Sleep Medicine

For researchers involved with sleep disorders, developing a pharmacologic treatment for obstructive sleep apnea (OSA) is a bit like searching for the holy grail. P K Schweitzer and colleagues have published the results of the randomized MARIPOSA study assessing a combination of two medicinal products known as AD109, one of the products having an antimuscarinic effect (aroxybutynin), and the other a noradrenergic effect (atomoxetine), in treating this condition. These molecules increase the activity of the dilator muscles in the upper airways by activating the genioglossus muscle with a synergic effect on the upper respiratory tract during sleep.
 

MARIPOSA Methodology 

The trial included 209 patients, 176 of whom completed the 4-week protocol. The trial was double-blinded according to four parallel arms: participants in the first and second arms received AD109 containing doses of 2.5 mg/75 mg and 5 mg/75 mg of aroxybutynin and atomoxetine, respectively. The third arm received atomoxetine alone (75 mg), and the fourth arm was given a placebo. 

Two polysomnograms (PSGs) were carried out at the start and end of the trial, allowing researchers to calculate the apnea-hypopnea index (AHI) and to quantify nocturnal desaturation. The impact of these variables are now being deemed as the primary marker of the risk for cardiovascular complications secondary to OSA. Finally, questionnaires that evaluated excessive daytime sleepiness, fatigue, and sleep quality were completed. 

The median age varied from 5 to 57 years, depending on the arm of the study, and body mass index varied between 31.2 and 34.5. Inclusion criteria comprised an AHI between 10 and 45 events per hour, of which, at least 75% were described as obstructive. Where continuous positive airway pressure (CPAP) was used (21%-30% of cases), it was abandoned during the trial (in a time frame that is perhaps too short to consider these patients as treatment naive).

 

Combination Brought Improvements 

After the 4 weeks of treatment, the AHI measured via follow-up PSG went from a median of 20.5 to 10.8 (in arm one and from 19.4 to 9.5  in arm two (P < .0001 vs placebo in these two arms). For participants in arm three, AHI went from 19.0 to 11.8 (P < .01 vs placebo). 

The rate of nocturnal desaturation (in percentage per hour) declined from -12.7 in arm one (P = .03), from -16.6 in arm two (P = .005), and from -5.2 in arm three (P = .003) compared with the placebo. The fatigue score was significantly improved by AD109 2.5 mg/75 mg. The use of atomoxetine alone slightly worsened the sleep disturbance score.

The main side effects were dry mouth sensation (which was markedly more common with AD109 5 mg/75 mg), difficulty passing urine in 7%-22% of cases, tachycardia in all trial arms, and increased diastolic blood pressure at the 2.5-mg/75-mg dose. The authors concluded that AD109, a combination of noradrenergic and antimuscarinic molecules, is effective in correcting mild to severe OSA. 

The 2.5-mg/75-mg dose was as effective as the 5-mg/75-mg dose. Atomoxetine alone is less effective, has more side effects, and is associated with lower quality sleep. Finally, it is reported that compliance with oral treatment was not checked, yet the argument of patient noncompliance with CPAP is largely used by the authors in their presentation of their study. A phase 3 trial is underway. 

Nevertheless, these results herald important scientific benefits if we consider that Colin Sullivan’s original 1981 research paper, which ushered in the CPAP era, presented the results of just five participants. 

This article was translated from JIM, which is part of the Medscape professional network. 

A version of this article appeared on Medscape.com.

For researchers involved with sleep disorders, developing a pharmacologic treatment for obstructive sleep apnea (OSA) is a bit like searching for the holy grail. P K Schweitzer and colleagues have published the results of the randomized MARIPOSA study assessing a combination of two medicinal products known as AD109, one of the products having an antimuscarinic effect (aroxybutynin), and the other a noradrenergic effect (atomoxetine), in treating this condition. These molecules increase the activity of the dilator muscles in the upper airways by activating the genioglossus muscle with a synergic effect on the upper respiratory tract during sleep.
 

MARIPOSA Methodology 

The trial included 209 patients, 176 of whom completed the 4-week protocol. The trial was double-blinded according to four parallel arms: participants in the first and second arms received AD109 containing doses of 2.5 mg/75 mg and 5 mg/75 mg of aroxybutynin and atomoxetine, respectively. The third arm received atomoxetine alone (75 mg), and the fourth arm was given a placebo. 

Two polysomnograms (PSGs) were carried out at the start and end of the trial, allowing researchers to calculate the apnea-hypopnea index (AHI) and to quantify nocturnal desaturation. The impact of these variables are now being deemed as the primary marker of the risk for cardiovascular complications secondary to OSA. Finally, questionnaires that evaluated excessive daytime sleepiness, fatigue, and sleep quality were completed. 

The median age varied from 5 to 57 years, depending on the arm of the study, and body mass index varied between 31.2 and 34.5. Inclusion criteria comprised an AHI between 10 and 45 events per hour, of which, at least 75% were described as obstructive. Where continuous positive airway pressure (CPAP) was used (21%-30% of cases), it was abandoned during the trial (in a time frame that is perhaps too short to consider these patients as treatment naive).

 

Combination Brought Improvements 

After the 4 weeks of treatment, the AHI measured via follow-up PSG went from a median of 20.5 to 10.8 (in arm one and from 19.4 to 9.5  in arm two (P < .0001 vs placebo in these two arms). For participants in arm three, AHI went from 19.0 to 11.8 (P < .01 vs placebo). 

The rate of nocturnal desaturation (in percentage per hour) declined from -12.7 in arm one (P = .03), from -16.6 in arm two (P = .005), and from -5.2 in arm three (P = .003) compared with the placebo. The fatigue score was significantly improved by AD109 2.5 mg/75 mg. The use of atomoxetine alone slightly worsened the sleep disturbance score.

The main side effects were dry mouth sensation (which was markedly more common with AD109 5 mg/75 mg), difficulty passing urine in 7%-22% of cases, tachycardia in all trial arms, and increased diastolic blood pressure at the 2.5-mg/75-mg dose. The authors concluded that AD109, a combination of noradrenergic and antimuscarinic molecules, is effective in correcting mild to severe OSA. 

The 2.5-mg/75-mg dose was as effective as the 5-mg/75-mg dose. Atomoxetine alone is less effective, has more side effects, and is associated with lower quality sleep. Finally, it is reported that compliance with oral treatment was not checked, yet the argument of patient noncompliance with CPAP is largely used by the authors in their presentation of their study. A phase 3 trial is underway. 

Nevertheless, these results herald important scientific benefits if we consider that Colin Sullivan’s original 1981 research paper, which ushered in the CPAP era, presented the results of just five participants. 

This article was translated from JIM, which is part of the Medscape professional network. 

A version of this article appeared on Medscape.com.

For researchers involved with sleep disorders, developing a pharmacologic treatment for obstructive sleep apnea (OSA) is a bit like searching for the holy grail. P K Schweitzer and colleagues have published the results of the randomized MARIPOSA study assessing a combination of two medicinal products known as AD109, one of the products having an antimuscarinic effect (aroxybutynin), and the other a noradrenergic effect (atomoxetine), in treating this condition. These molecules increase the activity of the dilator muscles in the upper airways by activating the genioglossus muscle with a synergic effect on the upper respiratory tract during sleep.
 

MARIPOSA Methodology 

The trial included 209 patients, 176 of whom completed the 4-week protocol. The trial was double-blinded according to four parallel arms: participants in the first and second arms received AD109 containing doses of 2.5 mg/75 mg and 5 mg/75 mg of aroxybutynin and atomoxetine, respectively. The third arm received atomoxetine alone (75 mg), and the fourth arm was given a placebo. 

Two polysomnograms (PSGs) were carried out at the start and end of the trial, allowing researchers to calculate the apnea-hypopnea index (AHI) and to quantify nocturnal desaturation. The impact of these variables are now being deemed as the primary marker of the risk for cardiovascular complications secondary to OSA. Finally, questionnaires that evaluated excessive daytime sleepiness, fatigue, and sleep quality were completed. 

The median age varied from 5 to 57 years, depending on the arm of the study, and body mass index varied between 31.2 and 34.5. Inclusion criteria comprised an AHI between 10 and 45 events per hour, of which, at least 75% were described as obstructive. Where continuous positive airway pressure (CPAP) was used (21%-30% of cases), it was abandoned during the trial (in a time frame that is perhaps too short to consider these patients as treatment naive).

 

Combination Brought Improvements 

After the 4 weeks of treatment, the AHI measured via follow-up PSG went from a median of 20.5 to 10.8 (in arm one and from 19.4 to 9.5  in arm two (P < .0001 vs placebo in these two arms). For participants in arm three, AHI went from 19.0 to 11.8 (P < .01 vs placebo). 

The rate of nocturnal desaturation (in percentage per hour) declined from -12.7 in arm one (P = .03), from -16.6 in arm two (P = .005), and from -5.2 in arm three (P = .003) compared with the placebo. The fatigue score was significantly improved by AD109 2.5 mg/75 mg. The use of atomoxetine alone slightly worsened the sleep disturbance score.

The main side effects were dry mouth sensation (which was markedly more common with AD109 5 mg/75 mg), difficulty passing urine in 7%-22% of cases, tachycardia in all trial arms, and increased diastolic blood pressure at the 2.5-mg/75-mg dose. The authors concluded that AD109, a combination of noradrenergic and antimuscarinic molecules, is effective in correcting mild to severe OSA. 

The 2.5-mg/75-mg dose was as effective as the 5-mg/75-mg dose. Atomoxetine alone is less effective, has more side effects, and is associated with lower quality sleep. Finally, it is reported that compliance with oral treatment was not checked, yet the argument of patient noncompliance with CPAP is largely used by the authors in their presentation of their study. A phase 3 trial is underway. 

