD.¹³ In small retrospective studies, clonidine decreased sleep latency and nighttime awakenings in addition to increasing sleep duration.¹⁴ Also, clonidine was well tolerated but associated with daytime somnolence. Guanfacine—a selective alpha-2 agonist—is also commonly prescribed for insomnia in youth, although results of trials have been equivocal.¹⁵ Given the more rapid absorption and shorter Tmax of clonidine relative to guanfacine, the former may be preferred as a soporific.

Melatonin and melatonin agonists. The primary regulator of the sleep-wake cycle is melatonin, an endogenous hormone produced by the pineal gland in response to changes in retinal light perception. Exogenous melatonin supplementation may be the preferred initial pharmacotherapy for sleep-onset insomnia due to its chronobiotic properties.¹⁶ In clinical studies, both immediate-release^17,18 and extended-release¹⁹ melatonin reduced sleep-onset latency and increased total sleep duration in pediatric patients, although the increase in total duration of sleep was greater with extended-release preparations. Additionally, tolerability data for melatonin in pediatric patients are encouraging. A 2-year randomized trial of prolonged-release melatonin for insomnia in pediatric patients found no adverse effects with regard to growth, body mass index, or pubertal development.²⁰ Additionally, significant improvements in sleep quality, sleep patterns, and caregiver satisfaction were maintained throughout the trial, and no withdrawal symptoms were observed upon discontinuation.

Melatonin may have a particularly important role in circadian rhythm sleep disorders. In this regard, low-dose melatonin (0.5 mg), when timed relative to the endogenous dim light melatonin onset (DLMO), is more effective in shifting sleep phase than higher doses, which suggests that timing may have greater impact than dosage.²¹ Data regarding melatonin administration with respect to DLMO suggest that the optimal administration time is 4 to 6 hours before a child’s preferred bedtime, and doses of 0.5 to 1 mg have been effective when given in this window.²² Variation across studies has contributed to a lack of consensus regarding pediatric melatonin dosing. For example, .05 mg/kg may be a minimal effective dose when given 1 to 2 hours before bedtime¹⁸; however, in surveys doses vary considerably, with typical doses of 2.5 to 3 mg for prepubertal children and 5 mg for adolescents.⁵ Of note, in patients with decreased cytochrome P450 (CYP) 1A2 activity, lack of diurnal variation in melatonin serum concentration may decrease the effectiveness of melatonin.¹⁶Ramelteon is a potent agonist of the melatonin MT1 and MT2 receptors, with a significantly higher binding affinity than melatonin in vitro. In case reports, ramelteon was well-tolerated, improved delayed sleep onset, and decreased nighttime awakenings.²³

Zolpidem, eszopiclone and zaleplon. Studies of selective GABAergic modulators and benzodiazepines have not produced positive results in prospective trials of youth with insomnia. Zolpidem was studied in children and adolescents (N = 201) with ADHD; although sleep latency did not differ between zolpidem and placebo, some significant improvements were observed in adolescents.²⁴ Zolpidem was generally well tolerated, with approximately 10% of youth discontinuing due to adverse effects. Additionally, eszopiclone—which has a longer duration of action compared with zolpidem—has been studied in children and adolescents with ADHD (N = 486) who were also evaluated with a sleep study. No differences were observed between placebo and eszopiclone in terms of sleep latency and approximately 10% of patients discontinued treatment as a result of adverse events.²⁵ We were unable to locate any prospective trials of zaleplon or benzodiazepine receptor agonists for insomnia in youth, although some reports suggest that clonazepam may have a possible role for specific parasomnias.^26,27Dual orexin receptor antagonists. Suvorexant, an antagonist of the wakefulness-promoting neuropeptide orexin, improved subjective sleep quality in a prospective trial of adolescents with insomnia (N = 30), although dropout was high (44%).²⁸ Of those patients, reasons for discontinuation included loss to follow-up, lack of effectiveness, and abnormal dreams. We were unable to locate any trials of lemborexant in pediatric patients.

Atypical antidepressants. Trazodone is commonly prescribed for insomnia in pediatric patients with comorbid mood or anxiety disorders. In open-label studies of children and toddlers, trazodone may be well-tolerated and improve sleep.²⁹ Additionally, development of a physiologically based pharmacokinetic model to inform trazodone dosing for youth with insomnia is underway.³⁰ Some studies in adolescents with depression suggest that caution should be used when combining trazodone with medications that inhibit CYP2D6. In the Treatment of SSRI-Resistant Depression in Adolescents study, none of the patients who were treated with trazodone (vs other soporifics) improved.³¹ This may relate to CYP2D6 interactions and accumulation of methyl-chloro-piperazine (mCPP), a trazodone metabolite that is associated with dysphoria, irritability, and depression.³¹ This finding has been replicated in a separate cohort of depressed adolescents.³²

Because of its antihistaminergic effects, mirtazapine has been used to treat insomnia in adults. One open-label study of mirtazapine in children and young adults ages 3 to 23 with neurodevelopmental disorders suggested that mirtazapine improved behavioral symptoms and insomnia, and was associated with few treatment-limiting adverse effects.³³

Tricyclic antidepressants. In a retrospective study of youth with insomnia who failed behavioral interventions and melatonin (N = 29), doxepin, a potent H1 antagonist, improved subjective sleep in one-half of patients.³⁴

Continue to: Consultation with pediatric sleep medicine specialists...

Consultation with pediatric sleep medicine specialists

It often will behoove the psychiatric clinician to review their concerns with a behavioral sleep medicine specialist or a psychologist with specific expertise in the psychotherapeutic treatment of sleep who can provide important guidance regarding the key aspects of treatment. When discussing a particular patient’s presentation with the pediatric behavioral sleep psychologist/specialist, consider the following questions:

• Is the child’s sleep disorder the primary problem, or is the child’s insomnia secondary to another diagnosis (psychiatric or nonpsychiatric)?
• What are the primary sleep-related problems the child/family presents with? How long have the symptoms been present?
• Is the sleep disorder interfering with the child’s functioning, either academically or socially? Does the child’s sleep problem interfere with other family members’ sleep?
• Does the child have a comorbid psychological conditions such as ADHD, depression, or anxiety, and/or is undergoing treatment for these disorders, which may play a role in the sleep problem?
• Is a sleep study warranted?

A sleep study, also known as polysomnography (PSG), is a diagnostic test in which physiologic parameters are continuously recorded during a period of sleep via electroencephalography, electromyography, electrooculogram, electrocardiogram, airflow sensors, pulse oximeter, body position monitors, and video. In 2012, the American Academy of Sleep Medicine published evidenced-based practice parameters for respiratory and nonrespiratory indications for PSG.³⁵ It is most commonly indicated to rule out obstructive sleep apnea in pediatric patients who exhibit snoring, gasping, irregular breathing, witnessed apneic events, unusual head positioning, or other signs of obstructive breathing during sleep. Nonrespiratory indications for PSG include children suspected of having periodic limb movement disorder and suspected narcolepsy. Children with frequent parasomnias, epilepsy, or nocturnal enuresis should be clinically screened for presence of comorbid sleep disorders, and PSG would be indicated if there are concerns about a possible sleep-disordered breathing disorder. PSG is also recommended for children with hypersomnia, to differentiate a parasomnia from sleep-related epilepsy, and for children suspected of having restless leg syndrome.³⁶ PSG is not typically indicated in the initial evaluation of insomnia (unless there is evidence of a comorbid sleep disorder), circadian rhythm disorders (ie, delayed sleep phase syndrome), or for evaluation of children with sleep-related bruxism.³ Special considerations for PSG in children include ensuring a parent or guardian is always with the child, providing developmentally appropriate sleeping arrangements, arranging family tours of the sleep lab prior to the study, and accommodating for earlier bedtimes.³⁷

Bottom Line

Techniques to promote healthy sleep in pediatric patients include behavioral interventions such as setting a developmentally appropriate bedtime and a consistent wake time, establishing bedtime routines, and encouraging relaxation/ wind-down period before bed. Cognitive-behavioral therapy for insomnia (CBT-I) may include cognitive restructuring of anxious thoughts, relaxation training, stimulus control, and sleep restriction. Use of medications may be indicated for children and teens who have not responded to CBT-I or soporific dosing of melatonin.

Children and adolescents who do not receive sufficient sleep can experience worsening inattention, daytime fatigue, and cognitive and behavioral difficulties. Assessment and treatment of insomnia and other sleep difficulties in young patients is critical as poor sleep increases their risk for depression, self-harm, and suicide.

In Part 1 of this article (Pediatric insomnia: Assessment and diagnosis, Current Psychiatry, December 2021, p. 9-13,24-25), we described sleep architecture, sleep in healthy youth and in those with certain psychiatric disorders, and how to assess sleep in pediatric patients. In Part 2, we focus on psychotherapeutic and psychopharmacologic interventions for youth with insomnia, and describe an effective approach to consultation with pediatric behavioral sleep medicine specialists.

Psychotherapeutic interventions

Regardless of the source of a child’s insomnia or co-occurring disorders, healthy sleep practices are the first line behavioral treatment, including for youth with attention-deficit/hyperactivity disorder (ADHD), anxiety disorders, obsessive-compulsive disorder, and depressive disorders.

Healthy sleep practices/sleep hygiene

Developmentally appropriate bedtimes and routines (Table). Helping children establish a regular, consistent bedtime is key in promoting healthy sleep. Ideally, the bedtime routine involves 3 to 4 activities each night in the same order, and these activities should be relaxing and soothing (eg, taking a bath, putting on pajamas, reading books). Setting age-appropriate bedtimes also is important. If an older child is asked to go to bed at 8 pm but cannot fall asleep for an hour, they may not have insomnia but instead a developmentally inappropriate bedtime. Several studies found that children younger than age 10 should go to bed no later than 9 pm. Bedtimes later than 9 pm for young children are correlated with shorter sleep duration.¹

Consistent sleep schedules. Another important aspect of healthy sleep is working with parents to enforce a consistent bedtime and wake-up time, including weekdays and weekends. Ideally, bedtime on weekdays and weekends should not vary by more than 1 hour. Helping children wake up at the same time each day helps to set and regulate their circadian rhythm. Keeping these schedules consistent on vacations and school holidays also is helpful. For adolescents, the weekday/weekend bedtimes can vary by up to 2 hours because adolescents have a delayed circadian rhythm and wake-up times for high school can be early.

Environmental factors. An important piece of parental education is stimulus control and the ingredients of healthy sleep. Healthy sleep ingredients include a dark, quiet, consistent, and cool bedroom; a comfortable bed, the child feeling safe, and limited environmental stimuli.

Continue to: Cognitive-behavioral therapy for insomnia...

Cognitive-behavioral therapy for insomnia

Relaxation. Pediatric patients can be taught relaxation, mindfulness, meditation, and progressive muscle relaxation techniques to help lower overall stress. This can be especially helpful for youth with sleep disorders or anxiety. Guided relaxation apps are popular among children and teens, and various apps offer soothing sounds, deep breathing, progressive muscle relaxation, and guided imagery. This can be taught in psychotherapy sessions and used at home to promote gains in between sessions.

Stimulus control. Stimulus control involves using the bed exclusively for sleep and avoiding nonsleep activities in bed (eg, reading, watching television, using a computer, worrying). These activities promote wakefulness and insomnia. This may mean the child does not get into bed until they cannot keep their eyes open, even if that delays bedtime. If the child is still awake within 15 to 20 minutes, they should be encouraged to get out of bed and engage in a nonstimulating activity such as meditation, reading, or sitting quietly in the dark or low light. This recommendation can run counter to parents’ intuition that children with sleep problems should go to bed earlier. Using the bed only for sleep conditions the child to falling asleep or being asleep when in bed.

Sleep restriction. Sleep restriction involves restricting sleep to a set number of hours in order to increase their sleep efficiency (time slept in bed divided by total time spent in bed x 100). Restricting sleep to 6 to 7 hours increases sleep efficiency, consolidates sleep, and extinguishes the association of being awake in bed. For older adolescents, sleep restriction may help to limit their time in bed to either falling asleep or being asleep. This is intended to be used as a short-term strategy and only after other sleep hygiene measures (bedtime routine, environmental factors, etc) have been put into place for several weeks. While this strategy sounds unappealing to most individuals with insomnia, it can lead to lasting change due to the use of behavioral conditioning in bed. Because sleep restriction can lead to significant daytime sleepiness and impairment during the day, sleep should not be restricted to <6 hours a day for children and adolescents. Once the adolescent is sleeping more consistently and sleep efficiency reaches 85% or higher, time in bed for sleep is increased.²

Cognitive restructuring. Some children and adolescents develop maladaptive thoughts about sleep that further promote insomnia. These thoughts might include “I will never get to sleep,” “I am going to have a terrible day if I cannot fall asleep,” or “I will fail my test tomorrow if I am unable to sleep.” Such maladaptive thoughts are often untrue but promote wakefulness in the early or middle part of the night. Cognitive restructuring involves helping the child identify each problematic thought, challenge how accurate each thought is with evidence, and replace the problematic thought with a more helpful thought. For instance, an adolescent can recognize that even if they have a sleepless night, their catastrophic outcome (eg, “I will not be able to function”) is likely untrue. A psychologist can help review evidence for this, including previous times when the adolescent has not slept well and managed to get through the next day.

When is pharmacologic treatment needed?

Pharmacologic treatment may be indicated if a child does not show significant improvement following behavioral intervention (Figure). However, it is critical to exclude other primary causes of dyssomnia (eg, obstructive sleep apnea, iron deficiency anemia) before pursuing pharmacotherapy, because pharmacotherapy could mask an underlying disorder. Moreover, while there is relatively limited evidence for psychopharmacologic interventions for sleep difficulties in children and adolescents, a large survey of child and adolescent psychiatrists (N = 1,273) suggested that medications were considered for one-quarter of pediatric patients with insomnia.³ Further, patients with specific comorbidities such as neurodevelopmental disorders may be more likely to be prescribed soporifics.⁴

Continue to: What is the evidence for pharmacotherapy?...

What is the evidence for pharmacotherapy?

Antihistamines. Histamine antagonists—which promote sleep by blocking the wakefulness-promoting and circadian-related effects of histamine—are the most commonly used medications to treat pediatric insomnia, despite a dearth of data from prospective trials.^5,6 In 1 small study, Russo et al⁷ found diphenhydramine, 1 mg/kg at bedtime, reduced sleep latency and nighttime awakenings, and increased sleep duration in patients ages 2 to 12; similar effects have been observed in pediatric burn patients.⁸ There are some limited data for other H1 antagonists (eg, hydroxyzine) in pediatric insomnia.^9-11

Alpha-2 agonists increase rapid eye movement sleep via dose-dependent downregulation of noradrenergic signaling¹² and thus have been commonly prescribed for insomnia in children and adolescents. In fact, the nonselective alpha-2 agonist clonidine is among the most prescribed medications for youth with insomnia, and may be efficacious in youth with neurodevelopmental disorders and ADHD.¹³ In small retrospective studies, clonidine decreased sleep latency and nighttime awakenings in addition to increasing sleep duration.¹⁴ Also, clonidine was well tolerated but associated with daytime somnolence. Guanfacine—a selective alpha-2 agonist—is also commonly prescribed for insomnia in youth, although results of trials have been equivocal.¹⁵ Given the more rapid absorption and shorter Tmax of clonidine relative to guanfacine, the former may be preferred as a soporific.

