Late-to-bed adolescents may be early-to-diabetes

Article Type
Changed
Fri, 01/18/2019 - 16:49

 

– Late chronotype may have a deleterious impact on glucose homeostasis independent of obesity in preadolescents aged 10-13 years, according to a small study.

Late chronotype – or an individual’s preference for later sleep and food intake – is associated with higher body mass index (BMI), risk incidence of type 2 diabetes mellitus, hemoglobin A1c, and risk of hypertension in adults. It is also associated with higher BMI, lower dietary restraint, and lower HDL cholesterol in adolescents. This study was the first to focus on chronotype and glycemic control in children on the cusp of or in early puberty.

In participants tested during the summer months, the actigraphy-derived mid-sleep time on free days – an objective measure of chronotype – was associated positively with fasting plasma glucose (P = 0.048). “This is an important point because it highlights the objective measure of chronotype, whereas questionnaires can be more subjective,” said Magdalena Dumin, MD, at the annual meeting of Associated Professional Sleep Societies.

Dr. Magdalena Dumin, University of Chicago Medical Center
Debra L. Beck/Frontline Medical News
Dr. Magdalena Dumin
An additional finding included HbA1c having been positively associated with late chronotype questionnaire scores. This suggested “that a later chronotype has an adverse effect on glucose homeostasis,” reported Dr. Dumin, who was one of the investigators in this study and is a pediatric endocrinologist at the University of Chicago Medical Center. Furthermore, higher Children’s ChronoType Questionnaire scores (a more subjective indicator of eveningness) tended to be associated with higher plasma glucose.

The researcher also noted that higher sleep fragmentation and lower sleep efficiency were both associated with hyperglycemia and hyperinsulinemia, independent of obesity.

“Our preliminary findings suggest that having a late chronotype and less efficient and more fragmented sleep in pre- and early adolescence may have a deleterious glycemic impact independent of obesity and pubertal stage,” she said.

“Advancing bedtimes may reduce glucose levels in preadolescents and adolescents,” Dr. Dumin surmised.

This study included 24 adolescents, 13 of whom were normal weight and 11 of whom were obese. They all underwent anthropometric measurements with fasting glucose, insulin, C-peptide, HbA1c, and lipid levels. Exclusion criteria included a clinical diagnosis of sleep, behavioral, or dietary problems. The obese subjects also underwent a 180-minute glucose tolerance test.

Chronotype was assessed via actigraphy over 1 week to provide mid-sleep time on free days, and secondarily through administration to chronotype questionnaires – the Children’s ChronoType Questionnaire and the Morningness-Eveningness Scale for Children.

Among the normal-weight participants, 31% were morning and 23% evening chronotype (the rest being neutral chronotype), and, in the obese subjects, 27% were morning and 36% were evening chronotype.

The obese subjects were more likely to be in puberty, and had higher systolic blood pressures, higher fasting plasma insulin and levels of insulin resistance, as measured by Homeostatic Model Assessment of Insulin Resistance. Hemoglobin A1c tended to be higher in the obese subjects (P = .06), but fasting plasma glucose did not differ significantly between the obese and normal-weight participants (P = .68).

“We chose this population due to the shift from morningness to eveningness that occurs during adolescence followed by a progressive return to an intermediate or early chronotype at the end of adolescence,” Dr. Dumin said.

Bedtime, wake time, and total sleep time were nearly identical between the two groups (7.84 hours and 7.62 hours; P = .49), although sleep efficiency was numerically lower in the obese subjects (87.0 vs. 89.8; P = .14), while sleep fragmentation was somewhat greater (20.16 vs. 17.38; P = .18).

Dr. Dumin suggested that a continuation of her research with more patients would be useful.

This study is supported by the Endocrine Fellows Foundation and the University of Chicago Institute of Translational Medicine. Dr. Dumin reported having no financial disclosures.

Meeting/Event
Publications
Topics
Sections
Meeting/Event
Meeting/Event

 

– Late chronotype may have a deleterious impact on glucose homeostasis independent of obesity in preadolescents aged 10-13 years, according to a small study.

Late chronotype – or an individual’s preference for later sleep and food intake – is associated with higher body mass index (BMI), risk incidence of type 2 diabetes mellitus, hemoglobin A1c, and risk of hypertension in adults. It is also associated with higher BMI, lower dietary restraint, and lower HDL cholesterol in adolescents. This study was the first to focus on chronotype and glycemic control in children on the cusp of or in early puberty.

In participants tested during the summer months, the actigraphy-derived mid-sleep time on free days – an objective measure of chronotype – was associated positively with fasting plasma glucose (P = 0.048). “This is an important point because it highlights the objective measure of chronotype, whereas questionnaires can be more subjective,” said Magdalena Dumin, MD, at the annual meeting of Associated Professional Sleep Societies.

Dr. Magdalena Dumin, University of Chicago Medical Center
Debra L. Beck/Frontline Medical News
Dr. Magdalena Dumin
An additional finding included HbA1c having been positively associated with late chronotype questionnaire scores. This suggested “that a later chronotype has an adverse effect on glucose homeostasis,” reported Dr. Dumin, who was one of the investigators in this study and is a pediatric endocrinologist at the University of Chicago Medical Center. Furthermore, higher Children’s ChronoType Questionnaire scores (a more subjective indicator of eveningness) tended to be associated with higher plasma glucose.

The researcher also noted that higher sleep fragmentation and lower sleep efficiency were both associated with hyperglycemia and hyperinsulinemia, independent of obesity.

“Our preliminary findings suggest that having a late chronotype and less efficient and more fragmented sleep in pre- and early adolescence may have a deleterious glycemic impact independent of obesity and pubertal stage,” she said.

“Advancing bedtimes may reduce glucose levels in preadolescents and adolescents,” Dr. Dumin surmised.

This study included 24 adolescents, 13 of whom were normal weight and 11 of whom were obese. They all underwent anthropometric measurements with fasting glucose, insulin, C-peptide, HbA1c, and lipid levels. Exclusion criteria included a clinical diagnosis of sleep, behavioral, or dietary problems. The obese subjects also underwent a 180-minute glucose tolerance test.

Chronotype was assessed via actigraphy over 1 week to provide mid-sleep time on free days, and secondarily through administration to chronotype questionnaires – the Children’s ChronoType Questionnaire and the Morningness-Eveningness Scale for Children.

Among the normal-weight participants, 31% were morning and 23% evening chronotype (the rest being neutral chronotype), and, in the obese subjects, 27% were morning and 36% were evening chronotype.

The obese subjects were more likely to be in puberty, and had higher systolic blood pressures, higher fasting plasma insulin and levels of insulin resistance, as measured by Homeostatic Model Assessment of Insulin Resistance. Hemoglobin A1c tended to be higher in the obese subjects (P = .06), but fasting plasma glucose did not differ significantly between the obese and normal-weight participants (P = .68).

“We chose this population due to the shift from morningness to eveningness that occurs during adolescence followed by a progressive return to an intermediate or early chronotype at the end of adolescence,” Dr. Dumin said.

Bedtime, wake time, and total sleep time were nearly identical between the two groups (7.84 hours and 7.62 hours; P = .49), although sleep efficiency was numerically lower in the obese subjects (87.0 vs. 89.8; P = .14), while sleep fragmentation was somewhat greater (20.16 vs. 17.38; P = .18).

Dr. Dumin suggested that a continuation of her research with more patients would be useful.

This study is supported by the Endocrine Fellows Foundation and the University of Chicago Institute of Translational Medicine. Dr. Dumin reported having no financial disclosures.

 

– Late chronotype may have a deleterious impact on glucose homeostasis independent of obesity in preadolescents aged 10-13 years, according to a small study.

Late chronotype – or an individual’s preference for later sleep and food intake – is associated with higher body mass index (BMI), risk incidence of type 2 diabetes mellitus, hemoglobin A1c, and risk of hypertension in adults. It is also associated with higher BMI, lower dietary restraint, and lower HDL cholesterol in adolescents. This study was the first to focus on chronotype and glycemic control in children on the cusp of or in early puberty.

In participants tested during the summer months, the actigraphy-derived mid-sleep time on free days – an objective measure of chronotype – was associated positively with fasting plasma glucose (P = 0.048). “This is an important point because it highlights the objective measure of chronotype, whereas questionnaires can be more subjective,” said Magdalena Dumin, MD, at the annual meeting of Associated Professional Sleep Societies.

Dr. Magdalena Dumin, University of Chicago Medical Center
Debra L. Beck/Frontline Medical News
Dr. Magdalena Dumin
An additional finding included HbA1c having been positively associated with late chronotype questionnaire scores. This suggested “that a later chronotype has an adverse effect on glucose homeostasis,” reported Dr. Dumin, who was one of the investigators in this study and is a pediatric endocrinologist at the University of Chicago Medical Center. Furthermore, higher Children’s ChronoType Questionnaire scores (a more subjective indicator of eveningness) tended to be associated with higher plasma glucose.

The researcher also noted that higher sleep fragmentation and lower sleep efficiency were both associated with hyperglycemia and hyperinsulinemia, independent of obesity.

“Our preliminary findings suggest that having a late chronotype and less efficient and more fragmented sleep in pre- and early adolescence may have a deleterious glycemic impact independent of obesity and pubertal stage,” she said.

“Advancing bedtimes may reduce glucose levels in preadolescents and adolescents,” Dr. Dumin surmised.

This study included 24 adolescents, 13 of whom were normal weight and 11 of whom were obese. They all underwent anthropometric measurements with fasting glucose, insulin, C-peptide, HbA1c, and lipid levels. Exclusion criteria included a clinical diagnosis of sleep, behavioral, or dietary problems. The obese subjects also underwent a 180-minute glucose tolerance test.

Chronotype was assessed via actigraphy over 1 week to provide mid-sleep time on free days, and secondarily through administration to chronotype questionnaires – the Children’s ChronoType Questionnaire and the Morningness-Eveningness Scale for Children.

Among the normal-weight participants, 31% were morning and 23% evening chronotype (the rest being neutral chronotype), and, in the obese subjects, 27% were morning and 36% were evening chronotype.

The obese subjects were more likely to be in puberty, and had higher systolic blood pressures, higher fasting plasma insulin and levels of insulin resistance, as measured by Homeostatic Model Assessment of Insulin Resistance. Hemoglobin A1c tended to be higher in the obese subjects (P = .06), but fasting plasma glucose did not differ significantly between the obese and normal-weight participants (P = .68).

“We chose this population due to the shift from morningness to eveningness that occurs during adolescence followed by a progressive return to an intermediate or early chronotype at the end of adolescence,” Dr. Dumin said.

Bedtime, wake time, and total sleep time were nearly identical between the two groups (7.84 hours and 7.62 hours; P = .49), although sleep efficiency was numerically lower in the obese subjects (87.0 vs. 89.8; P = .14), while sleep fragmentation was somewhat greater (20.16 vs. 17.38; P = .18).

Dr. Dumin suggested that a continuation of her research with more patients would be useful.

This study is supported by the Endocrine Fellows Foundation and the University of Chicago Institute of Translational Medicine. Dr. Dumin reported having no financial disclosures.

Publications
Publications
Topics
Article Type
Sections
Article Source

AT SLEEP 2017

Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Vitals

 

Key clinical point: Preadolescents with a late chronotype show impaired glucose homeostasis independent of obesity.

Major finding: In participants tested during the summer months, the actigraphy-derived mid-sleep time on free days was positively associated with fasting plasma glucose (P = .048).

Data source: Observational study including 24 adolescents between 10 and 13 years of age. Thirteen were normal weight and 11 were obese.

Disclosures: Dr. Dumin reported having no financial disclosures. This study is supported by the Endocrine Fellows Foundation and the University of Chicago Institute of Translational Medicine.

Later school start tied to more sleep

Article Type
Changed
Sat, 12/08/2018 - 14:10

 

BOSTON – Teenagers slept more hours when they started school later, a new study found.

With 73% of high schoolers reporting receiving less than the recommended 8 hours of sleep per night, teens are among the most sleep-deprived members of society.

In this study, the later a teenager started school, the later he or she woke up, with average wake-up times having been just after 6:00 a.m. for those starting school between 7:00 and 7:30 a.m. and about 7:00 a.m. for those starting school after 8:30 a.m. But only those teens who started after 8:30 a.m. achieved the 8-hour recommended sleep duration, said Nicole Nahmod, during a presentation at the annual meeting of the Associated Professional Sleep Societies.

The students with the later school start times averaged 32 minutes of extra sleep, when compared with their early-rising colleagues, noted Ms. Nahmod, who is one of the study’s authors, a research technician, and study coordinator at Pennsylvania State University, Hershey. Specifically, adolescents who started school after 8:30 a.m. had a mean sleep duration of 8.1 hours, while those who started school earlier slept for only 7.5 hours a night.*

Nicole G. Nahmod
Nicole G. Nahmod
“Despite the teens with the earliest start times going to bed about 20 minutes before the other groups, they are still the most sleep-deprived group because of that 1-hour truncation in morning sleep,” Ms. Nahmod explained.

Acknowledging the importance of adequate sleep on teen health, mood, and school performance, the American Academy of Pediatrics recommends that middle schools and high schools begin at 8:30 a.m. or later. However, most school days start earlier than that, as evidenced by this dataset. While 72% of the study’s participants started school between 7:00 a.m. and 8:30 a.m., as many as 15% of the study participants began school during the narrower 7:00-7:30 a.m. window.

In this study, researchers from Penn State used data from 413 adolescents (mean age, 15.4 years; 46% male), who participated in a substudy of the Fragile Families & Child Wellbeing Study conducted across 20 large American cities. The study oversampled nonmarried pregnant mothers, resulting in a racially diverse sample and a high proportion of low-income families. The household income for 29% of the sample was below the poverty line.*

For this substudy, sleep duration was calculated from app-based daily diary reports of bed times, wake times, and school start times on days when a teen attended school.

The study was limited by its cross-sectional nature, but was enriched by a diverse range of school start times sampled from 20 U.S. cities, the high proportion of at-risk teens, and the use of a daily sleep diary.

“Current literature shows associations between later school start times and academic success, mood, and health. It also shows a decrease in motor vehicle accidents, tardiness, school dropout, and daytime sleepiness,” Ms. Nahmod noted.

Her continued research in this area involves analyzing the relationships between actigraphically assessed sleep measures in students and school start times.

Ms. Nahmod reported having no financial disclosures.

*This article was updated on June 6, 2017.

Meeting/Event
Publications
Topics
Sections
Meeting/Event
Meeting/Event

 

BOSTON – Teenagers slept more hours when they started school later, a new study found.

With 73% of high schoolers reporting receiving less than the recommended 8 hours of sleep per night, teens are among the most sleep-deprived members of society.

In this study, the later a teenager started school, the later he or she woke up, with average wake-up times having been just after 6:00 a.m. for those starting school between 7:00 and 7:30 a.m. and about 7:00 a.m. for those starting school after 8:30 a.m. But only those teens who started after 8:30 a.m. achieved the 8-hour recommended sleep duration, said Nicole Nahmod, during a presentation at the annual meeting of the Associated Professional Sleep Societies.

The students with the later school start times averaged 32 minutes of extra sleep, when compared with their early-rising colleagues, noted Ms. Nahmod, who is one of the study’s authors, a research technician, and study coordinator at Pennsylvania State University, Hershey. Specifically, adolescents who started school after 8:30 a.m. had a mean sleep duration of 8.1 hours, while those who started school earlier slept for only 7.5 hours a night.*

Nicole G. Nahmod
Nicole G. Nahmod
“Despite the teens with the earliest start times going to bed about 20 minutes before the other groups, they are still the most sleep-deprived group because of that 1-hour truncation in morning sleep,” Ms. Nahmod explained.

Acknowledging the importance of adequate sleep on teen health, mood, and school performance, the American Academy of Pediatrics recommends that middle schools and high schools begin at 8:30 a.m. or later. However, most school days start earlier than that, as evidenced by this dataset. While 72% of the study’s participants started school between 7:00 a.m. and 8:30 a.m., as many as 15% of the study participants began school during the narrower 7:00-7:30 a.m. window.

In this study, researchers from Penn State used data from 413 adolescents (mean age, 15.4 years; 46% male), who participated in a substudy of the Fragile Families & Child Wellbeing Study conducted across 20 large American cities. The study oversampled nonmarried pregnant mothers, resulting in a racially diverse sample and a high proportion of low-income families. The household income for 29% of the sample was below the poverty line.*

For this substudy, sleep duration was calculated from app-based daily diary reports of bed times, wake times, and school start times on days when a teen attended school.

The study was limited by its cross-sectional nature, but was enriched by a diverse range of school start times sampled from 20 U.S. cities, the high proportion of at-risk teens, and the use of a daily sleep diary.

“Current literature shows associations between later school start times and academic success, mood, and health. It also shows a decrease in motor vehicle accidents, tardiness, school dropout, and daytime sleepiness,” Ms. Nahmod noted.

Her continued research in this area involves analyzing the relationships between actigraphically assessed sleep measures in students and school start times.

Ms. Nahmod reported having no financial disclosures.

*This article was updated on June 6, 2017.

 

BOSTON – Teenagers slept more hours when they started school later, a new study found.

With 73% of high schoolers reporting receiving less than the recommended 8 hours of sleep per night, teens are among the most sleep-deprived members of society.

In this study, the later a teenager started school, the later he or she woke up, with average wake-up times having been just after 6:00 a.m. for those starting school between 7:00 and 7:30 a.m. and about 7:00 a.m. for those starting school after 8:30 a.m. But only those teens who started after 8:30 a.m. achieved the 8-hour recommended sleep duration, said Nicole Nahmod, during a presentation at the annual meeting of the Associated Professional Sleep Societies.

The students with the later school start times averaged 32 minutes of extra sleep, when compared with their early-rising colleagues, noted Ms. Nahmod, who is one of the study’s authors, a research technician, and study coordinator at Pennsylvania State University, Hershey. Specifically, adolescents who started school after 8:30 a.m. had a mean sleep duration of 8.1 hours, while those who started school earlier slept for only 7.5 hours a night.*

Nicole G. Nahmod
Nicole G. Nahmod
“Despite the teens with the earliest start times going to bed about 20 minutes before the other groups, they are still the most sleep-deprived group because of that 1-hour truncation in morning sleep,” Ms. Nahmod explained.

Acknowledging the importance of adequate sleep on teen health, mood, and school performance, the American Academy of Pediatrics recommends that middle schools and high schools begin at 8:30 a.m. or later. However, most school days start earlier than that, as evidenced by this dataset. While 72% of the study’s participants started school between 7:00 a.m. and 8:30 a.m., as many as 15% of the study participants began school during the narrower 7:00-7:30 a.m. window.

In this study, researchers from Penn State used data from 413 adolescents (mean age, 15.4 years; 46% male), who participated in a substudy of the Fragile Families & Child Wellbeing Study conducted across 20 large American cities. The study oversampled nonmarried pregnant mothers, resulting in a racially diverse sample and a high proportion of low-income families. The household income for 29% of the sample was below the poverty line.*

For this substudy, sleep duration was calculated from app-based daily diary reports of bed times, wake times, and school start times on days when a teen attended school.

The study was limited by its cross-sectional nature, but was enriched by a diverse range of school start times sampled from 20 U.S. cities, the high proportion of at-risk teens, and the use of a daily sleep diary.

“Current literature shows associations between later school start times and academic success, mood, and health. It also shows a decrease in motor vehicle accidents, tardiness, school dropout, and daytime sleepiness,” Ms. Nahmod noted.

Her continued research in this area involves analyzing the relationships between actigraphically assessed sleep measures in students and school start times.

Ms. Nahmod reported having no financial disclosures.

*This article was updated on June 6, 2017.

Publications
Publications
Topics
Article Type
Sections
Article Source

AT SLEEP 2017

Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Vitals

 

Key clinical point: Teenage students who start school after 8:30 a.m. are more likely to get the recommended 8 hours of sleep than are their counterparts with earlier start times.

Major finding: Adolescents who started school after 8:30 a.m. had a mean sleep duration of 8.1 hours, compared with 7.5 hours for students who started school earlier.

Data source: A national longitudinal birth cohort study of 413 adolescents.

Disclosures: Ms. Nahmod reported having no financial disclosures.

The USPSTF and screening for obstructive sleep apnea: Dispelling misconceptions

Article Type
Changed
Wed, 09/13/2017 - 14:36
Display Headline
The USPSTF and screening for obstructive sleep apnea: Dispelling misconceptions

Recent guidelines from the United States Preventive Services Task Force (USPSTF) say that there is insufficient evidence to recommend screening for obstructive sleep apnea in people who have no symptoms of it.1–3

The USPSTF committee systematically reviewed the evidence, sifting through 1,315 articles,3 and found no randomized controlled trials that compared screening with no screening in adults who have no symptoms (or no recognized symptoms) of obstructive sleep apnea. Conclusion: “The current evidence is insufficient to assess the balance of benefits and harms of screening for [obstructive sleep apnea] in asymptomatic adults.”1

This is logical, rigorous, and evidence-based. However, the conclusions might be misinterpreted and need to be put into context.

SCREENING IS WARRANTED IF PATIENTS HAVE SYMPTOMS

First, note that the USPSTF is referring to people who have no symptoms. The American Academy of Sleep Medicine has issued recommendations about screening and diagnostic testing in people who do have symptoms,4 in whom it is important to pursue screening and diagnostic testing.

Symptoms of obstructive sleep apnea include excessive daytime sleepiness, fatigue, drowsy driving, disrupted or fragmented sleep, nocturia, witnessed apnea, snoring, restless sleep, neurocognitive deficits, and depressed mood. Treating it improves these symptoms, as clinical trials have shown unequivocally and consistently.5

Moreover, the third edition of the International Classification of Sleep Disorders defines obstructive sleep apnea as an obstructive apnea-hypopnea index of 15 or more events per hour even in the absence of symptoms. This threshold recognizes the risk of adverse health outcomes observed in population-based studies (ie, in participants recruited irrespective of symptoms).6

ABSENCE OF EVIDENCE, NOT EVIDENCE OF ABSENCE

Second, the absence of sufficient evidence cited by the USPSTF does not necessarily mean that screening for obstructive sleep apnea in asymptomatic people is not beneficial—it has just not been systematically studied. There was insufficient evidence available to make a recommendation to allocate resources to screen all patients irrespective of symptoms.

The Sleep Heart Health Study suggested that few people with obstructive sleep apnea were diagnosed with it and that even fewer were treated for it.7 More recent data indicate that this underdiagnosis persists and is more pervasive in underserved minority groups.8,9

SCREENING VS CASE-FINDING

Moreover, screening is not the same as case-finding. The purpose of screening, as defined 50 years ago by Wilson and Jungner in a report for the World Health Organization, is “to discover those among the apparently well who are in fact suffering from disease.”10

Case-finding, on the other hand, focuses on those suspected of being at risk of the disease. In the case of obstructive sleep apnea, this is a lot of people. The overall prevalence of obstructive sleep apnea is about 26% by one estimate,11 and many more people have risk factors for it. For example, in one study, 69% of patients presenting to a primary care clinic were overweight or obese,12 and many primary care patients have diseases that obstructive sleep apnea can exacerbate. One can therefore argue that in clinical practice, testing for obstructive sleep apnea is more like case-finding than screening—most patients that you see have unrecognized symptoms of it or risk factors for it.

 

 

CRITERIA FOR A GOOD SCREENING TEST

Principles for screening outlined by Wilson and Jungner10 were:

  • The condition we are trying to detect should be important
  • There should be an accepted treatment for it
  • Facilities for diagnosis and treatment should be available
  • Testing should be acceptable to the population
  • There should be cost benefit to the expense of case-finding
  • There should be an agreed-upon policy on whom to treat as patients.