Nevertheless, these results herald important scientific benefits if we consider that Colin Sullivan’s original 1981 research paper, which ushered in the CPAP era, presented the results of just five participants. 

This article was translated from JIM, which is part of the Medscape professional network. 

A version of this article appeared on Medscape.com.

TOPLINE:

Patients with psoriasis had a 1.77-fold increased risk of having obstructive sleep apnea, in a study comparing patients with psoriasis with controls.

METHODOLOGY:

• Prior studies have established a link between psoriasis and obstructive sleep apnea (OSA), but some have suggested that confounders may drive the association.
• Using a case-control design, researchers analyzed data from 156,707 participants in the National Institutes of Health’s : 5140 with psoriasis and 151,567 controls.
• They used Pearson’s x 2 test to compare the prevalence of OSA among cases and controls, logistic regression to calculate odds ratios (ORs) in multivariable analysis, and two-sided t-tests to evaluate the significance between continuous variables.

TAKEAWAY:

• Compared with controls, patients with psoriasis were older (a mean of 62.4 vs 57.3 years, respectively), more likely to be White (86.1% vs 70.6%), reported higher annual household incomes (59.9% vs 52.6%), and were more likely to smoke (48.2% vs 43.4%).
• The rate of OSA was significantly higher among patients with psoriasis compared with controls (29.3% vs 17.1%; P < .001).
• On unadjusted multivariable logistic regression controlling for age, gender, and race, psoriasis was significantly associated with OSA (OR, 1.77, 95% CI, 1.66 - 1.89; P < .001).
• Psoriasis was also significantly associated with OSA in the adjusted model controlling for age, gender, race, BMI, and smoking status (OR, 1.66, 95% CI, 1.55 - 1.77; P < .001) and in the adjusted model controlling for age, gender, race, BMI, smoking status, type 2 diabetes, congestive heart failure, hypertension, history of myocardial infarction, angina, and peripheral artery disease (OR, 1.45, 95% CI, 1.35 - 1.55; P <.001).

IN PRACTICE:

“This study further substantiates the association between psoriasis and OSA, reinforcing the importance of evaluation for OSA when clinically appropriate given that both psoriasis and OSA contribute to adverse health outcomes,” the authors conclude.

SOURCE:

Corresponding author Jeffrey M. Cohen, MD, of the Department of Dermatology at Yale University, New Haven, Connecticut, led the research. The study was published online in the Journal of the American Academy of Dermatology.

LIMITATIONS:

Study limitations included the use of electronic health record data, a potential lack of generalizability to the US population, and reliance on survey data for certain variables such as income and smoking status.

DISCLOSURES:

The All of Us Research Program is supported by the National Institutes of Health. Cohen disclosed that he serves on a data safety and monitoring board for Advarra.

A version of this article appeared on Medscape.com.

TOPLINE:

Patients with psoriasis had a 1.77-fold increased risk of having obstructive sleep apnea, in a study comparing patients with psoriasis with controls.

METHODOLOGY:

• Prior studies have established a link between psoriasis and obstructive sleep apnea (OSA), but some have suggested that confounders may drive the association.
• Using a case-control design, researchers analyzed data from 156,707 participants in the National Institutes of Health’s : 5140 with psoriasis and 151,567 controls.
• They used Pearson’s x 2 test to compare the prevalence of OSA among cases and controls, logistic regression to calculate odds ratios (ORs) in multivariable analysis, and two-sided t-tests to evaluate the significance between continuous variables.

TAKEAWAY:

• Compared with controls, patients with psoriasis were older (a mean of 62.4 vs 57.3 years, respectively), more likely to be White (86.1% vs 70.6%), reported higher annual household incomes (59.9% vs 52.6%), and were more likely to smoke (48.2% vs 43.4%).
• The rate of OSA was significantly higher among patients with psoriasis compared with controls (29.3% vs 17.1%; P < .001).
• On unadjusted multivariable logistic regression controlling for age, gender, and race, psoriasis was significantly associated with OSA (OR, 1.77, 95% CI, 1.66 - 1.89; P < .001).
• Psoriasis was also significantly associated with OSA in the adjusted model controlling for age, gender, race, BMI, and smoking status (OR, 1.66, 95% CI, 1.55 - 1.77; P < .001) and in the adjusted model controlling for age, gender, race, BMI, smoking status, type 2 diabetes, congestive heart failure, hypertension, history of myocardial infarction, angina, and peripheral artery disease (OR, 1.45, 95% CI, 1.35 - 1.55; P <.001).

IN PRACTICE:

“This study further substantiates the association between psoriasis and OSA, reinforcing the importance of evaluation for OSA when clinically appropriate given that both psoriasis and OSA contribute to adverse health outcomes,” the authors conclude.

SOURCE:

Corresponding author Jeffrey M. Cohen, MD, of the Department of Dermatology at Yale University, New Haven, Connecticut, led the research. The study was published online in the Journal of the American Academy of Dermatology.

LIMITATIONS:

Study limitations included the use of electronic health record data, a potential lack of generalizability to the US population, and reliance on survey data for certain variables such as income and smoking status.

DISCLOSURES:

The All of Us Research Program is supported by the National Institutes of Health. Cohen disclosed that he serves on a data safety and monitoring board for Advarra.

A version of this article appeared on Medscape.com.

TOPLINE:

Patients with psoriasis had a 1.77-fold increased risk of having obstructive sleep apnea, in a study comparing patients with psoriasis with controls.

METHODOLOGY:

• Prior studies have established a link between psoriasis and obstructive sleep apnea (OSA), but some have suggested that confounders may drive the association.
• Using a case-control design, researchers analyzed data from 156,707 participants in the National Institutes of Health’s : 5140 with psoriasis and 151,567 controls.
• They used Pearson’s x 2 test to compare the prevalence of OSA among cases and controls, logistic regression to calculate odds ratios (ORs) in multivariable analysis, and two-sided t-tests to evaluate the significance between continuous variables.

TAKEAWAY:

• Compared with controls, patients with psoriasis were older (a mean of 62.4 vs 57.3 years, respectively), more likely to be White (86.1% vs 70.6%), reported higher annual household incomes (59.9% vs 52.6%), and were more likely to smoke (48.2% vs 43.4%).
• The rate of OSA was significantly higher among patients with psoriasis compared with controls (29.3% vs 17.1%; P < .001).
• On unadjusted multivariable logistic regression controlling for age, gender, and race, psoriasis was significantly associated with OSA (OR, 1.77, 95% CI, 1.66 - 1.89; P < .001).
• Psoriasis was also significantly associated with OSA in the adjusted model controlling for age, gender, race, BMI, and smoking status (OR, 1.66, 95% CI, 1.55 - 1.77; P < .001) and in the adjusted model controlling for age, gender, race, BMI, smoking status, type 2 diabetes, congestive heart failure, hypertension, history of myocardial infarction, angina, and peripheral artery disease (OR, 1.45, 95% CI, 1.35 - 1.55; P <.001).

IN PRACTICE:

“This study further substantiates the association between psoriasis and OSA, reinforcing the importance of evaluation for OSA when clinically appropriate given that both psoriasis and OSA contribute to adverse health outcomes,” the authors conclude.

SOURCE:

Corresponding author Jeffrey M. Cohen, MD, of the Department of Dermatology at Yale University, New Haven, Connecticut, led the research. The study was published online in the Journal of the American Academy of Dermatology.

LIMITATIONS:

Study limitations included the use of electronic health record data, a potential lack of generalizability to the US population, and reliance on survey data for certain variables such as income and smoking status.

DISCLOSURES:

The All of Us Research Program is supported by the National Institutes of Health. Cohen disclosed that he serves on a data safety and monitoring board for Advarra.

A version of this article appeared on Medscape.com.

In “Treating chronic insomnia: An alternating medication strategy” (Current Psychiatry, October 2023, p. 25-31, doi:10.12788/cp.0397), Dr. Kaplan correctly identified tolerance and tachyphylaxis as significant problems when prescribing traditional hypnotics, and proposed a solution of using 2 sleep medications, each having a different mechanism of action, on an alternating schedule. However, with the availability of the dual orexin receptor antagonists (DORAs) daridorexant, lemborexant, and suvorexant, this approach is unnecessary. Moreover, the mechanism of action of orexin receptor antagonism directly addresses extant hyperarousal by decreasing wake signaling, without any deleterious effect on sleep architecture.¹ Additionally, the DORAs are not associated with physiological dependence, withdrawal, or rebound. Their efficacy profile is as good as or better than other FDA-approved agents for insomnia disorder.¹ An obstacle to their use is that they are not yet available as generic products, but access is facilitated by the manufacturers’ patient assistance programs. Additional resources elaborate on indirect comparisons among agents using number needed to treat and number needed to harm, metrics that are helpful when clinically appraising new agents.^2-5

Leslie Citrome, MD, MPH
Valhalla, New York

In “Treating chronic insomnia: An alternating medication strategy” (Current Psychiatry, October 2023, p. 25-31, doi:10.12788/cp.0397), Dr. Kaplan correctly identified tolerance and tachyphylaxis as significant problems when prescribing traditional hypnotics, and proposed a solution of using 2 sleep medications, each having a different mechanism of action, on an alternating schedule. However, with the availability of the dual orexin receptor antagonists (DORAs) daridorexant, lemborexant, and suvorexant, this approach is unnecessary. Moreover, the mechanism of action of orexin receptor antagonism directly addresses extant hyperarousal by decreasing wake signaling, without any deleterious effect on sleep architecture.¹ Additionally, the DORAs are not associated with physiological dependence, withdrawal, or rebound. Their efficacy profile is as good as or better than other FDA-approved agents for insomnia disorder.¹ An obstacle to their use is that they are not yet available as generic products, but access is facilitated by the manufacturers’ patient assistance programs. Additional resources elaborate on indirect comparisons among agents using number needed to treat and number needed to harm, metrics that are helpful when clinically appraising new agents.^2-5