Melatonin and melatonin agonists. The primary regulator of the sleep-wake cycle is melatonin, an endogenous hormone produced by the pineal gland in response to changes in retinal light perception. Exogenous melatonin supplementation may be the preferred initial pharmacotherapy for sleep-onset insomnia due to its chronobiotic properties.¹⁶ In clinical studies, both immediate-release^17,18 and extended-release¹⁹ melatonin reduced sleep-onset latency and increased total sleep duration in pediatric patients, although the increase in total duration of sleep was greater with extended-release preparations. Additionally, tolerability data for melatonin in pediatric patients are encouraging. A 2-year randomized trial of prolonged-release melatonin for insomnia in pediatric patients found no adverse effects with regard to growth, body mass index, or pubertal development.²⁰ Additionally, significant improvements in sleep quality, sleep patterns, and caregiver satisfaction were maintained throughout the trial, and no withdrawal symptoms were observed upon discontinuation.

Melatonin may have a particularly important role in circadian rhythm sleep disorders. In this regard, low-dose melatonin (0.5 mg), when timed relative to the endogenous dim light melatonin onset (DLMO), is more effective in shifting sleep phase than higher doses, which suggests that timing may have greater impact than dosage.²¹ Data regarding melatonin administration with respect to DLMO suggest that the optimal administration time is 4 to 6 hours before a child’s preferred bedtime, and doses of 0.5 to 1 mg have been effective when given in this window.²² Variation across studies has contributed to a lack of consensus regarding pediatric melatonin dosing. For example, .05 mg/kg may be a minimal effective dose when given 1 to 2 hours before bedtime¹⁸; however, in surveys doses vary considerably, with typical doses of 2.5 to 3 mg for prepubertal children and 5 mg for adolescents.⁵ Of note, in patients with decreased cytochrome P450 (CYP) 1A2 activity, lack of diurnal variation in melatonin serum concentration may decrease the effectiveness of melatonin.¹⁶Ramelteon is a potent agonist of the melatonin MT1 and MT2 receptors, with a significantly higher binding affinity than melatonin in vitro. In case reports, ramelteon was well-tolerated, improved delayed sleep onset, and decreased nighttime awakenings.²³

Zolpidem, eszopiclone and zaleplon. Studies of selective GABAergic modulators and benzodiazepines have not produced positive results in prospective trials of youth with insomnia. Zolpidem was studied in children and adolescents (N = 201) with ADHD; although sleep latency did not differ between zolpidem and placebo, some significant improvements were observed in adolescents.²⁴ Zolpidem was generally well tolerated, with approximately 10% of youth discontinuing due to adverse effects. Additionally, eszopiclone—which has a longer duration of action compared with zolpidem—has been studied in children and adolescents with ADHD (N = 486) who were also evaluated with a sleep study. No differences were observed between placebo and eszopiclone in terms of sleep latency and approximately 10% of patients discontinued treatment as a result of adverse events.²⁵ We were unable to locate any prospective trials of zaleplon or benzodiazepine receptor agonists for insomnia in youth, although some reports suggest that clonazepam may have a possible role for specific parasomnias.^26,27Dual orexin receptor antagonists. Suvorexant, an antagonist of the wakefulness-promoting neuropeptide orexin, improved subjective sleep quality in a prospective trial of adolescents with insomnia (N = 30), although dropout was high (44%).²⁸ Of those patients, reasons for discontinuation included loss to follow-up, lack of effectiveness, and abnormal dreams. We were unable to locate any trials of lemborexant in pediatric patients.

Atypical antidepressants. Trazodone is commonly prescribed for insomnia in pediatric patients with comorbid mood or anxiety disorders. In open-label studies of children and toddlers, trazodone may be well-tolerated and improve sleep.²⁹ Additionally, development of a physiologically based pharmacokinetic model to inform trazodone dosing for youth with insomnia is underway.³⁰ Some studies in adolescents with depression suggest that caution should be used when combining trazodone with medications that inhibit CYP2D6. In the Treatment of SSRI-Resistant Depression in Adolescents study, none of the patients who were treated with trazodone (vs other soporifics) improved.³¹ This may relate to CYP2D6 interactions and accumulation of methyl-chloro-piperazine (mCPP), a trazodone metabolite that is associated with dysphoria, irritability, and depression.³¹ This finding has been replicated in a separate cohort of depressed adolescents.³²

Because of its antihistaminergic effects, mirtazapine has been used to treat insomnia in adults. One open-label study of mirtazapine in children and young adults ages 3 to 23 with neurodevelopmental disorders suggested that mirtazapine improved behavioral symptoms and insomnia, and was associated with few treatment-limiting adverse effects.³³

Tricyclic antidepressants. In a retrospective study of youth with insomnia who failed behavioral interventions and melatonin (N = 29), doxepin, a potent H1 antagonist, improved subjective sleep in one-half of patients.³⁴

Continue to: Consultation with pediatric sleep medicine specialists...

Consultation with pediatric sleep medicine specialists

It often will behoove the psychiatric clinician to review their concerns with a behavioral sleep medicine specialist or a psychologist with specific expertise in the psychotherapeutic treatment of sleep who can provide important guidance regarding the key aspects of treatment. When discussing a particular patient’s presentation with the pediatric behavioral sleep psychologist/specialist, consider the following questions:

• Is the child’s sleep disorder the primary problem, or is the child’s insomnia secondary to another diagnosis (psychiatric or nonpsychiatric)?
• What are the primary sleep-related problems the child/family presents with? How long have the symptoms been present?
• Is the sleep disorder interfering with the child’s functioning, either academically or socially? Does the child’s sleep problem interfere with other family members’ sleep?
• Does the child have a comorbid psychological conditions such as ADHD, depression, or anxiety, and/or is undergoing treatment for these disorders, which may play a role in the sleep problem?
• Is a sleep study warranted?

A sleep study, also known as polysomnography (PSG), is a diagnostic test in which physiologic parameters are continuously recorded during a period of sleep via electroencephalography, electromyography, electrooculogram, electrocardiogram, airflow sensors, pulse oximeter, body position monitors, and video. In 2012, the American Academy of Sleep Medicine published evidenced-based practice parameters for respiratory and nonrespiratory indications for PSG.³⁵ It is most commonly indicated to rule out obstructive sleep apnea in pediatric patients who exhibit snoring, gasping, irregular breathing, witnessed apneic events, unusual head positioning, or other signs of obstructive breathing during sleep. Nonrespiratory indications for PSG include children suspected of having periodic limb movement disorder and suspected narcolepsy. Children with frequent parasomnias, epilepsy, or nocturnal enuresis should be clinically screened for presence of comorbid sleep disorders, and PSG would be indicated if there are concerns about a possible sleep-disordered breathing disorder. PSG is also recommended for children with hypersomnia, to differentiate a parasomnia from sleep-related epilepsy, and for children suspected of having restless leg syndrome.³⁶ PSG is not typically indicated in the initial evaluation of insomnia (unless there is evidence of a comorbid sleep disorder), circadian rhythm disorders (ie, delayed sleep phase syndrome), or for evaluation of children with sleep-related bruxism.³ Special considerations for PSG in children include ensuring a parent or guardian is always with the child, providing developmentally appropriate sleeping arrangements, arranging family tours of the sleep lab prior to the study, and accommodating for earlier bedtimes.³⁷

Bottom Line

Techniques to promote healthy sleep in pediatric patients include behavioral interventions such as setting a developmentally appropriate bedtime and a consistent wake time, establishing bedtime routines, and encouraging relaxation/ wind-down period before bed. Cognitive-behavioral therapy for insomnia (CBT-I) may include cognitive restructuring of anxious thoughts, relaxation training, stimulus control, and sleep restriction. Use of medications may be indicated for children and teens who have not responded to CBT-I or soporific dosing of melatonin.

Children and adolescents who do not receive sufficient sleep can experience worsening inattention, daytime fatigue, and cognitive and behavioral difficulties. Assessment and treatment of insomnia and other sleep difficulties in young patients is critical as poor sleep increases their risk for depression, self-harm, and suicide.

In Part 1 of this article (Pediatric insomnia: Assessment and diagnosis, Current Psychiatry, December 2021, p. 9-13,24-25), we described sleep architecture, sleep in healthy youth and in those with certain psychiatric disorders, and how to assess sleep in pediatric patients. In Part 2, we focus on psychotherapeutic and psychopharmacologic interventions for youth with insomnia, and describe an effective approach to consultation with pediatric behavioral sleep medicine specialists.

Psychotherapeutic interventions

Regardless of the source of a child’s insomnia or co-occurring disorders, healthy sleep practices are the first line behavioral treatment, including for youth with attention-deficit/hyperactivity disorder (ADHD), anxiety disorders, obsessive-compulsive disorder, and depressive disorders.

Healthy sleep practices/sleep hygiene

Developmentally appropriate bedtimes and routines (Table). Helping children establish a regular, consistent bedtime is key in promoting healthy sleep. Ideally, the bedtime routine involves 3 to 4 activities each night in the same order, and these activities should be relaxing and soothing (eg, taking a bath, putting on pajamas, reading books). Setting age-appropriate bedtimes also is important. If an older child is asked to go to bed at 8 pm but cannot fall asleep for an hour, they may not have insomnia but instead a developmentally inappropriate bedtime. Several studies found that children younger than age 10 should go to bed no later than 9 pm. Bedtimes later than 9 pm for young children are correlated with shorter sleep duration.¹

Consistent sleep schedules. Another important aspect of healthy sleep is working with parents to enforce a consistent bedtime and wake-up time, including weekdays and weekends. Ideally, bedtime on weekdays and weekends should not vary by more than 1 hour. Helping children wake up at the same time each day helps to set and regulate their circadian rhythm. Keeping these schedules consistent on vacations and school holidays also is helpful. For adolescents, the weekday/weekend bedtimes can vary by up to 2 hours because adolescents have a delayed circadian rhythm and wake-up times for high school can be early.

Environmental factors. An important piece of parental education is stimulus control and the ingredients of healthy sleep. Healthy sleep ingredients include a dark, quiet, consistent, and cool bedroom; a comfortable bed, the child feeling safe, and limited environmental stimuli.

Continue to: Cognitive-behavioral therapy for insomnia...

Cognitive-behavioral therapy for insomnia

Relaxation. Pediatric patients can be taught relaxation, mindfulness, meditation, and progressive muscle relaxation techniques to help lower overall stress. This can be especially helpful for youth with sleep disorders or anxiety. Guided relaxation apps are popular among children and teens, and various apps offer soothing sounds, deep breathing, progressive muscle relaxation, and guided imagery. This can be taught in psychotherapy sessions and used at home to promote gains in between sessions.

Stimulus control. Stimulus control involves using the bed exclusively for sleep and avoiding nonsleep activities in bed (eg, reading, watching television, using a computer, worrying). These activities promote wakefulness and insomnia. This may mean the child does not get into bed until they cannot keep their eyes open, even if that delays bedtime. If the child is still awake within 15 to 20 minutes, they should be encouraged to get out of bed and engage in a nonstimulating activity such as meditation, reading, or sitting quietly in the dark or low light. This recommendation can run counter to parents’ intuition that children with sleep problems should go to bed earlier. Using the bed only for sleep conditions the child to falling asleep or being asleep when in bed.

Sleep restriction. Sleep restriction involves restricting sleep to a set number of hours in order to increase their sleep efficiency (time slept in bed divided by total time spent in bed x 100). Restricting sleep to 6 to 7 hours increases sleep efficiency, consolidates sleep, and extinguishes the association of being awake in bed. For older adolescents, sleep restriction may help to limit their time in bed to either falling asleep or being asleep. This is intended to be used as a short-term strategy and only after other sleep hygiene measures (bedtime routine, environmental factors, etc) have been put into place for several weeks. While this strategy sounds unappealing to most individuals with insomnia, it can lead to lasting change due to the use of behavioral conditioning in bed. Because sleep restriction can lead to significant daytime sleepiness and impairment during the day, sleep should not be restricted to <6 hours a day for children and adolescents. Once the adolescent is sleeping more consistently and sleep efficiency reaches 85% or higher, time in bed for sleep is increased.²

Cognitive restructuring. Some children and adolescents develop maladaptive thoughts about sleep that further promote insomnia. These thoughts might include “I will never get to sleep,” “I am going to have a terrible day if I cannot fall asleep,” or “I will fail my test tomorrow if I am unable to sleep.” Such maladaptive thoughts are often untrue but promote wakefulness in the early or middle part of the night. Cognitive restructuring involves helping the child identify each problematic thought, challenge how accurate each thought is with evidence, and replace the problematic thought with a more helpful thought. For instance, an adolescent can recognize that even if they have a sleepless night, their catastrophic outcome (eg, “I will not be able to function”) is likely untrue. A psychologist can help review evidence for this, including previous times when the adolescent has not slept well and managed to get through the next day.

When is pharmacologic treatment needed?

Pharmacologic treatment may be indicated if a child does not show significant improvement following behavioral intervention (Figure). However, it is critical to exclude other primary causes of dyssomnia (eg, obstructive sleep apnea, iron deficiency anemia) before pursuing pharmacotherapy, because pharmacotherapy could mask an underlying disorder. Moreover, while there is relatively limited evidence for psychopharmacologic interventions for sleep difficulties in children and adolescents, a large survey of child and adolescent psychiatrists (N = 1,273) suggested that medications were considered for one-quarter of pediatric patients with insomnia.³ Further, patients with specific comorbidities such as neurodevelopmental disorders may be more likely to be prescribed soporifics.⁴

Continue to: What is the evidence for pharmacotherapy?...

What is the evidence for pharmacotherapy?

Antihistamines. Histamine antagonists—which promote sleep by blocking the wakefulness-promoting and circadian-related effects of histamine—are the most commonly used medications to treat pediatric insomnia, despite a dearth of data from prospective trials.^5,6 In 1 small study, Russo et al⁷ found diphenhydramine, 1 mg/kg at bedtime, reduced sleep latency and nighttime awakenings, and increased sleep duration in patients ages 2 to 12; similar effects have been observed in pediatric burn patients.⁸ There are some limited data for other H1 antagonists (eg, hydroxyzine) in pediatric insomnia.^9-11

Alpha-2 agonists increase rapid eye movement sleep via dose-dependent downregulation of noradrenergic signaling¹² and thus have been commonly prescribed for insomnia in children and adolescents. In fact, the nonselective alpha-2 agonist clonidine is among the most prescribed medications for youth with insomnia, and may be efficacious in youth with neurodevelopmental disorders and ADHD.¹³ In small retrospective studies, clonidine decreased sleep latency and nighttime awakenings in addition to increasing sleep duration.¹⁴ Also, clonidine was well tolerated but associated with daytime somnolence. Guanfacine—a selective alpha-2 agonist—is also commonly prescribed for insomnia in youth, although results of trials have been equivocal.¹⁵ Given the more rapid absorption and shorter Tmax of clonidine relative to guanfacine, the former may be preferred as a soporific.