Screening for obstructive sleep apnea meets many of these criteria.

Obstructive sleep apnea is important

Solid evidence exists that obstructive sleep apnea exerts a bad effect on health and quality of life. Population-based studies that enrolled participants irrespective of symptoms indicate that the risk of death is about twice as high in those with severe obstructive sleep apnea as in those without, and treatment exerts benefit especially in those with cardiovascular risk.13,14 Therefore, the criterion for screening that says the disease must be important is met.

Pathophysiologic pathways by which obstructive sleep apnea causes harm include intermittent hypoxia, hypercapnia, intrathoracic pressure swings, and autonomic nervous system fluctuations. 

Treatment is beneficial

The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure recognized obstructive sleep apnea as a cause of hypertension.15

Treating obstructive sleep apnea lowers blood pressure, which in turn improves cardio­vascular outcomes. Effects are most pronounced in those with resistant hypertension. The reduction in blood pressure is only about 2 to 3 mm Hg, but this translates to a 4% to 8% reduction in future risk of stroke and coronary heart disease.16,17

The Continuous Positive Airway Pressure Treatment of Obstructive Sleep Apnea to Prevent Cardiovascular Disease multicenter randomized clinical trial investigated the impact of treating obstructive sleep apnea with continuous positive airway pressure (CPAP) compared with usual care.18 Although no statistically significant difference was seen in the composite cardiovascular outcome, propensity-score analysis in the subgroup adherent to CPAP demonstrated a lower composite of cerebral events in those who used CPAP for at least 4 hours a day.

The findings from this trial are difficult to interpret for several reasons. Adherence to CPAP was suboptimal, the severity of obstructive sleep apnea might not have been bad enough to permit observation of a significant treatment effect, and the generalizability of the findings is unclear, given that many of the participants were from underresourced regions.19

In a meta-analysis of cohort studies comprising more than 3 million participants, Fu et al found that the cardiovascular mortality rate was 63% lower in those with obstructive sleep apnea using CPAP than in untreated patients.20

APPLY CLINICAL JUDGMENT

Overall, the USPSTF report is intended to guide healthcare decision-makers. However, it includes a caveat to not substitute the findings for clinical judgment and to interpret the findings in the context of collateral pertinent information.2

Although no high-quality data exist to support or refute global screening for obstructive sleep apnea in the primary care setting, the high prevalence of this disease and its detrimental effects on health and quality of life if left untreated should not be dismissed.

Arguably, most patients who present to primary care clinics are not healthy, are not free of symptoms, and are at risk of obstructive sleep apnea because they are obese. Testing for it is therefore more like case-finding than screening.

In view of the serious consequences of obstructive sleep apnea, we should view the situation as an opportunity to examine the impact of screening. Perhaps using electronic medical records, we could collect sleep-specific measures, implement case-finding strategies, and perform pragmatic clinical trials to inform and guide optimal and cost-effective screening approaches.

Patients with common disorders such as obstructive sleep apnea are often considered asymptomatic until asked about symptoms. Therefore, careful review of systems incorporating sleep health is important, particularly as patients do not typically volunteer this information. Obtaining this history does not necessarily fall under the USPSTF’s recommendation not to screen.

Future efforts should focus on leveraging the electronic medical record platform to collect sleep-specific measures, implementing case-finding strategies, and performing pragmatic clinical trials in the primary care setting to inform and guide optimal and cost-effective approaches to screening.

References
  1. US Preventive Services Task Force, Bibbins-Domingo K, Grossman DC, Curry SJ, et al. Screening for obstructive sleep apnea in adults: US Preventive Services Task Force Recommendation Statement. JAMA 2017; 317:407–414.
  2. Jonas DE, Amick HR, Feltner C, et al. Screening for obstructive sleep apnea in adults: evidence report and systematic review for the US Preventive Services Task Force. JAMA 2017; 317:415–433.
  3. Jonas DE, Amick HR, Feltner C, et al. Screening for obstructive sleep apnea in adults: an evidence review for the U.S. Preventive Services Task Force. Evidence Synthesis No. 146. AHRQ Publication No. 14-05216-EF-1. Rockville, MD: Agency for Healthcare Research and Quality; 2017. www.uspreventiveservicestaskforce.org/Page/Document/final-evidence-review152/obstructive-sleep-apnea-in-adults-screening. Accessed May 2, 2017.
  4. Kapur VK, Auckley DH, Chowdhuri S, et al. Clinical practice guideline for diagnostic testing for adult obstructive sleep apnea: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med 2017; 13:479–504.
  5. Patel SR, White DP, Malhotra A, Stanchina ML, Ayas NT. Continuous positive airway pressure therapy for treating sleepiness in a diverse population with obstructive sleep apnea: results of a meta-analysis. Arch Intern Med 2003; 163:565–571.
  6. American Academy of Sleep Medicine. International Classification of Sleep Disorders, 3rd ed. Darien, IL: American Academy of Sleep Medicine; 2014.
  7. Kapur V, Strohl KP, Redline S, Iber C, O’Connor G, Nieto J. Underdiagnosis of sleep apnea syndrome in U.S. communities. Sleep Breath 2002; 6:49–54.
  8. Chen X, Wang R, Zee P, et al. Racial/ethnic differences in sleep disturbances: the Multi-Ethnic Study of Atherosclerosis (MESA). Sleep 2015; 38:877–888.
  9. Redline S, Sotres-Alvarez D, Loredo J, et al. Sleep-disordered breathing in Hispanic/Latino individuals of diverse backgrounds. The Hispanic Community Health Study/Study of Latinos. Am J Respir Crit Care Med 2014; 189:335–344.
  10. Wilson JMG, Jungner G. Principles and practice of screening for disease. Geneva: WHO; 1968. www.who.int/ionizing_radiation/medical_radiation_exposure/munich-WHO-1968-Screening-Disease.pdf?ua=1. Accessed May 2, 2017.
  11. Peppard PE, Young T, Barnet JH, Palta M, Hagen EW, Hla KM. Increased prevalence of sleep-disordered breathing in adults. Am J Epidemiol 2013; 177:1006–1014.
  12. Stecker T, Sparks S. Prevalence of obese patients in a primary care setting. Obesity (Silver Spring) 2006; 14:373–376.
  13. Zhao YY, Wang R, Gleason KJ, et al; BestAIR Investigators. Effect of continuous positive airway pressure treatment on health-related quality of life and sleepiness in high cardiovascular risk individuals with sleep apnea: Best Apnea Interventions for Research (BestAIR) Trial. Sleep 2017; Apr 17. doi: 10.1093/sleep/zsx040. [Epub ahead of print].
  14. Punjabi NM, Caffo BS, Goodwin JL, et al. Sleep-disordered breathing and mortality: a prospective cohort study. PLoS Med 2009 Aug;6(8) e1000132. doi: 10.1371/journal.pmed.1000132. Epub 2009 Aug 18.
  15. Chobanian AV, Bakris GL, Black HR, et al. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA 2003; 289:2560–2572.
  16. Schein AS, Kerkhoff AC, Coronel CC, Plentz RD, Sbruzzi G. Continuous positive airway pressure reduces blood pressure in patients with obstructive sleep apnea; a systematic review and meta-analysis with 1000 patients. J Hypertens 2014; 32:1762–1773.
  17. He J, Whelton PK. Elevated systolic blood pressure and risk of cardiovascular and renal disease: overview of evidence from observational epidemiologic studies and randomized controlled trials. Am Heart J 1999; 138:211–219.
  18. McEvoy RD, Antic NA, Heeley E, et al. CPAP for prevention of cardiovascular events in obstructive sleep apnea. N Engl J Med 2016; 375:919–931.
  19. Javaheri S, Barbe F, Campos-Rodriguez F, et al. Sleep apnea: types, mechanisms, and clinical cardiovascular consequences. J Am Coll Cardiol 2017; 69:841–858.
  20. Fu Y, Xia Y, Yi H, Xu H, Guan J, Yin S. Meta-analysis of all-cause and cardiovascular mortality in obstructive sleep apnea with or without continuous positive airway pressure treatment. Sleep Breath 2017; 21:181–189.
Article PDF
Author and Disclosure Information

Reena Mehra, MD, MS, FCCP, FAASM
Sleep Disorders Center, Neurologic Institute; Heart and Vascular Institute and Department of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic; Associate Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Nancy Foldvary-Schaefer, DO, MS
Sleep Disorders Center, Neurologic Institute, Cleveland Clinic; Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Address: Reena Mehra, MD, Cleveland Clinic Sleep Disorders Center at Fairhill, 11203 Stokes Boulevard, Cleveland, OH 44104; mehrar@ccf.org

Issue
Cleveland Clinic Journal of Medicine - 84(6)
Publications
Topics
Page Number
429-431
Legacy Keywords
sleep, US Preventive Services Task Force, USPSTF, screening, obstructive sleep apnea, OSA, continuous positive airway pressure, CPAP, Reena Mehra, Nancy Foldvary-Schaefer
Sections
Author and Disclosure Information

Reena Mehra, MD, MS, FCCP, FAASM
Sleep Disorders Center, Neurologic Institute; Heart and Vascular Institute and Department of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic; Associate Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Nancy Foldvary-Schaefer, DO, MS
Sleep Disorders Center, Neurologic Institute, Cleveland Clinic; Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Address: Reena Mehra, MD, Cleveland Clinic Sleep Disorders Center at Fairhill, 11203 Stokes Boulevard, Cleveland, OH 44104; mehrar@ccf.org

Author and Disclosure Information

Reena Mehra, MD, MS, FCCP, FAASM
Sleep Disorders Center, Neurologic Institute; Heart and Vascular Institute and Department of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic; Associate Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Nancy Foldvary-Schaefer, DO, MS
Sleep Disorders Center, Neurologic Institute, Cleveland Clinic; Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Address: Reena Mehra, MD, Cleveland Clinic Sleep Disorders Center at Fairhill, 11203 Stokes Boulevard, Cleveland, OH 44104; mehrar@ccf.org

Article PDF
Article PDF
Related Articles

Recent guidelines from the United States Preventive Services Task Force (USPSTF) say that there is insufficient evidence to recommend screening for obstructive sleep apnea in people who have no symptoms of it.1–3

The USPSTF committee systematically reviewed the evidence, sifting through 1,315 articles,3 and found no randomized controlled trials that compared screening with no screening in adults who have no symptoms (or no recognized symptoms) of obstructive sleep apnea. Conclusion: “The current evidence is insufficient to assess the balance of benefits and harms of screening for [obstructive sleep apnea] in asymptomatic adults.”1

This is logical, rigorous, and evidence-based. However, the conclusions might be misinterpreted and need to be put into context.

SCREENING IS WARRANTED IF PATIENTS HAVE SYMPTOMS

First, note that the USPSTF is referring to people who have no symptoms. The American Academy of Sleep Medicine has issued recommendations about screening and diagnostic testing in people who do have symptoms,4 in whom it is important to pursue screening and diagnostic testing.

Symptoms of obstructive sleep apnea include excessive daytime sleepiness, fatigue, drowsy driving, disrupted or fragmented sleep, nocturia, witnessed apnea, snoring, restless sleep, neurocognitive deficits, and depressed mood. Treating it improves these symptoms, as clinical trials have shown unequivocally and consistently.5

Moreover, the third edition of the International Classification of Sleep Disorders defines obstructive sleep apnea as an obstructive apnea-hypopnea index of 15 or more events per hour even in the absence of symptoms. This threshold recognizes the risk of adverse health outcomes observed in population-based studies (ie, in participants recruited irrespective of symptoms).6

ABSENCE OF EVIDENCE, NOT EVIDENCE OF ABSENCE

Second, the absence of sufficient evidence cited by the USPSTF does not necessarily mean that screening for obstructive sleep apnea in asymptomatic people is not beneficial—it has just not been systematically studied. There was insufficient evidence available to make a recommendation to allocate resources to screen all patients irrespective of symptoms.

The Sleep Heart Health Study suggested that few people with obstructive sleep apnea were diagnosed with it and that even fewer were treated for it.7 More recent data indicate that this underdiagnosis persists and is more pervasive in underserved minority groups.8,9

SCREENING VS CASE-FINDING

Moreover, screening is not the same as case-finding. The purpose of screening, as defined 50 years ago by Wilson and Jungner in a report for the World Health Organization, is “to discover those among the apparently well who are in fact suffering from disease.”10

Case-finding, on the other hand, focuses on those suspected of being at risk of the disease. In the case of obstructive sleep apnea, this is a lot of people. The overall prevalence of obstructive sleep apnea is about 26% by one estimate,11 and many more people have risk factors for it. For example, in one study, 69% of patients presenting to a primary care clinic were overweight or obese,12 and many primary care patients have diseases that obstructive sleep apnea can exacerbate. One can therefore argue that in clinical practice, testing for obstructive sleep apnea is more like case-finding than screening—most patients that you see have unrecognized symptoms of it or risk factors for it.

 

 

CRITERIA FOR A GOOD SCREENING TEST

Principles for screening outlined by Wilson and Jungner10 were:

  • The condition we are trying to detect should be important
  • There should be an accepted treatment for it
  • Facilities for diagnosis and treatment should be available
  • Testing should be acceptable to the population
  • There should be cost benefit to the expense of case-finding
  • There should be an agreed-upon policy on whom to treat as patients.

Screening for obstructive sleep apnea meets many of these criteria.

Obstructive sleep apnea is important

Solid evidence exists that obstructive sleep apnea exerts a bad effect on health and quality of life. Population-based studies that enrolled participants irrespective of symptoms indicate that the risk of death is about twice as high in those with severe obstructive sleep apnea as in those without, and treatment exerts benefit especially in those with cardiovascular risk.13,14 Therefore, the criterion for screening that says the disease must be important is met.

Pathophysiologic pathways by which obstructive sleep apnea causes harm include intermittent hypoxia, hypercapnia, intrathoracic pressure swings, and autonomic nervous system fluctuations. 

Treatment is beneficial

The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure recognized obstructive sleep apnea as a cause of hypertension.15

Treating obstructive sleep apnea lowers blood pressure, which in turn improves cardio­vascular outcomes. Effects are most pronounced in those with resistant hypertension. The reduction in blood pressure is only about 2 to 3 mm Hg, but this translates to a 4% to 8% reduction in future risk of stroke and coronary heart disease.16,17

The Continuous Positive Airway Pressure Treatment of Obstructive Sleep Apnea to Prevent Cardiovascular Disease multicenter randomized clinical trial investigated the impact of treating obstructive sleep apnea with continuous positive airway pressure (CPAP) compared with usual care.18 Although no statistically significant difference was seen in the composite cardiovascular outcome, propensity-score analysis in the subgroup adherent to CPAP demonstrated a lower composite of cerebral events in those who used CPAP for at least 4 hours a day.

The findings from this trial are difficult to interpret for several reasons. Adherence to CPAP was suboptimal, the severity of obstructive sleep apnea might not have been bad enough to permit observation of a significant treatment effect, and the generalizability of the findings is unclear, given that many of the participants were from underresourced regions.19

In a meta-analysis of cohort studies comprising more than 3 million participants, Fu et al found that the cardiovascular mortality rate was 63% lower in those with obstructive sleep apnea using CPAP than in untreated patients.20

APPLY CLINICAL JUDGMENT

Overall, the USPSTF report is intended to guide healthcare decision-makers. However, it includes a caveat to not substitute the findings for clinical judgment and to interpret the findings in the context of collateral pertinent information.2

Although no high-quality data exist to support or refute global screening for obstructive sleep apnea in the primary care setting, the high prevalence of this disease and its detrimental effects on health and quality of life if left untreated should not be dismissed.

Arguably, most patients who present to primary care clinics are not healthy, are not free of symptoms, and are at risk of obstructive sleep apnea because they are obese. Testing for it is therefore more like case-finding than screening.

In view of the serious consequences of obstructive sleep apnea, we should view the situation as an opportunity to examine the impact of screening. Perhaps using electronic medical records, we could collect sleep-specific measures, implement case-finding strategies, and perform pragmatic clinical trials to inform and guide optimal and cost-effective screening approaches.

Patients with common disorders such as obstructive sleep apnea are often considered asymptomatic until asked about symptoms. Therefore, careful review of systems incorporating sleep health is important, particularly as patients do not typically volunteer this information. Obtaining this history does not necessarily fall under the USPSTF’s recommendation not to screen.

Future efforts should focus on leveraging the electronic medical record platform to collect sleep-specific measures, implementing case-finding strategies, and performing pragmatic clinical trials in the primary care setting to inform and guide optimal and cost-effective approaches to screening.

Recent guidelines from the United States Preventive Services Task Force (USPSTF) say that there is insufficient evidence to recommend screening for obstructive sleep apnea in people who have no symptoms of it.1–3

The USPSTF committee systematically reviewed the evidence, sifting through 1,315 articles,3 and found no randomized controlled trials that compared screening with no screening in adults who have no symptoms (or no recognized symptoms) of obstructive sleep apnea. Conclusion: “The current evidence is insufficient to assess the balance of benefits and harms of screening for [obstructive sleep apnea] in asymptomatic adults.”1

This is logical, rigorous, and evidence-based. However, the conclusions might be misinterpreted and need to be put into context.

SCREENING IS WARRANTED IF PATIENTS HAVE SYMPTOMS

First, note that the USPSTF is referring to people who have no symptoms. The American Academy of Sleep Medicine has issued recommendations about screening and diagnostic testing in people who do have symptoms,4 in whom it is important to pursue screening and diagnostic testing.

Symptoms of obstructive sleep apnea include excessive daytime sleepiness, fatigue, drowsy driving, disrupted or fragmented sleep, nocturia, witnessed apnea, snoring, restless sleep, neurocognitive deficits, and depressed mood. Treating it improves these symptoms, as clinical trials have shown unequivocally and consistently.5

Moreover, the third edition of the International Classification of Sleep Disorders defines obstructive sleep apnea as an obstructive apnea-hypopnea index of 15 or more events per hour even in the absence of symptoms. This threshold recognizes the risk of adverse health outcomes observed in population-based studies (ie, in participants recruited irrespective of symptoms).6

ABSENCE OF EVIDENCE, NOT EVIDENCE OF ABSENCE

Second, the absence of sufficient evidence cited by the USPSTF does not necessarily mean that screening for obstructive sleep apnea in asymptomatic people is not beneficial—it has just not been systematically studied. There was insufficient evidence available to make a recommendation to allocate resources to screen all patients irrespective of symptoms.

The Sleep Heart Health Study suggested that few people with obstructive sleep apnea were diagnosed with it and that even fewer were treated for it.7 More recent data indicate that this underdiagnosis persists and is more pervasive in underserved minority groups.8,9

SCREENING VS CASE-FINDING

Moreover, screening is not the same as case-finding. The purpose of screening, as defined 50 years ago by Wilson and Jungner in a report for the World Health Organization, is “to discover those among the apparently well who are in fact suffering from disease.”10

Case-finding, on the other hand, focuses on those suspected of being at risk of the disease. In the case of obstructive sleep apnea, this is a lot of people. The overall prevalence of obstructive sleep apnea is about 26% by one estimate,11 and many more people have risk factors for it. For example, in one study, 69% of patients presenting to a primary care clinic were overweight or obese,12 and many primary care patients have diseases that obstructive sleep apnea can exacerbate. One can therefore argue that in clinical practice, testing for obstructive sleep apnea is more like case-finding than screening—most patients that you see have unrecognized symptoms of it or risk factors for it.

 

 

CRITERIA FOR A GOOD SCREENING TEST

Principles for screening outlined by Wilson and Jungner10 were:

  • The condition we are trying to detect should be important
  • There should be an accepted treatment for it
  • Facilities for diagnosis and treatment should be available
  • Testing should be acceptable to the population
  • There should be cost benefit to the expense of case-finding
  • There should be an agreed-upon policy on whom to treat as patients.

Screening for obstructive sleep apnea meets many of these criteria.

Obstructive sleep apnea is important

Solid evidence exists that obstructive sleep apnea exerts a bad effect on health and quality of life. Population-based studies that enrolled participants irrespective of symptoms indicate that the risk of death is about twice as high in those with severe obstructive sleep apnea as in those without, and treatment exerts benefit especially in those with cardiovascular risk.13,14 Therefore, the criterion for screening that says the disease must be important is met.

Pathophysiologic pathways by which obstructive sleep apnea causes harm include intermittent hypoxia, hypercapnia, intrathoracic pressure swings, and autonomic nervous system fluctuations. 

Treatment is beneficial

The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure recognized obstructive sleep apnea as a cause of hypertension.15

Treating obstructive sleep apnea lowers blood pressure, which in turn improves cardio­vascular outcomes. Effects are most pronounced in those with resistant hypertension. The reduction in blood pressure is only about 2 to 3 mm Hg, but this translates to a 4% to 8% reduction in future risk of stroke and coronary heart disease.16,17

The Continuous Positive Airway Pressure Treatment of Obstructive Sleep Apnea to Prevent Cardiovascular Disease multicenter randomized clinical trial investigated the impact of treating obstructive sleep apnea with continuous positive airway pressure (CPAP) compared with usual care.18 Although no statistically significant difference was seen in the composite cardiovascular outcome, propensity-score analysis in the subgroup adherent to CPAP demonstrated a lower composite of cerebral events in those who used CPAP for at least 4 hours a day.

The findings from this trial are difficult to interpret for several reasons. Adherence to CPAP was suboptimal, the severity of obstructive sleep apnea might not have been bad enough to permit observation of a significant treatment effect, and the generalizability of the findings is unclear, given that many of the participants were from underresourced regions.19

In a meta-analysis of cohort studies comprising more than 3 million participants, Fu et al found that the cardiovascular mortality rate was 63% lower in those with obstructive sleep apnea using CPAP than in untreated patients.20

APPLY CLINICAL JUDGMENT

Overall, the USPSTF report is intended to guide healthcare decision-makers. However, it includes a caveat to not substitute the findings for clinical judgment and to interpret the findings in the context of collateral pertinent information.2

Although no high-quality data exist to support or refute global screening for obstructive sleep apnea in the primary care setting, the high prevalence of this disease and its detrimental effects on health and quality of life if left untreated should not be dismissed.

Arguably, most patients who present to primary care clinics are not healthy, are not free of symptoms, and are at risk of obstructive sleep apnea because they are obese. Testing for it is therefore more like case-finding than screening.

In view of the serious consequences of obstructive sleep apnea, we should view the situation as an opportunity to examine the impact of screening. Perhaps using electronic medical records, we could collect sleep-specific measures, implement case-finding strategies, and perform pragmatic clinical trials to inform and guide optimal and cost-effective screening approaches.

Patients with common disorders such as obstructive sleep apnea are often considered asymptomatic until asked about symptoms. Therefore, careful review of systems incorporating sleep health is important, particularly as patients do not typically volunteer this information. Obtaining this history does not necessarily fall under the USPSTF’s recommendation not to screen.

Future efforts should focus on leveraging the electronic medical record platform to collect sleep-specific measures, implementing case-finding strategies, and performing pragmatic clinical trials in the primary care setting to inform and guide optimal and cost-effective approaches to screening.