Leslie Citrome, MD, MPH
Valhalla, New York

In “Treating chronic insomnia: An alternating medication strategy” (Current Psychiatry, October 2023, p. 25-31, doi:10.12788/cp.0397), Dr. Kaplan correctly identified tolerance and tachyphylaxis as significant problems when prescribing traditional hypnotics, and proposed a solution of using 2 sleep medications, each having a different mechanism of action, on an alternating schedule. However, with the availability of the dual orexin receptor antagonists (DORAs) daridorexant, lemborexant, and suvorexant, this approach is unnecessary. Moreover, the mechanism of action of orexin receptor antagonism directly addresses extant hyperarousal by decreasing wake signaling, without any deleterious effect on sleep architecture.¹ Additionally, the DORAs are not associated with physiological dependence, withdrawal, or rebound. Their efficacy profile is as good as or better than other FDA-approved agents for insomnia disorder.¹ An obstacle to their use is that they are not yet available as generic products, but access is facilitated by the manufacturers’ patient assistance programs. Additional resources elaborate on indirect comparisons among agents using number needed to treat and number needed to harm, metrics that are helpful when clinically appraising new agents.^2-5

Leslie Citrome, MD, MPH
Valhalla, New York

Women, particularly those who are postmenopausal, who sleep less than the recommended 7 hours per night may have impaired insulin sensitivity regardless of their degree of adiposity, a randomized crossover trial reveals.

The research was published recently in Diabetes Care.

Nearly 40 women were randomly assigned to either restricted sleep or adequate sleep for 6 weeks, then crossed over to the other sleep condition. During sleep restriction, women slept an average of 6.2 hours per night versus 7-9 hours per night.

Both fasting insulin levels and insulin resistance were significantly increased during sleep restriction, with the effect on insulin resistance particularly notable in postmenopausal women. This was independent of adiposity and changes in adiposity.

“What we’re seeing is that more insulin is needed to normalize glucose levels in the women under conditions of sleep restriction,” said senior author Marie-Pierre St-Onge, PhD, director of the Center of Excellence for Sleep and Circadian Research at Columbia University Vagelos College of Physicians and Surgeons, New York, in a release.

“Even then, the insulin may not have been doing enough to counteract rising blood glucose levels of postmenopausal women,” she stated.
 

Prolonged lack of sleep may accelerate diabetes progression

Dr. St-Onge added, “If that’s sustained over time, it is possible that prolonged insufficient sleep among individuals with prediabetes could accelerate the progression to type 2 diabetes.”

Dr. St-Onge said in an interview that it was crucial to show the impact of sleep restriction in a randomized study, because “observational studies don’t provide information on causality.”

The study did not rely on people “living in our clinical research facility,” but instead enrolled individuals who were “living their lives,” and the reduction in sleep achieved was “similar to what is seen in the general population with sleep,” she said.

Dr. St-Onge therefore believes the findings indicate that sleep has been overlooked as a contributory factor in insulin sensitivity.

Robert Gabbay, MD, PhD, chief scientific and medical officer at the American Diabetes Association, said in an interview that this is an “important study [that] builds on what we have seen on the importance of sleep for metabolic outcomes and diabetes.”

Joslin Diabetes Center

A version of this article appeared on Medscape.com.

Women, particularly those who are postmenopausal, who sleep less than the recommended 7 hours per night may have impaired insulin sensitivity regardless of their degree of adiposity, a randomized crossover trial reveals.

The research was published recently in Diabetes Care.

Nearly 40 women were randomly assigned to either restricted sleep or adequate sleep for 6 weeks, then crossed over to the other sleep condition. During sleep restriction, women slept an average of 6.2 hours per night versus 7-9 hours per night.

Both fasting insulin levels and insulin resistance were significantly increased during sleep restriction, with the effect on insulin resistance particularly notable in postmenopausal women. This was independent of adiposity and changes in adiposity.

“What we’re seeing is that more insulin is needed to normalize glucose levels in the women under conditions of sleep restriction,” said senior author Marie-Pierre St-Onge, PhD, director of the Center of Excellence for Sleep and Circadian Research at Columbia University Vagelos College of Physicians and Surgeons, New York, in a release.

“Even then, the insulin may not have been doing enough to counteract rising blood glucose levels of postmenopausal women,” she stated.
 

Prolonged lack of sleep may accelerate diabetes progression

Dr. St-Onge added, “If that’s sustained over time, it is possible that prolonged insufficient sleep among individuals with prediabetes could accelerate the progression to type 2 diabetes.”

Dr. St-Onge said in an interview that it was crucial to show the impact of sleep restriction in a randomized study, because “observational studies don’t provide information on causality.”

The study did not rely on people “living in our clinical research facility,” but instead enrolled individuals who were “living their lives,” and the reduction in sleep achieved was “similar to what is seen in the general population with sleep,” she said.

Dr. St-Onge therefore believes the findings indicate that sleep has been overlooked as a contributory factor in insulin sensitivity.

Robert Gabbay, MD, PhD, chief scientific and medical officer at the American Diabetes Association, said in an interview that this is an “important study [that] builds on what we have seen on the importance of sleep for metabolic outcomes and diabetes.”

Joslin Diabetes Center

A version of this article appeared on Medscape.com.

Women, particularly those who are postmenopausal, who sleep less than the recommended 7 hours per night may have impaired insulin sensitivity regardless of their degree of adiposity, a randomized crossover trial reveals.

The research was published recently in Diabetes Care.

Nearly 40 women were randomly assigned to either restricted sleep or adequate sleep for 6 weeks, then crossed over to the other sleep condition. During sleep restriction, women slept an average of 6.2 hours per night versus 7-9 hours per night.

Both fasting insulin levels and insulin resistance were significantly increased during sleep restriction, with the effect on insulin resistance particularly notable in postmenopausal women. This was independent of adiposity and changes in adiposity.

“What we’re seeing is that more insulin is needed to normalize glucose levels in the women under conditions of sleep restriction,” said senior author Marie-Pierre St-Onge, PhD, director of the Center of Excellence for Sleep and Circadian Research at Columbia University Vagelos College of Physicians and Surgeons, New York, in a release.

“Even then, the insulin may not have been doing enough to counteract rising blood glucose levels of postmenopausal women,” she stated.
 

Prolonged lack of sleep may accelerate diabetes progression

Dr. St-Onge added, “If that’s sustained over time, it is possible that prolonged insufficient sleep among individuals with prediabetes could accelerate the progression to type 2 diabetes.”

Dr. St-Onge said in an interview that it was crucial to show the impact of sleep restriction in a randomized study, because “observational studies don’t provide information on causality.”

The study did not rely on people “living in our clinical research facility,” but instead enrolled individuals who were “living their lives,” and the reduction in sleep achieved was “similar to what is seen in the general population with sleep,” she said.

Dr. St-Onge therefore believes the findings indicate that sleep has been overlooked as a contributory factor in insulin sensitivity.

Robert Gabbay, MD, PhD, chief scientific and medical officer at the American Diabetes Association, said in an interview that this is an “important study [that] builds on what we have seen on the importance of sleep for metabolic outcomes and diabetes.”

Joslin Diabetes Center

A version of this article appeared on Medscape.com.

Melatonin usage has become increasingly common among children in the United States, with almost one in five kids over the age of 5 having taken the sleep aid in the past 30 days, according to a recent study.

These findings should prompt clinicians to discuss with parents the various factors that could be driving sleep disturbances, and potential safety issues associated with melatonin usage, lead author Lauren E. Hartstein, PhD, a postdoctoral fellow in the Sleep and Development Lab at the University of Colorado, Boulder, and colleagues reported.

Writing in JAMA Pediatrics, the investigators noted that melatonin products are notorious for mislabeling, with active ingredient quantities as much as three times higher than the labeled amount. This issue is particularly concerning, they added, as calls to poison control for melatonin ingestion jumped more than fivefold from 2012 to 2021, with most cases involving children younger than 5 years. Meanwhile, scant evidence is available to characterize intentional usage in the same population.

“Current data are lacking on the prevalence of melatonin use and the frequency, dosing, and timing of melatonin administration in U.S. youth,” Dr. Hartstein and colleagues wrote.

To address this knowledge gap, the investigators conducted an online survey of parents with children and adolescents aged 1.0-13.9 years. The survey asked parents to report any melatonin usage in their children in the past 30 days.

Parents reporting melatonin usage were asked about frequency, dose, timing of administration before bedtime, and duration of use.

Findings were reported within three age groups: preschool (1-4 years), school aged (5-9 years), and preteen (10-13 years).

The survey revealed that almost one in five children in the older age groups were using melatonin, with a rate of 18.5% in the school-aged group and 19.4% in the preteen group. In comparison, 5.6% of preschool children had received melatonin for sleep in the past 30 days.
 

A significant uptick in usage

These findings point to a significant uptick in usage, according to Dr. Hartstein and colleagues, who cited a 2017-2018 study that found just 1.3% of U.S. children had taken melatonin in the past 30 days.

In the present study, melatonin was typically administered 30 minutes before bedtime, most often as a gummy (64.3%) or chewable tablet (27.0%).

Frequency of administration was similar between age groups and trended toward a bimodal pattern, with melatonin often given either 1 day per week or 7 days per week.

Median dose increased significantly with age, from 0.5 mg in the preschool group to 1.0 mg in the school-aged group and 2.0 mg in the preteen group. Median duration also showed a significant upward trend, with 12-month, 18-month, and 21-month durations, respectively, for ascending age groups.