Melatonin and melatonin agonists. The primary regulator of the sleep-wake cycle is melatonin, an endogenous hormone produced by the pineal gland in response to changes in retinal light perception. Exogenous melatonin supplementation may be the preferred initial pharmacotherapy for sleep-onset insomnia due to its chronobiotic properties.¹⁶ In clinical studies, both immediate-release^17,18 and extended-release¹⁹ melatonin reduced sleep-onset latency and increased total sleep duration in pediatric patients, although the increase in total duration of sleep was greater with extended-release preparations. Additionally, tolerability data for melatonin in pediatric patients are encouraging. A 2-year randomized trial of prolonged-release melatonin for insomnia in pediatric patients found no adverse effects with regard to growth, body mass index, or pubertal development.²⁰ Additionally, significant improvements in sleep quality, sleep patterns, and caregiver satisfaction were maintained throughout the trial, and no withdrawal symptoms were observed upon discontinuation.

Melatonin may have a particularly important role in circadian rhythm sleep disorders. In this regard, low-dose melatonin (0.5 mg), when timed relative to the endogenous dim light melatonin onset (DLMO), is more effective in shifting sleep phase than higher doses, which suggests that timing may have greater impact than dosage.²¹ Data regarding melatonin administration with respect to DLMO suggest that the optimal administration time is 4 to 6 hours before a child’s preferred bedtime, and doses of 0.5 to 1 mg have been effective when given in this window.²² Variation across studies has contributed to a lack of consensus regarding pediatric melatonin dosing. For example, .05 mg/kg may be a minimal effective dose when given 1 to 2 hours before bedtime¹⁸; however, in surveys doses vary considerably, with typical doses of 2.5 to 3 mg for prepubertal children and 5 mg for adolescents.⁵ Of note, in patients with decreased cytochrome P450 (CYP) 1A2 activity, lack of diurnal variation in melatonin serum concentration may decrease the effectiveness of melatonin.¹⁶Ramelteon is a potent agonist of the melatonin MT1 and MT2 receptors, with a significantly higher binding affinity than melatonin in vitro. In case reports, ramelteon was well-tolerated, improved delayed sleep onset, and decreased nighttime awakenings.²³

Zolpidem, eszopiclone and zaleplon. Studies of selective GABAergic modulators and benzodiazepines have not produced positive results in prospective trials of youth with insomnia. Zolpidem was studied in children and adolescents (N = 201) with ADHD; although sleep latency did not differ between zolpidem and placebo, some significant improvements were observed in adolescents.²⁴ Zolpidem was generally well tolerated, with approximately 10% of youth discontinuing due to adverse effects. Additionally, eszopiclone—which has a longer duration of action compared with zolpidem—has been studied in children and adolescents with ADHD (N = 486) who were also evaluated with a sleep study. No differences were observed between placebo and eszopiclone in terms of sleep latency and approximately 10% of patients discontinued treatment as a result of adverse events.²⁵ We were unable to locate any prospective trials of zaleplon or benzodiazepine receptor agonists for insomnia in youth, although some reports suggest that clonazepam may have a possible role for specific parasomnias.^26,27Dual orexin receptor antagonists. Suvorexant, an antagonist of the wakefulness-promoting neuropeptide orexin, improved subjective sleep quality in a prospective trial of adolescents with insomnia (N = 30), although dropout was high (44%).²⁸ Of those patients, reasons for discontinuation included loss to follow-up, lack of effectiveness, and abnormal dreams. We were unable to locate any trials of lemborexant in pediatric patients.

Atypical antidepressants. Trazodone is commonly prescribed for insomnia in pediatric patients with comorbid mood or anxiety disorders. In open-label studies of children and toddlers, trazodone may be well-tolerated and improve sleep.²⁹ Additionally, development of a physiologically based pharmacokinetic model to inform trazodone dosing for youth with insomnia is underway.³⁰ Some studies in adolescents with depression suggest that caution should be used when combining trazodone with medications that inhibit CYP2D6. In the Treatment of SSRI-Resistant Depression in Adolescents study, none of the patients who were treated with trazodone (vs other soporifics) improved.³¹ This may relate to CYP2D6 interactions and accumulation of methyl-chloro-piperazine (mCPP), a trazodone metabolite that is associated with dysphoria, irritability, and depression.³¹ This finding has been replicated in a separate cohort of depressed adolescents.³²

Because of its antihistaminergic effects, mirtazapine has been used to treat insomnia in adults. One open-label study of mirtazapine in children and young adults ages 3 to 23 with neurodevelopmental disorders suggested that mirtazapine improved behavioral symptoms and insomnia, and was associated with few treatment-limiting adverse effects.³³

Tricyclic antidepressants. In a retrospective study of youth with insomnia who failed behavioral interventions and melatonin (N = 29), doxepin, a potent H1 antagonist, improved subjective sleep in one-half of patients.³⁴

Continue to: Consultation with pediatric sleep medicine specialists...

Consultation with pediatric sleep medicine specialists

It often will behoove the psychiatric clinician to review their concerns with a behavioral sleep medicine specialist or a psychologist with specific expertise in the psychotherapeutic treatment of sleep who can provide important guidance regarding the key aspects of treatment. When discussing a particular patient’s presentation with the pediatric behavioral sleep psychologist/specialist, consider the following questions:

• Is the child’s sleep disorder the primary problem, or is the child’s insomnia secondary to another diagnosis (psychiatric or nonpsychiatric)?
• What are the primary sleep-related problems the child/family presents with? How long have the symptoms been present?
• Is the sleep disorder interfering with the child’s functioning, either academically or socially? Does the child’s sleep problem interfere with other family members’ sleep?
• Does the child have a comorbid psychological conditions such as ADHD, depression, or anxiety, and/or is undergoing treatment for these disorders, which may play a role in the sleep problem?
• Is a sleep study warranted?

A sleep study, also known as polysomnography (PSG), is a diagnostic test in which physiologic parameters are continuously recorded during a period of sleep via electroencephalography, electromyography, electrooculogram, electrocardiogram, airflow sensors, pulse oximeter, body position monitors, and video. In 2012, the American Academy of Sleep Medicine published evidenced-based practice parameters for respiratory and nonrespiratory indications for PSG.³⁵ It is most commonly indicated to rule out obstructive sleep apnea in pediatric patients who exhibit snoring, gasping, irregular breathing, witnessed apneic events, unusual head positioning, or other signs of obstructive breathing during sleep. Nonrespiratory indications for PSG include children suspected of having periodic limb movement disorder and suspected narcolepsy. Children with frequent parasomnias, epilepsy, or nocturnal enuresis should be clinically screened for presence of comorbid sleep disorders, and PSG would be indicated if there are concerns about a possible sleep-disordered breathing disorder. PSG is also recommended for children with hypersomnia, to differentiate a parasomnia from sleep-related epilepsy, and for children suspected of having restless leg syndrome.³⁶ PSG is not typically indicated in the initial evaluation of insomnia (unless there is evidence of a comorbid sleep disorder), circadian rhythm disorders (ie, delayed sleep phase syndrome), or for evaluation of children with sleep-related bruxism.³ Special considerations for PSG in children include ensuring a parent or guardian is always with the child, providing developmentally appropriate sleeping arrangements, arranging family tours of the sleep lab prior to the study, and accommodating for earlier bedtimes.³⁷

Bottom Line

Techniques to promote healthy sleep in pediatric patients include behavioral interventions such as setting a developmentally appropriate bedtime and a consistent wake time, establishing bedtime routines, and encouraging relaxation/ wind-down period before bed. Cognitive-behavioral therapy for insomnia (CBT-I) may include cognitive restructuring of anxious thoughts, relaxation training, stimulus control, and sleep restriction. Use of medications may be indicated for children and teens who have not responded to CBT-I or soporific dosing of melatonin.

Hormone therapy in breast cancer patients can lead to mood and sleep disorders. A new randomized, controlled trial shows that omega-3 supplementation improves these symptoms. After 4 weeks of treatment, patients who received omega-3 reported better sleep, depression, and mood outcomes than those who received placebo.

Estrogen-receptor inhibitors are used to treat breast cancer with positive hormone receptors in combination with other therapies. However, the drugs can lead to long-term side effects, including hot flashes, night sweats, and changes to mood and sleep.

These side effects are often treated with selective serotonin reuptake inhibitors and some anticonvulsant drugs. Omega-3 supplements contain various polyunsaturated fatty acids, which influence cell signaling and contribute to the production of bioactive fat mediators that counter inflammation. They are widely used in cardiovascular disease, breast cancer, rheumatoid arthritis, depression, and other cognitive disorders. They also appear to amplify the antitumor efficacy of tamoxifen through the inhibition of proliferative and antiapoptotic pathways that that are influenced by estrogen-receptor signaling.

“This study showed that omega-3 supplementation can improve mood and sleep disorder in women suffering from breast cancer while they (are) managing with antihormone drugs. … this supplement can be proposed for the treatment of these patients,” wrote researchers led by Azadeh Moghaddas, MD, PhD, who is an associate professor of clinical pharmacy and pharmacy practice at Isfahan (Iran) University of Medical Sciences.

The study was made available as a preprint on ResearchSquare and has not yet been peer reviewed. It included 60 patients who were screened for baseline mood disorders using the hospital anxiety and depression scale (HADS), then randomized to 2 mg omega-3 per day for 4 weeks, or placebo.

Studies have shown that omega-3 supplementation improves menopause and mood symptoms in postmenopausal women without cancer.

Omega-3 supplementation has neuroprotective effects and improved brain function and mood in rats, and a 2019 review suggested that the evidence is strong enough to warrant clinical studies.

To determine if the supplement was also safe and effective in women with breast cancer undergoing hormone therapy, the researchers analyzed data from 32 patients in the intervention group and 28 patients in the placebo group.

At 4 weeks of follow-up, patients in the intervention group had significantly lower values on the Center for Epidemiological Studies-Depression scale (mean, 22.8 vs. 30.8; P < .001), Profile of Mood State (mean, 30.8 versus 39.5; P<.001), and Pittsburgh Sleep Quality Index (mean, 4.6 vs. 5.9; P = .04). There were no statistically significant changes in these values in the placebo group.

At 4 weeks, paired samples t-test comparisons between the intervention and the placebo groups revealed lower scores in the intervention group for mean scores in the PSQI subscales subjective sleep quality (0.8 vs. 1.4; P = .002), delay in falling asleep (1.1 vs. 1.6; P = .02), and sleep disturbances (0.8 vs. 1.1; P = .005).

There were no significant adverse reactions in either group.

The study is limited by its small sample size and the short follow-up period.

The study was funded by Isfahan University of Medical Sciences. The authors declare no other conflicts of interest.

Hormone therapy in breast cancer patients can lead to mood and sleep disorders. A new randomized, controlled trial shows that omega-3 supplementation improves these symptoms. After 4 weeks of treatment, patients who received omega-3 reported better sleep, depression, and mood outcomes than those who received placebo.

Estrogen-receptor inhibitors are used to treat breast cancer with positive hormone receptors in combination with other therapies. However, the drugs can lead to long-term side effects, including hot flashes, night sweats, and changes to mood and sleep.

These side effects are often treated with selective serotonin reuptake inhibitors and some anticonvulsant drugs. Omega-3 supplements contain various polyunsaturated fatty acids, which influence cell signaling and contribute to the production of bioactive fat mediators that counter inflammation. They are widely used in cardiovascular disease, breast cancer, rheumatoid arthritis, depression, and other cognitive disorders. They also appear to amplify the antitumor efficacy of tamoxifen through the inhibition of proliferative and antiapoptotic pathways that that are influenced by estrogen-receptor signaling.

“This study showed that omega-3 supplementation can improve mood and sleep disorder in women suffering from breast cancer while they (are) managing with antihormone drugs. … this supplement can be proposed for the treatment of these patients,” wrote researchers led by Azadeh Moghaddas, MD, PhD, who is an associate professor of clinical pharmacy and pharmacy practice at Isfahan (Iran) University of Medical Sciences.

The study was made available as a preprint on ResearchSquare and has not yet been peer reviewed. It included 60 patients who were screened for baseline mood disorders using the hospital anxiety and depression scale (HADS), then randomized to 2 mg omega-3 per day for 4 weeks, or placebo.

Studies have shown that omega-3 supplementation improves menopause and mood symptoms in postmenopausal women without cancer.

Omega-3 supplementation has neuroprotective effects and improved brain function and mood in rats, and a 2019 review suggested that the evidence is strong enough to warrant clinical studies.

To determine if the supplement was also safe and effective in women with breast cancer undergoing hormone therapy, the researchers analyzed data from 32 patients in the intervention group and 28 patients in the placebo group.

At 4 weeks of follow-up, patients in the intervention group had significantly lower values on the Center for Epidemiological Studies-Depression scale (mean, 22.8 vs. 30.8; P < .001), Profile of Mood State (mean, 30.8 versus 39.5; P<.001), and Pittsburgh Sleep Quality Index (mean, 4.6 vs. 5.9; P = .04). There were no statistically significant changes in these values in the placebo group.

At 4 weeks, paired samples t-test comparisons between the intervention and the placebo groups revealed lower scores in the intervention group for mean scores in the PSQI subscales subjective sleep quality (0.8 vs. 1.4; P = .002), delay in falling asleep (1.1 vs. 1.6; P = .02), and sleep disturbances (0.8 vs. 1.1; P = .005).

There were no significant adverse reactions in either group.

The study is limited by its small sample size and the short follow-up period.

The study was funded by Isfahan University of Medical Sciences. The authors declare no other conflicts of interest.

Hormone therapy in breast cancer patients can lead to mood and sleep disorders. A new randomized, controlled trial shows that omega-3 supplementation improves these symptoms. After 4 weeks of treatment, patients who received omega-3 reported better sleep, depression, and mood outcomes than those who received placebo.

Estrogen-receptor inhibitors are used to treat breast cancer with positive hormone receptors in combination with other therapies. However, the drugs can lead to long-term side effects, including hot flashes, night sweats, and changes to mood and sleep.

These side effects are often treated with selective serotonin reuptake inhibitors and some anticonvulsant drugs. Omega-3 supplements contain various polyunsaturated fatty acids, which influence cell signaling and contribute to the production of bioactive fat mediators that counter inflammation. They are widely used in cardiovascular disease, breast cancer, rheumatoid arthritis, depression, and other cognitive disorders. They also appear to amplify the antitumor efficacy of tamoxifen through the inhibition of proliferative and antiapoptotic pathways that that are influenced by estrogen-receptor signaling.

“This study showed that omega-3 supplementation can improve mood and sleep disorder in women suffering from breast cancer while they (are) managing with antihormone drugs. … this supplement can be proposed for the treatment of these patients,” wrote researchers led by Azadeh Moghaddas, MD, PhD, who is an associate professor of clinical pharmacy and pharmacy practice at Isfahan (Iran) University of Medical Sciences.