References
  1. US Preventive Services Task Force, Bibbins-Domingo K, Grossman DC, Curry SJ, et al. Screening for obstructive sleep apnea in adults: US Preventive Services Task Force Recommendation Statement. JAMA 2017; 317:407–414.
  2. Jonas DE, Amick HR, Feltner C, et al. Screening for obstructive sleep apnea in adults: evidence report and systematic review for the US Preventive Services Task Force. JAMA 2017; 317:415–433.
  3. Jonas DE, Amick HR, Feltner C, et al. Screening for obstructive sleep apnea in adults: an evidence review for the U.S. Preventive Services Task Force. Evidence Synthesis No. 146. AHRQ Publication No. 14-05216-EF-1. Rockville, MD: Agency for Healthcare Research and Quality; 2017. www.uspreventiveservicestaskforce.org/Page/Document/final-evidence-review152/obstructive-sleep-apnea-in-adults-screening. Accessed May 2, 2017.
  4. Kapur VK, Auckley DH, Chowdhuri S, et al. Clinical practice guideline for diagnostic testing for adult obstructive sleep apnea: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med 2017; 13:479–504.
  5. Patel SR, White DP, Malhotra A, Stanchina ML, Ayas NT. Continuous positive airway pressure therapy for treating sleepiness in a diverse population with obstructive sleep apnea: results of a meta-analysis. Arch Intern Med 2003; 163:565–571.
  6. American Academy of Sleep Medicine. International Classification of Sleep Disorders, 3rd ed. Darien, IL: American Academy of Sleep Medicine; 2014.
  7. Kapur V, Strohl KP, Redline S, Iber C, O’Connor G, Nieto J. Underdiagnosis of sleep apnea syndrome in U.S. communities. Sleep Breath 2002; 6:49–54.
  8. Chen X, Wang R, Zee P, et al. Racial/ethnic differences in sleep disturbances: the Multi-Ethnic Study of Atherosclerosis (MESA). Sleep 2015; 38:877–888.
  9. Redline S, Sotres-Alvarez D, Loredo J, et al. Sleep-disordered breathing in Hispanic/Latino individuals of diverse backgrounds. The Hispanic Community Health Study/Study of Latinos. Am J Respir Crit Care Med 2014; 189:335–344.
  10. Wilson JMG, Jungner G. Principles and practice of screening for disease. Geneva: WHO; 1968. www.who.int/ionizing_radiation/medical_radiation_exposure/munich-WHO-1968-Screening-Disease.pdf?ua=1. Accessed May 2, 2017.
  11. Peppard PE, Young T, Barnet JH, Palta M, Hagen EW, Hla KM. Increased prevalence of sleep-disordered breathing in adults. Am J Epidemiol 2013; 177:1006–1014.
  12. Stecker T, Sparks S. Prevalence of obese patients in a primary care setting. Obesity (Silver Spring) 2006; 14:373–376.
  13. Zhao YY, Wang R, Gleason KJ, et al; BestAIR Investigators. Effect of continuous positive airway pressure treatment on health-related quality of life and sleepiness in high cardiovascular risk individuals with sleep apnea: Best Apnea Interventions for Research (BestAIR) Trial. Sleep 2017; Apr 17. doi: 10.1093/sleep/zsx040. [Epub ahead of print].
  14. Punjabi NM, Caffo BS, Goodwin JL, et al. Sleep-disordered breathing and mortality: a prospective cohort study. PLoS Med 2009 Aug;6(8) e1000132. doi: 10.1371/journal.pmed.1000132. Epub 2009 Aug 18.
  15. Chobanian AV, Bakris GL, Black HR, et al. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA 2003; 289:2560–2572.
  16. Schein AS, Kerkhoff AC, Coronel CC, Plentz RD, Sbruzzi G. Continuous positive airway pressure reduces blood pressure in patients with obstructive sleep apnea; a systematic review and meta-analysis with 1000 patients. J Hypertens 2014; 32:1762–1773.
  17. He J, Whelton PK. Elevated systolic blood pressure and risk of cardiovascular and renal disease: overview of evidence from observational epidemiologic studies and randomized controlled trials. Am Heart J 1999; 138:211–219.
  18. McEvoy RD, Antic NA, Heeley E, et al. CPAP for prevention of cardiovascular events in obstructive sleep apnea. N Engl J Med 2016; 375:919–931.
  19. Javaheri S, Barbe F, Campos-Rodriguez F, et al. Sleep apnea: types, mechanisms, and clinical cardiovascular consequences. J Am Coll Cardiol 2017; 69:841–858.
  20. Fu Y, Xia Y, Yi H, Xu H, Guan J, Yin S. Meta-analysis of all-cause and cardiovascular mortality in obstructive sleep apnea with or without continuous positive airway pressure treatment. Sleep Breath 2017; 21:181–189.
References
  1. US Preventive Services Task Force, Bibbins-Domingo K, Grossman DC, Curry SJ, et al. Screening for obstructive sleep apnea in adults: US Preventive Services Task Force Recommendation Statement. JAMA 2017; 317:407–414.
  2. Jonas DE, Amick HR, Feltner C, et al. Screening for obstructive sleep apnea in adults: evidence report and systematic review for the US Preventive Services Task Force. JAMA 2017; 317:415–433.
  3. Jonas DE, Amick HR, Feltner C, et al. Screening for obstructive sleep apnea in adults: an evidence review for the U.S. Preventive Services Task Force. Evidence Synthesis No. 146. AHRQ Publication No. 14-05216-EF-1. Rockville, MD: Agency for Healthcare Research and Quality; 2017. www.uspreventiveservicestaskforce.org/Page/Document/final-evidence-review152/obstructive-sleep-apnea-in-adults-screening. Accessed May 2, 2017.
  4. Kapur VK, Auckley DH, Chowdhuri S, et al. Clinical practice guideline for diagnostic testing for adult obstructive sleep apnea: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med 2017; 13:479–504.
  5. Patel SR, White DP, Malhotra A, Stanchina ML, Ayas NT. Continuous positive airway pressure therapy for treating sleepiness in a diverse population with obstructive sleep apnea: results of a meta-analysis. Arch Intern Med 2003; 163:565–571.
  6. American Academy of Sleep Medicine. International Classification of Sleep Disorders, 3rd ed. Darien, IL: American Academy of Sleep Medicine; 2014.
  7. Kapur V, Strohl KP, Redline S, Iber C, O’Connor G, Nieto J. Underdiagnosis of sleep apnea syndrome in U.S. communities. Sleep Breath 2002; 6:49–54.
  8. Chen X, Wang R, Zee P, et al. Racial/ethnic differences in sleep disturbances: the Multi-Ethnic Study of Atherosclerosis (MESA). Sleep 2015; 38:877–888.
  9. Redline S, Sotres-Alvarez D, Loredo J, et al. Sleep-disordered breathing in Hispanic/Latino individuals of diverse backgrounds. The Hispanic Community Health Study/Study of Latinos. Am J Respir Crit Care Med 2014; 189:335–344.
  10. Wilson JMG, Jungner G. Principles and practice of screening for disease. Geneva: WHO; 1968. www.who.int/ionizing_radiation/medical_radiation_exposure/munich-WHO-1968-Screening-Disease.pdf?ua=1. Accessed May 2, 2017.
  11. Peppard PE, Young T, Barnet JH, Palta M, Hagen EW, Hla KM. Increased prevalence of sleep-disordered breathing in adults. Am J Epidemiol 2013; 177:1006–1014.
  12. Stecker T, Sparks S. Prevalence of obese patients in a primary care setting. Obesity (Silver Spring) 2006; 14:373–376.
  13. Zhao YY, Wang R, Gleason KJ, et al; BestAIR Investigators. Effect of continuous positive airway pressure treatment on health-related quality of life and sleepiness in high cardiovascular risk individuals with sleep apnea: Best Apnea Interventions for Research (BestAIR) Trial. Sleep 2017; Apr 17. doi: 10.1093/sleep/zsx040. [Epub ahead of print].
  14. Punjabi NM, Caffo BS, Goodwin JL, et al. Sleep-disordered breathing and mortality: a prospective cohort study. PLoS Med 2009 Aug;6(8) e1000132. doi: 10.1371/journal.pmed.1000132. Epub 2009 Aug 18.
  15. Chobanian AV, Bakris GL, Black HR, et al. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA 2003; 289:2560–2572.
  16. Schein AS, Kerkhoff AC, Coronel CC, Plentz RD, Sbruzzi G. Continuous positive airway pressure reduces blood pressure in patients with obstructive sleep apnea; a systematic review and meta-analysis with 1000 patients. J Hypertens 2014; 32:1762–1773.
  17. He J, Whelton PK. Elevated systolic blood pressure and risk of cardiovascular and renal disease: overview of evidence from observational epidemiologic studies and randomized controlled trials. Am Heart J 1999; 138:211–219.
  18. McEvoy RD, Antic NA, Heeley E, et al. CPAP for prevention of cardiovascular events in obstructive sleep apnea. N Engl J Med 2016; 375:919–931.
  19. Javaheri S, Barbe F, Campos-Rodriguez F, et al. Sleep apnea: types, mechanisms, and clinical cardiovascular consequences. J Am Coll Cardiol 2017; 69:841–858.
  20. Fu Y, Xia Y, Yi H, Xu H, Guan J, Yin S. Meta-analysis of all-cause and cardiovascular mortality in obstructive sleep apnea with or without continuous positive airway pressure treatment. Sleep Breath 2017; 21:181–189.
Issue
Cleveland Clinic Journal of Medicine - 84(6)
Issue
Cleveland Clinic Journal of Medicine - 84(6)
Page Number
429-431
Page Number
429-431
Publications
Publications
Topics
Article Type
Display Headline
The USPSTF and screening for obstructive sleep apnea: Dispelling misconceptions
Display Headline
The USPSTF and screening for obstructive sleep apnea: Dispelling misconceptions
Legacy Keywords
sleep, US Preventive Services Task Force, USPSTF, screening, obstructive sleep apnea, OSA, continuous positive airway pressure, CPAP, Reena Mehra, Nancy Foldvary-Schaefer
Legacy Keywords
sleep, US Preventive Services Task Force, USPSTF, screening, obstructive sleep apnea, OSA, continuous positive airway pressure, CPAP, Reena Mehra, Nancy Foldvary-Schaefer
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Article PDF Media

Apps and fitness trackers that measure sleep: Are they useful?

Article Type
Changed
Mon, 07/31/2017 - 10:14
Display Headline
Apps and fitness trackers that measure sleep: Are they useful?

More and more consumers are using wearable devices and smartphones to monitor and measure various body functions, including sleep. Many patients now present their providers with sleep data obtained from their phones and other devices. But can these devices provide valid, useful clinical information?

This article describes common sleep tracking devices available to consumers and the mechanisms the devices probably use to distinguish sleep from wakefulness (their algorithms are secret), the studies evaluating the validity of device manufacturers’ claims, and their clinical utility and limitations.

DEVICES ARE COMMON

Close to 1 in 10 adults over age 18 owns an activity tracker, and sales are projected to reach $50 billion by 2018.1 Even more impressive, close to 69% of Americans own a smartphone,1 and more than half use it as an alarm clock.2

At the same time that these devices have become so popular, sleep medicine has come of age, and experts have been pushing to improve people’s sleep and increase awareness of sleep disorders.3,4 While the technology has significantly advanced, adoption of data from these devices for clinical evaluation has been limited. Studies examining the validity of these devices have only recently been conducted, and companies that make the devices have not been forthcoming with details of the specific algorithms they use to tell if the patient is asleep or awake or what stage of sleep the patient is in.

WHAT ARE THESE DEVICES?

Consumer tracking devices that claim to measure sleep are easily available for purchase and include wearable fitness trackers such as Fitbit, Jawbone UP, and Nike+ Fuelband. Other sleep tracking devices are catalogued by Ko et al.5 Various smartphone applications (apps) are also available.

Fitness trackers, usually worn as a wrist band, are primarily designed to measure movement and activity, but manufacturers now claim the trackers can also measure sleep. Collected data are available for the user to review the following day. In most cases, these trackers display sleep and wake times; others also claim to record sound sleep, light sleep, and the number and duration of awakenings. Most fitness trackers have complementary apps available for download that graphically display the data on smartphones and interact with social media to allow users to post their sleep and activity data.

More than 500 sleep-related apps are available for download to smartphones in the iTunes app store5; the Sleep Cycle alarm clock app was among the top 5 sleep-tracking apps downloaded in 2014.6 Because sleep data collection relies on the smartphone being placed on the user’s mattress, movements of bed partners, pets, and bedding may interfere with results. In most cases, the apps display data in a format similar to that of fitness trackers. Some claim to determine the optimal sleep phase for the alarm to wake the user.

HOW DOES THE TECHNOLOGY WORK?

Older activity-tracking devices used single-channel electroencephalographic recordings or multiple physiologic channels such as galvanic skin response, skin temperature, and heat flux to measure activity to determine transitions between periods of sleep and wakefulness.7,8

None of the currently available consumer sleep tracking devices discloses the exact mechanisms used to measure sleep and wakefulness, but most appear to rely on 3-axis accelerometers,9 ie, microelectromechanical devices that measure front-to-back, side-to-side, and up-and-down motion and convert the data into an activity count. Activity counts are acquired over 30- or 60-second intervals and are entered into algorithms that determine if the pattern indicates that the patient is awake or asleep. This is the same method that actigraphy uses to evaluate sleep, but most actigraphs used in medicine disclose their mechanisms and provide clinicians with the option of using various validated algorithms to classify the activity counts into sleep or awake periods.9–11

 

 

ARE THE MEASURES VALID?

Only a few studies have examined the validity and accuracy of current fitness trackers and apps for measuring sleep.

The available studies are difficult to compare; most have been small and used different actigraphy devices for comparison. Some tested healthy volunteers, others included people with suspected or confirmed sleep disorders, and some had both types of participants. In many studies, the device was compared with polysomnography for only 1 night, making the “first-night effect” likely to be a confounding factor, as people tend to sleep worse during the first night of testing. Technical failures for the devices were noted in some studies.12 In addition, some currently used apps may use different platforms than the devices used in these studies, limiting the extrapolation of results.

Two fitness tracking devices (Fitbit13,14  and Jawbone UP15–17) were compared with polysomnography and actigraphy in several studies in children and adults (Table 1). The devices tended to overestimate sleeping time, sleep efficiency, and latency to sleep onset and underestimate awake time after falling asleep. Some studies noted that differences were more pronounced for those with the most disturbed sleep.

As with fitness trackers, few studies have been done to examine the validity of smartphone apps.5 Findings of 3 studies are summarized in Table 2.17–19 In addition to tracking the duration and depth of sleep, some apps purport to detect snoring, sleep apnea, and periodic limb movements of sleep. Discussion of these apps is beyond the scope of this review.

In general, sleep tracking devices are fair to good at detecting sleep but poor at determining wakefulness. They are inaccurate for determining absolute sleep parameters (ie, total sleep time, sleep efficiency, wake time after sleep onset, and sleep onset latency) and in distinguishing the different sleep stages compared to polysomnography. Age-related differences have been found between consumer sleep devices compared with polysomnography and actigraphy-derived measures; because adults are likelier to lie still when awake, activity monitors are prone to overestimate sleep time in adults. Comparisons in patients with sleep apnea are conflicting.12,15 Claims that the “sensitive” mode may be appropriate for users with sleep disorders are thus far unsubstantiated.

ARE THE DEVICES CLINICALLY USEFUL?

Although a thorough history remains the cornerstone of a good evaluation of sleep problems, testing is sometimes essential, and in certain situations, objective data can complement the history and clarify the diagnosis.

Polysomnography remains the gold standard for telling when the patient is asleep vs awake, diagnosing sleep-disordered breathing, detecting periodic limb movements and parasomnias, and aiding in the diagnosis of narcolepsy.

Actigraphy, which uses technology similar to fitness trackers, can help distinguish sleep from wakefulness, reveal erratic sleep schedules, and help diagnose circadian rhythm sleep disorders. In patients with insomnia, actigraphy can help determine daily sleep patterns and response to treatment.20 It can be especially useful for patients who cannot provide a clear history, eg, children and those with developmental disabilities or cognitive dysfunction.

Consumer sleep tracking devices, like actigraphy, are portable and unobtrusive, providing a way to measure sleep duration and demonstrate sleep patterns in a patient’s natural environment. Being more accessible, cheaper, and less time-consuming than clinical tests, the commercially available devices could be clinically useful in some situations, eg, for monitoring overall sleep patterns to look for circadian sleep-wake disorders, commonly seen in shift workers (shift work disorder) or adolescents (delayed sleep-wake phase disorder); or in patients with poor motivation to maintain a sleep diary. Because of their poor performance in clinical trials, they should not be relied upon to distinguish sleep from wakefulness, quantify the amount of sleep, determine sleep stages, and awaken patients exclusively from light sleep.

Discerning poor sleep hygiene from insomnia

Patients with insomnia tend to take longer to go to sleep (have longer sleep latencies), wake up more (have more disturbed sleep with increased awakenings), and have shorter sleep times with reduced sleep efficiencies.21 Sleep tracking devices tend to be less accurate for patients with short sleep duration and disturbed sleep, limiting their usefulness in this group. Furthermore, patients with insomnia tend to underestimate their sleep time and overestimate sleep latency; some devices also tend to overestimate the time to fall asleep, reinforcing this common error made by patients.22,23

On the other hand, data from sleep tracking devices could help distinguish poor sleep hygiene from an insomnia disorder. For example, the data may indicate that a patient has poor sleep habits, such as taking long daytime naps or having significantly variable time in and out of bed from day to day. The total times asleep and awake in the middle of the night may also be substantially different on each night, which would also possibly indicate poor sleep hygiene.

 

 

Detecting circadian rhythms

A device may show that a patient has a clear circadian preference that is not in line with his or her daily routines, suggesting an underlying circadian rhythm sleep-wake disorder. This may be evident by bedtimes and wake times that are consistent but substantially out of sync with one’s social or occupational needs.

Measuring overall sleep duration

In people with normal sleep, fitness trackers perform reasonably well for measuring overall sleep duration. This information could be used to assess a patient with daytime sleepiness and fatigue to evaluate insufficient sleep as an etiologic factor.

Table 3 summarizes how to evaluate the data from sleep apps and fitness tracking devices for clinical use. While these features of consumer sleep tracking devices could conceivably help in the above clinical scenarios, further validation of devices in clinical populations is necessary before their use can be recommended without reservation.

ADVISING PATIENTS

Patients sometimes present to clinicians with concerns about the duration of sleep time and time spent in various sleep stages as delineated by their sleep tracking devices. Currently, these devices do not appear to be able to adequately distinguish various sleep stages, and in many users, they can substantially underestimate or overestimate sleep parameters such as time taken to fall asleep or duration of awakenings in the middle of the night. Patients can be reassured about this lack of evidence and should be advised to not place too much weight on such data alone.

Sleep “goals” set by many devices have not been scientifically validated. People without sleep problems should be discouraged from making substantial changes to their routines to accommodate sleep targets set by the devices. Patients should be counseled about the pitfalls of the data and can be reassured that little evidence suggests that time spent in various sleep stages correlates with adverse daytime consequences or with poor health outcomes.

Some of the apps used as alarm clocks claim to be able to tell what stage of sleep people are in and wait to awaken them until they are in a light stage, which is less jarring than being awakened from a deep stage, but the evidence for this is unclear. In the one study that tested this claim, the app did not awaken participants from light sleep more often than is likely to occur by chance.17 The utility of these apps as personalized alarm clocks is still extremely limited, and patients should be counseled to obtain an adequate amount of sleep rather than rely on devices to awaken them during specific sleep stages.

The rates for discontinuing the use of these devices are high, which could limit their utility. Some surveys have shown that close to 50% of users stop using fitness trackers; 33% stop using them within 6 months of obtaining the device.24 Also, there is little evidence that close monitoring of sleep results in behavior changes or improved sleep duration. Conversely, the potential harms of excessive monitoring of one’s sleep are currently unknown.

References
  1. Rock Health. The future of biosensing wearables. http://rockhealth.com/reports/the-future-of-biosensing-wearables/. Accessed March 16, 2017.
  2. Time, Inc. Your wireless life: results of Time’s mobility poll. http://content.time.com/time/interactive/0,31813,2122187,00.html. Accessed March 16, 2017.
  3. Office of Disease Prevention and Health Promotion (ODPHP). Healthy people 2020. Sleep health. www.healthypeople.gov/2020/topics-objectives/topic/sleep-health. Accessed March 16, 2017.
  4. Consensus Conference Panel; Watson NF, Badr MS, Belenky G, et al. Joint consensus statement of the American Academy of Sleep Medicine and Sleep Research Society on the recommended amount of sleep for a healthy adult: methodology and discussion. J Clin Sleep Med 2015; 11:931–952.
  5. Ko PT, Kientz JA, Choe EK, Kay M, Landis CA, Watson NF. Consumer sleep technologies: a review of the landscape. J Clin Sleep Med 2015; 11:1455–1461.
  6. Investor Place Media, LLC. Top iTunes picks: Apple names best apps of 2014. http://investorplace.com/2014/12/apple-best-apps-of-2014-aapl/#.VIYeE9LF98E/. Accessed April 13, 2017.
  7. Sunseri M, Liden CB, Farringdon J, et al. The SenseWear armband as a sleep detection device. Internal publication.
  8. Shambroom JR, Fábregas SE, Johnstone J. Validation of an automated wireless system to monitor sleep in healthy adults. J Sleep Res 2012; 21:221–230.
  9. John D, Freedson P. ActiGraph and Actical physical activity monitors: a peek under the hood. Med Sci Sports Exerc 2012; 44(suppl 1):S86–S89.
  10. Sadeh A, Sharkey KM, Carskadon MA. Activity-based sleep-wake identification: an empirical test of methodological issues. Sleep 1994; 17:201–207.
  11. Kripke DF, Hahn EK, Grizas AP, et al. Wrist actigraphic scoring for sleep laboratory patients: algorithm development. J Sleep Res 2010; 19:612–619.
  12. Meltzer LJ, Marcus CL. Reply: caffeine therapy for apnea of prematurity: long-term effect on sleep by actigraphy and polysomnography. Am J Respir Crit Care Med 2014; 190:1457–1458.
  13. Montgomery-Downs HE, Insana SP, Bond JA. Movement toward a novel activity monitoring device. Sleep Breath 2012; 16:913–917.
  14. Meltzer LJ, Hiruma LS, Avis K, Montgomery-Downs H, Valentin J. Comparison of a commercial accelerometer with polysomnography and actigraphy in children and adolescents. Sleep 2015; 38:1323–1330.
  15. de Zambotti M, Baker FC, Colrain IM. Validation of sleep-tracking technology compared with polysomnography in adolescents. Sleep 2015; 38:1461–1468.
  16. de Zambotti M, Claudatos S, Inkelis S, Colrain IM, Baker FC. Evaluation of a consumer fitness-tracking device to assess sleep in adults. Chronobiol Int 2015; 32:1024–1028.
  17. Toon E, Davey MJ, Hollis SL, Nixon GM, Horne RS, Biggs SN. Comparison of commercial wrist-based and smartphone accelerometers, actigraphy, and PSG in a clinical cohort of children and adolescents. J Clin Sleep Med 2016; 12:343–350.
  18. Bhat S, Ferraris A, Gupta D, et al. Is there a clinical role for smartphone sleep apps? Comparison of sleep cycle detection by a smartphone application to polysomnography. J Clin Sleep Med 2015; 11:709–715.
  19. Min JK, Doryab A, Wiese J, Amini S, Zimmerman J, Hong JI. Toss ‘n’ turn: smartphone as sleep and sleep quality detector. Proceedings of the SIGCHI Conference on Human Factors in Computing Systems. Toronto, Ontario, Canada: ACM; 2014:477-486.
  20. Morgenthaler T, Alessi C, Friedman L, et al; Standards of Practice Committee; American Academy of Sleep Medicine. Practice parameters for the use of actigraphy in the assessment of sleep and sleep disorders: an update for 2007. Sleep 2007; 30:519-529.
  21. Lichstein KL, Durrence HH, Taylor DJ, Bush AJ, Riedel BW. Quantitative criteria for insomnia. Behav Res Ther 2003; 41:427–445.
  22. Carskadon MA, Dement WC, Mitler MM, Guilleminault C, Zarcone VP, Spiegel R. Self-reports versus sleep laboratory findings in 122 drug-free subjects with complaints of chronic insomnia. Am J Psychiatry 1976; 133:1382–1388.
  23. Perlis ML, Giles DE, Mendelson WB, Bootzin RR, Wyatt JK. Psychophysiological insomnia: the behavioural model and a neurocognitive perspective. J Sleep Res 1997; 6:179–188.
  24. Endeavour Partners LLC. Inside wearables: how the science of human behavior change offers the secret to long-term engagement. http://endeavourpartners.net/assets/Wearables-and-the-Science-of-Human-Behavior-Change-EP4.pdf. Accessed March 16, 2017.
Article PDF
Author and Disclosure Information

Meghna P. Mansukhani, MD
Center for Sleep Medicine, Mayo Clinic, Rochester, MN

Bhanu Prakash Kolla, MD, MRCPsych
Center for Sleep Medicine and Department of Psychiatry and Psychology, Mayo Clinic, Rochester, MN

Address: Meghna P. Mansukhani, MD, Center for Sleep Medicine, Mayo Clinic, 2nd Street SW, Rochester, MN 55905; Mansukhani.Meghna@mayo.edu

Dr. Mansukhani has disclosed research funding from ResMed.