The investigators concluded that melatonin usage among U.S. adolescents and children is “exceedingly common,” despite a lack of evidence to support long-term safety or guide optimal dosing.
 

Is melatonin use masking other sleep issues?

“Widespread melatonin use across developmental stages may suggest a high prevalence of sleep disruption, which deserves accurate diagnosis and effective treatment,” Dr. Hartstein and colleagues wrote. “Dissemination of information regarding safety concerns, such as overdose and supplement mislabeling, is necessary. Clinicians should discuss with parents the factors associated with sleep difficulties and effective behavioral strategies.”

Large-scale, long-term studies are needed, they added, to generate relevant safety and efficacy data, and to characterize the factors driving melatonin administration by parents.

courtesy UCLA

“Studies like these add to our knowledge base and give us insight into what patients or parents may be doing that can impact overall health,” said Alfonso J. Padilla, MD, assistant clinical professor of sleep medicine at the University of California, Los Angeles, in a written comment. “Often, in normal encounters with our patients we may not be able to gather this information easily. It may help open conversations about sleep issues that are not being addressed.”

Dr. Padilla suggested that parents may believe that melatonin is safe because it is not regulated by the Food and Drug Administration, when in fact they could be negatively impacting their children’s sleep. He noted that short-term risks include altered circadian rhythm and vivid dreams or nightmares, while long-term safety remains unclear.

“As a sleep physician, I use melatonin for specific indications only,” Dr. Padilla said. “I may use it in small children that are having difficulty falling asleep, especially in children with autism or special needs. I also use it for help in adjustment in circadian rhythm, especially in adolescents.”

He recommends melatonin, he added, if he has a complete case history, and melatonin is suitable for that patient.

Typically, it’s not.

“Most often a medication is not the answer for the sleep concern that parents are having about their child,” he said.

The investigators disclosed grants from the Eunice Kennedy Shriver National Institute of Child Health and Human Development and the Colorado Clinical and Translational Science Award Program of the National Center for Advancing Translational Sciences of the National Institutes of Health. They reported no conflicts of interest.

Melatonin usage has become increasingly common among children in the United States, with almost one in five kids over the age of 5 having taken the sleep aid in the past 30 days, according to a recent study.

These findings should prompt clinicians to discuss with parents the various factors that could be driving sleep disturbances, and potential safety issues associated with melatonin usage, lead author Lauren E. Hartstein, PhD, a postdoctoral fellow in the Sleep and Development Lab at the University of Colorado, Boulder, and colleagues reported.

Writing in JAMA Pediatrics, the investigators noted that melatonin products are notorious for mislabeling, with active ingredient quantities as much as three times higher than the labeled amount. This issue is particularly concerning, they added, as calls to poison control for melatonin ingestion jumped more than fivefold from 2012 to 2021, with most cases involving children younger than 5 years. Meanwhile, scant evidence is available to characterize intentional usage in the same population.

“Current data are lacking on the prevalence of melatonin use and the frequency, dosing, and timing of melatonin administration in U.S. youth,” Dr. Hartstein and colleagues wrote.

To address this knowledge gap, the investigators conducted an online survey of parents with children and adolescents aged 1.0-13.9 years. The survey asked parents to report any melatonin usage in their children in the past 30 days.

Parents reporting melatonin usage were asked about frequency, dose, timing of administration before bedtime, and duration of use.

Findings were reported within three age groups: preschool (1-4 years), school aged (5-9 years), and preteen (10-13 years).

The survey revealed that almost one in five children in the older age groups were using melatonin, with a rate of 18.5% in the school-aged group and 19.4% in the preteen group. In comparison, 5.6% of preschool children had received melatonin for sleep in the past 30 days.
 

A significant uptick in usage

These findings point to a significant uptick in usage, according to Dr. Hartstein and colleagues, who cited a 2017-2018 study that found just 1.3% of U.S. children had taken melatonin in the past 30 days.

In the present study, melatonin was typically administered 30 minutes before bedtime, most often as a gummy (64.3%) or chewable tablet (27.0%).

Frequency of administration was similar between age groups and trended toward a bimodal pattern, with melatonin often given either 1 day per week or 7 days per week.

Median dose increased significantly with age, from 0.5 mg in the preschool group to 1.0 mg in the school-aged group and 2.0 mg in the preteen group. Median duration also showed a significant upward trend, with 12-month, 18-month, and 21-month durations, respectively, for ascending age groups.

The investigators concluded that melatonin usage among U.S. adolescents and children is “exceedingly common,” despite a lack of evidence to support long-term safety or guide optimal dosing.
 

Is melatonin use masking other sleep issues?

“Widespread melatonin use across developmental stages may suggest a high prevalence of sleep disruption, which deserves accurate diagnosis and effective treatment,” Dr. Hartstein and colleagues wrote. “Dissemination of information regarding safety concerns, such as overdose and supplement mislabeling, is necessary. Clinicians should discuss with parents the factors associated with sleep difficulties and effective behavioral strategies.”

Large-scale, long-term studies are needed, they added, to generate relevant safety and efficacy data, and to characterize the factors driving melatonin administration by parents.

courtesy UCLA

“Studies like these add to our knowledge base and give us insight into what patients or parents may be doing that can impact overall health,” said Alfonso J. Padilla, MD, assistant clinical professor of sleep medicine at the University of California, Los Angeles, in a written comment. “Often, in normal encounters with our patients we may not be able to gather this information easily. It may help open conversations about sleep issues that are not being addressed.”

Dr. Padilla suggested that parents may believe that melatonin is safe because it is not regulated by the Food and Drug Administration, when in fact they could be negatively impacting their children’s sleep. He noted that short-term risks include altered circadian rhythm and vivid dreams or nightmares, while long-term safety remains unclear.

“As a sleep physician, I use melatonin for specific indications only,” Dr. Padilla said. “I may use it in small children that are having difficulty falling asleep, especially in children with autism or special needs. I also use it for help in adjustment in circadian rhythm, especially in adolescents.”

He recommends melatonin, he added, if he has a complete case history, and melatonin is suitable for that patient.

Typically, it’s not.

“Most often a medication is not the answer for the sleep concern that parents are having about their child,” he said.

The investigators disclosed grants from the Eunice Kennedy Shriver National Institute of Child Health and Human Development and the Colorado Clinical and Translational Science Award Program of the National Center for Advancing Translational Sciences of the National Institutes of Health. They reported no conflicts of interest.

Melatonin usage has become increasingly common among children in the United States, with almost one in five kids over the age of 5 having taken the sleep aid in the past 30 days, according to a recent study.

These findings should prompt clinicians to discuss with parents the various factors that could be driving sleep disturbances, and potential safety issues associated with melatonin usage, lead author Lauren E. Hartstein, PhD, a postdoctoral fellow in the Sleep and Development Lab at the University of Colorado, Boulder, and colleagues reported.

Writing in JAMA Pediatrics, the investigators noted that melatonin products are notorious for mislabeling, with active ingredient quantities as much as three times higher than the labeled amount. This issue is particularly concerning, they added, as calls to poison control for melatonin ingestion jumped more than fivefold from 2012 to 2021, with most cases involving children younger than 5 years. Meanwhile, scant evidence is available to characterize intentional usage in the same population.

“Current data are lacking on the prevalence of melatonin use and the frequency, dosing, and timing of melatonin administration in U.S. youth,” Dr. Hartstein and colleagues wrote.

To address this knowledge gap, the investigators conducted an online survey of parents with children and adolescents aged 1.0-13.9 years. The survey asked parents to report any melatonin usage in their children in the past 30 days.

Parents reporting melatonin usage were asked about frequency, dose, timing of administration before bedtime, and duration of use.

Findings were reported within three age groups: preschool (1-4 years), school aged (5-9 years), and preteen (10-13 years).

The survey revealed that almost one in five children in the older age groups were using melatonin, with a rate of 18.5% in the school-aged group and 19.4% in the preteen group. In comparison, 5.6% of preschool children had received melatonin for sleep in the past 30 days.
 

A significant uptick in usage

These findings point to a significant uptick in usage, according to Dr. Hartstein and colleagues, who cited a 2017-2018 study that found just 1.3% of U.S. children had taken melatonin in the past 30 days.

In the present study, melatonin was typically administered 30 minutes before bedtime, most often as a gummy (64.3%) or chewable tablet (27.0%).

Frequency of administration was similar between age groups and trended toward a bimodal pattern, with melatonin often given either 1 day per week or 7 days per week.

Median dose increased significantly with age, from 0.5 mg in the preschool group to 1.0 mg in the school-aged group and 2.0 mg in the preteen group. Median duration also showed a significant upward trend, with 12-month, 18-month, and 21-month durations, respectively, for ascending age groups.

The investigators concluded that melatonin usage among U.S. adolescents and children is “exceedingly common,” despite a lack of evidence to support long-term safety or guide optimal dosing.
 

Is melatonin use masking other sleep issues?

“Widespread melatonin use across developmental stages may suggest a high prevalence of sleep disruption, which deserves accurate diagnosis and effective treatment,” Dr. Hartstein and colleagues wrote. “Dissemination of information regarding safety concerns, such as overdose and supplement mislabeling, is necessary. Clinicians should discuss with parents the factors associated with sleep difficulties and effective behavioral strategies.”

Large-scale, long-term studies are needed, they added, to generate relevant safety and efficacy data, and to characterize the factors driving melatonin administration by parents.

courtesy UCLA

“Studies like these add to our knowledge base and give us insight into what patients or parents may be doing that can impact overall health,” said Alfonso J. Padilla, MD, assistant clinical professor of sleep medicine at the University of California, Los Angeles, in a written comment. “Often, in normal encounters with our patients we may not be able to gather this information easily. It may help open conversations about sleep issues that are not being addressed.”