The study was made available as a preprint on ResearchSquare and has not yet been peer reviewed. It included 60 patients who were screened for baseline mood disorders using the hospital anxiety and depression scale (HADS), then randomized to 2 mg omega-3 per day for 4 weeks, or placebo.

Studies have shown that omega-3 supplementation improves menopause and mood symptoms in postmenopausal women without cancer.

Omega-3 supplementation has neuroprotective effects and improved brain function and mood in rats, and a 2019 review suggested that the evidence is strong enough to warrant clinical studies.

To determine if the supplement was also safe and effective in women with breast cancer undergoing hormone therapy, the researchers analyzed data from 32 patients in the intervention group and 28 patients in the placebo group.

At 4 weeks of follow-up, patients in the intervention group had significantly lower values on the Center for Epidemiological Studies-Depression scale (mean, 22.8 vs. 30.8; P < .001), Profile of Mood State (mean, 30.8 versus 39.5; P<.001), and Pittsburgh Sleep Quality Index (mean, 4.6 vs. 5.9; P = .04). There were no statistically significant changes in these values in the placebo group.

At 4 weeks, paired samples t-test comparisons between the intervention and the placebo groups revealed lower scores in the intervention group for mean scores in the PSQI subscales subjective sleep quality (0.8 vs. 1.4; P = .002), delay in falling asleep (1.1 vs. 1.6; P = .02), and sleep disturbances (0.8 vs. 1.1; P = .005).

There were no significant adverse reactions in either group.

The study is limited by its small sample size and the short follow-up period.

The study was funded by Isfahan University of Medical Sciences. The authors declare no other conflicts of interest.

Patients ages 65 years and older with atopic dermatitis (AD) have similar disease severity when compared with younger adult patients, but they have more profound sleep disturbances, especially trouble staying asleep.

Those are key findings from a cross-sectional study that Jaya Manjunath, BS, and Jonathan I. Silverberg, MD, PhD, MPH, presented during a poster session at the Revolutionizing Atopic Dermatitis symposium.

“Atopic dermatitis is a chronic, pruritic skin disease associated with sleep disturbance and fatigue affecting adults of all ages,” they wrote. “When caring for geriatric patients, several factors such as sleep disturbance, polypharmacy, cognition, social support, and mobility should be considered. However, little is known about the characteristics of atopic dermatitis in the geriatric population.”

Ms. Manjunath, a student at George Washington University, Washington, and Dr. Silverberg, director of clinical research in the department of dermatology at GWU, recruited patients with AD aged 18 years and older diagnosed by Hanifin-Rajka criteria who were evaluated at an academic medical center between 2014 and 2019. They underwent full body skin exams and completed electronic questionnaires. AD severity was assessed with the Eczema Area and Severity Index (EASI), Scoring Atopic Dermatitis (SCORAD) total and itch subscores, Investigator’s Global Assessment (IGA), patient-reported Global Assessment of AD severity, and the Patient-Oriented Eczema Measure (POEM).

The researchers also assessed the frequency of sleep disturbances, including difficulty falling asleep and staying asleep, and used multivariable logistic regression models to evaluate associations of age (65 and older vs. 18-64 years) with AD severity, sleep disturbance or fatigue, controlling for total POEM score, sex, and race.

Using adjusted odds ratios, Ms. Manjunath and Dr. Silverberg found that being 65 or older was not associated with AD severity on the EASI (adjusted odds ratio, 1.47); total SCORAD (aOR, 1.10), and itch subscore (aOR, 1.00); IGA (aOR, 1.87); patient-reported Global Assessment of AD severity (aOR, 0.80), or the patient-oriented eczema measure (aOR, 0.55), associations that were not statistically significant.

However, the researchers found that older adult age was associated with an increased number of nights of sleep disturbance from AD in the past week (aOR, 2.14; P = .0142), as well as increased fatigue in the past 7 days (aOR, 1.81; P = .0313), trouble sleeping in the past 7 days (aOR, 1.98; P = .0118), and trouble staying asleep in the past 7 days (aOR, 2.26; P = .0030), but not with difficulty falling asleep in the last 7 days (aOR, 1.16; P = .5996).

“Future studies are needed to determine why geriatric AD patients have increased sleep disturbance and optimal interventions to address their sleep disturbance,” the researchers concluded.

The study was supported by the Agency for Healthcare Research and Quality, the Dermatology Foundation, and by an unrestricted grant from Galderma. Ms. Manjunath disclosed no relevant financial relationships. Dr. Silverberg reported that he is a consultant to and/or an advisory board member for several pharmaceutical companies. He is also a speaker for Regeneron and Sanofi and has received a grant from Galderma.

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

Patients ages 65 years and older with atopic dermatitis (AD) have similar disease severity when compared with younger adult patients, but they have more profound sleep disturbances, especially trouble staying asleep.

Those are key findings from a cross-sectional study that Jaya Manjunath, BS, and Jonathan I. Silverberg, MD, PhD, MPH, presented during a poster session at the Revolutionizing Atopic Dermatitis symposium.

“Atopic dermatitis is a chronic, pruritic skin disease associated with sleep disturbance and fatigue affecting adults of all ages,” they wrote. “When caring for geriatric patients, several factors such as sleep disturbance, polypharmacy, cognition, social support, and mobility should be considered. However, little is known about the characteristics of atopic dermatitis in the geriatric population.”

Ms. Manjunath, a student at George Washington University, Washington, and Dr. Silverberg, director of clinical research in the department of dermatology at GWU, recruited patients with AD aged 18 years and older diagnosed by Hanifin-Rajka criteria who were evaluated at an academic medical center between 2014 and 2019. They underwent full body skin exams and completed electronic questionnaires. AD severity was assessed with the Eczema Area and Severity Index (EASI), Scoring Atopic Dermatitis (SCORAD) total and itch subscores, Investigator’s Global Assessment (IGA), patient-reported Global Assessment of AD severity, and the Patient-Oriented Eczema Measure (POEM).

The researchers also assessed the frequency of sleep disturbances, including difficulty falling asleep and staying asleep, and used multivariable logistic regression models to evaluate associations of age (65 and older vs. 18-64 years) with AD severity, sleep disturbance or fatigue, controlling for total POEM score, sex, and race.

Using adjusted odds ratios, Ms. Manjunath and Dr. Silverberg found that being 65 or older was not associated with AD severity on the EASI (adjusted odds ratio, 1.47); total SCORAD (aOR, 1.10), and itch subscore (aOR, 1.00); IGA (aOR, 1.87); patient-reported Global Assessment of AD severity (aOR, 0.80), or the patient-oriented eczema measure (aOR, 0.55), associations that were not statistically significant.

However, the researchers found that older adult age was associated with an increased number of nights of sleep disturbance from AD in the past week (aOR, 2.14; P = .0142), as well as increased fatigue in the past 7 days (aOR, 1.81; P = .0313), trouble sleeping in the past 7 days (aOR, 1.98; P = .0118), and trouble staying asleep in the past 7 days (aOR, 2.26; P = .0030), but not with difficulty falling asleep in the last 7 days (aOR, 1.16; P = .5996).

“Future studies are needed to determine why geriatric AD patients have increased sleep disturbance and optimal interventions to address their sleep disturbance,” the researchers concluded.

The study was supported by the Agency for Healthcare Research and Quality, the Dermatology Foundation, and by an unrestricted grant from Galderma. Ms. Manjunath disclosed no relevant financial relationships. Dr. Silverberg reported that he is a consultant to and/or an advisory board member for several pharmaceutical companies. He is also a speaker for Regeneron and Sanofi and has received a grant from Galderma.

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

Patients ages 65 years and older with atopic dermatitis (AD) have similar disease severity when compared with younger adult patients, but they have more profound sleep disturbances, especially trouble staying asleep.

Those are key findings from a cross-sectional study that Jaya Manjunath, BS, and Jonathan I. Silverberg, MD, PhD, MPH, presented during a poster session at the Revolutionizing Atopic Dermatitis symposium.

“Atopic dermatitis is a chronic, pruritic skin disease associated with sleep disturbance and fatigue affecting adults of all ages,” they wrote. “When caring for geriatric patients, several factors such as sleep disturbance, polypharmacy, cognition, social support, and mobility should be considered. However, little is known about the characteristics of atopic dermatitis in the geriatric population.”

Ms. Manjunath, a student at George Washington University, Washington, and Dr. Silverberg, director of clinical research in the department of dermatology at GWU, recruited patients with AD aged 18 years and older diagnosed by Hanifin-Rajka criteria who were evaluated at an academic medical center between 2014 and 2019. They underwent full body skin exams and completed electronic questionnaires. AD severity was assessed with the Eczema Area and Severity Index (EASI), Scoring Atopic Dermatitis (SCORAD) total and itch subscores, Investigator’s Global Assessment (IGA), patient-reported Global Assessment of AD severity, and the Patient-Oriented Eczema Measure (POEM).

The researchers also assessed the frequency of sleep disturbances, including difficulty falling asleep and staying asleep, and used multivariable logistic regression models to evaluate associations of age (65 and older vs. 18-64 years) with AD severity, sleep disturbance or fatigue, controlling for total POEM score, sex, and race.

Using adjusted odds ratios, Ms. Manjunath and Dr. Silverberg found that being 65 or older was not associated with AD severity on the EASI (adjusted odds ratio, 1.47); total SCORAD (aOR, 1.10), and itch subscore (aOR, 1.00); IGA (aOR, 1.87); patient-reported Global Assessment of AD severity (aOR, 0.80), or the patient-oriented eczema measure (aOR, 0.55), associations that were not statistically significant.

However, the researchers found that older adult age was associated with an increased number of nights of sleep disturbance from AD in the past week (aOR, 2.14; P = .0142), as well as increased fatigue in the past 7 days (aOR, 1.81; P = .0313), trouble sleeping in the past 7 days (aOR, 1.98; P = .0118), and trouble staying asleep in the past 7 days (aOR, 2.26; P = .0030), but not with difficulty falling asleep in the last 7 days (aOR, 1.16; P = .5996).

“Future studies are needed to determine why geriatric AD patients have increased sleep disturbance and optimal interventions to address their sleep disturbance,” the researchers concluded.

The study was supported by the Agency for Healthcare Research and Quality, the Dermatology Foundation, and by an unrestricted grant from Galderma. Ms. Manjunath disclosed no relevant financial relationships. Dr. Silverberg reported that he is a consultant to and/or an advisory board member for several pharmaceutical companies. He is also a speaker for Regeneron and Sanofi and has received a grant from Galderma.

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

A nose for the tooth

Have you ever had a stuffy nose that just wouldn’t go away? Those irritating head colds have nothing on the stuffy nose a man in New York recently had to go through. A stuffy nose to top all stuffy noses. One stuffy nose to rule them all, as it were.

John Oliver/Pixabay

This man went to a Mount Sinai clinic with difficulty breathing through his right nostril, a problem that had been going on for years. Let us repeat that: A stuffy nose that lasted for years. The exam revealed a white mass jutting through the back of the septum and a CT scan confirmed the diagnosis. Perhaps you’ve already guessed, since the headline does give things away. Yes, this man had a tooth growing into his nose.

The problem was a half-inch-long ectopic tooth. Ectopic teeth are rare, occurring in less than 1% of people, but an ectopic tooth growing backward into the nasal cavity? Well, that’s so uncommon that this man got a case report in the New England Journal of Medicine.

This story does have a happy ending. Not all ectopic teeth need to be treated, but this one really did have to go. The offending tooth was surgically removed and, at a 3-month follow-up, the stuffy nose issue was completely resolved. So our friend gets the best of both worlds: His issue gets cured and he gets a case report in a major medical publication. If that’s not living the dream, we don’t know what is, and that’s the tooth.
 

Lettuce recommend you a sleep aid

Lettuce is great for many things. The star in a salad? Of course. The fresh element in a BLT? Yep. A sleep aid? According to a TikTok hack with almost 5 million views, the pinch hitter in a sandwich is switching leagues to be used like a tea for faster sleep. But, does it really work? Researchers say yes and no, according to a recent report at Tyla.com.

PxHere

Studies conducted in 2013 and 2017 pointed toward a compound called lactucin, which is found in the plant’s n-butanol fraction. In the 2013 study, mice that received n-butanol fraction fell asleep faster and stayed asleep longer. In 2017, researchers found that lettuce made mice sleep longer and helped protect against cell inflammation and damage.

OK, so it works on mice. But what about humans? In the TikTok video, user Shapla Hoque pours hot water on a few lettuce leaves in a mug with a peppermint tea bag (for flavor). After 10 minutes, when the leaves are soaked and soggy, she removes them and drinks the lettuce tea. By the end of the video she’s visibly drowsy and ready to crash. Does this hold water?

Here’s the no. Dr. Charlotte Norton of the Slimming Clinic told Tyla.com that yeah, there are some properties in lettuce that will help you fall asleep, such as lactucarium, which is prominent in romaine. But you would need a massive amount of lettuce to get any effect. The TikTok video, she said, is an example of the placebo effect.
 

Brains get a rise out of Viagra

A lot of medications are used off label. Antidepressants for COVID have taken the cake recently, but here’s a new one: Viagra for Alzheimer’s disease.

©roberthyrons/thinkstockphotos.com

Omicron is not a social-distancing robot

COVID, safe to say, has not been your typical, run-of-the-mill pandemic. People have protested social distancing. People have protested lockdowns. People have protested mask mandates. People have protested vaccine mandates. People have protested people protesting vaccine mandates.

neo tam/Pixabay

Someone used a fake arm to get a COVID vaccine card. People have tried to reverse their COVID vaccinations. People had COVID contamination parties.

The common denominator? People. Humans. Maybe what we need is a nonhuman intervention. To fight COVID, we need a hero. A robotic hero.

And where can we find such a hero? The University of Maryland, of course, where computer scientists and engineers are working on an autonomous mobile robot to enforce indoor social-distancing rules.

Their robot can detect lapses in social distancing using cameras, both thermal and visual, along with a LiDAR (Light Detection and Ranging) sensor. It then sorts the offenders into various groups depending on whether they are standing still or moving and predicts their future movement using a state-of-the-art hybrid collision avoidance method known as Frozone, Adarsh Jagan Sathyamoorthy and associates explained in PLOS One.

“Once it reaches the breach, the robot encourages people to move apart via text that appears on a mounted display,” ScienceDaily said.

Maybe you were expecting a Terminator-type robot coming to enforce social distancing requirements rather than a simple text message. Let’s just hope that all COVID guidelines are followed, including social distancing, so the pandemic will finally end and won’t “be back.”

A nose for the tooth

Have you ever had a stuffy nose that just wouldn’t go away? Those irritating head colds have nothing on the stuffy nose a man in New York recently had to go through. A stuffy nose to top all stuffy noses. One stuffy nose to rule them all, as it were.