Issue
Cleveland Clinic Journal of Medicine - 84(6)
Publications
Topics
Page Number
451-456
Legacy Keywords
sleep, sleep monitor, polysomnography, sleep study, fitness tracker, phone app, Fitbit, Jawbone, Nike, Fuelband, insomnia, Meghna Mansukhani, Bhanu Kolla
Sections
Author and Disclosure Information

Meghna P. Mansukhani, MD
Center for Sleep Medicine, Mayo Clinic, Rochester, MN

Bhanu Prakash Kolla, MD, MRCPsych
Center for Sleep Medicine and Department of Psychiatry and Psychology, Mayo Clinic, Rochester, MN

Address: Meghna P. Mansukhani, MD, Center for Sleep Medicine, Mayo Clinic, 2nd Street SW, Rochester, MN 55905; Mansukhani.Meghna@mayo.edu

Dr. Mansukhani has disclosed research funding from ResMed.

Author and Disclosure Information

Meghna P. Mansukhani, MD
Center for Sleep Medicine, Mayo Clinic, Rochester, MN

Bhanu Prakash Kolla, MD, MRCPsych
Center for Sleep Medicine and Department of Psychiatry and Psychology, Mayo Clinic, Rochester, MN

Address: Meghna P. Mansukhani, MD, Center for Sleep Medicine, Mayo Clinic, 2nd Street SW, Rochester, MN 55905; Mansukhani.Meghna@mayo.edu

Dr. Mansukhani has disclosed research funding from ResMed.

Article PDF
Article PDF
Related Articles

More and more consumers are using wearable devices and smartphones to monitor and measure various body functions, including sleep. Many patients now present their providers with sleep data obtained from their phones and other devices. But can these devices provide valid, useful clinical information?

This article describes common sleep tracking devices available to consumers and the mechanisms the devices probably use to distinguish sleep from wakefulness (their algorithms are secret), the studies evaluating the validity of device manufacturers’ claims, and their clinical utility and limitations.

DEVICES ARE COMMON

Close to 1 in 10 adults over age 18 owns an activity tracker, and sales are projected to reach $50 billion by 2018.1 Even more impressive, close to 69% of Americans own a smartphone,1 and more than half use it as an alarm clock.2

At the same time that these devices have become so popular, sleep medicine has come of age, and experts have been pushing to improve people’s sleep and increase awareness of sleep disorders.3,4 While the technology has significantly advanced, adoption of data from these devices for clinical evaluation has been limited. Studies examining the validity of these devices have only recently been conducted, and companies that make the devices have not been forthcoming with details of the specific algorithms they use to tell if the patient is asleep or awake or what stage of sleep the patient is in.

WHAT ARE THESE DEVICES?

Consumer tracking devices that claim to measure sleep are easily available for purchase and include wearable fitness trackers such as Fitbit, Jawbone UP, and Nike+ Fuelband. Other sleep tracking devices are catalogued by Ko et al.5 Various smartphone applications (apps) are also available.

Fitness trackers, usually worn as a wrist band, are primarily designed to measure movement and activity, but manufacturers now claim the trackers can also measure sleep. Collected data are available for the user to review the following day. In most cases, these trackers display sleep and wake times; others also claim to record sound sleep, light sleep, and the number and duration of awakenings. Most fitness trackers have complementary apps available for download that graphically display the data on smartphones and interact with social media to allow users to post their sleep and activity data.

More than 500 sleep-related apps are available for download to smartphones in the iTunes app store5; the Sleep Cycle alarm clock app was among the top 5 sleep-tracking apps downloaded in 2014.6 Because sleep data collection relies on the smartphone being placed on the user’s mattress, movements of bed partners, pets, and bedding may interfere with results. In most cases, the apps display data in a format similar to that of fitness trackers. Some claim to determine the optimal sleep phase for the alarm to wake the user.

HOW DOES THE TECHNOLOGY WORK?

Older activity-tracking devices used single-channel electroencephalographic recordings or multiple physiologic channels such as galvanic skin response, skin temperature, and heat flux to measure activity to determine transitions between periods of sleep and wakefulness.7,8

None of the currently available consumer sleep tracking devices discloses the exact mechanisms used to measure sleep and wakefulness, but most appear to rely on 3-axis accelerometers,9 ie, microelectromechanical devices that measure front-to-back, side-to-side, and up-and-down motion and convert the data into an activity count. Activity counts are acquired over 30- or 60-second intervals and are entered into algorithms that determine if the pattern indicates that the patient is awake or asleep. This is the same method that actigraphy uses to evaluate sleep, but most actigraphs used in medicine disclose their mechanisms and provide clinicians with the option of using various validated algorithms to classify the activity counts into sleep or awake periods.9–11

 

 

ARE THE MEASURES VALID?

Only a few studies have examined the validity and accuracy of current fitness trackers and apps for measuring sleep.

The available studies are difficult to compare; most have been small and used different actigraphy devices for comparison. Some tested healthy volunteers, others included people with suspected or confirmed sleep disorders, and some had both types of participants. In many studies, the device was compared with polysomnography for only 1 night, making the “first-night effect” likely to be a confounding factor, as people tend to sleep worse during the first night of testing. Technical failures for the devices were noted in some studies.12 In addition, some currently used apps may use different platforms than the devices used in these studies, limiting the extrapolation of results.

Two fitness tracking devices (Fitbit13,14  and Jawbone UP15–17) were compared with polysomnography and actigraphy in several studies in children and adults (Table 1). The devices tended to overestimate sleeping time, sleep efficiency, and latency to sleep onset and underestimate awake time after falling asleep. Some studies noted that differences were more pronounced for those with the most disturbed sleep.

As with fitness trackers, few studies have been done to examine the validity of smartphone apps.5 Findings of 3 studies are summarized in Table 2.17–19 In addition to tracking the duration and depth of sleep, some apps purport to detect snoring, sleep apnea, and periodic limb movements of sleep. Discussion of these apps is beyond the scope of this review.

In general, sleep tracking devices are fair to good at detecting sleep but poor at determining wakefulness. They are inaccurate for determining absolute sleep parameters (ie, total sleep time, sleep efficiency, wake time after sleep onset, and sleep onset latency) and in distinguishing the different sleep stages compared to polysomnography. Age-related differences have been found between consumer sleep devices compared with polysomnography and actigraphy-derived measures; because adults are likelier to lie still when awake, activity monitors are prone to overestimate sleep time in adults. Comparisons in patients with sleep apnea are conflicting.12,15 Claims that the “sensitive” mode may be appropriate for users with sleep disorders are thus far unsubstantiated.

ARE THE DEVICES CLINICALLY USEFUL?

Although a thorough history remains the cornerstone of a good evaluation of sleep problems, testing is sometimes essential, and in certain situations, objective data can complement the history and clarify the diagnosis.

Polysomnography remains the gold standard for telling when the patient is asleep vs awake, diagnosing sleep-disordered breathing, detecting periodic limb movements and parasomnias, and aiding in the diagnosis of narcolepsy.

Actigraphy, which uses technology similar to fitness trackers, can help distinguish sleep from wakefulness, reveal erratic sleep schedules, and help diagnose circadian rhythm sleep disorders. In patients with insomnia, actigraphy can help determine daily sleep patterns and response to treatment.20 It can be especially useful for patients who cannot provide a clear history, eg, children and those with developmental disabilities or cognitive dysfunction.

Consumer sleep tracking devices, like actigraphy, are portable and unobtrusive, providing a way to measure sleep duration and demonstrate sleep patterns in a patient’s natural environment. Being more accessible, cheaper, and less time-consuming than clinical tests, the commercially available devices could be clinically useful in some situations, eg, for monitoring overall sleep patterns to look for circadian sleep-wake disorders, commonly seen in shift workers (shift work disorder) or adolescents (delayed sleep-wake phase disorder); or in patients with poor motivation to maintain a sleep diary. Because of their poor performance in clinical trials, they should not be relied upon to distinguish sleep from wakefulness, quantify the amount of sleep, determine sleep stages, and awaken patients exclusively from light sleep.

Discerning poor sleep hygiene from insomnia

Patients with insomnia tend to take longer to go to sleep (have longer sleep latencies), wake up more (have more disturbed sleep with increased awakenings), and have shorter sleep times with reduced sleep efficiencies.21 Sleep tracking devices tend to be less accurate for patients with short sleep duration and disturbed sleep, limiting their usefulness in this group. Furthermore, patients with insomnia tend to underestimate their sleep time and overestimate sleep latency; some devices also tend to overestimate the time to fall asleep, reinforcing this common error made by patients.22,23

On the other hand, data from sleep tracking devices could help distinguish poor sleep hygiene from an insomnia disorder. For example, the data may indicate that a patient has poor sleep habits, such as taking long daytime naps or having significantly variable time in and out of bed from day to day. The total times asleep and awake in the middle of the night may also be substantially different on each night, which would also possibly indicate poor sleep hygiene.

 

 

Detecting circadian rhythms

A device may show that a patient has a clear circadian preference that is not in line with his or her daily routines, suggesting an underlying circadian rhythm sleep-wake disorder. This may be evident by bedtimes and wake times that are consistent but substantially out of sync with one’s social or occupational needs.

Measuring overall sleep duration

In people with normal sleep, fitness trackers perform reasonably well for measuring overall sleep duration. This information could be used to assess a patient with daytime sleepiness and fatigue to evaluate insufficient sleep as an etiologic factor.

Table 3 summarizes how to evaluate the data from sleep apps and fitness tracking devices for clinical use. While these features of consumer sleep tracking devices could conceivably help in the above clinical scenarios, further validation of devices in clinical populations is necessary before their use can be recommended without reservation.

ADVISING PATIENTS

Patients sometimes present to clinicians with concerns about the duration of sleep time and time spent in various sleep stages as delineated by their sleep tracking devices. Currently, these devices do not appear to be able to adequately distinguish various sleep stages, and in many users, they can substantially underestimate or overestimate sleep parameters such as time taken to fall asleep or duration of awakenings in the middle of the night. Patients can be reassured about this lack of evidence and should be advised to not place too much weight on such data alone.

Sleep “goals” set by many devices have not been scientifically validated. People without sleep problems should be discouraged from making substantial changes to their routines to accommodate sleep targets set by the devices. Patients should be counseled about the pitfalls of the data and can be reassured that little evidence suggests that time spent in various sleep stages correlates with adverse daytime consequences or with poor health outcomes.

Some of the apps used as alarm clocks claim to be able to tell what stage of sleep people are in and wait to awaken them until they are in a light stage, which is less jarring than being awakened from a deep stage, but the evidence for this is unclear. In the one study that tested this claim, the app did not awaken participants from light sleep more often than is likely to occur by chance.17 The utility of these apps as personalized alarm clocks is still extremely limited, and patients should be counseled to obtain an adequate amount of sleep rather than rely on devices to awaken them during specific sleep stages.

The rates for discontinuing the use of these devices are high, which could limit their utility. Some surveys have shown that close to 50% of users stop using fitness trackers; 33% stop using them within 6 months of obtaining the device.24 Also, there is little evidence that close monitoring of sleep results in behavior changes or improved sleep duration. Conversely, the potential harms of excessive monitoring of one’s sleep are currently unknown.

More and more consumers are using wearable devices and smartphones to monitor and measure various body functions, including sleep. Many patients now present their providers with sleep data obtained from their phones and other devices. But can these devices provide valid, useful clinical information?

This article describes common sleep tracking devices available to consumers and the mechanisms the devices probably use to distinguish sleep from wakefulness (their algorithms are secret), the studies evaluating the validity of device manufacturers’ claims, and their clinical utility and limitations.

DEVICES ARE COMMON

Close to 1 in 10 adults over age 18 owns an activity tracker, and sales are projected to reach $50 billion by 2018.1 Even more impressive, close to 69% of Americans own a smartphone,1 and more than half use it as an alarm clock.2

At the same time that these devices have become so popular, sleep medicine has come of age, and experts have been pushing to improve people’s sleep and increase awareness of sleep disorders.3,4 While the technology has significantly advanced, adoption of data from these devices for clinical evaluation has been limited. Studies examining the validity of these devices have only recently been conducted, and companies that make the devices have not been forthcoming with details of the specific algorithms they use to tell if the patient is asleep or awake or what stage of sleep the patient is in.

WHAT ARE THESE DEVICES?

Consumer tracking devices that claim to measure sleep are easily available for purchase and include wearable fitness trackers such as Fitbit, Jawbone UP, and Nike+ Fuelband. Other sleep tracking devices are catalogued by Ko et al.5 Various smartphone applications (apps) are also available.

Fitness trackers, usually worn as a wrist band, are primarily designed to measure movement and activity, but manufacturers now claim the trackers can also measure sleep. Collected data are available for the user to review the following day. In most cases, these trackers display sleep and wake times; others also claim to record sound sleep, light sleep, and the number and duration of awakenings. Most fitness trackers have complementary apps available for download that graphically display the data on smartphones and interact with social media to allow users to post their sleep and activity data.

More than 500 sleep-related apps are available for download to smartphones in the iTunes app store5; the Sleep Cycle alarm clock app was among the top 5 sleep-tracking apps downloaded in 2014.6 Because sleep data collection relies on the smartphone being placed on the user’s mattress, movements of bed partners, pets, and bedding may interfere with results. In most cases, the apps display data in a format similar to that of fitness trackers. Some claim to determine the optimal sleep phase for the alarm to wake the user.

HOW DOES THE TECHNOLOGY WORK?

Older activity-tracking devices used single-channel electroencephalographic recordings or multiple physiologic channels such as galvanic skin response, skin temperature, and heat flux to measure activity to determine transitions between periods of sleep and wakefulness.7,8

None of the currently available consumer sleep tracking devices discloses the exact mechanisms used to measure sleep and wakefulness, but most appear to rely on 3-axis accelerometers,9 ie, microelectromechanical devices that measure front-to-back, side-to-side, and up-and-down motion and convert the data into an activity count. Activity counts are acquired over 30- or 60-second intervals and are entered into algorithms that determine if the pattern indicates that the patient is awake or asleep. This is the same method that actigraphy uses to evaluate sleep, but most actigraphs used in medicine disclose their mechanisms and provide clinicians with the option of using various validated algorithms to classify the activity counts into sleep or awake periods.9–11

 

 

ARE THE MEASURES VALID?

Only a few studies have examined the validity and accuracy of current fitness trackers and apps for measuring sleep.

The available studies are difficult to compare; most have been small and used different actigraphy devices for comparison. Some tested healthy volunteers, others included people with suspected or confirmed sleep disorders, and some had both types of participants. In many studies, the device was compared with polysomnography for only 1 night, making the “first-night effect” likely to be a confounding factor, as people tend to sleep worse during the first night of testing. Technical failures for the devices were noted in some studies.12 In addition, some currently used apps may use different platforms than the devices used in these studies, limiting the extrapolation of results.

Two fitness tracking devices (Fitbit13,14  and Jawbone UP15–17) were compared with polysomnography and actigraphy in several studies in children and adults (Table 1). The devices tended to overestimate sleeping time, sleep efficiency, and latency to sleep onset and underestimate awake time after falling asleep. Some studies noted that differences were more pronounced for those with the most disturbed sleep.

As with fitness trackers, few studies have been done to examine the validity of smartphone apps.5 Findings of 3 studies are summarized in Table 2.17–19 In addition to tracking the duration and depth of sleep, some apps purport to detect snoring, sleep apnea, and periodic limb movements of sleep. Discussion of these apps is beyond the scope of this review.

In general, sleep tracking devices are fair to good at detecting sleep but poor at determining wakefulness. They are inaccurate for determining absolute sleep parameters (ie, total sleep time, sleep efficiency, wake time after sleep onset, and sleep onset latency) and in distinguishing the different sleep stages compared to polysomnography. Age-related differences have been found between consumer sleep devices compared with polysomnography and actigraphy-derived measures; because adults are likelier to lie still when awake, activity monitors are prone to overestimate sleep time in adults. Comparisons in patients with sleep apnea are conflicting.12,15 Claims that the “sensitive” mode may be appropriate for users with sleep disorders are thus far unsubstantiated.

ARE THE DEVICES CLINICALLY USEFUL?

Although a thorough history remains the cornerstone of a good evaluation of sleep problems, testing is sometimes essential, and in certain situations, objective data can complement the history and clarify the diagnosis.

Polysomnography remains the gold standard for telling when the patient is asleep vs awake, diagnosing sleep-disordered breathing, detecting periodic limb movements and parasomnias, and aiding in the diagnosis of narcolepsy.

Actigraphy, which uses technology similar to fitness trackers, can help distinguish sleep from wakefulness, reveal erratic sleep schedules, and help diagnose circadian rhythm sleep disorders. In patients with insomnia, actigraphy can help determine daily sleep patterns and response to treatment.20 It can be especially useful for patients who cannot provide a clear history, eg, children and those with developmental disabilities or cognitive dysfunction.

Consumer sleep tracking devices, like actigraphy, are portable and unobtrusive, providing a way to measure sleep duration and demonstrate sleep patterns in a patient’s natural environment. Being more accessible, cheaper, and less time-consuming than clinical tests, the commercially available devices could be clinically useful in some situations, eg, for monitoring overall sleep patterns to look for circadian sleep-wake disorders, commonly seen in shift workers (shift work disorder) or adolescents (delayed sleep-wake phase disorder); or in patients with poor motivation to maintain a sleep diary. Because of their poor performance in clinical trials, they should not be relied upon to distinguish sleep from wakefulness, quantify the amount of sleep, determine sleep stages, and awaken patients exclusively from light sleep.

Discerning poor sleep hygiene from insomnia

Patients with insomnia tend to take longer to go to sleep (have longer sleep latencies), wake up more (have more disturbed sleep with increased awakenings), and have shorter sleep times with reduced sleep efficiencies.21 Sleep tracking devices tend to be less accurate for patients with short sleep duration and disturbed sleep, limiting their usefulness in this group. Furthermore, patients with insomnia tend to underestimate their sleep time and overestimate sleep latency; some devices also tend to overestimate the time to fall asleep, reinforcing this common error made by patients.22,23

On the other hand, data from sleep tracking devices could help distinguish poor sleep hygiene from an insomnia disorder. For example, the data may indicate that a patient has poor sleep habits, such as taking long daytime naps or having significantly variable time in and out of bed from day to day. The total times asleep and awake in the middle of the night may also be substantially different on each night, which would also possibly indicate poor sleep hygiene.

 

 

Detecting circadian rhythms

A device may show that a patient has a clear circadian preference that is not in line with his or her daily routines, suggesting an underlying circadian rhythm sleep-wake disorder. This may be evident by bedtimes and wake times that are consistent but substantially out of sync with one’s social or occupational needs.

Measuring overall sleep duration

In people with normal sleep, fitness trackers perform reasonably well for measuring overall sleep duration. This information could be used to assess a patient with daytime sleepiness and fatigue to evaluate insufficient sleep as an etiologic factor.

Table 3 summarizes how to evaluate the data from sleep apps and fitness tracking devices for clinical use. While these features of consumer sleep tracking devices could conceivably help in the above clinical scenarios, further validation of devices in clinical populations is necessary before their use can be recommended without reservation.

ADVISING PATIENTS

Patients sometimes present to clinicians with concerns about the duration of sleep time and time spent in various sleep stages as delineated by their sleep tracking devices. Currently, these devices do not appear to be able to adequately distinguish various sleep stages, and in many users, they can substantially underestimate or overestimate sleep parameters such as time taken to fall asleep or duration of awakenings in the middle of the night. Patients can be reassured about this lack of evidence and should be advised to not place too much weight on such data alone.

Sleep “goals” set by many devices have not been scientifically validated. People without sleep problems should be discouraged from making substantial changes to their routines to accommodate sleep targets set by the devices. Patients should be counseled about the pitfalls of the data and can be reassured that little evidence suggests that time spent in various sleep stages correlates with adverse daytime consequences or with poor health outcomes.

Some of the apps used as alarm clocks claim to be able to tell what stage of sleep people are in and wait to awaken them until they are in a light stage, which is less jarring than being awakened from a deep stage, but the evidence for this is unclear. In the one study that tested this claim, the app did not awaken participants from light sleep more often than is likely to occur by chance.17 The utility of these apps as personalized alarm clocks is still extremely limited, and patients should be counseled to obtain an adequate amount of sleep rather than rely on devices to awaken them during specific sleep stages.

The rates for discontinuing the use of these devices are high, which could limit their utility. Some surveys have shown that close to 50% of users stop using fitness trackers; 33% stop using them within 6 months of obtaining the device.24 Also, there is little evidence that close monitoring of sleep results in behavior changes or improved sleep duration. Conversely, the potential harms of excessive monitoring of one’s sleep are currently unknown.