Dr. Padilla suggested that parents may believe that melatonin is safe because it is not regulated by the Food and Drug Administration, when in fact they could be negatively impacting their children’s sleep. He noted that short-term risks include altered circadian rhythm and vivid dreams or nightmares, while long-term safety remains unclear.

“As a sleep physician, I use melatonin for specific indications only,” Dr. Padilla said. “I may use it in small children that are having difficulty falling asleep, especially in children with autism or special needs. I also use it for help in adjustment in circadian rhythm, especially in adolescents.”

He recommends melatonin, he added, if he has a complete case history, and melatonin is suitable for that patient.

Typically, it’s not.

“Most often a medication is not the answer for the sleep concern that parents are having about their child,” he said.

The investigators disclosed grants from the Eunice Kennedy Shriver National Institute of Child Health and Human Development and the Colorado Clinical and Translational Science Award Program of the National Center for Advancing Translational Sciences of the National Institutes of Health. They reported no conflicts of interest.

More children and preteens are taking melatonin to help them sleep, a new study found, while experts cautioned parents may be unaware of some risks, particularly with long-term use. 

The investigators noted not all melatonin supplements contain what they say they do – some tested in a separate study contained two to three times the amount of melatonin on the label, and one supplement contained none at all.
 

A matter of timing?

While not completely advising against the sleep supplement, the study researchers pointed out that short-term use is likely safer. 

“We are not saying that melatonin is necessarily harmful to children. But much more research needs to be done before we can state with confidence that it is safe for kids to be taking long term,” lead study author Lauren Hartstein, PhD, a postdoctoral fellow in the Sleep and Development Lab at the University of Colorado in Boulder, said in a news release.

“If, after weighing potential risks and benefits, melatonin is recommended as the appropriate treatment, [a sleep medicine specialist] can recommend a dose and timing to treat the sleep issue,” said Raj Bhui, MD, a sleep medicine specialist and American Academy of Sleep Medicine spokesperson, who was not involved in the study.
 

An increasing trend

From 2017 to 2018, only about 1.3% of parents reported their children used melatonin in national data looking at supplement use in children and teenagers. In fact, usage more than doubled in this younger population from 2017 to 2020, another study revealed. “All of a sudden, in 2022, we started noticing a lot of parents telling us that their healthy child was regularly taking melatonin,” Dr. Hartstein said.

She and colleagues surveyed the parents of 993 children, aged 1 to less than 14, from January to April 2023. They found about 20% of these school-aged children and preteens took melatonin as a sleep aid. The findings, published in the journal JAMA Pediatrics, also suggest that some parents routinely give their preschool children melatonin.

They found nearly 6% of preschoolers aged 1-4, 18.5% of children aged 5-9, and 19.4% of kids aged 10-13 had taken melatonin in the previous month. 

The researchers also discovered that many took melatonin for longer than a few nights. Preschool children took the supplement for a median of 1 year, grade school children for a median 18 months, and preteens for 21 months. 
 

What’s in your supplement? 

In a different study published April 25 (JAMA. 2023. doi: 10.1001/jama.2023.2296), researchers looked at 25 melatonin gummy products and found that 22 of them contained different amounts of melatonin than listed on the label. In fact, one called Sleep Plus Immune contained more than three times the amount, and with a supplement called Sleep Support, researchers could not detect any melatonin. 

There is a general misconception that supplements are natural and therefore safe, Dr. Bhui said. “Multiple investigations of commercially available supplements have shown we cannot assume that what is on the label is in the pill or that what is in the pill is disclosed on the label. Formal laboratory testing has revealed some supplements to be adulterated with unapproved pharmaceutical ingredients, contaminated with microbes, or even tainted with toxins like arsenic, lead, and mercury.”

Choosing a product with the “USP Verified Mark” may give parents some comfort regarding melatonin content and consistency with labeling, Dr. Bhui said. Taking steps to safeguard the supply at home is also important in making sure children don’t take the supplements by accident. “With the increased use of melatonin, this has been a growing problem.”

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

More children and preteens are taking melatonin to help them sleep, a new study found, while experts cautioned parents may be unaware of some risks, particularly with long-term use. 

The investigators noted not all melatonin supplements contain what they say they do – some tested in a separate study contained two to three times the amount of melatonin on the label, and one supplement contained none at all.
 

A matter of timing?

While not completely advising against the sleep supplement, the study researchers pointed out that short-term use is likely safer. 

“We are not saying that melatonin is necessarily harmful to children. But much more research needs to be done before we can state with confidence that it is safe for kids to be taking long term,” lead study author Lauren Hartstein, PhD, a postdoctoral fellow in the Sleep and Development Lab at the University of Colorado in Boulder, said in a news release.

“If, after weighing potential risks and benefits, melatonin is recommended as the appropriate treatment, [a sleep medicine specialist] can recommend a dose and timing to treat the sleep issue,” said Raj Bhui, MD, a sleep medicine specialist and American Academy of Sleep Medicine spokesperson, who was not involved in the study.
 

An increasing trend

From 2017 to 2018, only about 1.3% of parents reported their children used melatonin in national data looking at supplement use in children and teenagers. In fact, usage more than doubled in this younger population from 2017 to 2020, another study revealed. “All of a sudden, in 2022, we started noticing a lot of parents telling us that their healthy child was regularly taking melatonin,” Dr. Hartstein said.

She and colleagues surveyed the parents of 993 children, aged 1 to less than 14, from January to April 2023. They found about 20% of these school-aged children and preteens took melatonin as a sleep aid. The findings, published in the journal JAMA Pediatrics, also suggest that some parents routinely give their preschool children melatonin.

They found nearly 6% of preschoolers aged 1-4, 18.5% of children aged 5-9, and 19.4% of kids aged 10-13 had taken melatonin in the previous month. 

The researchers also discovered that many took melatonin for longer than a few nights. Preschool children took the supplement for a median of 1 year, grade school children for a median 18 months, and preteens for 21 months. 
 

What’s in your supplement? 

In a different study published April 25 (JAMA. 2023. doi: 10.1001/jama.2023.2296), researchers looked at 25 melatonin gummy products and found that 22 of them contained different amounts of melatonin than listed on the label. In fact, one called Sleep Plus Immune contained more than three times the amount, and with a supplement called Sleep Support, researchers could not detect any melatonin. 

There is a general misconception that supplements are natural and therefore safe, Dr. Bhui said. “Multiple investigations of commercially available supplements have shown we cannot assume that what is on the label is in the pill or that what is in the pill is disclosed on the label. Formal laboratory testing has revealed some supplements to be adulterated with unapproved pharmaceutical ingredients, contaminated with microbes, or even tainted with toxins like arsenic, lead, and mercury.”

Choosing a product with the “USP Verified Mark” may give parents some comfort regarding melatonin content and consistency with labeling, Dr. Bhui said. Taking steps to safeguard the supply at home is also important in making sure children don’t take the supplements by accident. “With the increased use of melatonin, this has been a growing problem.”

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

More children and preteens are taking melatonin to help them sleep, a new study found, while experts cautioned parents may be unaware of some risks, particularly with long-term use. 

The investigators noted not all melatonin supplements contain what they say they do – some tested in a separate study contained two to three times the amount of melatonin on the label, and one supplement contained none at all.
 

A matter of timing?

While not completely advising against the sleep supplement, the study researchers pointed out that short-term use is likely safer. 

“We are not saying that melatonin is necessarily harmful to children. But much more research needs to be done before we can state with confidence that it is safe for kids to be taking long term,” lead study author Lauren Hartstein, PhD, a postdoctoral fellow in the Sleep and Development Lab at the University of Colorado in Boulder, said in a news release.

“If, after weighing potential risks and benefits, melatonin is recommended as the appropriate treatment, [a sleep medicine specialist] can recommend a dose and timing to treat the sleep issue,” said Raj Bhui, MD, a sleep medicine specialist and American Academy of Sleep Medicine spokesperson, who was not involved in the study.
 

An increasing trend

From 2017 to 2018, only about 1.3% of parents reported their children used melatonin in national data looking at supplement use in children and teenagers. In fact, usage more than doubled in this younger population from 2017 to 2020, another study revealed. “All of a sudden, in 2022, we started noticing a lot of parents telling us that their healthy child was regularly taking melatonin,” Dr. Hartstein said.

She and colleagues surveyed the parents of 993 children, aged 1 to less than 14, from January to April 2023. They found about 20% of these school-aged children and preteens took melatonin as a sleep aid. The findings, published in the journal JAMA Pediatrics, also suggest that some parents routinely give their preschool children melatonin.

They found nearly 6% of preschoolers aged 1-4, 18.5% of children aged 5-9, and 19.4% of kids aged 10-13 had taken melatonin in the previous month. 

The researchers also discovered that many took melatonin for longer than a few nights. Preschool children took the supplement for a median of 1 year, grade school children for a median 18 months, and preteens for 21 months. 
 

What’s in your supplement? 

In a different study published April 25 (JAMA. 2023. doi: 10.1001/jama.2023.2296), researchers looked at 25 melatonin gummy products and found that 22 of them contained different amounts of melatonin than listed on the label. In fact, one called Sleep Plus Immune contained more than three times the amount, and with a supplement called Sleep Support, researchers could not detect any melatonin. 

There is a general misconception that supplements are natural and therefore safe, Dr. Bhui said. “Multiple investigations of commercially available supplements have shown we cannot assume that what is on the label is in the pill or that what is in the pill is disclosed on the label. Formal laboratory testing has revealed some supplements to be adulterated with unapproved pharmaceutical ingredients, contaminated with microbes, or even tainted with toxins like arsenic, lead, and mercury.”