John Oliver/Pixabay

This man went to a Mount Sinai clinic with difficulty breathing through his right nostril, a problem that had been going on for years. Let us repeat that: A stuffy nose that lasted for years. The exam revealed a white mass jutting through the back of the septum and a CT scan confirmed the diagnosis. Perhaps you’ve already guessed, since the headline does give things away. Yes, this man had a tooth growing into his nose.

The problem was a half-inch-long ectopic tooth. Ectopic teeth are rare, occurring in less than 1% of people, but an ectopic tooth growing backward into the nasal cavity? Well, that’s so uncommon that this man got a case report in the New England Journal of Medicine.

This story does have a happy ending. Not all ectopic teeth need to be treated, but this one really did have to go. The offending tooth was surgically removed and, at a 3-month follow-up, the stuffy nose issue was completely resolved. So our friend gets the best of both worlds: His issue gets cured and he gets a case report in a major medical publication. If that’s not living the dream, we don’t know what is, and that’s the tooth.
 

Lettuce recommend you a sleep aid

Lettuce is great for many things. The star in a salad? Of course. The fresh element in a BLT? Yep. A sleep aid? According to a TikTok hack with almost 5 million views, the pinch hitter in a sandwich is switching leagues to be used like a tea for faster sleep. But, does it really work? Researchers say yes and no, according to a recent report at Tyla.com.

PxHere

Studies conducted in 2013 and 2017 pointed toward a compound called lactucin, which is found in the plant’s n-butanol fraction. In the 2013 study, mice that received n-butanol fraction fell asleep faster and stayed asleep longer. In 2017, researchers found that lettuce made mice sleep longer and helped protect against cell inflammation and damage.

OK, so it works on mice. But what about humans? In the TikTok video, user Shapla Hoque pours hot water on a few lettuce leaves in a mug with a peppermint tea bag (for flavor). After 10 minutes, when the leaves are soaked and soggy, she removes them and drinks the lettuce tea. By the end of the video she’s visibly drowsy and ready to crash. Does this hold water?

Here’s the no. Dr. Charlotte Norton of the Slimming Clinic told Tyla.com that yeah, there are some properties in lettuce that will help you fall asleep, such as lactucarium, which is prominent in romaine. But you would need a massive amount of lettuce to get any effect. The TikTok video, she said, is an example of the placebo effect.
 

Brains get a rise out of Viagra

A lot of medications are used off label. Antidepressants for COVID have taken the cake recently, but here’s a new one: Viagra for Alzheimer’s disease.

©roberthyrons/thinkstockphotos.com

Omicron is not a social-distancing robot

COVID, safe to say, has not been your typical, run-of-the-mill pandemic. People have protested social distancing. People have protested lockdowns. People have protested mask mandates. People have protested vaccine mandates. People have protested people protesting vaccine mandates.

neo tam/Pixabay

Someone used a fake arm to get a COVID vaccine card. People have tried to reverse their COVID vaccinations. People had COVID contamination parties.

The common denominator? People. Humans. Maybe what we need is a nonhuman intervention. To fight COVID, we need a hero. A robotic hero.

And where can we find such a hero? The University of Maryland, of course, where computer scientists and engineers are working on an autonomous mobile robot to enforce indoor social-distancing rules.

Their robot can detect lapses in social distancing using cameras, both thermal and visual, along with a LiDAR (Light Detection and Ranging) sensor. It then sorts the offenders into various groups depending on whether they are standing still or moving and predicts their future movement using a state-of-the-art hybrid collision avoidance method known as Frozone, Adarsh Jagan Sathyamoorthy and associates explained in PLOS One.

“Once it reaches the breach, the robot encourages people to move apart via text that appears on a mounted display,” ScienceDaily said.

Maybe you were expecting a Terminator-type robot coming to enforce social distancing requirements rather than a simple text message. Let’s just hope that all COVID guidelines are followed, including social distancing, so the pandemic will finally end and won’t “be back.”

A nose for the tooth

Have you ever had a stuffy nose that just wouldn’t go away? Those irritating head colds have nothing on the stuffy nose a man in New York recently had to go through. A stuffy nose to top all stuffy noses. One stuffy nose to rule them all, as it were.

John Oliver/Pixabay

This man went to a Mount Sinai clinic with difficulty breathing through his right nostril, a problem that had been going on for years. Let us repeat that: A stuffy nose that lasted for years. The exam revealed a white mass jutting through the back of the septum and a CT scan confirmed the diagnosis. Perhaps you’ve already guessed, since the headline does give things away. Yes, this man had a tooth growing into his nose.

The problem was a half-inch-long ectopic tooth. Ectopic teeth are rare, occurring in less than 1% of people, but an ectopic tooth growing backward into the nasal cavity? Well, that’s so uncommon that this man got a case report in the New England Journal of Medicine.

This story does have a happy ending. Not all ectopic teeth need to be treated, but this one really did have to go. The offending tooth was surgically removed and, at a 3-month follow-up, the stuffy nose issue was completely resolved. So our friend gets the best of both worlds: His issue gets cured and he gets a case report in a major medical publication. If that’s not living the dream, we don’t know what is, and that’s the tooth.
 

Lettuce recommend you a sleep aid

Lettuce is great for many things. The star in a salad? Of course. The fresh element in a BLT? Yep. A sleep aid? According to a TikTok hack with almost 5 million views, the pinch hitter in a sandwich is switching leagues to be used like a tea for faster sleep. But, does it really work? Researchers say yes and no, according to a recent report at Tyla.com.

PxHere

Studies conducted in 2013 and 2017 pointed toward a compound called lactucin, which is found in the plant’s n-butanol fraction. In the 2013 study, mice that received n-butanol fraction fell asleep faster and stayed asleep longer. In 2017, researchers found that lettuce made mice sleep longer and helped protect against cell inflammation and damage.

OK, so it works on mice. But what about humans? In the TikTok video, user Shapla Hoque pours hot water on a few lettuce leaves in a mug with a peppermint tea bag (for flavor). After 10 minutes, when the leaves are soaked and soggy, she removes them and drinks the lettuce tea. By the end of the video she’s visibly drowsy and ready to crash. Does this hold water?

Here’s the no. Dr. Charlotte Norton of the Slimming Clinic told Tyla.com that yeah, there are some properties in lettuce that will help you fall asleep, such as lactucarium, which is prominent in romaine. But you would need a massive amount of lettuce to get any effect. The TikTok video, she said, is an example of the placebo effect.
 

Brains get a rise out of Viagra

A lot of medications are used off label. Antidepressants for COVID have taken the cake recently, but here’s a new one: Viagra for Alzheimer’s disease.

©roberthyrons/thinkstockphotos.com

Omicron is not a social-distancing robot

COVID, safe to say, has not been your typical, run-of-the-mill pandemic. People have protested social distancing. People have protested lockdowns. People have protested mask mandates. People have protested vaccine mandates. People have protested people protesting vaccine mandates.

neo tam/Pixabay

Someone used a fake arm to get a COVID vaccine card. People have tried to reverse their COVID vaccinations. People had COVID contamination parties.

The common denominator? People. Humans. Maybe what we need is a nonhuman intervention. To fight COVID, we need a hero. A robotic hero.

And where can we find such a hero? The University of Maryland, of course, where computer scientists and engineers are working on an autonomous mobile robot to enforce indoor social-distancing rules.

Their robot can detect lapses in social distancing using cameras, both thermal and visual, along with a LiDAR (Light Detection and Ranging) sensor. It then sorts the offenders into various groups depending on whether they are standing still or moving and predicts their future movement using a state-of-the-art hybrid collision avoidance method known as Frozone, Adarsh Jagan Sathyamoorthy and associates explained in PLOS One.

“Once it reaches the breach, the robot encourages people to move apart via text that appears on a mounted display,” ScienceDaily said.

Maybe you were expecting a Terminator-type robot coming to enforce social distancing requirements rather than a simple text message. Let’s just hope that all COVID guidelines are followed, including social distancing, so the pandemic will finally end and won’t “be back.”

In 2011, the Mayo Clinic began surveying physicians about burnout and found 45% of physicians experienced at least one symptom, such as emotional exhaustion, finding work no longer meaningful, feelings of ineffectiveness, and depersonalizing patients. Associated manifestations can range from headache and insomnia to impaired memory and decreased attention. 

Marija Jovovic/Getty Images

Fast forward 10 years to the Medscape National Physician Burnout and Suicide Report, which found that a similar number of physicians (42%) feel burned out. The COVID-19 pandemic only added insult to injury. A Medscape survey that included nearly 5,000 U.S. physicians revealed that about two-thirds (64%) of them reported burnout had intensified during the crisis.

These elevated numbers are being labeled as “a public health crisis” for the impact widespread physician burnout could have on the health of the doctor and patient safety. The relatively consistent levels across the decade seem to suggest that, if health organizations are attempting to improve physician well-being, it doesn’t appear to be working, forcing doctors to find solutions for themselves.

Jill Wener, MD, considers herself part of the 45% burned out 10 years ago. She was working as an internist at Rush University Medical Center in Chicago, but the “existential reality of being a doctor in this world” was wearing on her. “Staying up with the literature, knowing that every day you’re going to go into work without knowing what you’re going to find, threats of lawsuits, the pressure of perfectionism,” Dr. Wener told this news organization. “By the time I hit burnout, everything made me feel like the world was crashing down on me.”

When Dr. Wener encountered someone who meditated twice a day, she was intrigued, even though the self-described “most Type-A, inside-the-box, nonspiritual type, anxious, linear-path doctor” didn’t think people like her could meditate. Dr. Wener is not alone in her hesitation to explore meditation as a means to help prevent burnout because the causes of burnout are primarily linked to external rather than internal factors. Issues including a loss of autonomy, the burden and distraction of electronic health records, and the intense pressure to comply with rules from the government are not things mindfulness can fix. 

And because the sources of burnout are primarily environmental and inherent to the current medical system, the suggestion that physicians need to fix themselves with meditation can come as a slap in the face. However, when up against a system slow to change, mindfulness can provide physicians access to the one thing they can control: How they perceive and react to what’s in front of them.

At the recommendation of an acquaintance, Dr. Wener enrolled in a Vedic Meditation (also known as Conscious Health Meditation) course taught by Light Watkins, a well-known traveling instructor, author, and speaker. By the second meeting she was successfully practicing 20 minutes twice a day. This form of mediation traces its roots to the Vedas, ancient Indian texts (also the foundation for yoga), and uses a mantra to settle the mind, transitioning to an awake state of inner contentment. 

Three weeks later, Dr. Wener’s daily crying jags ended as did her propensity for road rage. “I felt like I was on the cusp of something life-changing, I just didn’t understand it,” she recalled. “But I knew I was never going to give it up.”
 

Defining mindfulness

“Mindfulness is being able to be present in the moment that you’re in with acceptance of what it is and without judging it,” said Donna Rockwell, PsyD, a leading mindfulness meditation teacher. The practice of mindfulness is really meditation. Dr. Rockwell explained that the noise of our mind is most often focused on either the past or the future. “We’re either bemoaning something that happened earlier or we’re catastrophizing the future,” she said, which prevents us from being present in the moment. 

Meditation allows you to notice when your mind has drifted from the present moment into the past or future. “You gently notice it, label it with a lot of self-compassion, and then bring your mind back by focusing on your breath – going out, going in – and the incoming stimuli through your five senses,” said Dr. Rockwell. “When you’re doing that, you can’t be in the past or future.”

Dr. Rockwell also pointed out that we constantly categorize incoming data of the moment as either “good for me or bad for me,” which gets in the way of simply being present for what you’re facing. “When you’re more fully present, you become more skillful and able to do what this moment is asking of you,” she said. Being mindful allows us to better navigate incoming stimuli, which could be a “code blue” in the ED or a patient who needs another 2 minutes during an office visit. 

When Dr. Wener was burned out, she felt unable to adapt whenever something unexpected happened. “When you have no emotional reserves, everything feels like a big deal,” she said. “The meditation gave me what we call adaptation energy; it filled up my tank and kept me from feeling like I was going to lose it at 10 o’clock in the morning.”

Dr. Rockwell explained burnout as an overactive fight or flight response activated by the amygdala. It starts pumping cortisol, our pupils dilate, and our pores open. The prefrontal cortex is offline when we’re experiencing this physiological response because they both can’t be operational at the same time. “When we’re constantly in a ‘fight or flight’ response and don’t have any access to our prefrontal cortex, we are coming from a brain that is pumping cortisol and that leads to burnout,” said Dr. Rockwell.

“Any fight or flight response leaves a mark on your body,” Dr. Wener echoed. “When we go into our state of deep rest in the meditation practice, which is two to five times more restful than sleep, it heals those stress scars.”
 

Making time for mindfulness

Prescribing mindfulness for physicians is not new. Molecular biologist Jon Kabat-Zinn, PhD, developed Mindfulness-Based Stress Reduction (MBSR) in 1979, a practice that incorporates mindfulness exercises to help people become familiar with their behavior patterns in stressful situations. Thus, instead of reacting, they can respond with a clearer understanding of the circumstance. Dr. Kabat-Zinn initially targeted people with chronic health problems to help them cope with the effects of pain and the condition of their illness, but it has expanded to anyone experiencing challenges in their life, including physicians. A standard MBSR course runs 8 weeks, making it a commitment for most people. 

Mindfulness training requires that physicians use what they already have so little of: time.

Dr. Wener was able to take a sabbatical, embarking on a 3-month trip to India to immerse herself in the study of Vedic Meditation. Upon her return, Dr. Wener took a position at Emory University, Atlanta, and has launched a number of CME-accredited meditation courses and retreats. Unlike Dr. Kabat-Zinn, her programs are by physicians and for physicians. She also created an online version of the meditation course to make it more accessible. 

For these reasons, Kara Pepper, MD, an internist in outpatient primary care in Atlanta, was drawn to the meditation course. Dr. Pepper was 7 years into practice when she burned out. “The program dovetailed into my burnout recovery,” she said. “It allowed me space to separate myself from the thoughts I was having about work and just recognize them as just that – as thoughts.”

In the course, Dr. Wener teaches the REST Technique, which she says is different than mindfulness in that she encourages the mind to run rampant. “Trying to control the mind can feel very uncomfortable because we always have thoughts,” she says. “We can’t tell the mind to stop thinking just like we can’t tell the heart to stop beating.” Dr. Wener said the REST Technique lets “the mind swim downstream,” allowing the brain to go into a deep state of rest and start to heal from the scars caused by stress. 

Dr. Pepper said the self-paced online course gave her all the tools she needed, and it was pragmatic and evidence based. “I didn’t feel ‘woo’ or like another gimmick,” she said. Pepper, who continues to practice medicine, became a life coach in 2019 to teach others the skills she uses daily. 
 

An integrated strategy

Dr. Wener acknowledges that meditation is not the panacea for everyone’s burnout, which data support. In a review published in The American Journal of Medicine in 2019, Scott Yates, MD, MBA, from the Center for Executive Medicine in Plano, Tex., found that physicians who had adopted mediation and mindfulness training to decrease anxiety and perceived work stress only experienced modest benefits. In fact, Dr. Yates claims that there’s little data to suggest the long-term benefit of any particular stress management intervention in the prevention of burnout symptoms. 