References
  1. Rock Health. The future of biosensing wearables. http://rockhealth.com/reports/the-future-of-biosensing-wearables/. Accessed March 16, 2017.
  2. Time, Inc. Your wireless life: results of Time’s mobility poll. http://content.time.com/time/interactive/0,31813,2122187,00.html. Accessed March 16, 2017.
  3. Office of Disease Prevention and Health Promotion (ODPHP). Healthy people 2020. Sleep health. www.healthypeople.gov/2020/topics-objectives/topic/sleep-health. Accessed March 16, 2017.
  4. Consensus Conference Panel; Watson NF, Badr MS, Belenky G, et al. Joint consensus statement of the American Academy of Sleep Medicine and Sleep Research Society on the recommended amount of sleep for a healthy adult: methodology and discussion. J Clin Sleep Med 2015; 11:931–952.
  5. Ko PT, Kientz JA, Choe EK, Kay M, Landis CA, Watson NF. Consumer sleep technologies: a review of the landscape. J Clin Sleep Med 2015; 11:1455–1461.
  6. Investor Place Media, LLC. Top iTunes picks: Apple names best apps of 2014. http://investorplace.com/2014/12/apple-best-apps-of-2014-aapl/#.VIYeE9LF98E/. Accessed April 13, 2017.
  7. Sunseri M, Liden CB, Farringdon J, et al. The SenseWear armband as a sleep detection device. Internal publication.
  8. Shambroom JR, Fábregas SE, Johnstone J. Validation of an automated wireless system to monitor sleep in healthy adults. J Sleep Res 2012; 21:221–230.
  9. John D, Freedson P. ActiGraph and Actical physical activity monitors: a peek under the hood. Med Sci Sports Exerc 2012; 44(suppl 1):S86–S89.
  10. Sadeh A, Sharkey KM, Carskadon MA. Activity-based sleep-wake identification: an empirical test of methodological issues. Sleep 1994; 17:201–207.
  11. Kripke DF, Hahn EK, Grizas AP, et al. Wrist actigraphic scoring for sleep laboratory patients: algorithm development. J Sleep Res 2010; 19:612–619.
  12. Meltzer LJ, Marcus CL. Reply: caffeine therapy for apnea of prematurity: long-term effect on sleep by actigraphy and polysomnography. Am J Respir Crit Care Med 2014; 190:1457–1458.
  13. Montgomery-Downs HE, Insana SP, Bond JA. Movement toward a novel activity monitoring device. Sleep Breath 2012; 16:913–917.
  14. Meltzer LJ, Hiruma LS, Avis K, Montgomery-Downs H, Valentin J. Comparison of a commercial accelerometer with polysomnography and actigraphy in children and adolescents. Sleep 2015; 38:1323–1330.
  15. de Zambotti M, Baker FC, Colrain IM. Validation of sleep-tracking technology compared with polysomnography in adolescents. Sleep 2015; 38:1461–1468.
  16. de Zambotti M, Claudatos S, Inkelis S, Colrain IM, Baker FC. Evaluation of a consumer fitness-tracking device to assess sleep in adults. Chronobiol Int 2015; 32:1024–1028.
  17. Toon E, Davey MJ, Hollis SL, Nixon GM, Horne RS, Biggs SN. Comparison of commercial wrist-based and smartphone accelerometers, actigraphy, and PSG in a clinical cohort of children and adolescents. J Clin Sleep Med 2016; 12:343–350.
  18. Bhat S, Ferraris A, Gupta D, et al. Is there a clinical role for smartphone sleep apps? Comparison of sleep cycle detection by a smartphone application to polysomnography. J Clin Sleep Med 2015; 11:709–715.
  19. Min JK, Doryab A, Wiese J, Amini S, Zimmerman J, Hong JI. Toss ‘n’ turn: smartphone as sleep and sleep quality detector. Proceedings of the SIGCHI Conference on Human Factors in Computing Systems. Toronto, Ontario, Canada: ACM; 2014:477-486.
  20. Morgenthaler T, Alessi C, Friedman L, et al; Standards of Practice Committee; American Academy of Sleep Medicine. Practice parameters for the use of actigraphy in the assessment of sleep and sleep disorders: an update for 2007. Sleep 2007; 30:519-529.
  21. Lichstein KL, Durrence HH, Taylor DJ, Bush AJ, Riedel BW. Quantitative criteria for insomnia. Behav Res Ther 2003; 41:427–445.
  22. Carskadon MA, Dement WC, Mitler MM, Guilleminault C, Zarcone VP, Spiegel R. Self-reports versus sleep laboratory findings in 122 drug-free subjects with complaints of chronic insomnia. Am J Psychiatry 1976; 133:1382–1388.
  23. Perlis ML, Giles DE, Mendelson WB, Bootzin RR, Wyatt JK. Psychophysiological insomnia: the behavioural model and a neurocognitive perspective. J Sleep Res 1997; 6:179–188.
  24. Endeavour Partners LLC. Inside wearables: how the science of human behavior change offers the secret to long-term engagement. http://endeavourpartners.net/assets/Wearables-and-the-Science-of-Human-Behavior-Change-EP4.pdf. Accessed March 16, 2017.
References
  1. Rock Health. The future of biosensing wearables. http://rockhealth.com/reports/the-future-of-biosensing-wearables/. Accessed March 16, 2017.
  2. Time, Inc. Your wireless life: results of Time’s mobility poll. http://content.time.com/time/interactive/0,31813,2122187,00.html. Accessed March 16, 2017.
  3. Office of Disease Prevention and Health Promotion (ODPHP). Healthy people 2020. Sleep health. www.healthypeople.gov/2020/topics-objectives/topic/sleep-health. Accessed March 16, 2017.
  4. Consensus Conference Panel; Watson NF, Badr MS, Belenky G, et al. Joint consensus statement of the American Academy of Sleep Medicine and Sleep Research Society on the recommended amount of sleep for a healthy adult: methodology and discussion. J Clin Sleep Med 2015; 11:931–952.
  5. Ko PT, Kientz JA, Choe EK, Kay M, Landis CA, Watson NF. Consumer sleep technologies: a review of the landscape. J Clin Sleep Med 2015; 11:1455–1461.
  6. Investor Place Media, LLC. Top iTunes picks: Apple names best apps of 2014. http://investorplace.com/2014/12/apple-best-apps-of-2014-aapl/#.VIYeE9LF98E/. Accessed April 13, 2017.
  7. Sunseri M, Liden CB, Farringdon J, et al. The SenseWear armband as a sleep detection device. Internal publication.
  8. Shambroom JR, Fábregas SE, Johnstone J. Validation of an automated wireless system to monitor sleep in healthy adults. J Sleep Res 2012; 21:221–230.
  9. John D, Freedson P. ActiGraph and Actical physical activity monitors: a peek under the hood. Med Sci Sports Exerc 2012; 44(suppl 1):S86–S89.
  10. Sadeh A, Sharkey KM, Carskadon MA. Activity-based sleep-wake identification: an empirical test of methodological issues. Sleep 1994; 17:201–207.
  11. Kripke DF, Hahn EK, Grizas AP, et al. Wrist actigraphic scoring for sleep laboratory patients: algorithm development. J Sleep Res 2010; 19:612–619.
  12. Meltzer LJ, Marcus CL. Reply: caffeine therapy for apnea of prematurity: long-term effect on sleep by actigraphy and polysomnography. Am J Respir Crit Care Med 2014; 190:1457–1458.
  13. Montgomery-Downs HE, Insana SP, Bond JA. Movement toward a novel activity monitoring device. Sleep Breath 2012; 16:913–917.
  14. Meltzer LJ, Hiruma LS, Avis K, Montgomery-Downs H, Valentin J. Comparison of a commercial accelerometer with polysomnography and actigraphy in children and adolescents. Sleep 2015; 38:1323–1330.
  15. de Zambotti M, Baker FC, Colrain IM. Validation of sleep-tracking technology compared with polysomnography in adolescents. Sleep 2015; 38:1461–1468.
  16. de Zambotti M, Claudatos S, Inkelis S, Colrain IM, Baker FC. Evaluation of a consumer fitness-tracking device to assess sleep in adults. Chronobiol Int 2015; 32:1024–1028.
  17. Toon E, Davey MJ, Hollis SL, Nixon GM, Horne RS, Biggs SN. Comparison of commercial wrist-based and smartphone accelerometers, actigraphy, and PSG in a clinical cohort of children and adolescents. J Clin Sleep Med 2016; 12:343–350.
  18. Bhat S, Ferraris A, Gupta D, et al. Is there a clinical role for smartphone sleep apps? Comparison of sleep cycle detection by a smartphone application to polysomnography. J Clin Sleep Med 2015; 11:709–715.
  19. Min JK, Doryab A, Wiese J, Amini S, Zimmerman J, Hong JI. Toss ‘n’ turn: smartphone as sleep and sleep quality detector. Proceedings of the SIGCHI Conference on Human Factors in Computing Systems. Toronto, Ontario, Canada: ACM; 2014:477-486.
  20. Morgenthaler T, Alessi C, Friedman L, et al; Standards of Practice Committee; American Academy of Sleep Medicine. Practice parameters for the use of actigraphy in the assessment of sleep and sleep disorders: an update for 2007. Sleep 2007; 30:519-529.
  21. Lichstein KL, Durrence HH, Taylor DJ, Bush AJ, Riedel BW. Quantitative criteria for insomnia. Behav Res Ther 2003; 41:427–445.
  22. Carskadon MA, Dement WC, Mitler MM, Guilleminault C, Zarcone VP, Spiegel R. Self-reports versus sleep laboratory findings in 122 drug-free subjects with complaints of chronic insomnia. Am J Psychiatry 1976; 133:1382–1388.
  23. Perlis ML, Giles DE, Mendelson WB, Bootzin RR, Wyatt JK. Psychophysiological insomnia: the behavioural model and a neurocognitive perspective. J Sleep Res 1997; 6:179–188.
  24. Endeavour Partners LLC. Inside wearables: how the science of human behavior change offers the secret to long-term engagement. http://endeavourpartners.net/assets/Wearables-and-the-Science-of-Human-Behavior-Change-EP4.pdf. Accessed March 16, 2017.
Issue
Cleveland Clinic Journal of Medicine - 84(6)
Issue
Cleveland Clinic Journal of Medicine - 84(6)
Page Number
451-456
Page Number
451-456
Publications
Publications
Topics
Article Type
Display Headline
Apps and fitness trackers that measure sleep: Are they useful?
Display Headline
Apps and fitness trackers that measure sleep: Are they useful?
Legacy Keywords
sleep, sleep monitor, polysomnography, sleep study, fitness tracker, phone app, Fitbit, Jawbone, Nike, Fuelband, insomnia, Meghna Mansukhani, Bhanu Kolla
Legacy Keywords
sleep, sleep monitor, polysomnography, sleep study, fitness tracker, phone app, Fitbit, Jawbone, Nike, Fuelband, insomnia, Meghna Mansukhani, Bhanu Kolla
Sections
Inside the Article

KEY POINTS

  • Wearable fitness trackers tend to perform better than smartphone applications, which are more prone to interference from bed partners and pets.
  • Sleep data from tracking devices are less reliable in patients with fragmented sleep and insomnia.
  • In normal sleepers, devices tend to measure sleep duration with reasonable accuracy, so that one can tell if a patient is getting too little sleep or reassure someone who is getting enough sleep.
  • Devices may help identify patients with poor sleep hygiene or atypical circadian rhythms.
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Article PDF Media

Mole count predicted melanoma death, especially among men

Article Type
Changed
Fri, 01/18/2019 - 16:47

 

– Among white men, the presence of at least one cutaneous nevus measuring 3 mm or more significantly predicted death from melanoma, in an adjusted analysis of a large prospective cohort study.

Dr. Eunyoung Cho
Dr. Eunyoung Cho
Although melanoma has the worst prognosis of all skin cancers, only limited data are available on phenotypic risk factors for melanoma death, said Dr. Cho of the department of dermatology, Brown University, Providence, R.I. She and her associates analyzed data from 77,288 white women from the Nurses’ Health Study and 32,455 white men from the Health Professionals Follow-Up Study from 1986 through 2012. In 1986, participants reported their number of moles measuring at least 3 mm in diameter. Subsequent melanoma diagnoses were confirmed pathologically, and deaths were confirmed either by next of kin or through the National Death Index.

In the Nurses’ Health Study, white women with at least three moles measuring at least 3 mm in diameter were at significantly increased risk of dying of melanoma, compared with those with no moles that size (hazard ratio, 2.5; 95% confidence interval, 1.5-4.1), even after the investigators controlled for many other potential confounders, including sunburn history, skin reaction to sun during childhood, tanning ability, family history of melanoma, personal history of nonmelanoma skin cancer, age, activity level, smoking, body mass index, alcohol intake, and hair color. Women with one or two moles also showed a trend toward increased risk of melanoma death (HR, 1.4), but the 95% confidence interval for the hazard ratio did not reach statistical significance (0.9-2.3).

The investigators estimated that among white women, each additional mole measuring 3 mm or more conferred about a 12% increase in the melanoma death rate, even after confounders were controlled for.

In the Health Professionals Follow-Up Study, men with one or two moles of at least 3 mm had about twice the melanoma death rate as men without moles of this size (HR, 2.0; 95% CI, 1.3-3.3), even after investigators controlled for potential confounders. The risk of melanoma death was even greater among men with at least three moles (HR, 4.0; 95% CI, 2.5-6.2), and the difference in rates was statistically significant (P less than .0001). After confounders were accounted for, each additional mole measuring at least 3 mm conferred a 20% increase in the rate of melanoma death.

A different picture emerged after narrowing the adjusted analyses to include only people diagnosed with melanoma: In this group, mole count did not predict melanoma death among women, but continued to do so among men with melanoma who had at least three moles at baseline (HR, 1.8; 95% CI, 1.1-3.0), Dr. Cho reported. Among men, higher mole count also predicted melanoma of at least 1-mm Breslow thickness, an important prognostic factor, she added. Hazard ratios for these “thicker melanomas” were 1.9 (95% CI, 1.1-3.3) among men with one or two moles, and 2.5 (95% CI, 1.5-4.4) among men with three or more moles. Among women with melanoma, mole count did not predict Breslow thickness.

The extent to which sex affected trends in this analysis highlights the need for more studies of sex and other phenotypic risk factors for melanoma death, Dr. Cho concluded. She presented on behalf of lead author Wen-Qing Li, PhD, also of Brown University.

The National Institutes of Health and the Dermatology Foundation provided funding. Dr. Cho and Dr. Li had no relevant financial disclosures.

Meeting/Event
Publications
Topics
Sections
Meeting/Event
Meeting/Event

 

– Among white men, the presence of at least one cutaneous nevus measuring 3 mm or more significantly predicted death from melanoma, in an adjusted analysis of a large prospective cohort study.

Dr. Eunyoung Cho
Dr. Eunyoung Cho
Although melanoma has the worst prognosis of all skin cancers, only limited data are available on phenotypic risk factors for melanoma death, said Dr. Cho of the department of dermatology, Brown University, Providence, R.I. She and her associates analyzed data from 77,288 white women from the Nurses’ Health Study and 32,455 white men from the Health Professionals Follow-Up Study from 1986 through 2012. In 1986, participants reported their number of moles measuring at least 3 mm in diameter. Subsequent melanoma diagnoses were confirmed pathologically, and deaths were confirmed either by next of kin or through the National Death Index.

In the Nurses’ Health Study, white women with at least three moles measuring at least 3 mm in diameter were at significantly increased risk of dying of melanoma, compared with those with no moles that size (hazard ratio, 2.5; 95% confidence interval, 1.5-4.1), even after the investigators controlled for many other potential confounders, including sunburn history, skin reaction to sun during childhood, tanning ability, family history of melanoma, personal history of nonmelanoma skin cancer, age, activity level, smoking, body mass index, alcohol intake, and hair color. Women with one or two moles also showed a trend toward increased risk of melanoma death (HR, 1.4), but the 95% confidence interval for the hazard ratio did not reach statistical significance (0.9-2.3).

The investigators estimated that among white women, each additional mole measuring 3 mm or more conferred about a 12% increase in the melanoma death rate, even after confounders were controlled for.

In the Health Professionals Follow-Up Study, men with one or two moles of at least 3 mm had about twice the melanoma death rate as men without moles of this size (HR, 2.0; 95% CI, 1.3-3.3), even after investigators controlled for potential confounders. The risk of melanoma death was even greater among men with at least three moles (HR, 4.0; 95% CI, 2.5-6.2), and the difference in rates was statistically significant (P less than .0001). After confounders were accounted for, each additional mole measuring at least 3 mm conferred a 20% increase in the rate of melanoma death.

A different picture emerged after narrowing the adjusted analyses to include only people diagnosed with melanoma: In this group, mole count did not predict melanoma death among women, but continued to do so among men with melanoma who had at least three moles at baseline (HR, 1.8; 95% CI, 1.1-3.0), Dr. Cho reported. Among men, higher mole count also predicted melanoma of at least 1-mm Breslow thickness, an important prognostic factor, she added. Hazard ratios for these “thicker melanomas” were 1.9 (95% CI, 1.1-3.3) among men with one or two moles, and 2.5 (95% CI, 1.5-4.4) among men with three or more moles. Among women with melanoma, mole count did not predict Breslow thickness.

The extent to which sex affected trends in this analysis highlights the need for more studies of sex and other phenotypic risk factors for melanoma death, Dr. Cho concluded. She presented on behalf of lead author Wen-Qing Li, PhD, also of Brown University.

The National Institutes of Health and the Dermatology Foundation provided funding. Dr. Cho and Dr. Li had no relevant financial disclosures.

 

– Among white men, the presence of at least one cutaneous nevus measuring 3 mm or more significantly predicted death from melanoma, in an adjusted analysis of a large prospective cohort study.

Dr. Eunyoung Cho
Dr. Eunyoung Cho
Although melanoma has the worst prognosis of all skin cancers, only limited data are available on phenotypic risk factors for melanoma death, said Dr. Cho of the department of dermatology, Brown University, Providence, R.I. She and her associates analyzed data from 77,288 white women from the Nurses’ Health Study and 32,455 white men from the Health Professionals Follow-Up Study from 1986 through 2012. In 1986, participants reported their number of moles measuring at least 3 mm in diameter. Subsequent melanoma diagnoses were confirmed pathologically, and deaths were confirmed either by next of kin or through the National Death Index.

In the Nurses’ Health Study, white women with at least three moles measuring at least 3 mm in diameter were at significantly increased risk of dying of melanoma, compared with those with no moles that size (hazard ratio, 2.5; 95% confidence interval, 1.5-4.1), even after the investigators controlled for many other potential confounders, including sunburn history, skin reaction to sun during childhood, tanning ability, family history of melanoma, personal history of nonmelanoma skin cancer, age, activity level, smoking, body mass index, alcohol intake, and hair color. Women with one or two moles also showed a trend toward increased risk of melanoma death (HR, 1.4), but the 95% confidence interval for the hazard ratio did not reach statistical significance (0.9-2.3).

The investigators estimated that among white women, each additional mole measuring 3 mm or more conferred about a 12% increase in the melanoma death rate, even after confounders were controlled for.

In the Health Professionals Follow-Up Study, men with one or two moles of at least 3 mm had about twice the melanoma death rate as men without moles of this size (HR, 2.0; 95% CI, 1.3-3.3), even after investigators controlled for potential confounders. The risk of melanoma death was even greater among men with at least three moles (HR, 4.0; 95% CI, 2.5-6.2), and the difference in rates was statistically significant (P less than .0001). After confounders were accounted for, each additional mole measuring at least 3 mm conferred a 20% increase in the rate of melanoma death.

A different picture emerged after narrowing the adjusted analyses to include only people diagnosed with melanoma: In this group, mole count did not predict melanoma death among women, but continued to do so among men with melanoma who had at least three moles at baseline (HR, 1.8; 95% CI, 1.1-3.0), Dr. Cho reported. Among men, higher mole count also predicted melanoma of at least 1-mm Breslow thickness, an important prognostic factor, she added. Hazard ratios for these “thicker melanomas” were 1.9 (95% CI, 1.1-3.3) among men with one or two moles, and 2.5 (95% CI, 1.5-4.4) among men with three or more moles. Among women with melanoma, mole count did not predict Breslow thickness.

The extent to which sex affected trends in this analysis highlights the need for more studies of sex and other phenotypic risk factors for melanoma death, Dr. Cho concluded. She presented on behalf of lead author Wen-Qing Li, PhD, also of Brown University.

The National Institutes of Health and the Dermatology Foundation provided funding. Dr. Cho and Dr. Li had no relevant financial disclosures.

Publications
Publications
Topics
Article Type
Click for Credit Status
Active
Sections
Article Source

AT SID 2017

Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
CME ID
138997
Vitals

 

Key clinical point: Mole count was an independent risk factor for melanoma death among men and, to a lesser extent, among women.

Major finding: Adjusted hazard ratios were 2.0 among white men with one or two moles at least 3 mm in diameter and 4.0 among those with at least three moles, but among white women, the association was not significant unless they had at least three moles (HR, 2.5).

Data source: Adjusted analyses of 77,288 white women from the Nurses’ Health Study and 32,455 white men from the Health Professionals Follow-Up Study for 1986 through 2012.

Disclosures: The National Institutes of Health and the Dermatology Foundation provided funding for the study. Dr. Cho and Dr. Li had no relevant financial disclosures.

Adolescents and sleep, or the lack thereof

Article Type
Changed
Fri, 01/18/2019 - 16:46

 

Every parent will attest that bright-eyed children grow into sleepy adolescents, and the science confirms their observations. There are multiple factors that prevent adolescents from getting the sleep they need, and inadequate sleep has serious consequences – from impaired learning to depressive symptoms, obesity to deadly accidents – all of which are potentially preventable with some practical strategies to promote adequate sleep.

Adolescence is a period of intense growth and development, so it is no surprise that adolescents require a lot of sleep, over 9 hours nightly. But surveys have shown that only 3% of American adolescents get 9 hours of sleep nightly, and the average amount of weeknight sleep is only 6 hours.1 Sleep deprivation is not a problem in childhood, so why can’t adolescents get enough sleep?

Dr. Susan D. Swick
Dr. Susan D. Swick
Some of the reasons are biological. Adolescent sleep is marked by a phase change in circadian rhythm, so that teens become sleepy about 2 hours later than younger children and need to sleep later to get adequate sleep. There also is a change in sleep homeostasis, so that it takes a teenager longer to feel sleepy after waking. These biological forces are compounded by external forces: school work, athletics, jobs, and the gravitational pull of friendships provide multiple reasons to stay up rather than sleep. Most high schools in the United States start by 7:30 a.m., meaning teens must get up after only 6-7 hours of sleep. Ambitious teenagers are often involved in sports and extracurricular activities which take several hours after every school day. Homework can consume several hours every night. Even with exquisite organization and discipline, it is challenging to fulfill these commitments and still get 9 hours of sleep nightly.

Over the last 15 years, a new factor – screen time – has worsened the adolescent sleep situation. Most teens have an electronic device in their bedroom and use it for homework, entertainment, and socializing well into the night. Multiple studies have confirmed that electronic exposure in the evening is associated with less sleep at night and more day time sleepiness,by competing with sleep and suppression of nocturnal melatonin release, which can delay the onset of sleep.2

It is ironic that many teens are staying up late for homework, when their lack of sleep can interfere with consolidation of learning. It also has powerful effects on working memory and reaction time, making both academic and athletic performance suffer. Chronically sleep-deprived teenagers often complain of difficulty with initiating and sustaining attention, which may lead to a mistaken diagnosis of ADHD, and stimulant treatment may further complicate sleep.

Dr. Michael S. Jellinek, professor emeritus of psychiatry and pediatrics, Harvard Medical School, Boston
Dr. Michael S. Jellinek
Even a few days of inadequate sleep can lead to anxiety and depressive symptoms, and chronic sleep deprivation is associated with a higher incidence of clinical depression. The relationship between inadequate sleep and depression is also two-way – disrupted sleep is a hallmark of depression. Beyond the links with depression, there appears to be an association between suicide attempts and inadequate sleep. One recent study found a threefold increase in the rate of suicide attempts in those adolescents who were getting less than 8 hours of sleep nightly, compared with their peers who were getting 8 or more hours of nightly sleep. The degree of risk is inversely related to the amount of sleep.3

Good mental health is not the only casualty of inadequate sleep. A growing body of evidence links short sleep duration with an increased risk of obesity. This appears to be mediated by alterations in neurohormones associated with sleep, leading to higher carbohydrate and fat intake, more snacking and insulin resistance.

Anything that compromises attention and reaction time, including sleep deprivation, adds risk to driving, particularly for inexperienced and impulsive adolescent drivers. The National Highway Transportation Safety Administration estimates that drivers 25 and younger cause more than half of all “fall asleep” crashes.

Teenagers generally know that they are exhausted, but the strategies they might use to manage their fatigue can actually make things worse. Sleepy teenagers often consume large amounts of caffeine to get through their days and their homework at night. Caffeine, in turn, interferes with both the onset and quality of sleep, perpetuating the cycle. Even “catch-up” sleep on weekends is a strategy that can contribute to the problem, as it can lead to more disrupted sleep by pushing the onset of school night sleepiness even later.