Choosing a product with the “USP Verified Mark” may give parents some comfort regarding melatonin content and consistency with labeling, Dr. Bhui said. Taking steps to safeguard the supply at home is also important in making sure children don’t take the supplements by accident. “With the increased use of melatonin, this has been a growing problem.”

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

TOPLINE:

A genetic predisposition to sleep 5 or fewer hours per night is associated with a significantly higher risk for subsequent depression. However, a genetic propensity to depression is not associated with suboptimal sleep patterns later on, new research shows.

METHODOLOGY:

• The analysis included participants in the English Longitudinal Study of Ageing (ELSA), a prospective cohort study of a representative U.K. sample (mean age, 65 years) that is assessed biennially.
• Researchers collected data on sleep duration and depression through nursing home visits and computer-assisted personal interviews and used combined ELSA waves from 2004 to 2008, when collection of genetic data began.
• Using genome-wide association studies from the U.K. Biobank, the authors constructed polygenic scores (PGSs) to predict an individual’s genetic risk over an average of 8 years for a disease or outcome, overall sleep duration, short sleep (≤ 5 hours nightly), long sleep (≥ 9 hours of sleep nightly), and depression.
• The analysis included two analytic samples; one involved 6,521 persons to determine the role of baseline sleep on depression (assessed using the Center for Epidemiologic Studies Depression Scale) at follow-up, and the other involved 6,070 persons to determine the role of baseline depression on suboptimal sleep at follow-up.

TAKEAWAY:

• After adjustments, including for age and sex, a 1–standard deviation increase in PGS for short sleep was associated with an increase of 14% in odds of developing depression during the follow-up period (odds ratio, 1.14; P = .008).
• There was no significant association of the PGS for sleep duration (P = .053) or long sleep (P = .544) with the onset of depression.
• There were no significant associations between PGS for depression and future overall sleep duration, short sleep, and long sleep by the end of the follow-up, suggesting that different mechanisms underlie the relationship between depression and subsequent onset of suboptimal sleep in older adults.
• Several sensitivity analyses – including additional adjustment for socioeconomic, environmental, and behavioral factors – upheld the findings of the main analysis, highlighting the robustness of the results.

IN PRACTICE:

The study showed that common genetic markers for short sleep play an important role in the incidence of depression in older adults, the authors note, adding that the new findings “support a growing view that short-sleep is more salient to the experience of depression than long sleep” across the lifespan.

SOURCE:

The study was led by Odessa S. Hamilton, department of behavioral science and health, University College London. It was published online  in Translational Psychiatry.

LIMITATIONS:

There are probably intraindividual differences in sleep duration that were not assessed in the study. The depression scale used may be indicative of subclinical depression and not major depressive disorder. The phenotypic sensitivity analyses did not account for comorbidities or medications that can affect sleep duration and depression.

DISCLOSURES:

ELSA is funded by the National Institute on Aging and by a consortium of U.K. government departments coordinated by the National Institute for Health and Care Research. The authors report no relevant conflicts of interests.

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

TOPLINE:

A genetic predisposition to sleep 5 or fewer hours per night is associated with a significantly higher risk for subsequent depression. However, a genetic propensity to depression is not associated with suboptimal sleep patterns later on, new research shows.

METHODOLOGY:

• The analysis included participants in the English Longitudinal Study of Ageing (ELSA), a prospective cohort study of a representative U.K. sample (mean age, 65 years) that is assessed biennially.
• Researchers collected data on sleep duration and depression through nursing home visits and computer-assisted personal interviews and used combined ELSA waves from 2004 to 2008, when collection of genetic data began.
• Using genome-wide association studies from the U.K. Biobank, the authors constructed polygenic scores (PGSs) to predict an individual’s genetic risk over an average of 8 years for a disease or outcome, overall sleep duration, short sleep (≤ 5 hours nightly), long sleep (≥ 9 hours of sleep nightly), and depression.
• The analysis included two analytic samples; one involved 6,521 persons to determine the role of baseline sleep on depression (assessed using the Center for Epidemiologic Studies Depression Scale) at follow-up, and the other involved 6,070 persons to determine the role of baseline depression on suboptimal sleep at follow-up.

TAKEAWAY:

• After adjustments, including for age and sex, a 1–standard deviation increase in PGS for short sleep was associated with an increase of 14% in odds of developing depression during the follow-up period (odds ratio, 1.14; P = .008).
• There was no significant association of the PGS for sleep duration (P = .053) or long sleep (P = .544) with the onset of depression.
• There were no significant associations between PGS for depression and future overall sleep duration, short sleep, and long sleep by the end of the follow-up, suggesting that different mechanisms underlie the relationship between depression and subsequent onset of suboptimal sleep in older adults.
• Several sensitivity analyses – including additional adjustment for socioeconomic, environmental, and behavioral factors – upheld the findings of the main analysis, highlighting the robustness of the results.

IN PRACTICE:

The study showed that common genetic markers for short sleep play an important role in the incidence of depression in older adults, the authors note, adding that the new findings “support a growing view that short-sleep is more salient to the experience of depression than long sleep” across the lifespan.

SOURCE:

The study was led by Odessa S. Hamilton, department of behavioral science and health, University College London. It was published online  in Translational Psychiatry.

LIMITATIONS:

There are probably intraindividual differences in sleep duration that were not assessed in the study. The depression scale used may be indicative of subclinical depression and not major depressive disorder. The phenotypic sensitivity analyses did not account for comorbidities or medications that can affect sleep duration and depression.

DISCLOSURES:

ELSA is funded by the National Institute on Aging and by a consortium of U.K. government departments coordinated by the National Institute for Health and Care Research. The authors report no relevant conflicts of interests.

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

TOPLINE:

A genetic predisposition to sleep 5 or fewer hours per night is associated with a significantly higher risk for subsequent depression. However, a genetic propensity to depression is not associated with suboptimal sleep patterns later on, new research shows.

METHODOLOGY:

• The analysis included participants in the English Longitudinal Study of Ageing (ELSA), a prospective cohort study of a representative U.K. sample (mean age, 65 years) that is assessed biennially.
• Researchers collected data on sleep duration and depression through nursing home visits and computer-assisted personal interviews and used combined ELSA waves from 2004 to 2008, when collection of genetic data began.
• Using genome-wide association studies from the U.K. Biobank, the authors constructed polygenic scores (PGSs) to predict an individual’s genetic risk over an average of 8 years for a disease or outcome, overall sleep duration, short sleep (≤ 5 hours nightly), long sleep (≥ 9 hours of sleep nightly), and depression.
• The analysis included two analytic samples; one involved 6,521 persons to determine the role of baseline sleep on depression (assessed using the Center for Epidemiologic Studies Depression Scale) at follow-up, and the other involved 6,070 persons to determine the role of baseline depression on suboptimal sleep at follow-up.

TAKEAWAY:

• After adjustments, including for age and sex, a 1–standard deviation increase in PGS for short sleep was associated with an increase of 14% in odds of developing depression during the follow-up period (odds ratio, 1.14; P = .008).
• There was no significant association of the PGS for sleep duration (P = .053) or long sleep (P = .544) with the onset of depression.
• There were no significant associations between PGS for depression and future overall sleep duration, short sleep, and long sleep by the end of the follow-up, suggesting that different mechanisms underlie the relationship between depression and subsequent onset of suboptimal sleep in older adults.
• Several sensitivity analyses – including additional adjustment for socioeconomic, environmental, and behavioral factors – upheld the findings of the main analysis, highlighting the robustness of the results.

IN PRACTICE:

The study showed that common genetic markers for short sleep play an important role in the incidence of depression in older adults, the authors note, adding that the new findings “support a growing view that short-sleep is more salient to the experience of depression than long sleep” across the lifespan.

SOURCE:

The study was led by Odessa S. Hamilton, department of behavioral science and health, University College London. It was published online  in Translational Psychiatry.

LIMITATIONS:

There are probably intraindividual differences in sleep duration that were not assessed in the study. The depression scale used may be indicative of subclinical depression and not major depressive disorder. The phenotypic sensitivity analyses did not account for comorbidities or medications that can affect sleep duration and depression.

DISCLOSURES:

ELSA is funded by the National Institute on Aging and by a consortium of U.K. government departments coordinated by the National Institute for Health and Care Research. The authors report no relevant conflicts of interests.

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

“On which side of the bed did you get up this morning?” Obviously, your inquisitor assumes that to avoid clumsily crawling over your sleeping partner you always get up on the side with the table stacked with unread books.

You know as well as I do that you have just received a totally undisguised comment on your recent behavior that has been several shades less than cheery. You may have already sensed your own grumpiness. Do you have an explanation? Did the commute leave you with a case of unresolved road rage? Did you wake up feeling unrested? How often does that happen? Do you think you are getting enough sleep?

A few weeks ago I wrote a Letters From Maine column in which I shared a study suggesting that the regularity of an individual’s sleep pattern may, in many cases, be more important than his or her total number of hours slept. In that same column I wrote that sleep scientists don’t as yet have a good definition of sleep irregularity, nor can they give us any more than a broad range for the total number of hours a person needs to maintain wellness.

How do you determine whether you are getting enough sleep? Do you keep a chart of how many times you were asked which side of the bed you got up on in a week? Or is it how you feel in the morning? Is it when you instantly doze off any time you sit down in a quiet place?

Although many adults are clueless (or in denial) that they are sleep deprived, generally if you ask them and take a brief history they will tell you. On the other hand, determining when a child, particularly one who is preverbal, is sleep deprived is a bit more difficult. Asking the patient isn’t going to give you the answer. You must rely on parental observations. And, to some extent, this can be difficult because parents are, by definition, learning on the job. They may not realize the symptoms and behaviors they are seeing in their child are the result of sleep deficiency.

Over the last half century of observing children, I have developed a very low threshold for diagnosing sleep deprivation. Basically, any child who is cranky and not obviously sick is overtired until proven otherwise. For example, colic does not appear on my frequently used, or in fact ever used, list of diagnoses. Colicky is an adjective that I may use to describe some episodic pain or behavior, but colic as a working diagnosis? Never.

When presented with a child who has already been diagnosed with “colic” by its aunt or the lady next door, this is when the astute pediatrician must be at his or her best. If a thorough history, including sleep pattern, yields no obvious evidence of illness, the next step should be some sleep coaching. However, this is where the “until proven otherwise” thing becomes important, because not providing close follow-up and continuing to keep an open mind for the less likely coexisting conditions can be dangerous and certainly not in the patient’s best interest.

For the older child crankiness, temper tantrums, mood disorders and signs and symptoms often (some might say too often) associated with attention-deficit disorder should trigger an immediate investigation of sleep habits and appropriate advice. Less well-known conditions associated with sleep deprivation are migraine and nocturnal leg pains, often mislabeled as growing pains.

The physicians planning on using sleep as a therapeutic modality is going to quickly run into several challenges. First is convincing the parents, the patient, and the family that the condition is to a greater or lesser degree the result of sleep deprivation. Because sleep is still underappreciated as a component of wellness, this is often not an easy sell.

Second, everyone must accept that altering sleep patterns regardless of age is often not easy and will not be achieved in 1 night or 2. Keeping up the drumbeat of encouragement with close follow-up is critical. Parents must be continually reminded that sleep is being used as a medicine and the dose is not measured in hours. The improvement in symptoms will tell us when enough is enough.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

“On which side of the bed did you get up this morning?” Obviously, your inquisitor assumes that to avoid clumsily crawling over your sleeping partner you always get up on the side with the table stacked with unread books.

You know as well as I do that you have just received a totally undisguised comment on your recent behavior that has been several shades less than cheery. You may have already sensed your own grumpiness. Do you have an explanation? Did the commute leave you with a case of unresolved road rage? Did you wake up feeling unrested? How often does that happen? Do you think you are getting enough sleep?

A few weeks ago I wrote a Letters From Maine column in which I shared a study suggesting that the regularity of an individual’s sleep pattern may, in many cases, be more important than his or her total number of hours slept. In that same column I wrote that sleep scientists don’t as yet have a good definition of sleep irregularity, nor can they give us any more than a broad range for the total number of hours a person needs to maintain wellness.

How do you determine whether you are getting enough sleep? Do you keep a chart of how many times you were asked which side of the bed you got up on in a week? Or is it how you feel in the morning? Is it when you instantly doze off any time you sit down in a quiet place?

Although many adults are clueless (or in denial) that they are sleep deprived, generally if you ask them and take a brief history they will tell you. On the other hand, determining when a child, particularly one who is preverbal, is sleep deprived is a bit more difficult. Asking the patient isn’t going to give you the answer. You must rely on parental observations. And, to some extent, this can be difficult because parents are, by definition, learning on the job. They may not realize the symptoms and behaviors they are seeing in their child are the result of sleep deficiency.

Over the last half century of observing children, I have developed a very low threshold for diagnosing sleep deprivation. Basically, any child who is cranky and not obviously sick is overtired until proven otherwise. For example, colic does not appear on my frequently used, or in fact ever used, list of diagnoses. Colicky is an adjective that I may use to describe some episodic pain or behavior, but colic as a working diagnosis? Never.

When presented with a child who has already been diagnosed with “colic” by its aunt or the lady next door, this is when the astute pediatrician must be at his or her best. If a thorough history, including sleep pattern, yields no obvious evidence of illness, the next step should be some sleep coaching. However, this is where the “until proven otherwise” thing becomes important, because not providing close follow-up and continuing to keep an open mind for the less likely coexisting conditions can be dangerous and certainly not in the patient’s best interest.

For the older child crankiness, temper tantrums, mood disorders and signs and symptoms often (some might say too often) associated with attention-deficit disorder should trigger an immediate investigation of sleep habits and appropriate advice. Less well-known conditions associated with sleep deprivation are migraine and nocturnal leg pains, often mislabeled as growing pains.

The physicians planning on using sleep as a therapeutic modality is going to quickly run into several challenges. First is convincing the parents, the patient, and the family that the condition is to a greater or lesser degree the result of sleep deprivation. Because sleep is still underappreciated as a component of wellness, this is often not an easy sell.

Second, everyone must accept that altering sleep patterns regardless of age is often not easy and will not be achieved in 1 night or 2. Keeping up the drumbeat of encouragement with close follow-up is critical. Parents must be continually reminded that sleep is being used as a medicine and the dose is not measured in hours. The improvement in symptoms will tell us when enough is enough.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

“On which side of the bed did you get up this morning?” Obviously, your inquisitor assumes that to avoid clumsily crawling over your sleeping partner you always get up on the side with the table stacked with unread books.

You know as well as I do that you have just received a totally undisguised comment on your recent behavior that has been several shades less than cheery. You may have already sensed your own grumpiness. Do you have an explanation? Did the commute leave you with a case of unresolved road rage? Did you wake up feeling unrested? How often does that happen? Do you think you are getting enough sleep?

A few weeks ago I wrote a Letters From Maine column in which I shared a study suggesting that the regularity of an individual’s sleep pattern may, in many cases, be more important than his or her total number of hours slept. In that same column I wrote that sleep scientists don’t as yet have a good definition of sleep irregularity, nor can they give us any more than a broad range for the total number of hours a person needs to maintain wellness.

How do you determine whether you are getting enough sleep? Do you keep a chart of how many times you were asked which side of the bed you got up on in a week? Or is it how you feel in the morning? Is it when you instantly doze off any time you sit down in a quiet place?

Although many adults are clueless (or in denial) that they are sleep deprived, generally if you ask them and take a brief history they will tell you. On the other hand, determining when a child, particularly one who is preverbal, is sleep deprived is a bit more difficult. Asking the patient isn’t going to give you the answer. You must rely on parental observations. And, to some extent, this can be difficult because parents are, by definition, learning on the job. They may not realize the symptoms and behaviors they are seeing in their child are the result of sleep deficiency.

Over the last half century of observing children, I have developed a very low threshold for diagnosing sleep deprivation. Basically, any child who is cranky and not obviously sick is overtired until proven otherwise. For example, colic does not appear on my frequently used, or in fact ever used, list of diagnoses. Colicky is an adjective that I may use to describe some episodic pain or behavior, but colic as a working diagnosis? Never.

When presented with a child who has already been diagnosed with “colic” by its aunt or the lady next door, this is when the astute pediatrician must be at his or her best. If a thorough history, including sleep pattern, yields no obvious evidence of illness, the next step should be some sleep coaching. However, this is where the “until proven otherwise” thing becomes important, because not providing close follow-up and continuing to keep an open mind for the less likely coexisting conditions can be dangerous and certainly not in the patient’s best interest.

For the older child crankiness, temper tantrums, mood disorders and signs and symptoms often (some might say too often) associated with attention-deficit disorder should trigger an immediate investigation of sleep habits and appropriate advice. Less well-known conditions associated with sleep deprivation are migraine and nocturnal leg pains, often mislabeled as growing pains.

The physicians planning on using sleep as a therapeutic modality is going to quickly run into several challenges. First is convincing the parents, the patient, and the family that the condition is to a greater or lesser degree the result of sleep deprivation. Because sleep is still underappreciated as a component of wellness, this is often not an easy sell.

Second, everyone must accept that altering sleep patterns regardless of age is often not easy and will not be achieved in 1 night or 2. Keeping up the drumbeat of encouragement with close follow-up is critical. Parents must be continually reminded that sleep is being used as a medicine and the dose is not measured in hours. The improvement in symptoms will tell us when enough is enough.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Children with obstructive sleep apnea syndrome showed significantly reduced nasal ventilation function, compared with healthy controls, based on data from more than 200 individuals.

Previous research has shown an increased risk of obstructive sleep apnea syndrome (OSAS) in patients with compromised nasal respiration, but the association between increased nasal resistance (NR) and OSAS in children is controversial and remains unclear, wrote Ying Pang, MD, of Children’s Hospital of Chongqing Medical University, China, and colleagues.

In a study published in the Ear, Nose & Throat Journal, the researchers enrolled 109 children aged 6-12 years with OSAS and 116 healthy control children, with the goal of examining the role of nasal ventilation function on OSAS. Participants underwent acoustic rhinometry (AR) following polysomnography, and measurements of the nasal minimal cross-sectional area (NMCA) were taken in 3 segments, as were nasal cavity volume (NCV) from 0 cm to 5 cm, nasopharyngeal volume (NPV) from 6 cm to 8 cm, and distance of the minimal cross-sectional area to the nostril (DCAN). The children also underwent NR testing in both nostrils while awake and lying in a supine position.

Overall, the NR of children with OSAS were significantly higher than that of controls (P < .05). For AR, children with OSAS had significantly lower measures of NMCA, NCV, and NPV, but DCAN values were between the groups. Both AR and NR measures were similar among children with mild, moderate, or severe OSAS.

A subset of 90 children with mild or moderate OSAS were treated with intranasal corticosteroids (ICS) and oral montelukast for 12 weeks. Of these, 69 completed the study and were divided into three groups: effectively cured (group A), successfully treated (group B), and treatment failure (group C). The researchers compared the size of the tonsil adenoids, the polysomnography, NR, and AR before and after treatment and found significant differences in NR, NMCA, and NCV for the A and B groups but no significant changes in DCAN following treatment.

For group A, treatment was associated with a significant reduction in adenoid size and increase in NPV, but these changes did not occur in group B.

The findings were limited by several factors, including the small sample size and measurement of NR when patients were awake and sitting upright, and larger studies are needed to confirm the results, the researchers noted.