“The often-repeated goals of the Triple Aim [enhancing patient experience, improving population health, and reducing costs] may be unreachable until we recognize and address burnout in health care providers,” Dr. Yates wrote. He recommends adding a fourth goal to specifically address physician wellness, which certainly could include mindfulness training and meditation.

Burnout coach, trainer, and consultant Dike Drummond, MD, also professes that physician wellness must be added as the key fourth ingredient to improving health care. “Burnout is a dilemma, a balancing act,” he said. “It takes an integrated strategy.” The CEO and founder of TheHappyMD.com, Dr. Drummond’s integrated strategy to stop physician burnout has been taught to more than 40,000 physicians in 175 organizations, and one element of that strategy can be mindfulness training. 

Dr. Drummond said he doesn’t use the word meditation “because that scares most people”; it takes a commitment and isn’t accessible for a lot of doctors. Instead, he coaches doctors to use a ‘single-breath’ technique to help them reset multiple times throughout the day. “I teach people how to breathe up to the top of their head and then down to the bottom of their feet,” Dr. Drummond said. He calls it the Squeegee Breath Technique because when they exhale, they “wipe away” anything that doesn’t need to be there right now. “If you happen to have a mindfulness practice like meditation, they work synergistically because the calmness you feel in your mediation is available to you at the bottom of these releasing breaths.”

Various studies and surveys provide great detail as to the “why” of physician burnout. And while mindfulness is not the sole answer, it’s something physicians can explore for themselves while health care as an industry looks for a more comprehensive solution. 

“It’s not rocket science,” Dr. Drummond insisted. “You want a different result? You’re not satisfied with the way things are now and you want to feel different? You absolutely must do something different.”

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

In 2011, the Mayo Clinic began surveying physicians about burnout and found 45% of physicians experienced at least one symptom, such as emotional exhaustion, finding work no longer meaningful, feelings of ineffectiveness, and depersonalizing patients. Associated manifestations can range from headache and insomnia to impaired memory and decreased attention. 

Marija Jovovic/Getty Images

Fast forward 10 years to the Medscape National Physician Burnout and Suicide Report, which found that a similar number of physicians (42%) feel burned out. The COVID-19 pandemic only added insult to injury. A Medscape survey that included nearly 5,000 U.S. physicians revealed that about two-thirds (64%) of them reported burnout had intensified during the crisis.

These elevated numbers are being labeled as “a public health crisis” for the impact widespread physician burnout could have on the health of the doctor and patient safety. The relatively consistent levels across the decade seem to suggest that, if health organizations are attempting to improve physician well-being, it doesn’t appear to be working, forcing doctors to find solutions for themselves.

Jill Wener, MD, considers herself part of the 45% burned out 10 years ago. She was working as an internist at Rush University Medical Center in Chicago, but the “existential reality of being a doctor in this world” was wearing on her. “Staying up with the literature, knowing that every day you’re going to go into work without knowing what you’re going to find, threats of lawsuits, the pressure of perfectionism,” Dr. Wener told this news organization. “By the time I hit burnout, everything made me feel like the world was crashing down on me.”

When Dr. Wener encountered someone who meditated twice a day, she was intrigued, even though the self-described “most Type-A, inside-the-box, nonspiritual type, anxious, linear-path doctor” didn’t think people like her could meditate. Dr. Wener is not alone in her hesitation to explore meditation as a means to help prevent burnout because the causes of burnout are primarily linked to external rather than internal factors. Issues including a loss of autonomy, the burden and distraction of electronic health records, and the intense pressure to comply with rules from the government are not things mindfulness can fix. 

And because the sources of burnout are primarily environmental and inherent to the current medical system, the suggestion that physicians need to fix themselves with meditation can come as a slap in the face. However, when up against a system slow to change, mindfulness can provide physicians access to the one thing they can control: How they perceive and react to what’s in front of them.

At the recommendation of an acquaintance, Dr. Wener enrolled in a Vedic Meditation (also known as Conscious Health Meditation) course taught by Light Watkins, a well-known traveling instructor, author, and speaker. By the second meeting she was successfully practicing 20 minutes twice a day. This form of mediation traces its roots to the Vedas, ancient Indian texts (also the foundation for yoga), and uses a mantra to settle the mind, transitioning to an awake state of inner contentment. 

Three weeks later, Dr. Wener’s daily crying jags ended as did her propensity for road rage. “I felt like I was on the cusp of something life-changing, I just didn’t understand it,” she recalled. “But I knew I was never going to give it up.”
 

Defining mindfulness

“Mindfulness is being able to be present in the moment that you’re in with acceptance of what it is and without judging it,” said Donna Rockwell, PsyD, a leading mindfulness meditation teacher. The practice of mindfulness is really meditation. Dr. Rockwell explained that the noise of our mind is most often focused on either the past or the future. “We’re either bemoaning something that happened earlier or we’re catastrophizing the future,” she said, which prevents us from being present in the moment. 

Meditation allows you to notice when your mind has drifted from the present moment into the past or future. “You gently notice it, label it with a lot of self-compassion, and then bring your mind back by focusing on your breath – going out, going in – and the incoming stimuli through your five senses,” said Dr. Rockwell. “When you’re doing that, you can’t be in the past or future.”

Dr. Rockwell also pointed out that we constantly categorize incoming data of the moment as either “good for me or bad for me,” which gets in the way of simply being present for what you’re facing. “When you’re more fully present, you become more skillful and able to do what this moment is asking of you,” she said. Being mindful allows us to better navigate incoming stimuli, which could be a “code blue” in the ED or a patient who needs another 2 minutes during an office visit. 

When Dr. Wener was burned out, she felt unable to adapt whenever something unexpected happened. “When you have no emotional reserves, everything feels like a big deal,” she said. “The meditation gave me what we call adaptation energy; it filled up my tank and kept me from feeling like I was going to lose it at 10 o’clock in the morning.”

Dr. Rockwell explained burnout as an overactive fight or flight response activated by the amygdala. It starts pumping cortisol, our pupils dilate, and our pores open. The prefrontal cortex is offline when we’re experiencing this physiological response because they both can’t be operational at the same time. “When we’re constantly in a ‘fight or flight’ response and don’t have any access to our prefrontal cortex, we are coming from a brain that is pumping cortisol and that leads to burnout,” said Dr. Rockwell.

“Any fight or flight response leaves a mark on your body,” Dr. Wener echoed. “When we go into our state of deep rest in the meditation practice, which is two to five times more restful than sleep, it heals those stress scars.”
 

Making time for mindfulness

Prescribing mindfulness for physicians is not new. Molecular biologist Jon Kabat-Zinn, PhD, developed Mindfulness-Based Stress Reduction (MBSR) in 1979, a practice that incorporates mindfulness exercises to help people become familiar with their behavior patterns in stressful situations. Thus, instead of reacting, they can respond with a clearer understanding of the circumstance. Dr. Kabat-Zinn initially targeted people with chronic health problems to help them cope with the effects of pain and the condition of their illness, but it has expanded to anyone experiencing challenges in their life, including physicians. A standard MBSR course runs 8 weeks, making it a commitment for most people. 

Mindfulness training requires that physicians use what they already have so little of: time.

Dr. Wener was able to take a sabbatical, embarking on a 3-month trip to India to immerse herself in the study of Vedic Meditation. Upon her return, Dr. Wener took a position at Emory University, Atlanta, and has launched a number of CME-accredited meditation courses and retreats. Unlike Dr. Kabat-Zinn, her programs are by physicians and for physicians. She also created an online version of the meditation course to make it more accessible. 

For these reasons, Kara Pepper, MD, an internist in outpatient primary care in Atlanta, was drawn to the meditation course. Dr. Pepper was 7 years into practice when she burned out. “The program dovetailed into my burnout recovery,” she said. “It allowed me space to separate myself from the thoughts I was having about work and just recognize them as just that – as thoughts.”

In the course, Dr. Wener teaches the REST Technique, which she says is different than mindfulness in that she encourages the mind to run rampant. “Trying to control the mind can feel very uncomfortable because we always have thoughts,” she says. “We can’t tell the mind to stop thinking just like we can’t tell the heart to stop beating.” Dr. Wener said the REST Technique lets “the mind swim downstream,” allowing the brain to go into a deep state of rest and start to heal from the scars caused by stress. 

Dr. Pepper said the self-paced online course gave her all the tools she needed, and it was pragmatic and evidence based. “I didn’t feel ‘woo’ or like another gimmick,” she said. Pepper, who continues to practice medicine, became a life coach in 2019 to teach others the skills she uses daily. 
 

An integrated strategy

Dr. Wener acknowledges that meditation is not the panacea for everyone’s burnout, which data support. In a review published in The American Journal of Medicine in 2019, Scott Yates, MD, MBA, from the Center for Executive Medicine in Plano, Tex., found that physicians who had adopted mediation and mindfulness training to decrease anxiety and perceived work stress only experienced modest benefits. In fact, Dr. Yates claims that there’s little data to suggest the long-term benefit of any particular stress management intervention in the prevention of burnout symptoms. 

“The often-repeated goals of the Triple Aim [enhancing patient experience, improving population health, and reducing costs] may be unreachable until we recognize and address burnout in health care providers,” Dr. Yates wrote. He recommends adding a fourth goal to specifically address physician wellness, which certainly could include mindfulness training and meditation.

Burnout coach, trainer, and consultant Dike Drummond, MD, also professes that physician wellness must be added as the key fourth ingredient to improving health care. “Burnout is a dilemma, a balancing act,” he said. “It takes an integrated strategy.” The CEO and founder of TheHappyMD.com, Dr. Drummond’s integrated strategy to stop physician burnout has been taught to more than 40,000 physicians in 175 organizations, and one element of that strategy can be mindfulness training. 

Dr. Drummond said he doesn’t use the word meditation “because that scares most people”; it takes a commitment and isn’t accessible for a lot of doctors. Instead, he coaches doctors to use a ‘single-breath’ technique to help them reset multiple times throughout the day. “I teach people how to breathe up to the top of their head and then down to the bottom of their feet,” Dr. Drummond said. He calls it the Squeegee Breath Technique because when they exhale, they “wipe away” anything that doesn’t need to be there right now. “If you happen to have a mindfulness practice like meditation, they work synergistically because the calmness you feel in your mediation is available to you at the bottom of these releasing breaths.”

Various studies and surveys provide great detail as to the “why” of physician burnout. And while mindfulness is not the sole answer, it’s something physicians can explore for themselves while health care as an industry looks for a more comprehensive solution. 

“It’s not rocket science,” Dr. Drummond insisted. “You want a different result? You’re not satisfied with the way things are now and you want to feel different? You absolutely must do something different.”

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

In 2011, the Mayo Clinic began surveying physicians about burnout and found 45% of physicians experienced at least one symptom, such as emotional exhaustion, finding work no longer meaningful, feelings of ineffectiveness, and depersonalizing patients. Associated manifestations can range from headache and insomnia to impaired memory and decreased attention. 

Marija Jovovic/Getty Images

Fast forward 10 years to the Medscape National Physician Burnout and Suicide Report, which found that a similar number of physicians (42%) feel burned out. The COVID-19 pandemic only added insult to injury. A Medscape survey that included nearly 5,000 U.S. physicians revealed that about two-thirds (64%) of them reported burnout had intensified during the crisis.

These elevated numbers are being labeled as “a public health crisis” for the impact widespread physician burnout could have on the health of the doctor and patient safety. The relatively consistent levels across the decade seem to suggest that, if health organizations are attempting to improve physician well-being, it doesn’t appear to be working, forcing doctors to find solutions for themselves.

Jill Wener, MD, considers herself part of the 45% burned out 10 years ago. She was working as an internist at Rush University Medical Center in Chicago, but the “existential reality of being a doctor in this world” was wearing on her. “Staying up with the literature, knowing that every day you’re going to go into work without knowing what you’re going to find, threats of lawsuits, the pressure of perfectionism,” Dr. Wener told this news organization. “By the time I hit burnout, everything made me feel like the world was crashing down on me.”

When Dr. Wener encountered someone who meditated twice a day, she was intrigued, even though the self-described “most Type-A, inside-the-box, nonspiritual type, anxious, linear-path doctor” didn’t think people like her could meditate. Dr. Wener is not alone in her hesitation to explore meditation as a means to help prevent burnout because the causes of burnout are primarily linked to external rather than internal factors. Issues including a loss of autonomy, the burden and distraction of electronic health records, and the intense pressure to comply with rules from the government are not things mindfulness can fix. 

And because the sources of burnout are primarily environmental and inherent to the current medical system, the suggestion that physicians need to fix themselves with meditation can come as a slap in the face. However, when up against a system slow to change, mindfulness can provide physicians access to the one thing they can control: How they perceive and react to what’s in front of them.

At the recommendation of an acquaintance, Dr. Wener enrolled in a Vedic Meditation (also known as Conscious Health Meditation) course taught by Light Watkins, a well-known traveling instructor, author, and speaker. By the second meeting she was successfully practicing 20 minutes twice a day. This form of mediation traces its roots to the Vedas, ancient Indian texts (also the foundation for yoga), and uses a mantra to settle the mind, transitioning to an awake state of inner contentment. 

Three weeks later, Dr. Wener’s daily crying jags ended as did her propensity for road rage. “I felt like I was on the cusp of something life-changing, I just didn’t understand it,” she recalled. “But I knew I was never going to give it up.”
 

Defining mindfulness

“Mindfulness is being able to be present in the moment that you’re in with acceptance of what it is and without judging it,” said Donna Rockwell, PsyD, a leading mindfulness meditation teacher. The practice of mindfulness is really meditation. Dr. Rockwell explained that the noise of our mind is most often focused on either the past or the future. “We’re either bemoaning something that happened earlier or we’re catastrophizing the future,” she said, which prevents us from being present in the moment. 

Meditation allows you to notice when your mind has drifted from the present moment into the past or future. “You gently notice it, label it with a lot of self-compassion, and then bring your mind back by focusing on your breath – going out, going in – and the incoming stimuli through your five senses,” said Dr. Rockwell. “When you’re doing that, you can’t be in the past or future.”

Dr. Rockwell also pointed out that we constantly categorize incoming data of the moment as either “good for me or bad for me,” which gets in the way of simply being present for what you’re facing. “When you’re more fully present, you become more skillful and able to do what this moment is asking of you,” she said. Being mindful allows us to better navigate incoming stimuli, which could be a “code blue” in the ED or a patient who needs another 2 minutes during an office visit. 

When Dr. Wener was burned out, she felt unable to adapt whenever something unexpected happened. “When you have no emotional reserves, everything feels like a big deal,” she said. “The meditation gave me what we call adaptation energy; it filled up my tank and kept me from feeling like I was going to lose it at 10 o’clock in the morning.”