While growing autonomy is part of why teenagers are sleep deprived, they will consider the caring and informed guidance of their pediatricians about their health. Ask your teenage patients how much sleep they usually get on a school night. It can be validating to show them how sleep deprived they are, and point out how strategies like caffeine and oversleeping might be making it worse. Explain that people (adults, too!) need to make time for sleep just as they might for exercise or friends. Tell them about “good sleep hygiene,” the practice of having consistent sleep times and routines that are conducive to restful sleep. This can include a hot shower before bed, reading for the last 30 minutes before lights out, and no screen time for at least 1 hour before bed. Indeed, it can be powerful to urge that everyone in the family takes screens out of their bedrooms.

Additionally, while they might sleep in on weekends, it shouldn’t be much more than an hour longer than on weekdays. And no naps after school! It is common for teens to feel overwhelmed by their commitments and that sleep must be the first thing to go. Use their growing sense of autonomy to remind them that they get to choose how to use their time, and balance will pay off much more than sacrificing sleep. A practical conversation about sleep can help them to make informed choices and thoughtfully take care of themselves before they head off to college.

 

 

Dr. Swick is an attending psychiatrist in the division of child psychiatry at Massachusetts General Hospital, Boston, and director of the Parenting at a Challenging Time (PACT) Program at the Vernon Cancer Center at Newton Wellesley Hospital, also in Boston. Dr. Jellinek is professor emeritus of psychiatry and pediatrics, Harvard Medical School, Boston. Email them at pdnews@frontlinemedcom.com.

Resources

1. “Adolescent Sleep Needs and Patterns: Research Report and Resource Guide.” (Arlington, Va.: National Sleep Foundation, 2000.)

2. Pediatrics. 2014 Sep;134(3):e921-32.

3. Sleep. 2004 Nov 1;27(7):1351-8.

Publications
Topics
Sections

 

Every parent will attest that bright-eyed children grow into sleepy adolescents, and the science confirms their observations. There are multiple factors that prevent adolescents from getting the sleep they need, and inadequate sleep has serious consequences – from impaired learning to depressive symptoms, obesity to deadly accidents – all of which are potentially preventable with some practical strategies to promote adequate sleep.

Adolescence is a period of intense growth and development, so it is no surprise that adolescents require a lot of sleep, over 9 hours nightly. But surveys have shown that only 3% of American adolescents get 9 hours of sleep nightly, and the average amount of weeknight sleep is only 6 hours.1 Sleep deprivation is not a problem in childhood, so why can’t adolescents get enough sleep?

Dr. Susan D. Swick
Dr. Susan D. Swick
Some of the reasons are biological. Adolescent sleep is marked by a phase change in circadian rhythm, so that teens become sleepy about 2 hours later than younger children and need to sleep later to get adequate sleep. There also is a change in sleep homeostasis, so that it takes a teenager longer to feel sleepy after waking. These biological forces are compounded by external forces: school work, athletics, jobs, and the gravitational pull of friendships provide multiple reasons to stay up rather than sleep. Most high schools in the United States start by 7:30 a.m., meaning teens must get up after only 6-7 hours of sleep. Ambitious teenagers are often involved in sports and extracurricular activities which take several hours after every school day. Homework can consume several hours every night. Even with exquisite organization and discipline, it is challenging to fulfill these commitments and still get 9 hours of sleep nightly.

Over the last 15 years, a new factor – screen time – has worsened the adolescent sleep situation. Most teens have an electronic device in their bedroom and use it for homework, entertainment, and socializing well into the night. Multiple studies have confirmed that electronic exposure in the evening is associated with less sleep at night and more day time sleepiness,by competing with sleep and suppression of nocturnal melatonin release, which can delay the onset of sleep.2

It is ironic that many teens are staying up late for homework, when their lack of sleep can interfere with consolidation of learning. It also has powerful effects on working memory and reaction time, making both academic and athletic performance suffer. Chronically sleep-deprived teenagers often complain of difficulty with initiating and sustaining attention, which may lead to a mistaken diagnosis of ADHD, and stimulant treatment may further complicate sleep.

Dr. Michael S. Jellinek, professor emeritus of psychiatry and pediatrics, Harvard Medical School, Boston
Dr. Michael S. Jellinek
Even a few days of inadequate sleep can lead to anxiety and depressive symptoms, and chronic sleep deprivation is associated with a higher incidence of clinical depression. The relationship between inadequate sleep and depression is also two-way – disrupted sleep is a hallmark of depression. Beyond the links with depression, there appears to be an association between suicide attempts and inadequate sleep. One recent study found a threefold increase in the rate of suicide attempts in those adolescents who were getting less than 8 hours of sleep nightly, compared with their peers who were getting 8 or more hours of nightly sleep. The degree of risk is inversely related to the amount of sleep.3

Good mental health is not the only casualty of inadequate sleep. A growing body of evidence links short sleep duration with an increased risk of obesity. This appears to be mediated by alterations in neurohormones associated with sleep, leading to higher carbohydrate and fat intake, more snacking and insulin resistance.

Anything that compromises attention and reaction time, including sleep deprivation, adds risk to driving, particularly for inexperienced and impulsive adolescent drivers. The National Highway Transportation Safety Administration estimates that drivers 25 and younger cause more than half of all “fall asleep” crashes.

Teenagers generally know that they are exhausted, but the strategies they might use to manage their fatigue can actually make things worse. Sleepy teenagers often consume large amounts of caffeine to get through their days and their homework at night. Caffeine, in turn, interferes with both the onset and quality of sleep, perpetuating the cycle. Even “catch-up” sleep on weekends is a strategy that can contribute to the problem, as it can lead to more disrupted sleep by pushing the onset of school night sleepiness even later.

While growing autonomy is part of why teenagers are sleep deprived, they will consider the caring and informed guidance of their pediatricians about their health. Ask your teenage patients how much sleep they usually get on a school night. It can be validating to show them how sleep deprived they are, and point out how strategies like caffeine and oversleeping might be making it worse. Explain that people (adults, too!) need to make time for sleep just as they might for exercise or friends. Tell them about “good sleep hygiene,” the practice of having consistent sleep times and routines that are conducive to restful sleep. This can include a hot shower before bed, reading for the last 30 minutes before lights out, and no screen time for at least 1 hour before bed. Indeed, it can be powerful to urge that everyone in the family takes screens out of their bedrooms.

Additionally, while they might sleep in on weekends, it shouldn’t be much more than an hour longer than on weekdays. And no naps after school! It is common for teens to feel overwhelmed by their commitments and that sleep must be the first thing to go. Use their growing sense of autonomy to remind them that they get to choose how to use their time, and balance will pay off much more than sacrificing sleep. A practical conversation about sleep can help them to make informed choices and thoughtfully take care of themselves before they head off to college.

 

 

Dr. Swick is an attending psychiatrist in the division of child psychiatry at Massachusetts General Hospital, Boston, and director of the Parenting at a Challenging Time (PACT) Program at the Vernon Cancer Center at Newton Wellesley Hospital, also in Boston. Dr. Jellinek is professor emeritus of psychiatry and pediatrics, Harvard Medical School, Boston. Email them at pdnews@frontlinemedcom.com.

Resources

1. “Adolescent Sleep Needs and Patterns: Research Report and Resource Guide.” (Arlington, Va.: National Sleep Foundation, 2000.)

2. Pediatrics. 2014 Sep;134(3):e921-32.

3. Sleep. 2004 Nov 1;27(7):1351-8.

 

Every parent will attest that bright-eyed children grow into sleepy adolescents, and the science confirms their observations. There are multiple factors that prevent adolescents from getting the sleep they need, and inadequate sleep has serious consequences – from impaired learning to depressive symptoms, obesity to deadly accidents – all of which are potentially preventable with some practical strategies to promote adequate sleep.

Adolescence is a period of intense growth and development, so it is no surprise that adolescents require a lot of sleep, over 9 hours nightly. But surveys have shown that only 3% of American adolescents get 9 hours of sleep nightly, and the average amount of weeknight sleep is only 6 hours.1 Sleep deprivation is not a problem in childhood, so why can’t adolescents get enough sleep?

Dr. Susan D. Swick
Dr. Susan D. Swick
Some of the reasons are biological. Adolescent sleep is marked by a phase change in circadian rhythm, so that teens become sleepy about 2 hours later than younger children and need to sleep later to get adequate sleep. There also is a change in sleep homeostasis, so that it takes a teenager longer to feel sleepy after waking. These biological forces are compounded by external forces: school work, athletics, jobs, and the gravitational pull of friendships provide multiple reasons to stay up rather than sleep. Most high schools in the United States start by 7:30 a.m., meaning teens must get up after only 6-7 hours of sleep. Ambitious teenagers are often involved in sports and extracurricular activities which take several hours after every school day. Homework can consume several hours every night. Even with exquisite organization and discipline, it is challenging to fulfill these commitments and still get 9 hours of sleep nightly.

Over the last 15 years, a new factor – screen time – has worsened the adolescent sleep situation. Most teens have an electronic device in their bedroom and use it for homework, entertainment, and socializing well into the night. Multiple studies have confirmed that electronic exposure in the evening is associated with less sleep at night and more day time sleepiness,by competing with sleep and suppression of nocturnal melatonin release, which can delay the onset of sleep.2

It is ironic that many teens are staying up late for homework, when their lack of sleep can interfere with consolidation of learning. It also has powerful effects on working memory and reaction time, making both academic and athletic performance suffer. Chronically sleep-deprived teenagers often complain of difficulty with initiating and sustaining attention, which may lead to a mistaken diagnosis of ADHD, and stimulant treatment may further complicate sleep.

Dr. Michael S. Jellinek, professor emeritus of psychiatry and pediatrics, Harvard Medical School, Boston
Dr. Michael S. Jellinek
Even a few days of inadequate sleep can lead to anxiety and depressive symptoms, and chronic sleep deprivation is associated with a higher incidence of clinical depression. The relationship between inadequate sleep and depression is also two-way – disrupted sleep is a hallmark of depression. Beyond the links with depression, there appears to be an association between suicide attempts and inadequate sleep. One recent study found a threefold increase in the rate of suicide attempts in those adolescents who were getting less than 8 hours of sleep nightly, compared with their peers who were getting 8 or more hours of nightly sleep. The degree of risk is inversely related to the amount of sleep.3

Good mental health is not the only casualty of inadequate sleep. A growing body of evidence links short sleep duration with an increased risk of obesity. This appears to be mediated by alterations in neurohormones associated with sleep, leading to higher carbohydrate and fat intake, more snacking and insulin resistance.

Anything that compromises attention and reaction time, including sleep deprivation, adds risk to driving, particularly for inexperienced and impulsive adolescent drivers. The National Highway Transportation Safety Administration estimates that drivers 25 and younger cause more than half of all “fall asleep” crashes.

Teenagers generally know that they are exhausted, but the strategies they might use to manage their fatigue can actually make things worse. Sleepy teenagers often consume large amounts of caffeine to get through their days and their homework at night. Caffeine, in turn, interferes with both the onset and quality of sleep, perpetuating the cycle. Even “catch-up” sleep on weekends is a strategy that can contribute to the problem, as it can lead to more disrupted sleep by pushing the onset of school night sleepiness even later.

While growing autonomy is part of why teenagers are sleep deprived, they will consider the caring and informed guidance of their pediatricians about their health. Ask your teenage patients how much sleep they usually get on a school night. It can be validating to show them how sleep deprived they are, and point out how strategies like caffeine and oversleeping might be making it worse. Explain that people (adults, too!) need to make time for sleep just as they might for exercise or friends. Tell them about “good sleep hygiene,” the practice of having consistent sleep times and routines that are conducive to restful sleep. This can include a hot shower before bed, reading for the last 30 minutes before lights out, and no screen time for at least 1 hour before bed. Indeed, it can be powerful to urge that everyone in the family takes screens out of their bedrooms.

Additionally, while they might sleep in on weekends, it shouldn’t be much more than an hour longer than on weekdays. And no naps after school! It is common for teens to feel overwhelmed by their commitments and that sleep must be the first thing to go. Use their growing sense of autonomy to remind them that they get to choose how to use their time, and balance will pay off much more than sacrificing sleep. A practical conversation about sleep can help them to make informed choices and thoughtfully take care of themselves before they head off to college.

 

 

Dr. Swick is an attending psychiatrist in the division of child psychiatry at Massachusetts General Hospital, Boston, and director of the Parenting at a Challenging Time (PACT) Program at the Vernon Cancer Center at Newton Wellesley Hospital, also in Boston. Dr. Jellinek is professor emeritus of psychiatry and pediatrics, Harvard Medical School, Boston. Email them at pdnews@frontlinemedcom.com.

Resources

1. “Adolescent Sleep Needs and Patterns: Research Report and Resource Guide.” (Arlington, Va.: National Sleep Foundation, 2000.)

2. Pediatrics. 2014 Sep;134(3):e921-32.

3. Sleep. 2004 Nov 1;27(7):1351-8.

Publications
Publications
Topics
Article Type
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME

Women less likely to be diagnosed with sleep disorders

Article Type
Changed
Fri, 01/18/2019 - 16:45

 

Women are less likely to be diagnosed with and treated for sleep-disordered breathing, despite having symptoms similar to those of men, a Swedish study showed.

In a survey of 10,854 subjects, 14% of women reported being diagnosed with obstructive sleep apnea (OSA), compared with 25% of men (P less than .001), and 9% of women reported having any OSA treatment, compared with 16% of men (Sleep Med. 2017. doi: 10.1016/j.sleep.2017.02.032).

Underdiagnosis of sleep-disordered breathing (SDB) in women may have dire consequences, as symptoms, specifically snoring and excessive daytime sleepiness (EDS), correlate with increased risk for hypertension and diabetes, regardless of gender, according to Eva Lindberg, PhD, professor in the department of medical sciences, respiratory, allergy, and sleep research at Uppsala (Sweden) University, and her colleagues.

The mean age of the patients at baseline was 41 years. Mean body mass index was 25.4 kg/m2 for men and 24 kg/m2 for women.

On initial testing, approximately three times the percentage of men reported having issues with snoring and no EDS, compared with women (19% vs. 6% respectively), while more women reported the opposite, EDS but no snoring (19% vs. 11%). A slightly larger percentage of men reported having both symptoms (7.3% vs. 4.5%).

Investigators hypothesized the disparity between women and men reporting problems with snoring may be caused by gender expectations.


“It is more probable that SDB is still assumed to be a condition associated predominantly with men, and women feel ashamed of reporting these symptoms and seeking medical advice,” said Dr. Lindberg and her coinvestigators. These gender expectations may “contribute to females being less inclined to seek medical advice due to SDB symptoms.”

In a follow-up survey conducted 11 years after the initial one, doctors found 1,716 and 319 patients had received a new diagnosis for hypertension and diabetes, respectively.

While incidence was greater in men than in women for both (hypertension: 18.6% vs. 15.8% [P less than .001] and 3.6 vs. 2.4% [P less than .001], respectively), the investigators found “after adjusting for BMI and snoring at baseline, none of these gender differences remained significant.”


Physicians’ perception of SDB is partially responsible for the number of women who go undiagnosed, according to the researchers. Because SDB is considered to occur predominantly in males, doctors may overlook symptoms in female patients that would otherwise be a cause for further testing, they noted.

“[Even] among health professionals, SDB is still usually attributed to a male population, and female patients are therefore less frequently asked about the cardinal symptoms of snoring and sleepiness and do not therefore undergo sleep recordings. ... Also, among patients with obesity hypoventilation syndrome, females are generally diagnosed when the disease is more advanced and significantly more frequently develop acute disease before achieving treatment,” the investigators wrote.

“[Even] among health professionals, SDB is still usually attributed to a male population and female patients are therefore less frequently asked about the cardinal symptoms of snoring and sleepiness and do not therefore undergo sleep recordings ... Also, among patients with obesity hypoventilation syndrome, females are generally diagnosed when the disease is more advanced and significantly more frequently develop acute disease before achieving treatment,” the investigators claimed.

Dr. Lindberg and her team suggested engaging female patients more frequently about SDB symptoms, as well as referring patients with positive symptoms to participate in a sleep study.

The current study was limited by the nature of the data, which were self-reported. Patients were not surveyed via the Epworth Sleepiness Scale.

The study was funded by grants from the Norwegian Research Council, the Icelandic Research Council, Aarhus University, the Swedish Heart-Lung Foundation, and the Estonian Science Foundation.

The investigators reported no relevant financial disclosures.

ezimmerman@frontlinemedcom.com

Body

Krishna M. Sundar, MD, FCCP Associate Professor (Clinical), Pulmonary, Critical Care & Sleep Medicine
Dr. Krishna Sundar
Krishna Sundar, MD, FCCP, comments: The authors discuss the important topic of differing expression of OSA in male versus female subjects that may lead to under-recognition of sleep apnea in women.

Publications
Topics
Sections
Body

Krishna M. Sundar, MD, FCCP Associate Professor (Clinical), Pulmonary, Critical Care & Sleep Medicine
Dr. Krishna Sundar
Krishna Sundar, MD, FCCP, comments: The authors discuss the important topic of differing expression of OSA in male versus female subjects that may lead to under-recognition of sleep apnea in women.

Body

Krishna M. Sundar, MD, FCCP Associate Professor (Clinical), Pulmonary, Critical Care & Sleep Medicine
Dr. Krishna Sundar
Krishna Sundar, MD, FCCP, comments: The authors discuss the important topic of differing expression of OSA in male versus female subjects that may lead to under-recognition of sleep apnea in women.

 

Women are less likely to be diagnosed with and treated for sleep-disordered breathing, despite having symptoms similar to those of men, a Swedish study showed.

In a survey of 10,854 subjects, 14% of women reported being diagnosed with obstructive sleep apnea (OSA), compared with 25% of men (P less than .001), and 9% of women reported having any OSA treatment, compared with 16% of men (Sleep Med. 2017. doi: 10.1016/j.sleep.2017.02.032).

Underdiagnosis of sleep-disordered breathing (SDB) in women may have dire consequences, as symptoms, specifically snoring and excessive daytime sleepiness (EDS), correlate with increased risk for hypertension and diabetes, regardless of gender, according to Eva Lindberg, PhD, professor in the department of medical sciences, respiratory, allergy, and sleep research at Uppsala (Sweden) University, and her colleagues.

The mean age of the patients at baseline was 41 years. Mean body mass index was 25.4 kg/m2 for men and 24 kg/m2 for women.

On initial testing, approximately three times the percentage of men reported having issues with snoring and no EDS, compared with women (19% vs. 6% respectively), while more women reported the opposite, EDS but no snoring (19% vs. 11%). A slightly larger percentage of men reported having both symptoms (7.3% vs. 4.5%).

Investigators hypothesized the disparity between women and men reporting problems with snoring may be caused by gender expectations.


“It is more probable that SDB is still assumed to be a condition associated predominantly with men, and women feel ashamed of reporting these symptoms and seeking medical advice,” said Dr. Lindberg and her coinvestigators. These gender expectations may “contribute to females being less inclined to seek medical advice due to SDB symptoms.”

In a follow-up survey conducted 11 years after the initial one, doctors found 1,716 and 319 patients had received a new diagnosis for hypertension and diabetes, respectively.

While incidence was greater in men than in women for both (hypertension: 18.6% vs. 15.8% [P less than .001] and 3.6 vs. 2.4% [P less than .001], respectively), the investigators found “after adjusting for BMI and snoring at baseline, none of these gender differences remained significant.”


Physicians’ perception of SDB is partially responsible for the number of women who go undiagnosed, according to the researchers. Because SDB is considered to occur predominantly in males, doctors may overlook symptoms in female patients that would otherwise be a cause for further testing, they noted.

“[Even] among health professionals, SDB is still usually attributed to a male population, and female patients are therefore less frequently asked about the cardinal symptoms of snoring and sleepiness and do not therefore undergo sleep recordings. ... Also, among patients with obesity hypoventilation syndrome, females are generally diagnosed when the disease is more advanced and significantly more frequently develop acute disease before achieving treatment,” the investigators wrote.

“[Even] among health professionals, SDB is still usually attributed to a male population and female patients are therefore less frequently asked about the cardinal symptoms of snoring and sleepiness and do not therefore undergo sleep recordings ... Also, among patients with obesity hypoventilation syndrome, females are generally diagnosed when the disease is more advanced and significantly more frequently develop acute disease before achieving treatment,” the investigators claimed.

Dr. Lindberg and her team suggested engaging female patients more frequently about SDB symptoms, as well as referring patients with positive symptoms to participate in a sleep study.

The current study was limited by the nature of the data, which were self-reported. Patients were not surveyed via the Epworth Sleepiness Scale.

The study was funded by grants from the Norwegian Research Council, the Icelandic Research Council, Aarhus University, the Swedish Heart-Lung Foundation, and the Estonian Science Foundation.

The investigators reported no relevant financial disclosures.

ezimmerman@frontlinemedcom.com

 

Women are less likely to be diagnosed with and treated for sleep-disordered breathing, despite having symptoms similar to those of men, a Swedish study showed.

In a survey of 10,854 subjects, 14% of women reported being diagnosed with obstructive sleep apnea (OSA), compared with 25% of men (P less than .001), and 9% of women reported having any OSA treatment, compared with 16% of men (Sleep Med. 2017. doi: 10.1016/j.sleep.2017.02.032).

Underdiagnosis of sleep-disordered breathing (SDB) in women may have dire consequences, as symptoms, specifically snoring and excessive daytime sleepiness (EDS), correlate with increased risk for hypertension and diabetes, regardless of gender, according to Eva Lindberg, PhD, professor in the department of medical sciences, respiratory, allergy, and sleep research at Uppsala (Sweden) University, and her colleagues.

The mean age of the patients at baseline was 41 years. Mean body mass index was 25.4 kg/m2 for men and 24 kg/m2 for women.

On initial testing, approximately three times the percentage of men reported having issues with snoring and no EDS, compared with women (19% vs. 6% respectively), while more women reported the opposite, EDS but no snoring (19% vs. 11%). A slightly larger percentage of men reported having both symptoms (7.3% vs. 4.5%).

Investigators hypothesized the disparity between women and men reporting problems with snoring may be caused by gender expectations.


“It is more probable that SDB is still assumed to be a condition associated predominantly with men, and women feel ashamed of reporting these symptoms and seeking medical advice,” said Dr. Lindberg and her coinvestigators. These gender expectations may “contribute to females being less inclined to seek medical advice due to SDB symptoms.”

In a follow-up survey conducted 11 years after the initial one, doctors found 1,716 and 319 patients had received a new diagnosis for hypertension and diabetes, respectively.

While incidence was greater in men than in women for both (hypertension: 18.6% vs. 15.8% [P less than .001] and 3.6 vs. 2.4% [P less than .001], respectively), the investigators found “after adjusting for BMI and snoring at baseline, none of these gender differences remained significant.”


Physicians’ perception of SDB is partially responsible for the number of women who go undiagnosed, according to the researchers. Because SDB is considered to occur predominantly in males, doctors may overlook symptoms in female patients that would otherwise be a cause for further testing, they noted.

“[Even] among health professionals, SDB is still usually attributed to a male population, and female patients are therefore less frequently asked about the cardinal symptoms of snoring and sleepiness and do not therefore undergo sleep recordings. ... Also, among patients with obesity hypoventilation syndrome, females are generally diagnosed when the disease is more advanced and significantly more frequently develop acute disease before achieving treatment,” the investigators wrote.

“[Even] among health professionals, SDB is still usually attributed to a male population and female patients are therefore less frequently asked about the cardinal symptoms of snoring and sleepiness and do not therefore undergo sleep recordings ... Also, among patients with obesity hypoventilation syndrome, females are generally diagnosed when the disease is more advanced and significantly more frequently develop acute disease before achieving treatment,” the investigators claimed.