However, the results suggest that NVF plays a role in the pathogenesis of OSAS in children and suggest a need to improve NVF in treating these patients they concluded.

This study was supported by the Medical Project of Chongqing Municipal Science and Health Bureau of China. The researchers had no financial conflicts to disclose.

Children with obstructive sleep apnea syndrome showed significantly reduced nasal ventilation function, compared with healthy controls, based on data from more than 200 individuals.

Previous research has shown an increased risk of obstructive sleep apnea syndrome (OSAS) in patients with compromised nasal respiration, but the association between increased nasal resistance (NR) and OSAS in children is controversial and remains unclear, wrote Ying Pang, MD, of Children’s Hospital of Chongqing Medical University, China, and colleagues.

In a study published in the Ear, Nose & Throat Journal, the researchers enrolled 109 children aged 6-12 years with OSAS and 116 healthy control children, with the goal of examining the role of nasal ventilation function on OSAS. Participants underwent acoustic rhinometry (AR) following polysomnography, and measurements of the nasal minimal cross-sectional area (NMCA) were taken in 3 segments, as were nasal cavity volume (NCV) from 0 cm to 5 cm, nasopharyngeal volume (NPV) from 6 cm to 8 cm, and distance of the minimal cross-sectional area to the nostril (DCAN). The children also underwent NR testing in both nostrils while awake and lying in a supine position.

Overall, the NR of children with OSAS were significantly higher than that of controls (P < .05). For AR, children with OSAS had significantly lower measures of NMCA, NCV, and NPV, but DCAN values were between the groups. Both AR and NR measures were similar among children with mild, moderate, or severe OSAS.

A subset of 90 children with mild or moderate OSAS were treated with intranasal corticosteroids (ICS) and oral montelukast for 12 weeks. Of these, 69 completed the study and were divided into three groups: effectively cured (group A), successfully treated (group B), and treatment failure (group C). The researchers compared the size of the tonsil adenoids, the polysomnography, NR, and AR before and after treatment and found significant differences in NR, NMCA, and NCV for the A and B groups but no significant changes in DCAN following treatment.

For group A, treatment was associated with a significant reduction in adenoid size and increase in NPV, but these changes did not occur in group B.

The findings were limited by several factors, including the small sample size and measurement of NR when patients were awake and sitting upright, and larger studies are needed to confirm the results, the researchers noted.

However, the results suggest that NVF plays a role in the pathogenesis of OSAS in children and suggest a need to improve NVF in treating these patients they concluded.

This study was supported by the Medical Project of Chongqing Municipal Science and Health Bureau of China. The researchers had no financial conflicts to disclose.

Children with obstructive sleep apnea syndrome showed significantly reduced nasal ventilation function, compared with healthy controls, based on data from more than 200 individuals.

Previous research has shown an increased risk of obstructive sleep apnea syndrome (OSAS) in patients with compromised nasal respiration, but the association between increased nasal resistance (NR) and OSAS in children is controversial and remains unclear, wrote Ying Pang, MD, of Children’s Hospital of Chongqing Medical University, China, and colleagues.

In a study published in the Ear, Nose & Throat Journal, the researchers enrolled 109 children aged 6-12 years with OSAS and 116 healthy control children, with the goal of examining the role of nasal ventilation function on OSAS. Participants underwent acoustic rhinometry (AR) following polysomnography, and measurements of the nasal minimal cross-sectional area (NMCA) were taken in 3 segments, as were nasal cavity volume (NCV) from 0 cm to 5 cm, nasopharyngeal volume (NPV) from 6 cm to 8 cm, and distance of the minimal cross-sectional area to the nostril (DCAN). The children also underwent NR testing in both nostrils while awake and lying in a supine position.

Overall, the NR of children with OSAS were significantly higher than that of controls (P < .05). For AR, children with OSAS had significantly lower measures of NMCA, NCV, and NPV, but DCAN values were between the groups. Both AR and NR measures were similar among children with mild, moderate, or severe OSAS.

A subset of 90 children with mild or moderate OSAS were treated with intranasal corticosteroids (ICS) and oral montelukast for 12 weeks. Of these, 69 completed the study and were divided into three groups: effectively cured (group A), successfully treated (group B), and treatment failure (group C). The researchers compared the size of the tonsil adenoids, the polysomnography, NR, and AR before and after treatment and found significant differences in NR, NMCA, and NCV for the A and B groups but no significant changes in DCAN following treatment.

For group A, treatment was associated with a significant reduction in adenoid size and increase in NPV, but these changes did not occur in group B.

The findings were limited by several factors, including the small sample size and measurement of NR when patients were awake and sitting upright, and larger studies are needed to confirm the results, the researchers noted.

However, the results suggest that NVF plays a role in the pathogenesis of OSAS in children and suggest a need to improve NVF in treating these patients they concluded.

This study was supported by the Medical Project of Chongqing Municipal Science and Health Bureau of China. The researchers had no financial conflicts to disclose.

Sleep Network

Non-Respiratory Sleep Section

Do you feel like you sleep worse in the spring and have more difficulty keeping your schedule on track? There are new data to support the way you feel based on our deeper understanding of seasonal variations in sleep architecture.

Patients in a recent study had 43 minutes less total sleep time and approximately 30 less minutes of REM sleep in the late spring when compared with the winter (Seidler A, et al. Front Neurosci. 2023 Feb 17:17:1105233). Accumulation of decreased sleep time and quality can lead to the sensation of ‘running-on-empty’ by early spring.

Experts believe these seasonal variations in sleep architecture are mainly secondary to circadian shifts. Our social synchronization overrides our natural alignment with daylight patterns and can lead to known consequences of circadian misalignment. Common consequences of poor circadian alignment include worsening sleep disturbances, cognitive impairments, occupational mistakes, and metabolic and mental health disturbances (Schmal C, et al. Front Physiol. 2020 Apr 28:11:334; Boivin D, et al. J Biol Rhythms. 2022 Feb;37[1]:3-28).

The effects of circadian misalignment can be particularly dramatic in children receiving less than their age-appropriate hours of sleep. Children with sleep deprivation are at increased risk of attention, behavior, and learning problems (Paruthi S, et al. J Clinl Sleep Med. 2016;12[6]:785-6).

To improve circadian alignment in spring, it is recommended to achieve morning bright light exposure and perform regular exercise. The elimination of daylight savings time to a consensus of permanent standard time will optimize circadian alignment.

Christopher Izzo, DO – Section Fellow-in-Training

William Healy, MD – Section Member-at-Large

Mariam Louis, MD – Section Chair

Sleep Network

Non-Respiratory Sleep Section

Do you feel like you sleep worse in the spring and have more difficulty keeping your schedule on track? There are new data to support the way you feel based on our deeper understanding of seasonal variations in sleep architecture.

Patients in a recent study had 43 minutes less total sleep time and approximately 30 less minutes of REM sleep in the late spring when compared with the winter (Seidler A, et al. Front Neurosci. 2023 Feb 17:17:1105233). Accumulation of decreased sleep time and quality can lead to the sensation of ‘running-on-empty’ by early spring.

Experts believe these seasonal variations in sleep architecture are mainly secondary to circadian shifts. Our social synchronization overrides our natural alignment with daylight patterns and can lead to known consequences of circadian misalignment. Common consequences of poor circadian alignment include worsening sleep disturbances, cognitive impairments, occupational mistakes, and metabolic and mental health disturbances (Schmal C, et al. Front Physiol. 2020 Apr 28:11:334; Boivin D, et al. J Biol Rhythms. 2022 Feb;37[1]:3-28).

The effects of circadian misalignment can be particularly dramatic in children receiving less than their age-appropriate hours of sleep. Children with sleep deprivation are at increased risk of attention, behavior, and learning problems (Paruthi S, et al. J Clinl Sleep Med. 2016;12[6]:785-6).

To improve circadian alignment in spring, it is recommended to achieve morning bright light exposure and perform regular exercise. The elimination of daylight savings time to a consensus of permanent standard time will optimize circadian alignment.

Christopher Izzo, DO – Section Fellow-in-Training

William Healy, MD – Section Member-at-Large

Mariam Louis, MD – Section Chair

Sleep Network

Non-Respiratory Sleep Section

Do you feel like you sleep worse in the spring and have more difficulty keeping your schedule on track? There are new data to support the way you feel based on our deeper understanding of seasonal variations in sleep architecture.

Patients in a recent study had 43 minutes less total sleep time and approximately 30 less minutes of REM sleep in the late spring when compared with the winter (Seidler A, et al. Front Neurosci. 2023 Feb 17:17:1105233). Accumulation of decreased sleep time and quality can lead to the sensation of ‘running-on-empty’ by early spring.

Experts believe these seasonal variations in sleep architecture are mainly secondary to circadian shifts. Our social synchronization overrides our natural alignment with daylight patterns and can lead to known consequences of circadian misalignment. Common consequences of poor circadian alignment include worsening sleep disturbances, cognitive impairments, occupational mistakes, and metabolic and mental health disturbances (Schmal C, et al. Front Physiol. 2020 Apr 28:11:334; Boivin D, et al. J Biol Rhythms. 2022 Feb;37[1]:3-28).

The effects of circadian misalignment can be particularly dramatic in children receiving less than their age-appropriate hours of sleep. Children with sleep deprivation are at increased risk of attention, behavior, and learning problems (Paruthi S, et al. J Clinl Sleep Med. 2016;12[6]:785-6).

To improve circadian alignment in spring, it is recommended to achieve morning bright light exposure and perform regular exercise. The elimination of daylight savings time to a consensus of permanent standard time will optimize circadian alignment.

Christopher Izzo, DO – Section Fellow-in-Training

William Healy, MD – Section Member-at-Large

Mariam Louis, MD – Section Chair