Dr. Rockwell explained burnout as an overactive fight or flight response activated by the amygdala. It starts pumping cortisol, our pupils dilate, and our pores open. The prefrontal cortex is offline when we’re experiencing this physiological response because they both can’t be operational at the same time. “When we’re constantly in a ‘fight or flight’ response and don’t have any access to our prefrontal cortex, we are coming from a brain that is pumping cortisol and that leads to burnout,” said Dr. Rockwell.

“Any fight or flight response leaves a mark on your body,” Dr. Wener echoed. “When we go into our state of deep rest in the meditation practice, which is two to five times more restful than sleep, it heals those stress scars.”
 

Making time for mindfulness

Prescribing mindfulness for physicians is not new. Molecular biologist Jon Kabat-Zinn, PhD, developed Mindfulness-Based Stress Reduction (MBSR) in 1979, a practice that incorporates mindfulness exercises to help people become familiar with their behavior patterns in stressful situations. Thus, instead of reacting, they can respond with a clearer understanding of the circumstance. Dr. Kabat-Zinn initially targeted people with chronic health problems to help them cope with the effects of pain and the condition of their illness, but it has expanded to anyone experiencing challenges in their life, including physicians. A standard MBSR course runs 8 weeks, making it a commitment for most people. 

Mindfulness training requires that physicians use what they already have so little of: time.

Dr. Wener was able to take a sabbatical, embarking on a 3-month trip to India to immerse herself in the study of Vedic Meditation. Upon her return, Dr. Wener took a position at Emory University, Atlanta, and has launched a number of CME-accredited meditation courses and retreats. Unlike Dr. Kabat-Zinn, her programs are by physicians and for physicians. She also created an online version of the meditation course to make it more accessible. 

For these reasons, Kara Pepper, MD, an internist in outpatient primary care in Atlanta, was drawn to the meditation course. Dr. Pepper was 7 years into practice when she burned out. “The program dovetailed into my burnout recovery,” she said. “It allowed me space to separate myself from the thoughts I was having about work and just recognize them as just that – as thoughts.”

In the course, Dr. Wener teaches the REST Technique, which she says is different than mindfulness in that she encourages the mind to run rampant. “Trying to control the mind can feel very uncomfortable because we always have thoughts,” she says. “We can’t tell the mind to stop thinking just like we can’t tell the heart to stop beating.” Dr. Wener said the REST Technique lets “the mind swim downstream,” allowing the brain to go into a deep state of rest and start to heal from the scars caused by stress. 

Dr. Pepper said the self-paced online course gave her all the tools she needed, and it was pragmatic and evidence based. “I didn’t feel ‘woo’ or like another gimmick,” she said. Pepper, who continues to practice medicine, became a life coach in 2019 to teach others the skills she uses daily. 
 

An integrated strategy

Dr. Wener acknowledges that meditation is not the panacea for everyone’s burnout, which data support. In a review published in The American Journal of Medicine in 2019, Scott Yates, MD, MBA, from the Center for Executive Medicine in Plano, Tex., found that physicians who had adopted mediation and mindfulness training to decrease anxiety and perceived work stress only experienced modest benefits. In fact, Dr. Yates claims that there’s little data to suggest the long-term benefit of any particular stress management intervention in the prevention of burnout symptoms. 

“The often-repeated goals of the Triple Aim [enhancing patient experience, improving population health, and reducing costs] may be unreachable until we recognize and address burnout in health care providers,” Dr. Yates wrote. He recommends adding a fourth goal to specifically address physician wellness, which certainly could include mindfulness training and meditation.

Burnout coach, trainer, and consultant Dike Drummond, MD, also professes that physician wellness must be added as the key fourth ingredient to improving health care. “Burnout is a dilemma, a balancing act,” he said. “It takes an integrated strategy.” The CEO and founder of TheHappyMD.com, Dr. Drummond’s integrated strategy to stop physician burnout has been taught to more than 40,000 physicians in 175 organizations, and one element of that strategy can be mindfulness training. 

Dr. Drummond said he doesn’t use the word meditation “because that scares most people”; it takes a commitment and isn’t accessible for a lot of doctors. Instead, he coaches doctors to use a ‘single-breath’ technique to help them reset multiple times throughout the day. “I teach people how to breathe up to the top of their head and then down to the bottom of their feet,” Dr. Drummond said. He calls it the Squeegee Breath Technique because when they exhale, they “wipe away” anything that doesn’t need to be there right now. “If you happen to have a mindfulness practice like meditation, they work synergistically because the calmness you feel in your mediation is available to you at the bottom of these releasing breaths.”

Various studies and surveys provide great detail as to the “why” of physician burnout. And while mindfulness is not the sole answer, it’s something physicians can explore for themselves while health care as an industry looks for a more comprehensive solution. 

“It’s not rocket science,” Dr. Drummond insisted. “You want a different result? You’re not satisfied with the way things are now and you want to feel different? You absolutely must do something different.”

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

Evidence summary

Multiple analyses suggest short sleep increases obesity risk

Three recent, large systematic reviews of prospective cohort studies with meta-analyses in infants, children, and adolescents all found associations between short sleep at intake and later excessive weight.

The largest meta-analysis included 42 prospective studies with 75,499 patients ranging in age from infancy to adolescence and with follow-up ranging from 1 to 27 years. In a pooled analysis, short sleep—variously defined across trials and mostly assessed by parental report—was associated with an increased risk of obesity or overweight (relative risk [RR] = 1.58; 95% CI, 1.35-1.85; I²= 92%), compared to normal and long sleep. When the authors adjusted for suspected publication bias using a “trim and fill” method, short sleep remained associated with later overweight or obesity (RR = 1.42; 95% CI, 1.12-1.81). Short sleep was associated with later unhealthy weight status in all age groups: 0 to < 3 years (RR = 1.4; 95% CI, 1.19-1.65); 3 to < 9 years (RR = 1.57; 95% CI, 1.4-1.76);9 to < 12 years (RR = 2.23; 95% CI, 2.18-2.27); and 12 to 18 years (RR = 1.3; 95% CI, 1.11-1.53). In addition to high heterogeneity, limitations of the review included variability in the definition of short sleep, use of parent- or self-reported sleep duration, and variability in classification of overweight and obesity in primary studies.¹

A second systematic review and meta-analysis included 25 longitudinal studies (20 of which overlapped with the previously discussed meta-analysis) of children and adolescents (N = 56,584). Patients ranged in age from infancy to 16 years, and follow-up ranged from 6 months to 10 years (mean, 3.4 years). Children and adolescents with the shortest sleep duration were more likely to be overweight or obese at follow-up (pooled odds ratio [OR] = 1.76; 95% CI, 1.39-2.23; I² = 70.5%) than those with the longest sleep duration. Due to the overlap in studies, the limitations of this analysis were similar to those already mentioned. Lack of a linear association between sleep duration and weight was cited as evidence of possible publication bias; the authors did not attempt to correct for it.²

Three large systematic reviews all found associations between short sleep at intake and later excessive weight.

The third systematic review and meta-analysis included 22 longitudinal studies (18 overlapped with first meta-analysis and 17 with the second) of children and adolescents (N = 24,821) ages 6 months to 18 years. Follow-up ranged from 1 to 27 years. This meta-analysis standardized the categories of sleep duration using recommendations from the Sleep Health Foundation. Patients with short sleep duration had an increased risk of overweight or obesity compared with patients sleeping “normal” or “longer than normal” durations (pooled OR = 2.15; 95% CI, 1.64-2.81; I² = 67%). The authors indicated that their analysis could have been more robust if information about daytime sleep (ie, napping) had been available, but it was not collected in many of the included studies.³

Accelerometer data quantify the sleep/obesity association

A subsequent cohort study (N = 202) sought to better examine the association between sleep characteristics and adiposity by measuring sleep duration using accelerometers. Toddlers (ages 12 to 26 months) without previous medical history were recruited from early childhood education centers. Patients wore accelerometers for 7 consecutive days and then returned to the clinic after 12 months for collection of biometric information. Researchers measured body morphology with the BMI z-score (ie, the number of standard deviations from the mean). Every additional hour of total sleep time was associated with a 0.12-unit lower BMI z-score (95% CI, –0.23 to –0.01) at 1 year. However, every hour increase in nap duration was associated with a 0.41-unit higher BMI z-score (95% CI, 0.14-0.68).⁴

Recommendations from others

In 2016, the American Academy of Sleep Medicine (AASM) recommended the following sleep durations (per 24 hours): infants ages 4 to 12 months, 12-16 hours; children 1 to 2 years, 11-14 hours; children 3 to 5 years, 10-13 hours; children 6 to 12 years, 9-12 hours; and teenagers 13 to 18 years, 8-10 hours. The AASM further stated that sleeping the recommended number of hours was associated with better health outcomes, and that sleeping too few hours increased the risk of various health conditions, including obesity.⁵ In 2015, the American Academy of Pediatrics Committee on Nutrition acknowledged the association between obesity and short sleep duration and recommended that health care professionals counsel parents about age-appropriate sleep guidelines.⁶

Editor’s takeaway

Studies demonstrate that short sleep duration in pediatric patients is associated with later weight gain. However, associations do not prove a causal link, and other factors may contribute to both weight gain and poor sleep.

Evidence summary

Multiple analyses suggest short sleep increases obesity risk

Three recent, large systematic reviews of prospective cohort studies with meta-analyses in infants, children, and adolescents all found associations between short sleep at intake and later excessive weight.

The largest meta-analysis included 42 prospective studies with 75,499 patients ranging in age from infancy to adolescence and with follow-up ranging from 1 to 27 years. In a pooled analysis, short sleep—variously defined across trials and mostly assessed by parental report—was associated with an increased risk of obesity or overweight (relative risk [RR] = 1.58; 95% CI, 1.35-1.85; I²= 92%), compared to normal and long sleep. When the authors adjusted for suspected publication bias using a “trim and fill” method, short sleep remained associated with later overweight or obesity (RR = 1.42; 95% CI, 1.12-1.81). Short sleep was associated with later unhealthy weight status in all age groups: 0 to < 3 years (RR = 1.4; 95% CI, 1.19-1.65); 3 to < 9 years (RR = 1.57; 95% CI, 1.4-1.76);9 to < 12 years (RR = 2.23; 95% CI, 2.18-2.27); and 12 to 18 years (RR = 1.3; 95% CI, 1.11-1.53). In addition to high heterogeneity, limitations of the review included variability in the definition of short sleep, use of parent- or self-reported sleep duration, and variability in classification of overweight and obesity in primary studies.¹

A second systematic review and meta-analysis included 25 longitudinal studies (20 of which overlapped with the previously discussed meta-analysis) of children and adolescents (N = 56,584). Patients ranged in age from infancy to 16 years, and follow-up ranged from 6 months to 10 years (mean, 3.4 years). Children and adolescents with the shortest sleep duration were more likely to be overweight or obese at follow-up (pooled odds ratio [OR] = 1.76; 95% CI, 1.39-2.23; I² = 70.5%) than those with the longest sleep duration. Due to the overlap in studies, the limitations of this analysis were similar to those already mentioned. Lack of a linear association between sleep duration and weight was cited as evidence of possible publication bias; the authors did not attempt to correct for it.²

Three large systematic reviews all found associations between short sleep at intake and later excessive weight.

The third systematic review and meta-analysis included 22 longitudinal studies (18 overlapped with first meta-analysis and 17 with the second) of children and adolescents (N = 24,821) ages 6 months to 18 years. Follow-up ranged from 1 to 27 years. This meta-analysis standardized the categories of sleep duration using recommendations from the Sleep Health Foundation. Patients with short sleep duration had an increased risk of overweight or obesity compared with patients sleeping “normal” or “longer than normal” durations (pooled OR = 2.15; 95% CI, 1.64-2.81; I² = 67%). The authors indicated that their analysis could have been more robust if information about daytime sleep (ie, napping) had been available, but it was not collected in many of the included studies.³

Accelerometer data quantify the sleep/obesity association

A subsequent cohort study (N = 202) sought to better examine the association between sleep characteristics and adiposity by measuring sleep duration using accelerometers. Toddlers (ages 12 to 26 months) without previous medical history were recruited from early childhood education centers. Patients wore accelerometers for 7 consecutive days and then returned to the clinic after 12 months for collection of biometric information. Researchers measured body morphology with the BMI z-score (ie, the number of standard deviations from the mean). Every additional hour of total sleep time was associated with a 0.12-unit lower BMI z-score (95% CI, –0.23 to –0.01) at 1 year. However, every hour increase in nap duration was associated with a 0.41-unit higher BMI z-score (95% CI, 0.14-0.68).⁴

Recommendations from others

In 2016, the American Academy of Sleep Medicine (AASM) recommended the following sleep durations (per 24 hours): infants ages 4 to 12 months, 12-16 hours; children 1 to 2 years, 11-14 hours; children 3 to 5 years, 10-13 hours; children 6 to 12 years, 9-12 hours; and teenagers 13 to 18 years, 8-10 hours. The AASM further stated that sleeping the recommended number of hours was associated with better health outcomes, and that sleeping too few hours increased the risk of various health conditions, including obesity.⁵ In 2015, the American Academy of Pediatrics Committee on Nutrition acknowledged the association between obesity and short sleep duration and recommended that health care professionals counsel parents about age-appropriate sleep guidelines.⁶

Editor’s takeaway

Studies demonstrate that short sleep duration in pediatric patients is associated with later weight gain. However, associations do not prove a causal link, and other factors may contribute to both weight gain and poor sleep.

Evidence summary

Multiple analyses suggest short sleep increases obesity risk

Three recent, large systematic reviews of prospective cohort studies with meta-analyses in infants, children, and adolescents all found associations between short sleep at intake and later excessive weight.

The largest meta-analysis included 42 prospective studies with 75,499 patients ranging in age from infancy to adolescence and with follow-up ranging from 1 to 27 years. In a pooled analysis, short sleep—variously defined across trials and mostly assessed by parental report—was associated with an increased risk of obesity or overweight (relative risk [RR] = 1.58; 95% CI, 1.35-1.85; I²= 92%), compared to normal and long sleep. When the authors adjusted for suspected publication bias using a “trim and fill” method, short sleep remained associated with later overweight or obesity (RR = 1.42; 95% CI, 1.12-1.81). Short sleep was associated with later unhealthy weight status in all age groups: 0 to < 3 years (RR = 1.4; 95% CI, 1.19-1.65); 3 to < 9 years (RR = 1.57; 95% CI, 1.4-1.76);9 to < 12 years (RR = 2.23; 95% CI, 2.18-2.27); and 12 to 18 years (RR = 1.3; 95% CI, 1.11-1.53). In addition to high heterogeneity, limitations of the review included variability in the definition of short sleep, use of parent- or self-reported sleep duration, and variability in classification of overweight and obesity in primary studies.¹

A second systematic review and meta-analysis included 25 longitudinal studies (20 of which overlapped with the previously discussed meta-analysis) of children and adolescents (N = 56,584). Patients ranged in age from infancy to 16 years, and follow-up ranged from 6 months to 10 years (mean, 3.4 years). Children and adolescents with the shortest sleep duration were more likely to be overweight or obese at follow-up (pooled odds ratio [OR] = 1.76; 95% CI, 1.39-2.23; I² = 70.5%) than those with the longest sleep duration. Due to the overlap in studies, the limitations of this analysis were similar to those already mentioned. Lack of a linear association between sleep duration and weight was cited as evidence of possible publication bias; the authors did not attempt to correct for it.²

Three large systematic reviews all found associations between short sleep at intake and later excessive weight.

The third systematic review and meta-analysis included 22 longitudinal studies (18 overlapped with first meta-analysis and 17 with the second) of children and adolescents (N = 24,821) ages 6 months to 18 years. Follow-up ranged from 1 to 27 years. This meta-analysis standardized the categories of sleep duration using recommendations from the Sleep Health Foundation. Patients with short sleep duration had an increased risk of overweight or obesity compared with patients sleeping “normal” or “longer than normal” durations (pooled OR = 2.15; 95% CI, 1.64-2.81; I² = 67%). The authors indicated that their analysis could have been more robust if information about daytime sleep (ie, napping) had been available, but it was not collected in many of the included studies.³

Accelerometer data quantify the sleep/obesity association

A subsequent cohort study (N = 202) sought to better examine the association between sleep characteristics and adiposity by measuring sleep duration using accelerometers. Toddlers (ages 12 to 26 months) without previous medical history were recruited from early childhood education centers. Patients wore accelerometers for 7 consecutive days and then returned to the clinic after 12 months for collection of biometric information. Researchers measured body morphology with the BMI z-score (ie, the number of standard deviations from the mean). Every additional hour of total sleep time was associated with a 0.12-unit lower BMI z-score (95% CI, –0.23 to –0.01) at 1 year. However, every hour increase in nap duration was associated with a 0.41-unit higher BMI z-score (95% CI, 0.14-0.68).⁴

Recommendations from others

In 2016, the American Academy of Sleep Medicine (AASM) recommended the following sleep durations (per 24 hours): infants ages 4 to 12 months, 12-16 hours; children 1 to 2 years, 11-14 hours; children 3 to 5 years, 10-13 hours; children 6 to 12 years, 9-12 hours; and teenagers 13 to 18 years, 8-10 hours. The AASM further stated that sleeping the recommended number of hours was associated with better health outcomes, and that sleeping too few hours increased the risk of various health conditions, including obesity.⁵ In 2015, the American Academy of Pediatrics Committee on Nutrition acknowledged the association between obesity and short sleep duration and recommended that health care professionals counsel parents about age-appropriate sleep guidelines.⁶

Editor’s takeaway

Studies demonstrate that short sleep duration in pediatric patients is associated with later weight gain. However, associations do not prove a causal link, and other factors may contribute to both weight gain and poor sleep.

Individuals diagnosed with obstructive sleep apnea (OSA) have higher volumes of white-matter hyperintensities (WMHs), according to a new analysis of data from the SHIP-Trend-0 cohort in Western Pomerania, Germany, which is part of the Study of Health In Pomerania. The association was true for individual measures of OSA, including apnea-hypopnea index (AHI) and oxygen desaturation index (ODI).

WMHs are often seen on MRI in older people and in patients with stroke or dementia, and they may be an indicator of cerebral small-vessel disease. They are linked to greater risk of abnormal gait, worsening balance, depression, cognitive decline, dementia, stroke, and death. Suggested mechanisms for harms from WMHs include ischemia, hypoxia, hypoperfusion, inflammation, and demyelination.

WMHs have been linked to vascular risk factors like smoking, diabetes, and hypertension. Brain pathology studies have found loss of myelin, axonal loss, and scarring close to WMHs.

Although a few studies have looked for associations between WMHs and OSA, they have yielded inconsistent results. The new work employed highly standardized data collection and more complete covariate adjustment. The results, published in JAMA Network Open, suggest a novel, and potentially treatable, pathological WMH mechanism, according to the authors.

“This is an important study. It has strong methodology. The automated analysis of WMH in a large population-based cohort helps to eliminate several biases that can occur in this type of assessment. The data analysis was massive, with adequate control of all potential confounders and testing for interactions. This generated robust results,” said Diego Z. Carvalho, MD, who was asked to comment on the findings. Dr. Carvalho is an assistant professor of neurology at the Center for Sleep Medicine at the Mayo Clinic, Rochester, Minn.
 

Worse apnea, worse hyperintensity

“The association varies according to the degree of apnea severity, so mild OSA is probably not associated with increased WMH, while severe OSA is mostly likely driving most of the associations,” said Dr. Carvalho.

If a causal mechanism were to be proven, it would “bring a stronger call for treatment of severe OSA patients, particularly those with increased risk for small-vessel disease, [such as] patients with metabolic syndrome. Likewise, patients with severe OSA would be the best candidates for therapeutic trials with [continuous positive airway pressure] with or without possible adjunctive neuroprotective treatment for halting or slowing down WMH progression,” said Dr. Carvalho.

Stuart McCarter, MD, who is an instructor of neurology at the Center for Sleep Medicine at the Mayo Clinic, Rochester, Minn., also found the results interesting but pointed out that much more work needs to be done. “While they found a relationship between OSA as well as OSA severity and WMH despite adjusting for other known confounders, it is unlikely that it is as simple as OSA is the main causal factor for WMH, given the complex relationship between OSA, hypertension, and metabolic syndrome. However, this data does highlight the importance of considering OSA in addition to other more traditional risk factors when considering modifiable risk factors for brain aging,” said Dr. McCarter. The study cohort was mostly of White European ancestry, so more work also needs to be done in other racial groups.

The study underlines the importance of screening among individuals with cognitive impairment. “If OSA represents a modifiable risk factor for WMH and associated cognitive decline, then it would represent one of the few potentially treatable etiologies, or at least contributors of cognitive impairment,” said Dr. McCarter.

The SHIP-Trend-0 cohort is drawn from adults in Western Pomerania. The researchers analyzed data from 529 patients who had WMH and for whom intracranial volume data were available. Each member of the cohort also underwent polysomnography.

Based on AHI criteria, 24% of the overall sample had mild OSA, 10% had moderate OSA, and 6% had severe OSA.

After adjustment for sex, age, intracranial volume, and body weight, WMH volume was associated with AHI (beta = 0.024; P < .001) and ODI (beta = 0.033; P < .001). WMH counts were also associated with AHI (beta = 0.008; P = .01) and ODI (beta = 0.011; P = .02).

The effect size increased with greater OSA severity, as measured by AHI for both WMH volume (beta = 0.312, 0.480, and 1.255 for mild, moderate, and severe OSA, respectively) and WMH count (beta = 0.129, 0.107, and 0.419). The ODI regression models showed similar associations for WMH volume (beta = 0.426, 1.030, and 1.130) and WMH count (beta = 0.141, 0.315, and 0.538).

Dr. Carvalho and Dr. McCarter disclosed no relevant financial relationships.
 

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

Individuals diagnosed with obstructive sleep apnea (OSA) have higher volumes of white-matter hyperintensities (WMHs), according to a new analysis of data from the SHIP-Trend-0 cohort in Western Pomerania, Germany, which is part of the Study of Health In Pomerania. The association was true for individual measures of OSA, including apnea-hypopnea index (AHI) and oxygen desaturation index (ODI).

WMHs are often seen on MRI in older people and in patients with stroke or dementia, and they may be an indicator of cerebral small-vessel disease. They are linked to greater risk of abnormal gait, worsening balance, depression, cognitive decline, dementia, stroke, and death. Suggested mechanisms for harms from WMHs include ischemia, hypoxia, hypoperfusion, inflammation, and demyelination.

WMHs have been linked to vascular risk factors like smoking, diabetes, and hypertension. Brain pathology studies have found loss of myelin, axonal loss, and scarring close to WMHs.

Although a few studies have looked for associations between WMHs and OSA, they have yielded inconsistent results. The new work employed highly standardized data collection and more complete covariate adjustment. The results, published in JAMA Network Open, suggest a novel, and potentially treatable, pathological WMH mechanism, according to the authors.

“This is an important study. It has strong methodology. The automated analysis of WMH in a large population-based cohort helps to eliminate several biases that can occur in this type of assessment. The data analysis was massive, with adequate control of all potential confounders and testing for interactions. This generated robust results,” said Diego Z. Carvalho, MD, who was asked to comment on the findings. Dr. Carvalho is an assistant professor of neurology at the Center for Sleep Medicine at the Mayo Clinic, Rochester, Minn.
 

Worse apnea, worse hyperintensity

“The association varies according to the degree of apnea severity, so mild OSA is probably not associated with increased WMH, while severe OSA is mostly likely driving most of the associations,” said Dr. Carvalho.

If a causal mechanism were to be proven, it would “bring a stronger call for treatment of severe OSA patients, particularly those with increased risk for small-vessel disease, [such as] patients with metabolic syndrome. Likewise, patients with severe OSA would be the best candidates for therapeutic trials with [continuous positive airway pressure] with or without possible adjunctive neuroprotective treatment for halting or slowing down WMH progression,” said Dr. Carvalho.

Stuart McCarter, MD, who is an instructor of neurology at the Center for Sleep Medicine at the Mayo Clinic, Rochester, Minn., also found the results interesting but pointed out that much more work needs to be done. “While they found a relationship between OSA as well as OSA severity and WMH despite adjusting for other known confounders, it is unlikely that it is as simple as OSA is the main causal factor for WMH, given the complex relationship between OSA, hypertension, and metabolic syndrome. However, this data does highlight the importance of considering OSA in addition to other more traditional risk factors when considering modifiable risk factors for brain aging,” said Dr. McCarter. The study cohort was mostly of White European ancestry, so more work also needs to be done in other racial groups.

The study underlines the importance of screening among individuals with cognitive impairment. “If OSA represents a modifiable risk factor for WMH and associated cognitive decline, then it would represent one of the few potentially treatable etiologies, or at least contributors of cognitive impairment,” said Dr. McCarter.

The SHIP-Trend-0 cohort is drawn from adults in Western Pomerania. The researchers analyzed data from 529 patients who had WMH and for whom intracranial volume data were available. Each member of the cohort also underwent polysomnography.

Based on AHI criteria, 24% of the overall sample had mild OSA, 10% had moderate OSA, and 6% had severe OSA.

After adjustment for sex, age, intracranial volume, and body weight, WMH volume was associated with AHI (beta = 0.024; P < .001) and ODI (beta = 0.033; P < .001). WMH counts were also associated with AHI (beta = 0.008; P = .01) and ODI (beta = 0.011; P = .02).

The effect size increased with greater OSA severity, as measured by AHI for both WMH volume (beta = 0.312, 0.480, and 1.255 for mild, moderate, and severe OSA, respectively) and WMH count (beta = 0.129, 0.107, and 0.419). The ODI regression models showed similar associations for WMH volume (beta = 0.426, 1.030, and 1.130) and WMH count (beta = 0.141, 0.315, and 0.538).

Dr. Carvalho and Dr. McCarter disclosed no relevant financial relationships.
 

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

Individuals diagnosed with obstructive sleep apnea (OSA) have higher volumes of white-matter hyperintensities (WMHs), according to a new analysis of data from the SHIP-Trend-0 cohort in Western Pomerania, Germany, which is part of the Study of Health In Pomerania. The association was true for individual measures of OSA, including apnea-hypopnea index (AHI) and oxygen desaturation index (ODI).

WMHs are often seen on MRI in older people and in patients with stroke or dementia, and they may be an indicator of cerebral small-vessel disease. They are linked to greater risk of abnormal gait, worsening balance, depression, cognitive decline, dementia, stroke, and death. Suggested mechanisms for harms from WMHs include ischemia, hypoxia, hypoperfusion, inflammation, and demyelination.

WMHs have been linked to vascular risk factors like smoking, diabetes, and hypertension. Brain pathology studies have found loss of myelin, axonal loss, and scarring close to WMHs.

Although a few studies have looked for associations between WMHs and OSA, they have yielded inconsistent results. The new work employed highly standardized data collection and more complete covariate adjustment. The results, published in JAMA Network Open, suggest a novel, and potentially treatable, pathological WMH mechanism, according to the authors.

“This is an important study. It has strong methodology. The automated analysis of WMH in a large population-based cohort helps to eliminate several biases that can occur in this type of assessment. The data analysis was massive, with adequate control of all potential confounders and testing for interactions. This generated robust results,” said Diego Z. Carvalho, MD, who was asked to comment on the findings. Dr. Carvalho is an assistant professor of neurology at the Center for Sleep Medicine at the Mayo Clinic, Rochester, Minn.
 

Worse apnea, worse hyperintensity

“The association varies according to the degree of apnea severity, so mild OSA is probably not associated with increased WMH, while severe OSA is mostly likely driving most of the associations,” said Dr. Carvalho.

If a causal mechanism were to be proven, it would “bring a stronger call for treatment of severe OSA patients, particularly those with increased risk for small-vessel disease, [such as] patients with metabolic syndrome. Likewise, patients with severe OSA would be the best candidates for therapeutic trials with [continuous positive airway pressure] with or without possible adjunctive neuroprotective treatment for halting or slowing down WMH progression,” said Dr. Carvalho.

Stuart McCarter, MD, who is an instructor of neurology at the Center for Sleep Medicine at the Mayo Clinic, Rochester, Minn., also found the results interesting but pointed out that much more work needs to be done. “While they found a relationship between OSA as well as OSA severity and WMH despite adjusting for other known confounders, it is unlikely that it is as simple as OSA is the main causal factor for WMH, given the complex relationship between OSA, hypertension, and metabolic syndrome. However, this data does highlight the importance of considering OSA in addition to other more traditional risk factors when considering modifiable risk factors for brain aging,” said Dr. McCarter. The study cohort was mostly of White European ancestry, so more work also needs to be done in other racial groups.

The study underlines the importance of screening among individuals with cognitive impairment. “If OSA represents a modifiable risk factor for WMH and associated cognitive decline, then it would represent one of the few potentially treatable etiologies, or at least contributors of cognitive impairment,” said Dr. McCarter.

The SHIP-Trend-0 cohort is drawn from adults in Western Pomerania. The researchers analyzed data from 529 patients who had WMH and for whom intracranial volume data were available. Each member of the cohort also underwent polysomnography.

Based on AHI criteria, 24% of the overall sample had mild OSA, 10% had moderate OSA, and 6% had severe OSA.

After adjustment for sex, age, intracranial volume, and body weight, WMH volume was associated with AHI (beta = 0.024; P < .001) and ODI (beta = 0.033; P < .001). WMH counts were also associated with AHI (beta = 0.008; P = .01) and ODI (beta = 0.011; P = .02).

The effect size increased with greater OSA severity, as measured by AHI for both WMH volume (beta = 0.312, 0.480, and 1.255 for mild, moderate, and severe OSA, respectively) and WMH count (beta = 0.129, 0.107, and 0.419). The ODI regression models showed similar associations for WMH volume (beta = 0.426, 1.030, and 1.130) and WMH count (beta = 0.141, 0.315, and 0.538).

Dr. Carvalho and Dr. McCarter disclosed no relevant financial relationships.
 

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