Dr. Lindberg and her team suggested engaging female patients more frequently about SDB symptoms, as well as referring patients with positive symptoms to participate in a sleep study.

The current study was limited by the nature of the data, which were self-reported. Patients were not surveyed via the Epworth Sleepiness Scale.

The study was funded by grants from the Norwegian Research Council, the Icelandic Research Council, Aarhus University, the Swedish Heart-Lung Foundation, and the Estonian Science Foundation.

The investigators reported no relevant financial disclosures.

ezimmerman@frontlinemedcom.com

Publications
Publications
Topics
Article Type
Click for Credit Status
Active
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
CME ID
138331
Vitals

 

Key clinical point: Women are less likely to be tested for sleep disorders, a factor leading to underdiagnoses and potential long-term health risks.

Major finding: Women were less likely than were men to be diagnosed with sleep apnea (14% vs. 25%, P = .001) or given treatment for any kind of sleep disordered breathing (9% vs. 16%, P = .01).

Data source: Survey of 10,854 subjects: 4,962 men and 5,892 women, gathered from the European Community Respiratory Health Survey with subsequent follow-up.

Disclosures: The study was funded by grants from the Norwegian Research Council, the Icelandic Research Council, Aarhus University, the Swedish Heart-Lung Foundation, and the Estonian Science Foundation. The investigators report no relevant financial disclosures.

Tools measuring oxygen desaturation produced disparate data

Article Type
Changed
Fri, 01/18/2019 - 16:45

 

WASHINGTON – Oxygen desaturation index (ODI) scores showed significant variation across two software systems, a study showed.


The researchers assessed the ODI scores of 106 patients using the ResMed ApneaLink Plus system (AL) and the Compumedics Grael Profusion PSG3 system (Comp). “AL ODI values tended to be higher than Comp ODI values, but with significant variability,” they said.


AL  showed a bias of an additional 4.4 events per hour (95% limits of agreement, –5.8 to 14.6 events per hour) for ODI scores at 4% desaturation and a bias of an additional 7.1 events per hour (95% limits of agreement, –6.4 to 20.6 events per hour) at 3% desaturation (J Clin Sleep Med. 2017;13[4]:599-605).


This may be problematic for physicians evaluating patients during sleep studies who rely on ODI scores at 3% and 4% desaturations to create accurate apnea severity assessments, the investigators said.


“[The] wide limits of agreement in our study highlight that clinicians cannot be confident that an ODI4% recorded in the AL is the same as that recorded in the Comp,” wrote Yvonne Ng, MBBS, of the department of lung and sleep medicine at Monash Health, Victoria, Australia, and her colleagues. “The differences are large enough to significantly affect diagnostic thresholds for OSA [obstructive sleep apnea] and, in particular, moderate-severe OSA.”


The researchers gathered data from patients undergoing sleep analysis at the Monash Medical Centre, who were, on average, 47 years of age, had a body mass index score of 32 kg/m2, and had an apnea hypopnea index (AHI) of 23.2.


ODI3% scores analyzed through Comp diagnosed 66 patients with OSA (ODI3% greater than or equal to 5 events per hour), while desaturation events analyzed through the AL system diagnosed 90 patients, a 36% increase over Comp (P = .0002).


When researchers tested for moderate to severe OSA (ODI3% greater than or equal to 15 events per hour), 32 patients were diagnosed using the Comp system, compared with 59 patients using the AL system.


Disparities in these measurements create uncertainty among clinicians, who rely on ODI measurements for scores that are accurate and can be easily replicated using an algorithm, the researchers said.


“The current work demonstrates that significantly more patients would receive a diagnosis of OSA, or more particularly, moderate-severe OSA, with the AL ODI, compared to the Comp ODI,” Dr. Ng and her colleagues wrote.


When sensitivity scores for Comp and AL were compared, AL ODI3% scores were significantly more sensitive than Comp, with sensitivity scores of 96% vs. 58%.


Using different fingers for measuring desaturation during the test or differences in algorithms used to assess ODI scores were possible sources of the disparities, the researchers noted.

Differences in internal processing between the two systems were the most likely causes of the discrepancies between the data collected using each system, they added.


Because there is no universal standard for ODI measurements, the researchers were unable to determine which system was more accurate.


Several of the researchers reported receiving financial support, research equipment, or consultancy fees from various entities.

Body

Krishna M. Sundar, MD, FCCP Associate Professor (Clinical), Pulmonary, Critical Care & Sleep Medicine
Dr. Krishna Sundar
Krishna Sundar, MD, FCCP, comments: This article raises significant concerns about the role of different oximeters in contributing to the variation in hypopnea scoring.

Publications
Topics
Sections
Body

Krishna M. Sundar, MD, FCCP Associate Professor (Clinical), Pulmonary, Critical Care & Sleep Medicine
Dr. Krishna Sundar
Krishna Sundar, MD, FCCP, comments: This article raises significant concerns about the role of different oximeters in contributing to the variation in hypopnea scoring.

Body

Krishna M. Sundar, MD, FCCP Associate Professor (Clinical), Pulmonary, Critical Care & Sleep Medicine
Dr. Krishna Sundar
Krishna Sundar, MD, FCCP, comments: This article raises significant concerns about the role of different oximeters in contributing to the variation in hypopnea scoring.

 

WASHINGTON – Oxygen desaturation index (ODI) scores showed significant variation across two software systems, a study showed.


The researchers assessed the ODI scores of 106 patients using the ResMed ApneaLink Plus system (AL) and the Compumedics Grael Profusion PSG3 system (Comp). “AL ODI values tended to be higher than Comp ODI values, but with significant variability,” they said.


AL  showed a bias of an additional 4.4 events per hour (95% limits of agreement, –5.8 to 14.6 events per hour) for ODI scores at 4% desaturation and a bias of an additional 7.1 events per hour (95% limits of agreement, –6.4 to 20.6 events per hour) at 3% desaturation (J Clin Sleep Med. 2017;13[4]:599-605).


This may be problematic for physicians evaluating patients during sleep studies who rely on ODI scores at 3% and 4% desaturations to create accurate apnea severity assessments, the investigators said.


“[The] wide limits of agreement in our study highlight that clinicians cannot be confident that an ODI4% recorded in the AL is the same as that recorded in the Comp,” wrote Yvonne Ng, MBBS, of the department of lung and sleep medicine at Monash Health, Victoria, Australia, and her colleagues. “The differences are large enough to significantly affect diagnostic thresholds for OSA [obstructive sleep apnea] and, in particular, moderate-severe OSA.”


The researchers gathered data from patients undergoing sleep analysis at the Monash Medical Centre, who were, on average, 47 years of age, had a body mass index score of 32 kg/m2, and had an apnea hypopnea index (AHI) of 23.2.


ODI3% scores analyzed through Comp diagnosed 66 patients with OSA (ODI3% greater than or equal to 5 events per hour), while desaturation events analyzed through the AL system diagnosed 90 patients, a 36% increase over Comp (P = .0002).


When researchers tested for moderate to severe OSA (ODI3% greater than or equal to 15 events per hour), 32 patients were diagnosed using the Comp system, compared with 59 patients using the AL system.


Disparities in these measurements create uncertainty among clinicians, who rely on ODI measurements for scores that are accurate and can be easily replicated using an algorithm, the researchers said.


“The current work demonstrates that significantly more patients would receive a diagnosis of OSA, or more particularly, moderate-severe OSA, with the AL ODI, compared to the Comp ODI,” Dr. Ng and her colleagues wrote.


When sensitivity scores for Comp and AL were compared, AL ODI3% scores were significantly more sensitive than Comp, with sensitivity scores of 96% vs. 58%.


Using different fingers for measuring desaturation during the test or differences in algorithms used to assess ODI scores were possible sources of the disparities, the researchers noted.

Differences in internal processing between the two systems were the most likely causes of the discrepancies between the data collected using each system, they added.


Because there is no universal standard for ODI measurements, the researchers were unable to determine which system was more accurate.


Several of the researchers reported receiving financial support, research equipment, or consultancy fees from various entities.

 

WASHINGTON – Oxygen desaturation index (ODI) scores showed significant variation across two software systems, a study showed.


The researchers assessed the ODI scores of 106 patients using the ResMed ApneaLink Plus system (AL) and the Compumedics Grael Profusion PSG3 system (Comp). “AL ODI values tended to be higher than Comp ODI values, but with significant variability,” they said.


AL  showed a bias of an additional 4.4 events per hour (95% limits of agreement, –5.8 to 14.6 events per hour) for ODI scores at 4% desaturation and a bias of an additional 7.1 events per hour (95% limits of agreement, –6.4 to 20.6 events per hour) at 3% desaturation (J Clin Sleep Med. 2017;13[4]:599-605).


This may be problematic for physicians evaluating patients during sleep studies who rely on ODI scores at 3% and 4% desaturations to create accurate apnea severity assessments, the investigators said.


“[The] wide limits of agreement in our study highlight that clinicians cannot be confident that an ODI4% recorded in the AL is the same as that recorded in the Comp,” wrote Yvonne Ng, MBBS, of the department of lung and sleep medicine at Monash Health, Victoria, Australia, and her colleagues. “The differences are large enough to significantly affect diagnostic thresholds for OSA [obstructive sleep apnea] and, in particular, moderate-severe OSA.”


The researchers gathered data from patients undergoing sleep analysis at the Monash Medical Centre, who were, on average, 47 years of age, had a body mass index score of 32 kg/m2, and had an apnea hypopnea index (AHI) of 23.2.


ODI3% scores analyzed through Comp diagnosed 66 patients with OSA (ODI3% greater than or equal to 5 events per hour), while desaturation events analyzed through the AL system diagnosed 90 patients, a 36% increase over Comp (P = .0002).


When researchers tested for moderate to severe OSA (ODI3% greater than or equal to 15 events per hour), 32 patients were diagnosed using the Comp system, compared with 59 patients using the AL system.


Disparities in these measurements create uncertainty among clinicians, who rely on ODI measurements for scores that are accurate and can be easily replicated using an algorithm, the researchers said.


“The current work demonstrates that significantly more patients would receive a diagnosis of OSA, or more particularly, moderate-severe OSA, with the AL ODI, compared to the Comp ODI,” Dr. Ng and her colleagues wrote.


When sensitivity scores for Comp and AL were compared, AL ODI3% scores were significantly more sensitive than Comp, with sensitivity scores of 96% vs. 58%.


Using different fingers for measuring desaturation during the test or differences in algorithms used to assess ODI scores were possible sources of the disparities, the researchers noted.

Differences in internal processing between the two systems were the most likely causes of the discrepancies between the data collected using each system, they added.


Because there is no universal standard for ODI measurements, the researchers were unable to determine which system was more accurate.


Several of the researchers reported receiving financial support, research equipment, or consultancy fees from various entities.

Publications
Publications
Topics
Article Type
Click for Credit Status
Ready
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Vitals

 

Key clinical point: Two software systems used for measuring patients’ oxygen desaturation indexes produced disparate results.

Major finding: ODI tests analyzed using the ResMed APneaLink Plus system vs. Compumedics Grael Profusion PSG3 system reported ODI4% bias = 4.4 events per hour (95% limits of agreement, –5.8 to 14.6 events per hour) and ODI3% bias = 7.1 events per hour (95% limits of agreement, –6.4 to 20.6 events per hour).

Data source: ODI test results for 106 participants in a sleep study at Monash Medical Centre.

Disclosures: Several of the researchers reported receiving financial support, research equipment, or consultancy fees from various entities.
 

Sleep Strategies: Sleep in adults with Down syndrome

Article Type
Changed
Tue, 10/23/2018 - 16:10

 

Down syndrome (DS) is the most common chromosomal disorder with an estimated 250,700 children, teens, and adults living with DS in the United States in 2008 (CDC.gov). The life expectancy for individuals with DS has increased due to improved medical care, educational interventions, and identification and management of underlying psychiatric and behavioral problems. This has resulted in increased median age to 49 years, and the life expectancy of a 1-year-old child with DS to more than 60 to 65 years (Bittles et al. Dev Med Child Neurol. 2004;46[4]:282).

Sleep medicine specialists have been very involved in the care of the pediatric DS population but with the improved survival, more adult patients with DS are presenting to sleep clinics for their care. The complexity of caring for adult patients with DS poses a challenge to sleep specialists, especially with the paucity of literature and clinical guidelines.

Dr. Fidaa Shaib
OSA is more prevalent in children with DS (30% to 55%) compared with control subjects (2%). This high OSA prevalence further increases to 90% in adults with DS and is associated with more oxygen desaturation, hypoventilation, and sleep disruption (Trois et al. J Clin Sleep Med. 2009;5[4]:317). Childhood risk factors for OSA in DS are mostly related to hypotonia, relatively large tongue, tonsillar and adenoid hypertrophy, and the small airway. Obesity, hypothyroidism, and, more importantly, advancing age contribute to the increased risk of OSA in adults with DS. Central sleep apnea is relatively rare in adults with DS (Esbensen. Int Rev Res Ment Retard. 2010;39(C):107).

A bidirectional relationship exists between sleep disorders and mood and cognitive problems in this population. The frequency of OSA diagnosis is increased in adults with DS who present with new-onset mood disorder or declining adaptive skills (Capone et al. Am J Med Genet A. 2013;161A[9]:2188). OSA in DS is associated with sleep disruption, decreased slow wave sleep, and intermittent hypoxemia that are thought to contribute to the mechanism of declining cognitive function and memory. Given that individuals with DS are genetically at increased risk for diffuse senile plaque formation in the brain (a characteristic pathologic finding in Alzheimer’s disease brain), the super-imposed sleep fragmentation and intermittent hypoxia may accelerate the cognitive decline (Fernandez et al. J Alzheimers Dis Parkinsonism. 2013;3[2]:124).

In addition, sleep in adults with DS is characterized by a high incidence of sleep fragmentation and circadian misalignment with delayed sleep onset and early morning awakenings (Esbensen. J Intellect Disabil Res. 2016;60[1]:68). The DS population is also at increased risk for developing depression, anxiety, obsessive-compulsive tendencies, and behavioral issues. It is also worth noting that there is a tenfold increase in autism spectrum disease in this population, and a rare condition of developmental regression in adolescents with DS has recently been recognized. Patients usually present with rapid, atypical loss of previously attained skills in cognition, socialization, and activities of daily living that may further complicate their care. The regression occurs with maladaptive behaviors that develop in relation to new transitions, hormonal or menstrual changes, or major life events (Jensen et al. Br Med J. 2014;349:g5596). As a result, new behavioral sleep problems may emerge, or challenges to the treatment of existing sleep disorders may ensue. All of the aforementioned conditions alone or in combination pose additional challenges for the management of sleep problems in this population.

Adults with DS continue to manifest the same spectrum of health problems as children with DS. Adults with DS also tend toward premature aging, which puts them at risk for additional health problems seen in the geriatric population (Covelli et al. Int J Rehabil Res. 2016;39[1]:20). Adults with DS will age earlier and two times faster than control subjects (Nakamura et al. Mech Ageing Dev. 1998;05:89). Coexisting obesity and worsening cognitive function that further increase after the age of 40 will make multiple aspects of medical management very challenging (Carfi et al. Front Med. 2014;1:51).

The care of the adult patient with DS can be best delivered through a multidisciplinary team, led by physicians well informed about the specific needs of this population. The role of the sleep specialist is essential, given the implications of sleep on health and cognitive and behavioral function. The approach to diagnosing disorders of sleep timing, quality, and duration includes a focused history. Incorporating actigraphic monitoring provides additional information that can be relevant and useful. The value of the parent-reported sleep diary becomes less and less reliable as patients enter adolescence and adulthood. Attended sleep studies are widely utilized for diagnosing sleep-disordered breathing, but their value in guiding therapy is debatable. There are multiple factors that can affect the validity of a single night of sleep testing for the individual patient. Such factors include poor sleep achieved in a strange environment and sleep position variations when compared with sleep at home. There is no evidence yet to support the use of portable sleep testing in this population.

Establishing and maintaining routines are critical in different aspects of the care of this special population, particularly in relation to behavioral sleep problems. Success is dependent on the caregiver’s approach and level of involvement in their care, the individual’s intellectual ability, and the presence of other comorbidities. Management of obesity with counseling on healthy diet and participation in exercise programs are also integral parts of their care.

Although treatment with positive airway pressure (PAP) is thought to be effective in treating OSA in DS, little data are available to support its efficacy and benefits. Treatment of OSA with PAP can be very challenging. Our sleep center experience incorporates a personalized approach with gradual PAP desensitization in addition to positive feedback and a reward system to encourage and maintain use. We also utilize behavioral therapy to encourage avoidance of supine sleep in order to decrease the severity of OSA in patients who do not accept or tolerate PAP. Surgical interventions based on assessment of the upper airway during sleep through dynamic imaging or sleep endoscopy may also be considered. A recent report of hypoglossal nerve stimulation therapy in an adolescent with severe OSA suggests a potentially new alternative option for therapy (Diercks et al. Pediatrics. 2016;137(5). doi: 10.1542/peds.2015-3663.

It seems intuitive that the management of sleep disorders in adult patients with DS positively contributes to their care and promotes their overall wellbeing. Adult patients with DS continue to present particular diagnostic and therapeutic challenges that have become even more complex as their life expectancy has increased. Further research and clinical guidelines are momentously needed in order to guide the management of sleep disorders for this particularly challenging patient population.

 

 

Dr. Shaib is Associate Professor of Medicine, Medical Director, Baylor St Luke’s Center for Sleep Medicine, Department of Medicine, Section of Pulmonary, Critical Care, and Sleep Medicine, Baylor College of Medicine, Houston, Texas.

Publications
Topics
Sections

 

Down syndrome (DS) is the most common chromosomal disorder with an estimated 250,700 children, teens, and adults living with DS in the United States in 2008 (CDC.gov). The life expectancy for individuals with DS has increased due to improved medical care, educational interventions, and identification and management of underlying psychiatric and behavioral problems. This has resulted in increased median age to 49 years, and the life expectancy of a 1-year-old child with DS to more than 60 to 65 years (Bittles et al. Dev Med Child Neurol. 2004;46[4]:282).

Sleep medicine specialists have been very involved in the care of the pediatric DS population but with the improved survival, more adult patients with DS are presenting to sleep clinics for their care. The complexity of caring for adult patients with DS poses a challenge to sleep specialists, especially with the paucity of literature and clinical guidelines.

Dr. Fidaa Shaib
OSA is more prevalent in children with DS (30% to 55%) compared with control subjects (2%). This high OSA prevalence further increases to 90% in adults with DS and is associated with more oxygen desaturation, hypoventilation, and sleep disruption (Trois et al. J Clin Sleep Med. 2009;5[4]:317). Childhood risk factors for OSA in DS are mostly related to hypotonia, relatively large tongue, tonsillar and adenoid hypertrophy, and the small airway. Obesity, hypothyroidism, and, more importantly, advancing age contribute to the increased risk of OSA in adults with DS. Central sleep apnea is relatively rare in adults with DS (Esbensen. Int Rev Res Ment Retard. 2010;39(C):107).

A bidirectional relationship exists between sleep disorders and mood and cognitive problems in this population. The frequency of OSA diagnosis is increased in adults with DS who present with new-onset mood disorder or declining adaptive skills (Capone et al. Am J Med Genet A. 2013;161A[9]:2188). OSA in DS is associated with sleep disruption, decreased slow wave sleep, and intermittent hypoxemia that are thought to contribute to the mechanism of declining cognitive function and memory. Given that individuals with DS are genetically at increased risk for diffuse senile plaque formation in the brain (a characteristic pathologic finding in Alzheimer’s disease brain), the super-imposed sleep fragmentation and intermittent hypoxia may accelerate the cognitive decline (Fernandez et al. J Alzheimers Dis Parkinsonism. 2013;3[2]:124).

In addition, sleep in adults with DS is characterized by a high incidence of sleep fragmentation and circadian misalignment with delayed sleep onset and early morning awakenings (Esbensen. J Intellect Disabil Res. 2016;60[1]:68). The DS population is also at increased risk for developing depression, anxiety, obsessive-compulsive tendencies, and behavioral issues. It is also worth noting that there is a tenfold increase in autism spectrum disease in this population, and a rare condition of developmental regression in adolescents with DS has recently been recognized. Patients usually present with rapid, atypical loss of previously attained skills in cognition, socialization, and activities of daily living that may further complicate their care. The regression occurs with maladaptive behaviors that develop in relation to new transitions, hormonal or menstrual changes, or major life events (Jensen et al. Br Med J. 2014;349:g5596). As a result, new behavioral sleep problems may emerge, or challenges to the treatment of existing sleep disorders may ensue. All of the aforementioned conditions alone or in combination pose additional challenges for the management of sleep problems in this population.

Adults with DS continue to manifest the same spectrum of health problems as children with DS. Adults with DS also tend toward premature aging, which puts them at risk for additional health problems seen in the geriatric population (Covelli et al. Int J Rehabil Res. 2016;39[1]:20). Adults with DS will age earlier and two times faster than control subjects (Nakamura et al. Mech Ageing Dev. 1998;05:89). Coexisting obesity and worsening cognitive function that further increase after the age of 40 will make multiple aspects of medical management very challenging (Carfi et al. Front Med. 2014;1:51).

The care of the adult patient with DS can be best delivered through a multidisciplinary team, led by physicians well informed about the specific needs of this population. The role of the sleep specialist is essential, given the implications of sleep on health and cognitive and behavioral function. The approach to diagnosing disorders of sleep timing, quality, and duration includes a focused history. Incorporating actigraphic monitoring provides additional information that can be relevant and useful. The value of the parent-reported sleep diary becomes less and less reliable as patients enter adolescence and adulthood. Attended sleep studies are widely utilized for diagnosing sleep-disordered breathing, but their value in guiding therapy is debatable. There are multiple factors that can affect the validity of a single night of sleep testing for the individual patient. Such factors include poor sleep achieved in a strange environment and sleep position variations when compared with sleep at home. There is no evidence yet to support the use of portable sleep testing in this population.

Establishing and maintaining routines are critical in different aspects of the care of this special population, particularly in relation to behavioral sleep problems. Success is dependent on the caregiver’s approach and level of involvement in their care, the individual’s intellectual ability, and the presence of other comorbidities. Management of obesity with counseling on healthy diet and participation in exercise programs are also integral parts of their care.

Although treatment with positive airway pressure (PAP) is thought to be effective in treating OSA in DS, little data are available to support its efficacy and benefits. Treatment of OSA with PAP can be very challenging. Our sleep center experience incorporates a personalized approach with gradual PAP desensitization in addition to positive feedback and a reward system to encourage and maintain use. We also utilize behavioral therapy to encourage avoidance of supine sleep in order to decrease the severity of OSA in patients who do not accept or tolerate PAP. Surgical interventions based on assessment of the upper airway during sleep through dynamic imaging or sleep endoscopy may also be considered. A recent report of hypoglossal nerve stimulation therapy in an adolescent with severe OSA suggests a potentially new alternative option for therapy (Diercks et al. Pediatrics. 2016;137(5). doi: 10.1542/peds.2015-3663.

It seems intuitive that the management of sleep disorders in adult patients with DS positively contributes to their care and promotes their overall wellbeing. Adult patients with DS continue to present particular diagnostic and therapeutic challenges that have become even more complex as their life expectancy has increased. Further research and clinical guidelines are momentously needed in order to guide the management of sleep disorders for this particularly challenging patient population.

 

 

Dr. Shaib is Associate Professor of Medicine, Medical Director, Baylor St Luke’s Center for Sleep Medicine, Department of Medicine, Section of Pulmonary, Critical Care, and Sleep Medicine, Baylor College of Medicine, Houston, Texas.

 

Down syndrome (DS) is the most common chromosomal disorder with an estimated 250,700 children, teens, and adults living with DS in the United States in 2008 (CDC.gov). The life expectancy for individuals with DS has increased due to improved medical care, educational interventions, and identification and management of underlying psychiatric and behavioral problems. This has resulted in increased median age to 49 years, and the life expectancy of a 1-year-old child with DS to more than 60 to 65 years (Bittles et al. Dev Med Child Neurol. 2004;46[4]:282).

Sleep medicine specialists have been very involved in the care of the pediatric DS population but with the improved survival, more adult patients with DS are presenting to sleep clinics for their care. The complexity of caring for adult patients with DS poses a challenge to sleep specialists, especially with the paucity of literature and clinical guidelines.

Dr. Fidaa Shaib
OSA is more prevalent in children with DS (30% to 55%) compared with control subjects (2%). This high OSA prevalence further increases to 90% in adults with DS and is associated with more oxygen desaturation, hypoventilation, and sleep disruption (Trois et al. J Clin Sleep Med. 2009;5[4]:317). Childhood risk factors for OSA in DS are mostly related to hypotonia, relatively large tongue, tonsillar and adenoid hypertrophy, and the small airway. Obesity, hypothyroidism, and, more importantly, advancing age contribute to the increased risk of OSA in adults with DS. Central sleep apnea is relatively rare in adults with DS (Esbensen. Int Rev Res Ment Retard. 2010;39(C):107).

A bidirectional relationship exists between sleep disorders and mood and cognitive problems in this population. The frequency of OSA diagnosis is increased in adults with DS who present with new-onset mood disorder or declining adaptive skills (Capone et al. Am J Med Genet A. 2013;161A[9]:2188). OSA in DS is associated with sleep disruption, decreased slow wave sleep, and intermittent hypoxemia that are thought to contribute to the mechanism of declining cognitive function and memory. Given that individuals with DS are genetically at increased risk for diffuse senile plaque formation in the brain (a characteristic pathologic finding in Alzheimer’s disease brain), the super-imposed sleep fragmentation and intermittent hypoxia may accelerate the cognitive decline (Fernandez et al. J Alzheimers Dis Parkinsonism. 2013;3[2]:124).

In addition, sleep in adults with DS is characterized by a high incidence of sleep fragmentation and circadian misalignment with delayed sleep onset and early morning awakenings (Esbensen. J Intellect Disabil Res. 2016;60[1]:68). The DS population is also at increased risk for developing depression, anxiety, obsessive-compulsive tendencies, and behavioral issues. It is also worth noting that there is a tenfold increase in autism spectrum disease in this population, and a rare condition of developmental regression in adolescents with DS has recently been recognized. Patients usually present with rapid, atypical loss of previously attained skills in cognition, socialization, and activities of daily living that may further complicate their care. The regression occurs with maladaptive behaviors that develop in relation to new transitions, hormonal or menstrual changes, or major life events (Jensen et al. Br Med J. 2014;349:g5596). As a result, new behavioral sleep problems may emerge, or challenges to the treatment of existing sleep disorders may ensue. All of the aforementioned conditions alone or in combination pose additional challenges for the management of sleep problems in this population.

Adults with DS continue to manifest the same spectrum of health problems as children with DS. Adults with DS also tend toward premature aging, which puts them at risk for additional health problems seen in the geriatric population (Covelli et al. Int J Rehabil Res. 2016;39[1]:20). Adults with DS will age earlier and two times faster than control subjects (Nakamura et al. Mech Ageing Dev. 1998;05:89). Coexisting obesity and worsening cognitive function that further increase after the age of 40 will make multiple aspects of medical management very challenging (Carfi et al. Front Med. 2014;1:51).

The care of the adult patient with DS can be best delivered through a multidisciplinary team, led by physicians well informed about the specific needs of this population. The role of the sleep specialist is essential, given the implications of sleep on health and cognitive and behavioral function. The approach to diagnosing disorders of sleep timing, quality, and duration includes a focused history. Incorporating actigraphic monitoring provides additional information that can be relevant and useful. The value of the parent-reported sleep diary becomes less and less reliable as patients enter adolescence and adulthood. Attended sleep studies are widely utilized for diagnosing sleep-disordered breathing, but their value in guiding therapy is debatable. There are multiple factors that can affect the validity of a single night of sleep testing for the individual patient. Such factors include poor sleep achieved in a strange environment and sleep position variations when compared with sleep at home. There is no evidence yet to support the use of portable sleep testing in this population.

Establishing and maintaining routines are critical in different aspects of the care of this special population, particularly in relation to behavioral sleep problems. Success is dependent on the caregiver’s approach and level of involvement in their care, the individual’s intellectual ability, and the presence of other comorbidities. Management of obesity with counseling on healthy diet and participation in exercise programs are also integral parts of their care.

Although treatment with positive airway pressure (PAP) is thought to be effective in treating OSA in DS, little data are available to support its efficacy and benefits. Treatment of OSA with PAP can be very challenging. Our sleep center experience incorporates a personalized approach with gradual PAP desensitization in addition to positive feedback and a reward system to encourage and maintain use. We also utilize behavioral therapy to encourage avoidance of supine sleep in order to decrease the severity of OSA in patients who do not accept or tolerate PAP. Surgical interventions based on assessment of the upper airway during sleep through dynamic imaging or sleep endoscopy may also be considered. A recent report of hypoglossal nerve stimulation therapy in an adolescent with severe OSA suggests a potentially new alternative option for therapy (Diercks et al. Pediatrics. 2016;137(5). doi: 10.1542/peds.2015-3663.

It seems intuitive that the management of sleep disorders in adult patients with DS positively contributes to their care and promotes their overall wellbeing. Adult patients with DS continue to present particular diagnostic and therapeutic challenges that have become even more complex as their life expectancy has increased. Further research and clinical guidelines are momentously needed in order to guide the management of sleep disorders for this particularly challenging patient population.

 

 

Dr. Shaib is Associate Professor of Medicine, Medical Director, Baylor St Luke’s Center for Sleep Medicine, Department of Medicine, Section of Pulmonary, Critical Care, and Sleep Medicine, Baylor College of Medicine, Houston, Texas.

Publications
Publications
Topics
Article Type
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME

Management of chronic insomnia in adults

Article Type
Changed
Fri, 01/18/2019 - 16:42

 

Most adults experience problems with sleep from time to time, and 6%-10% meet diagnostic criteria for chronic insomnia. Many of these patients present to their primary care clinicians looking for help. This clinical practice guideline from the American College of Physicians provides recommendations based on a review of studies published during the previous decade, which were assessed in terms of the strength of the recommendation and the quality of evidence. The guideline resulted in two recommendations:

1: All adult patients should receive cognitive behavioral therapy for insomnia (CBT-I) as the initial treatment for chronic insomnia. (strong recommendation)

2: Clinicians should use a shared decision-making approach discussing the benefits, harms, and costs of short-term use of medications, to decide whether to add pharmacological therapy in adults with chronic insomnia in whom cognitive behavioral therapy for insomnia (CBT-I) alone was unsuccessful. (weak recommendation)

Cognitive behavioral therapy for insomnia (CBT-I)

Cognitive behavioral therapy for insomnia encompasses a variety of measures that aim to change patients’ habits and beliefs associated with sleep. These measures include general “sleep hygiene” interventions, as well as stimulus control, sleep restriction, relaxation training, and cognitive reframing. With sleep hygiene, patients are educated about environmental factors that affect sleep, such as avoiding caffeine late in the day, limiting alcohol intake, having a regular sleep schedule, avoiding napping, the importance of exercise, and the importance of a quiet dark room in which to sleep. Examples of stimulus control include going to bed only when sleepy, and avoiding reading and watching TV in the bedroom. Sleep restriction limits the time in bed with strict sleep and wake-up times, gradually increasing time in bed as sleep efficiency improves.

Dr. Neil Skolnik

Clinicians may find it surprising that this guideline makes such a strong, clear case for the primacy of behavioral measures in the treatment of chronic insomnia. The authors make a number of points in support of this position.

First, the effects of behavioral interventions appear to be robust – at least comparable to the short-term effects of medications – and often significantly better. For example, various studies of CBT-I show a decrease in sleep onset latency (how long it takes to fall asleep after going to bed) of between 12 and 31 minutes and an increase in total sleep time of 40 minutes. This compares favorably to the short-term effects of commonly used sleep medications.

Second, the effects of behavioral interventions are long-lasting compared with medications, which are usually approved for only short-term use, lose effectiveness over time, and have no benefit at all once they’re no longer being taken. Finally, there appear to be no harms associated with CBT-I, compared with significant adverse effects of medications.

One challenge is that access to effective behavioral interventions for insomnia can be an issue. On the other hand, a number of behavioral delivery methods were examined, and found to be effective, including in-person individual or group therapy, telephone- or Web-based modules or apps, and self-help books. An editorial accompanying the guidelines calls for efforts to increase the availability of behavioral modalities for insomnia.

Pharmacologic therapy

The recommendation to use pharmacologic therapy for insomnia is much more qualified than that for CBT-I, with language about shared decision-making, discussion of risks and benefits, emphasis on short-term use, and a provision that it be used only after an unsatisfactory trial of CBT-I alone. In addition, this recommendation is classified as “weak,” and the associated evidence “low-quality.” Medications reviewed included eszopiclone, zaleplon, zolpidem, orexin receptor antagonist, melatonin, ramelteon, and benzodiazepines.

There are several reasons why pharmacologic therapy is deemphasized. First, as noted above, the effects of commonly used medications are modest. As an example, typical patients with chronic insomnia will have sleep-onset latency of 60-70 minutes. Medications reviewed for this guideline decreased this time by approximately 10-20 minutes in short-term studies, so patients still took 40-60 minutes to fall asleep. Similar modest short-term effects were seen in terms of increasing total sleep time.

A second issue with pharmacologic therapy is that while many patients with chronic insomnia seek to use medications long term, the available studies have tended to look only at short-term use, and those studies with longer duration show a diminution of medication effect over time.

Finally, there are significant adverse effects associated with sedative-hypnotic medications, including somnolence, anxiety, confusion, and disturbance in attention. This is problematic, considering that these are precisely the symptoms that patients may be hoping to avoid when they take medications to help them sleep. Even patients who may not feel impaired often show demonstrable deficits in attention and performance following use of sleep medications; this issue is reflected in the boxed warnings that accompany several commonly prescribed agents.

It is noted in the evidence reviews that there are differences among the available medications. The nonbenzodiazepine hypnotics eszopiclone and zolpidem as well as the orexin receptor antagonist suvorexant improved short-term sleep quality, though the effect was small and there was significant evidence of harm as described above. Benzodiazepine hypnotics, melatonin agonists, and antidepressants studied had little or low-quality evidence to support efficacy on improving sleep. For melatonin and ramelteon, the evidence review notes that adverse effects did not differ between the medication and the placebo groups, though two open-label longer-term studies showed evidence of adverse effects with ramelteon. It is also important to note that patients studied in medication trials were mostly healthy middle-aged individuals; it is possible that the side effects of sleep medications may be greater in those who are older or more infirm.
 

 

 

Bottom line

This guideline from the American College of Physicians strongly endorses the use of tailored cognitive behavioral therapy modalities for the initial treatment of patients with chronic insomnia. Medications are given a weak recommendation for a limited back-up role.

Dr. Clark is associate director of the family medicine residency program at Abington (Pa.) Jefferson Health. Dr. Skolnik is professor of family and community medicine at Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, and associate director of the family medicine residency program at Abington Jefferson Health.

References

Qaseem A, et al. Management of Chronic Insomnia Disorder in Adults: A Clinical Practice Guideline From the American College of Physicians. Ann Intern Med. 2016;165:125-33.

Brasure M. Psychological and Behavioral Interventions for Managing Insomnia Disorder: An Evidence Report for a Clinical Practice Guideline by the American College of Physicians. Ann Intern Med. 2016;165:113-24.

Wilt TJ, et al. Pharmacologic Treatment of Insomnia Disorder: An Evidence Report for a Clinical Practice Guideline by the American College of Physicians. Ann Intern Med. 2016;165:103-12.

Publications
Topics
Sections

 

Most adults experience problems with sleep from time to time, and 6%-10% meet diagnostic criteria for chronic insomnia. Many of these patients present to their primary care clinicians looking for help. This clinical practice guideline from the American College of Physicians provides recommendations based on a review of studies published during the previous decade, which were assessed in terms of the strength of the recommendation and the quality of evidence. The guideline resulted in two recommendations:

1: All adult patients should receive cognitive behavioral therapy for insomnia (CBT-I) as the initial treatment for chronic insomnia. (strong recommendation)

2: Clinicians should use a shared decision-making approach discussing the benefits, harms, and costs of short-term use of medications, to decide whether to add pharmacological therapy in adults with chronic insomnia in whom cognitive behavioral therapy for insomnia (CBT-I) alone was unsuccessful. (weak recommendation)

Cognitive behavioral therapy for insomnia (CBT-I)

Cognitive behavioral therapy for insomnia encompasses a variety of measures that aim to change patients’ habits and beliefs associated with sleep. These measures include general “sleep hygiene” interventions, as well as stimulus control, sleep restriction, relaxation training, and cognitive reframing. With sleep hygiene, patients are educated about environmental factors that affect sleep, such as avoiding caffeine late in the day, limiting alcohol intake, having a regular sleep schedule, avoiding napping, the importance of exercise, and the importance of a quiet dark room in which to sleep. Examples of stimulus control include going to bed only when sleepy, and avoiding reading and watching TV in the bedroom. Sleep restriction limits the time in bed with strict sleep and wake-up times, gradually increasing time in bed as sleep efficiency improves.

Dr. Neil Skolnik

Clinicians may find it surprising that this guideline makes such a strong, clear case for the primacy of behavioral measures in the treatment of chronic insomnia. The authors make a number of points in support of this position.

First, the effects of behavioral interventions appear to be robust – at least comparable to the short-term effects of medications – and often significantly better. For example, various studies of CBT-I show a decrease in sleep onset latency (how long it takes to fall asleep after going to bed) of between 12 and 31 minutes and an increase in total sleep time of 40 minutes. This compares favorably to the short-term effects of commonly used sleep medications.

Second, the effects of behavioral interventions are long-lasting compared with medications, which are usually approved for only short-term use, lose effectiveness over time, and have no benefit at all once they’re no longer being taken. Finally, there appear to be no harms associated with CBT-I, compared with significant adverse effects of medications.

One challenge is that access to effective behavioral interventions for insomnia can be an issue. On the other hand, a number of behavioral delivery methods were examined, and found to be effective, including in-person individual or group therapy, telephone- or Web-based modules or apps, and self-help books. An editorial accompanying the guidelines calls for efforts to increase the availability of behavioral modalities for insomnia.

Pharmacologic therapy

The recommendation to use pharmacologic therapy for insomnia is much more qualified than that for CBT-I, with language about shared decision-making, discussion of risks and benefits, emphasis on short-term use, and a provision that it be used only after an unsatisfactory trial of CBT-I alone. In addition, this recommendation is classified as “weak,” and the associated evidence “low-quality.” Medications reviewed included eszopiclone, zaleplon, zolpidem, orexin receptor antagonist, melatonin, ramelteon, and benzodiazepines.

There are several reasons why pharmacologic therapy is deemphasized. First, as noted above, the effects of commonly used medications are modest. As an example, typical patients with chronic insomnia will have sleep-onset latency of 60-70 minutes. Medications reviewed for this guideline decreased this time by approximately 10-20 minutes in short-term studies, so patients still took 40-60 minutes to fall asleep. Similar modest short-term effects were seen in terms of increasing total sleep time.

A second issue with pharmacologic therapy is that while many patients with chronic insomnia seek to use medications long term, the available studies have tended to look only at short-term use, and those studies with longer duration show a diminution of medication effect over time.

Finally, there are significant adverse effects associated with sedative-hypnotic medications, including somnolence, anxiety, confusion, and disturbance in attention. This is problematic, considering that these are precisely the symptoms that patients may be hoping to avoid when they take medications to help them sleep. Even patients who may not feel impaired often show demonstrable deficits in attention and performance following use of sleep medications; this issue is reflected in the boxed warnings that accompany several commonly prescribed agents.

It is noted in the evidence reviews that there are differences among the available medications. The nonbenzodiazepine hypnotics eszopiclone and zolpidem as well as the orexin receptor antagonist suvorexant improved short-term sleep quality, though the effect was small and there was significant evidence of harm as described above. Benzodiazepine hypnotics, melatonin agonists, and antidepressants studied had little or low-quality evidence to support efficacy on improving sleep. For melatonin and ramelteon, the evidence review notes that adverse effects did not differ between the medication and the placebo groups, though two open-label longer-term studies showed evidence of adverse effects with ramelteon. It is also important to note that patients studied in medication trials were mostly healthy middle-aged individuals; it is possible that the side effects of sleep medications may be greater in those who are older or more infirm.
 

 

 

Bottom line

This guideline from the American College of Physicians strongly endorses the use of tailored cognitive behavioral therapy modalities for the initial treatment of patients with chronic insomnia. Medications are given a weak recommendation for a limited back-up role.

Dr. Clark is associate director of the family medicine residency program at Abington (Pa.) Jefferson Health. Dr. Skolnik is professor of family and community medicine at Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, and associate director of the family medicine residency program at Abington Jefferson Health.

References

Qaseem A, et al. Management of Chronic Insomnia Disorder in Adults: A Clinical Practice Guideline From the American College of Physicians. Ann Intern Med. 2016;165:125-33.

Brasure M. Psychological and Behavioral Interventions for Managing Insomnia Disorder: An Evidence Report for a Clinical Practice Guideline by the American College of Physicians. Ann Intern Med. 2016;165:113-24.

Wilt TJ, et al. Pharmacologic Treatment of Insomnia Disorder: An Evidence Report for a Clinical Practice Guideline by the American College of Physicians. Ann Intern Med. 2016;165:103-12.

 

Most adults experience problems with sleep from time to time, and 6%-10% meet diagnostic criteria for chronic insomnia. Many of these patients present to their primary care clinicians looking for help. This clinical practice guideline from the American College of Physicians provides recommendations based on a review of studies published during the previous decade, which were assessed in terms of the strength of the recommendation and the quality of evidence. The guideline resulted in two recommendations:

1: All adult patients should receive cognitive behavioral therapy for insomnia (CBT-I) as the initial treatment for chronic insomnia. (strong recommendation)

2: Clinicians should use a shared decision-making approach discussing the benefits, harms, and costs of short-term use of medications, to decide whether to add pharmacological therapy in adults with chronic insomnia in whom cognitive behavioral therapy for insomnia (CBT-I) alone was unsuccessful. (weak recommendation)

Cognitive behavioral therapy for insomnia (CBT-I)

Cognitive behavioral therapy for insomnia encompasses a variety of measures that aim to change patients’ habits and beliefs associated with sleep. These measures include general “sleep hygiene” interventions, as well as stimulus control, sleep restriction, relaxation training, and cognitive reframing. With sleep hygiene, patients are educated about environmental factors that affect sleep, such as avoiding caffeine late in the day, limiting alcohol intake, having a regular sleep schedule, avoiding napping, the importance of exercise, and the importance of a quiet dark room in which to sleep. Examples of stimulus control include going to bed only when sleepy, and avoiding reading and watching TV in the bedroom. Sleep restriction limits the time in bed with strict sleep and wake-up times, gradually increasing time in bed as sleep efficiency improves.

Dr. Neil Skolnik

Clinicians may find it surprising that this guideline makes such a strong, clear case for the primacy of behavioral measures in the treatment of chronic insomnia. The authors make a number of points in support of this position.

First, the effects of behavioral interventions appear to be robust – at least comparable to the short-term effects of medications – and often significantly better. For example, various studies of CBT-I show a decrease in sleep onset latency (how long it takes to fall asleep after going to bed) of between 12 and 31 minutes and an increase in total sleep time of 40 minutes. This compares favorably to the short-term effects of commonly used sleep medications.

Second, the effects of behavioral interventions are long-lasting compared with medications, which are usually approved for only short-term use, lose effectiveness over time, and have no benefit at all once they’re no longer being taken. Finally, there appear to be no harms associated with CBT-I, compared with significant adverse effects of medications.

One challenge is that access to effective behavioral interventions for insomnia can be an issue. On the other hand, a number of behavioral delivery methods were examined, and found to be effective, including in-person individual or group therapy, telephone- or Web-based modules or apps, and self-help books. An editorial accompanying the guidelines calls for efforts to increase the availability of behavioral modalities for insomnia.

Pharmacologic therapy

The recommendation to use pharmacologic therapy for insomnia is much more qualified than that for CBT-I, with language about shared decision-making, discussion of risks and benefits, emphasis on short-term use, and a provision that it be used only after an unsatisfactory trial of CBT-I alone. In addition, this recommendation is classified as “weak,” and the associated evidence “low-quality.” Medications reviewed included eszopiclone, zaleplon, zolpidem, orexin receptor antagonist, melatonin, ramelteon, and benzodiazepines.

There are several reasons why pharmacologic therapy is deemphasized. First, as noted above, the effects of commonly used medications are modest. As an example, typical patients with chronic insomnia will have sleep-onset latency of 60-70 minutes. Medications reviewed for this guideline decreased this time by approximately 10-20 minutes in short-term studies, so patients still took 40-60 minutes to fall asleep. Similar modest short-term effects were seen in terms of increasing total sleep time.

A second issue with pharmacologic therapy is that while many patients with chronic insomnia seek to use medications long term, the available studies have tended to look only at short-term use, and those studies with longer duration show a diminution of medication effect over time.

Finally, there are significant adverse effects associated with sedative-hypnotic medications, including somnolence, anxiety, confusion, and disturbance in attention. This is problematic, considering that these are precisely the symptoms that patients may be hoping to avoid when they take medications to help them sleep. Even patients who may not feel impaired often show demonstrable deficits in attention and performance following use of sleep medications; this issue is reflected in the boxed warnings that accompany several commonly prescribed agents.

It is noted in the evidence reviews that there are differences among the available medications. The nonbenzodiazepine hypnotics eszopiclone and zolpidem as well as the orexin receptor antagonist suvorexant improved short-term sleep quality, though the effect was small and there was significant evidence of harm as described above. Benzodiazepine hypnotics, melatonin agonists, and antidepressants studied had little or low-quality evidence to support efficacy on improving sleep. For melatonin and ramelteon, the evidence review notes that adverse effects did not differ between the medication and the placebo groups, though two open-label longer-term studies showed evidence of adverse effects with ramelteon. It is also important to note that patients studied in medication trials were mostly healthy middle-aged individuals; it is possible that the side effects of sleep medications may be greater in those who are older or more infirm.
 

 

 

Bottom line

This guideline from the American College of Physicians strongly endorses the use of tailored cognitive behavioral therapy modalities for the initial treatment of patients with chronic insomnia. Medications are given a weak recommendation for a limited back-up role.

Dr. Clark is associate director of the family medicine residency program at Abington (Pa.) Jefferson Health. Dr. Skolnik is professor of family and community medicine at Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, and associate director of the family medicine residency program at Abington Jefferson Health.

References

Qaseem A, et al. Management of Chronic Insomnia Disorder in Adults: A Clinical Practice Guideline From the American College of Physicians. Ann Intern Med. 2016;165:125-33.

Brasure M. Psychological and Behavioral Interventions for Managing Insomnia Disorder: An Evidence Report for a Clinical Practice Guideline by the American College of Physicians. Ann Intern Med. 2016;165:113-24.

Wilt TJ, et al. Pharmacologic Treatment of Insomnia Disorder: An Evidence Report for a Clinical Practice Guideline by the American College of Physicians. Ann Intern Med. 2016;165:103-12.

Publications
Publications
Topics
Article Type
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME