CPAP Pressure for Prediction of Oral Appliance Treatment Response in Obstructive Sleep Apnea

Notes from Dr. Norman Blumenstock
In Australian patients, the majority of whom are Caucasian, a higher therapeutic CPAP pressure requirement in conjunction with age and OSA severity characteristics may be useful to indicate likelihood of success with oral appliance (MAS) as an alternative therapy.

Scientific Investigations

CPAP Pressure for Prediction of Oral Appliance Treatment Response in Obstructive Sleep Apnea

http://dx.doi.org/10.5664/jcsm.4020

Kate Sutherland, Ph.D.1,2; Craig L. Phillips, Ph.D.1,2; Amanda Davies, B.Sc.(Hons)1,2; Vasanth K. Srinivasan, M.D.Sc.3; Oyku Dalci, Ph.D.3; Brendon J. Yee, M.D., Ph.D.1,4; M. Ali Darendeliler, Ph.D.3; Ronald R. Grunstein, M.D., Ph.D.1,4; Peter A. Cistulli, M.D., Ph.D.1,2

1NHMRC Centre for Sleep Health (CIRUS), University of Sydney, Australia; 2Centre for Sleep Health and Research, Department of Respiratory Medicine, Royal North Shore Hospital, Sydney, Australia; 3Discipline of Orthodontics, Faculty of Dentistry, University of Sydney, Sydney Dental Hospital, Australia; 4Department of Respiratory and Sleep Medicine, Royal Prince Alfred Hospital, Sydney, Australia

ABSTRACT

Study Objectives

Mandibular advancement splints (MAS) are often preferred to CPAP treatment for OSA but are not always equally efficacious. High therapeutic CPAP pressure has been associated with MAS treatment failure in a Japanese population. We sought to assess the relationship between CPAP pressure and MAS treatment response in an Australian population.

Methods

Therapeutic CPAP pressure and MAS treatment response were obtained from a one-month crossover trial of both treatments. Predictive utility of CPAP pressure to identify MAS treatment response was assessed.

Results

Seventy-eight OSA patients were included (age 49.3 ± 11.1 years, BMI 29.1 ± 5.8 kg/m2) with predominantly moderate-severe OSA (AHI 30.0 ± 12.7/h). CPAP pressure was lower in MAS responders (MAS AHI < 10/h) 9.7 ± 1.6 vs. 11.7 ± 2.4 cm H O, p < 0.01, with area under ROC curve of 0.74 (95% CI 0.63-0.86), p < 0.01. The best cutoff value of 10.5 cm H O useful for discriminating MAS responders and non-responders in the previous Japanese population, was inadequate for prediction in the current population (0.47 negative predictive value [NPV]). However a cutoff of 13 cm H O identified MAS non-responders (1.0 NPV). Multivariate regression identified CPAP pressure (odds ratio [95% confidence interval] 0.53 [0.33-0.87], age (0.93 [0.87-0.99]) and AHI (0.92 [0.86-0.97]) as predictors of MAS treatment response (model r2 = 0.54, p < 0.001).

Conclusions

In Australian patients, the majority of whom are Caucasian, a higher therapeutic CPAP pressure requirement in conjunction with age and OSA severity characteristics may be useful to indicate likelihood of success with MAS as an alternative therapy.

Citation

Sutherland K, Phillips CL, Davies A, Srinivasan VK, Dalci O, Yee BJ, Darendeliler MA, Grunstein RR, Cistulli PA. CPAP pressure for prediction of oral appliance treatment response in obstructive sleep apnea. J Clin Sleep Med 2014;10(9):943-949.

Continuous positive airway pressure (CPAP) is the standard treatment for obstructive sleep apnea (OSA). Although highly efficacious, CPAP is often hindered by poor tolerance and suboptimal adherence,1 limiting its effectiveness in the real world. Mandibular advancement splints (MAS) are an alternative option recommended as a first-line treatment for mild-moderate OSA.2 We have recently found that health outcome improvements, including sleepiness, are similar with MAS and CPAP treatments in patients with moderate-severe OSA.3 Superior patient adherence appears to offset any inferiority of MAS efficacy,3 and MAS may be considered a viable alternative for many patients.

However despite similar health benefits between treatments, approximately one-third of OSA patients will not respond to MAS.4–7 This is of significant concern in terms of resource wastage and treatment delays. Much attention has been given to understanding patient phenotypes which relate to MAS response such as gender, obesity, craniofacial structure, and type and severity of OSA.8 However, none of these factors are universal, and hence there is an unresolved need for reliable indicators of MAS treatment response.

A recent Japanese study has identified pressure requirement in CPAP users as a predictor of MAS response.9 In established CPAP users, a prescribed pressure of above 10.5 cm H2O indicated poor response to subsequent MAS therapy. This prediction method is, of course, restricted to patients who have used CPAP and wish to try MAS. However CPAP pressure would represent a simple predictor, either alone or possibly in combination with other patient characteristics to further improve prediction. This would be clinically useful in patients who have failed or are non-adherent to CPAP and would support implementation of MAS therapy as an alternative in such patients.

In this study, we aimed to firstly confirm a relationship between therapeutic CPAP pressure and MAS treatment response in treatment-naive OSA patients, and secondly to investigate the utility of therapeutic CPAP pressure as an indicator of MAS treatment outcome in an Australian population, predominantly comprised of Caucasians.

METHODS

Patients

OSA patients were participants in a previously published randomized crossover trial of one month of CPAP versus MAS to compare health effects.3 Inclusion criteria for this trial were a new diagnosis of OSA, aged ≥ 20 years, apnea-hypopnea index (AHI) > 10 events/h, ≥ 2 symptoms of OSA, and willingness to use both CPAP and MAS. No limits for body mass index (BMI) were set for inclusion. Exclusion criteria were central sleep apnea, previous OSA treatment, requiring immediate treatment, contraindications to MAS therapy, regular sedative or narcotic use, preexisting lung disease, or psychiatric disease. Self-reported ethnicity data was not collected in this study; however, the majority of patients likely have Caucasian ancestry.

Study Protocol

Patients underwent an acclimatization phase to both CPAP and MAS in a randomized order to optimize both treatments before the study. Subsequently patients were randomized to one month each of CPAP and MAS, with treatment response determined by polysomnography at end of each treatment. The study protocol in Figure 1 illustrates the acquisition of data utilized in this analysis.

BRIEF SUMMARY

Current Knowledge/Study Rationale: CPAP pressure has been shown to predict oral appliance treatment response in Japanese male OSA patients and could be a simple and useful clinical predictor for some OSA patients. We sought to assess the relationship between CPAP pressure and oral appliance treatment response in a predominantly Caucasian population.

Study Impact: We confirm a relationship between lower CPAP pressure and oral appliance treatment response, although not as strong as in the Japanese population and requiring a higher CPAP pressure cutoff value for best predictive utility. CPAP pressure requirement, in conjunction with patient characteristics of age and OSA severity, may be useful in indicating oral appliance treatment response in Caucasian OSA populations.

CPAP

All patients used the same CPAP device (ResMed Autoset S8, ResMed, Bella Vista, Australia). Patients were given the device to use in Autoset mode at home. Therapeutic pressure was determined by the 95th percentile pressure from usage exceeding 4 hours. Therapeutic CPAP pressure was confirmed by overnight polysomnography on CPAP treatment. Only participants who achieved AHI < 5 events/h on this night were included in the analysis as a stringent definition of therapeutic CPAP pressure.

MAS

The MAS used was a titratable two-piece customized device (SomnoDent, SomnoMed Ltd, Australia) with previously established clinical efficacy.4,10 Patients underwent a 6-week acclimatization period to incrementally advance the device until maximal comfortable jaw protrusion was reached and confirmed by the treating orthodontist.

Treatment Response Definitions

In order to assess generalizability, we used 3 definitions of treatment outcome that are used variably in clinical practice and to allow comparison with previous findings.9 MAS treatment response was most stringently defined as complete resolution of OSA defined by a treatment AHI < 5 events/h (definition 1). As baseline AHI was > 10/h in this sample, this also reflects a > 50% decrease in all patients. Secondly, treatment response was defined as a MAS treatment AHI < 10 events/h and > 50% reduction in AHI from baseline (definition 2). Thirdly, a more liberal definition of response was defined as ≥ 50% reduction in AHI from baseline regardless of the final AHI achieved (definition 3). These 3 alternate definitions of MAS treatment response are summarized in Table 1.

Statistical Analysis

Statistical analyses were performed using statistical software (SPSS version 21.0 for Windows; SPSS, Inc., IL, USA). Continuous variables (optimal CPAP pressure and other baseline characteristics) were compared between MAS treatment response groups using independent t-test and categorical variables with χ2 test. Univariate logistic regression was used to assess the predictive value of CPAP pressure for MAS response. Multivariate logistic regression analysis was used to identify the best prediction model from patient variables and therapeutic CPAP pressure. Predicted values of the models were assessed by receiver operating characteristic (ROC) curve analysis using the area under curve (AUC).

RESULTS

Patient Characteristics

Seventy-eight patients who completed both MAS and CPAP treatment arms were confirmed to have AHI < 5/h on CPAP and were therefore included in the analysis. Excluded patients (CPAP AHI > 5/h) did not differ in age, BMI, neck or waist circumference, AHI, MAS response, or CPAP pressure requirement compared to those included in the analysis. Eight patients had mild OSA (AHI 10-14.9/h), 33 moderate (AHI 15-29.9/h), and 37 had severe OSA (AHI > 30/h). Patients were predominantly Caucasian, mostly male (81%), middle-aged, and over-weight; 52.6 percent of patients had a complete response to MAS treatment (AHI < 5/h, definition 1). Baseline characteristics are shown in Table 2. MAS treatment responders were significantly younger and less obese with a tendency towards a lower baseline AHI than non-responders. However gender proportions and supine-predominant OSA frequency did not differ between responders and non-responders in this sample.

Therapeutic CPAP Pressure and MAS Treatment Response

Mean CPAP pressure was 10.4 ± 2.1 (± SD), with a range of 4-18 cm H2O. CPAP pressure did not significantly differ between responders and non-responders by definition 1 (10.0 ± 1.4 vs. 10.8 ± 2.6 cm H2O, p = 0.09). By definition 2, responders (AHI < 10/h on MAS) had a lower CPAP pressure requirement than non-responders (9.7 ± 1.6 vs. 11.7 ± 2.4 cm H2O, p < 0.01). Responders defined by ≥ 50% reduction in AHI (definition 3) also had a lower CPAP pressure (10.0 ± 2.0 vs. 11.6 ± 2.3 cm H2O, p < 0.05). CPAP pressures for responders and non-responders, by all 3 definitions, are shown in Figure 2. In univariate analysis CPAP pressure had predictive value in discriminating MAS treatment responders and non-responders by definitions 2 (AUC [95% CI] 0.74 [0.63-0.86], p < 0.01) and 3 (0.70 [0.55-0.84], p < 0.05) (Table 3). As post-treatment AHI < 10/h (definition 2) is probably the most clinically useful, we explored CPAP pressure cutoff values to correctly classify patients using this model (Table 4). A pressure cutoff value of 13 cm H2O most accurately identified non-responders to MAS therapy (negative predictive value = 1). However, patients requiring pressures ≥ 13 cm H2O represented < 10% of this patient sample. This cutoff value correctly classified 69.2% of patients as MAS responders or non-responders. Below 13 cm H2O there was much overlap in pressures between responders and non-responders making CPAP pressure alone inadequate to discriminate between these patients.

Prediction of MAS Treatment Response

Multivariate logistic regression was performed to assess the utility of baseline characteristics (age, gender, BMI, neck circumference, baseline AHI, in combination with CPAP pressure) in the prediction of MAS treatment response (Table 5). In the model for MAS response by definition 1 (MAS AHI < 5/h) only baseline AHI and age were significant predictors. In predicting MAS response by definition 2 (MAS AHI < 10/h), the combination of baseline AHI, age, and CPAP pressure were significant, with 54% of the variance in MAS response explained by the model. This multivariate model correctly classified more patients than the prediction model based on CPAP pressure alone (AUC [95%CI] 0.84[0.75-0.93], p < 0.001). By definition 3 of MAS response (≥ 50% AHI reduction), only age and neck circumference, but not CPAP pressure, had predictive value.

DISCUSSION

This is the largest study to assess the relationship between therapeutic CPAP pressure and MAS treatment response and the first study in a treatment-naive and a non-Japanese population. Our findings lend support to the previously reported relationship between CPAP pressure and MAS treatment response,9 and extend these findings by identifying a much higher CPAP pressure cutoff for negative prediction of MAS response in this population. The implication is that there may be population-specific characteristics that influence the cutoff pressure values for which CPAP is best predictive of MAS response. This could be attributed to differences in obesity and craniofacial phenotypes between Japanese and Australian populations.

Our data support the notion that there is some relationship between MAS treatment response and CPAP pressure requirement with MAS non-responders requiring higher pressures. However this relationship seems not to be as pronounced as in the previous Japanese study, with higher pressures only observed in nonresponders by definitions 2 and 3 (MAS AHI < 10/h and > 50% AHI reduction). The median difference in pressures between responders and non-responders was also much narrower in the current study at 1 cm H2O, compared to ≥ 4 cm H2O in the previous study. In the Japanese study, a CPAP pressure cutoff value of 10.5 cm H2O most reliably classified patients in terms of MAS response, with pressures higher than this generally indicating a negative response to MAS.9 This value was inadequate for use in our patient sample and correctly classified only 47% of patients as non-responders, due to a large overlap of MAS treatment responders and non-responders with therapeutic CPAP pressures in the < 12 cm H2O range. Our results indicate that application of this method of prediction to an Australian population requires a higher cutoff value of 13 cm H2O for best discrimination, with 100% of patients above this level correctly classified as non-responders and 75% of the patients below this level as responders. This substantial difference in CPAP cutoff values to best classify MAS responders and nonresponders between these two populations suggests that there may be an influence of ethnicity factors on the relationship between CPAP pressure and MAS treatment response.

There are recognized differences between ethnicities in craniofacial and obesity risk factors associated with OSA. For the same level of OSA severity, Caucasians have been shown to have more obesity compared to Asians with OSA, whereas Asians show a greater restriction in craniofacial skeletal measurements associated with OSA, such as restricted maxillary and dimensions and retro-positioning, compared to Caucasians.11–14 Therefore both populations appear to have an anatomical imbalance contributing to upper airway collapsibility,15,16 but this is primarily driven by excess soft tissues in Caucasians and bony restriction in Asians. Differences in the relationship between CPAP pressure and MAS response may relate to these different hard and soft tissue proportions. BMI was lower in MAS responders in our study and was a predictor of response in univariate analyses (data not shown); however, no such relationship was evident in the Japanese study,9 suggesting obesity was less of a factor in MAS treatment response. BMI and neck circumference also relate to CPAP pressure in Caucasian populations.17,18 Craniofacial measurements have additionally contributed to CPAP pressure determination in a Japanese study, whereas only soft palate length had any association with CPAP pressure in a French study.19,20 Therefore craniofacial/obesity factors may have also differentially contributed to MAS response and/or CPAP pressure requirements between the two populations, although craniofacial factors were not assessed in either study.

Differences in the relationship between CPAP pressure and MAS treatment response between these two studies may additionally relate to other factors. There was also a difference in gender between the two studies, with the study of Tsuiki and colleagues including only males. Nineteen percent of subjects in the current study population were female. However there was still not adequate numbers to determine if gender has an influence on the MAS response/CPAP pressure relationship, although there was no difference in pressure requirement between genders (data not shown). Treatment success rates were much higher in the current study, with a greater proportion of patients achieving AHI < 5/h with MAS (47.6% vs. 29%), which may relate to differences in MAS devices. In the current study a titratable, two-piece appliance was used which allows the jaw to be advanced incrementally over time to maximize efficacy.21,22 Our treatments were implemented as part of a one-month crossover trial of optimal forms of both MAS and CPAP treatment with a 2-week treatment washout period in between. This differs to the previous Japanese study in which long-term compliant CPAP users were invited to participate and try MAS therapy.9 Previous and consistent use of CPAP may have some effect on the subsequent relationship with MAS treatment outcome, as it is possible that long-term CPAP use may influence the efficacy of MAS therapy through changes in upper airway and soft tissues and craniofacial skeletal structure.23,24

Our study found CPAP pressure combined with patient age and OSA severity (AHI) in a multivariate model provided the best discrimination of MAS treatment responders and nonresponders in this OSA population. Patient factors such as younger age, less obesity, female gender, and supine-dependent OSA have variously been associated with MAS treatment success.6,25–28 A significant limitation of MAS therapy is the inability to pre-identify patients with a good treatment response. Overall it seems unlikely that MAS response can be determined by single patient characteristics alone. MAS response is influenced by multiple factors relating to both structural and functional aspects of the upper airway.29 Objectively validated tests of MAS treatment function may ultimately be required to accurately predict treatment response.10,30–33 For example a single-night titration study of mandibular advancement using an available commercial remotely controlled titration device or assessment of upper airway response to mandibular advancement via nasendoscopy to observe the airway response during drug-induced sleep or even wakefulness.34–36However in CPAP failure patients with known therapeutic pressure, this information in conjunction with age and OSA severity characteristics, may be useful to give an indication of the likelihood of success with MAS as an alternative therapy.

This study has extended investigation of a relationship between therapeutic CPAP pressure and MAS treatment response in a large sample of Australian OSA patients. However, potential study limitations include that although there was a range of pressures in the sample (4-18 cm H2O), only a minority of the sample (10%) required pressures higher than 13 cm H2O. Therefore we cannot confirm whether our negative predictive value would remain as high with the inclusion of more patients in the higher range. However, these pressures were confirmed to be therapeutic by polysomnography and they are within the range of commonly prescribed pressures. Furthermore, we were able to adequately demonstrate that the lower pressure cutoff value of 10.5 cm H2O is unsuitable for the studied population. Craniofacial factors are also implicated in MAS treatment response, but craniofacial assessment was not included in this analysis; however, a comprehensive cephalometric study in a similar OSA population suggests that craniofacial factors alone are not highly predictive of MAS response,37 and these can be difficult to assess in routine clinical practice. Finally, although our sample population likely included mostly patients with Caucasian ancestry, no ethnicity data was collected in this study.

In conclusion, therapeutic CPAP pressure was higher in MAS treatment non-responders compared to responders (depending on the definition of response used). CPAP pressure did have predictive utility in discriminating MAS treatment responders and non-responders in this sample of Australian OSA patients. However, the previously determined CPAP pressure threshold to identify MAS non-responders in a Japanese population was found to be inadequate for reliable prediction. Our results suggest CPAP pressures above 13 cm H2O are likely to indicate non-responsiveness to MAS treatment in the studied population. However prospective validation of CPAP pressure as a predictor of MAS response is still required. A combination of age, OSA severity, and CPAP pressure provided the best estimation of MAS treatment response, illustrating that one single patient variable is unlikely to provide a definitive indication in all patients. This study highlights the need to test reported prediction methods in different OSA populations in which relevant factors such as obesity and craniofacial phenotypes are likely to differ.

DISCLOSURE STATEMENT

ResMed Inc donated all continuous positive airway pressure equipment for the trial. SomnoMed Ltd. donated all oral appliances for the trial. Dr. Cistulli is a chief investigator on sponsored clinical trials in obstructive sleep apnea for ResMed Inc and Exploramed Inc. His department receives equipment support for oral appliance research from SomnoMed Ltd, and he has a pecuniary interest in the company from previous involvement in product development. He is a medical advisor to Exploramed Inc (a US medical device incubator) and Zephyr Sleep Technologies. He has received speaker fees/travel support from ResMed Inc Fisher & Paykel Healthcare. The other authors have indicated no financial conflicts of interest.

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12 Foods That Sabotage Sleep

Notes from Dr. Norman Blumenstock
Remember not to go to sleep on a "full stomach".

It's recommended that you have at least 3 hours after eating before you go to sleep in order to avoid any negative issues.

Sleep Better

The foods you eat for dinner or shortly before bed can prevent you from getting some much-needed zzz's. Here's what to shun for up to several hours before turning in if you want to sleep better and wake rested — from tomatoes and chocolate to cheddar cheese.

Celery

Steer clear of celery just before bed. Celery and other foods with a high water content (cucumbers, watermelon, radishes and such) are natural diuretics that may cause you to wake in the middle of the night with a full bladder.

Tomatoes

Tomatoes are rich in tyramine, an amino acid that triggers the brain to release norepinephrine, a stimulant that boosts brain activity and delays sleep. Other tyramine-rich foods include eggplant, soy sauce, red wine and aged cheeses, such as brie and Stilton.

Cheese Pizza

Foods high in fat and fried foods take longer to digest and can cause discomfort that interferes with sleep. They can also reduce the effectiveness of some medications taken at night, says Alon Avidan, a neurologist and director of UCLA's David Geffen School of Medicine Sleep Disorders Center.

Alcohol

Although a nightcap or a glass of wine before bed may help you doze off quicker, it disrupts sleep later in the night and robs you of rapid eye movement (REM) sleep. Lack of REM sleep harms concentration, memory and motor skills.

Black-bean chili

This dish could be a disaster if you eat it close to bedtime. The body has a hard time digesting beans, so stomach-rumbling gas pains will keep you from a good night's sleep, says Helen Rasmussen, a research nutritionist at Tufts University.

Dark chocolate

A small piece of dark chocolate each day helps keep your heart healthy — but don't nibble it right before you go to bed. Dark chocolate (though not white chocolate), hot cocoa and tea all contain caffeine, and if you're caffeine-sensitive, you may find yourself staring at the ceiling instead of sleeping.

Gumdrops

A handful of gumdrops (or any candy) may cause your blood sugar levels to spike and then fall rapidly as the body releases insulin to bring them under control. You may fall asleep easily, but these fluctuations make it difficult to stay asleep.

Tacos

A taco liberally sprinkled with hot sauce may set your taste buds tingling, but eating it within a few hours of lights-out can set you up for a bad case of heartburn and a restless night. Ditto for other spicy foods.

Steak

Save the leftover slice of steak for lunch tomorrow. Foods high in protein and marbled fats, such as steak and roast beef, are slow to digest. If your body is busy digesting food, there's more of a chance that you'll have a restless night.

Carbonated soft drinks

Caffeine, that sneak thief of sleep, can turn up in unexpected places, including root beer and lemon-lime soda. Added to a food or beverage, caffeine must be listed as an ingredient; if it occurs naturally (coffee, tea, chocolate), it doesn't. Check the label.

Dagwood sandwich

A heavy meal just before bed can rob you of the shut-eye you need. Allow at least three hours post-meal before you turn in so your body has a chance to digest the food and you don't feel too uncomfortable to sleep.

Broccoli

Broccoli is a nutrition powerhouse, but its slow-to-digest fiber will keep your body working hard into the night. Broccoli and its relatives cauliflower and brussels sprouts also contain an indigestible sugar that will produce large amounts of gas.

The Power of Sleep

Notes from Dr. Norman Blumenstock
New research shows a good night's rest isn't a luxury--it's critical for your brain and for your health

New research shows a good night's rest isn't a luxury--it's critical for your brain and for your health

When our heads hit the pillow every night, we tend to think we’re surrendering. Not just to exhaustion, though there is that. We’re also surrendering our mind, taking leave of our focus on sensory cues, like noise and smell and blinking lights. It’s as if we’re powering ourselves down like we do the electronics at our bedside–going idle for a while, only to spring back into action when the alarm blasts hours later.

That’s what we think is happening. But as scientists are now revealing, that couldn’t be further from the truth.

In fact, when the lights go out, our brains start working–but in an altogether different way than when we’re awake. At night, a legion of neurons springs into action, and like any well-trained platoon, the cells work in perfect synchrony, pulsing with electrical signals that wash over the brain with a soothing, hypnotic flow. Meanwhile, data processors sort through the reams of information that flooded the brain all day at a pace too overwhelming to handle in real time. The brain also runs checks on itself to ensure that the exquisite balance of hormones, enzymes and proteins isn’t too far off-kilter. And all the while, cleaners follow in close pursuit to sweep out the toxic detritus that the brain doesn’t need and which can cause all kinds of problems if it builds up.

This, scientists are just now learning, is the brain on sleep. It’s nature’s panacea, more powerful than any drug in its ability to restore and rejuvenate the human brain and body. Getting the recommended seven to eight hours each night can improve concentration, sharpen planning and memory skills and maintain the fat-burning systems that regulate our weight. If every one of us slept as much as we’re supposed to, we’d all be lighter, less prone to developing Type 2 diabetes and most likely better equipped to battle depression and anxiety. We might even lower our risk of Alzheimer’s disease, osteoporosis and cancer.

The trouble is, sleep works only if we get enough of it. While plenty of pills can knock us out, none so far can replicate all of sleep’s benefits, despite decades’ worth of attempts in high-tech pharmaceutical labs.

Which is why, after long treating rest as a good-if-you-can-get-it obligation, scientists are making the case that it matters much more than we think. They’re not alone in sounding the alarm. With up to 70 million of us not getting a good night’s sleep on a regular basis, the Centers for Disease Control and Prevention considers insufficient sleep a public-health epidemic. In fact, experts argue, sleep is emerging as so potent a factor in better health that we need a societal shift–and policies to support it–to make sleep a nonnegotiable priority.

THE CONSEQUENCES OF SKIMPING

Despite how great we feel after a night’s rest–and putting aside what we now know about sleep’s importance–we stubbornly refuse to swallow our medicine, pushing off bedtime and thinking that feeling a little drowsy during the day is an annoying but harmless consequence. It’s not. Nearly 40% of adults have nodded off unintentionally during the day in the past month, and 5% have done so while driving. Insomnia or interrupted sleep nearly doubles the chances that workers will call in sick. And half of Americans say their uneven sleep makes it harder to concentrate on tasks.

Those poor sleep habits are trickling down to the next generation: 45% of teens don’t sleep the recommended nine hours on school nights, leading 25% of them to report falling asleep in class at least once a week, according to a National Sleep Foundation survey. It’s a serious enough problem that the American Academy of Pediatrics recently endorsed the idea of starting middle and high schools later to allow for more adolescent shut-eye.

Health experts have been concerned about our sleep-deprived ways for some time, but the new insights about the role sleep plays in our overall health have brought an urgency to the message. Sleep, the experts are recognizing, is the only time the brain has to catch its breath. If it doesn’t, it may drown in its own biological debris–everything from toxic free radicals produced by hard-working fuel cells to spent molecules that have outlived their usefulness.

“We all want to push the system, to get the most out of our lives, and sleep gets in the way,” says Dr. Sigrid Veasey, a leading sleep researcher and a professor of medicine at Perelman School of Medicine at the University of Pennsylvania. “But we need to know how far we can really push that system and get away with it.”

Veasey is learning that brain cells that don’t get their needed break every night are like overworked employees on consecutive double shifts–eventually, they collapse. Working with mice, she found that neurons that fire constantly to keep the brain alert spew out toxic free radicals as a by-product of making energy. During sleep, they produce antioxidants that mop up these potential poisons. But even after short periods of sleep loss, “the cells are working hard but cannot make enough antioxidants, so they progressively build up free radicals and some of the neurons die off.” Once those brain cells are gone, they’re gone for good.

After several weeks of restricted sleep, says Veasey, the mice she studied–whose brains are considered a good proxy for human brains in lab research–“are more likely to be sleepy when they are supposed to be active and have more difficulty consolidating [the benefits of] sleep during their sleep period.”

It’s the same thing that happens in aging brains, she says, as nerve cells get less efficient at clearing away their garbage. “The real question is: What are we doing to our brains if we don’t get enough sleep? If we chronically sleep-deprive ourselves, are we really aging our brains?” she asks. Ultimately, the research suggests, it’s possible that a sleep-deprived brain belonging to a teen or a 20-year-old will start to look like that of a much older person.

“Chronic sleep restriction is a stress on the body,” says Dr. Peter Liu, professor of medicine at Harbor-UCLA Medical Center and L.A. Biomedical Research Institute. And the cause of that sleep deprivation doesn’t always originate in family strife, financial concerns or job-related problems. The way we live now–checking our phones every minute, hyperscheduling our days or our kids’ days, not taking time to relax without a screen in front of our faces–contributes to a regular flow of stress hormones like cortisol, and all that artificial light and screen time is disrupting our internal clocks. Simply put, our bodies don’t know when to go to sleep naturally anymore.

This is why researchers hope their new discoveries will change once and for all the way we think about–and prioritize–those 40 winks.

GARBAGEMEN FOR YOUR BRAIN

“I was nervous when I went to my first sleep conference,” says Dr. Maiken Nedergaard, the chatty and inquisitive co-director of the Center for Translational Neuromedicine at the University of Rochester. “I was not trained in sleep, and I came to it from the outside.” In fact, as a busy mother and career woman, she saw sleep the way most of us probably do: as a bother. “Every single night, I wanted to accomplish more and enjoy time with my family, and I was annoyed to have to go to bed.”

Because she’s a neuroscientist, however, Nedergaard was inclined to ask a seemingly basic question: Why do our brains need sleep at all? There are two competing evolutionary theories. One is that sleeping organisms are immobile and therefore less likely to be easy targets, so perhaps sleep provided some protection from prey. The time slumbering, however, took away from time spent finding food and reproducing. Another points out that sleeping organisms are oblivious to creeping predators, making them ripe for attack. Since both theories seem to put us at a disadvantage, Nedergaard thought there had to be some other reason the brain needs those hours offline.

All organs in the body use energy, and in the process, they spew out waste. Most take care of their garbage with an efficient local system, recruiting immune cells like macrophages to gobble up the garbage and break it down or linking up to the network of vessels that make up the lymph system, the body’s drainage pipes.

The brain is a tremendous consumer of energy, but it’s not blanketed in lymph vessels. So how does it get rid of its trash? “If the brain is not functioning optimally, you’re dead evolutionarily, so there must be an advantage to exporting the garbage to a less critical organ like the liver to take care of it,” says Nedergaard.

Indeed, that’s what her research shows. She found that an army of previously ignored cells in the brain, called glial cells, turn into a massive pump when the body sleeps. During the day, glial cells are the unsung personal assistants of the brain. They cannot conduct electrical impulses like other neurons, but they support them as they send signals zipping along nerve networks to register a smell here and an emotion there. For decades, they were dismissed by neuroscientists because they weren’t the actual drivers of neural connections.

But Nedergaard found in clinical trials on mice that glial cells change as soon as organisms fall asleep. The difference between the waking and sleeping brain is dramatic. When the brain is awake, it resembles a busy airport, swelling with the cumulative activity of individual messages traveling from one neuron to another. The activity inflates the size of brain cells until they take up 86% of the brain’s volume.

When daylight wanes and we eventually fall asleep, however, those glial cells kick into action, slowing the brain’s electrical activity to about a third of its peak frequency. During those first stages of sleep, called non-REM (rapid eye movement), the firing becomes more synchronized rather than haphazard. The repetitive cycle lulls the nerves into a state of quiet, so in the next stage, known as REM, the firing becomes almost nonexistent. The brain continues to toggle back and forth between non-REM and REM sleep throughout the night, once every hour and a half.

At the same time, the sleeping brain’s cells shrink, making more room for the brain and spinal cord’s fluid to slosh back and forth between them. “It’s like a dishwasher that keeps flushing through to wash the dirt away,” says Nedergaard. This cleansing also occurs in the brain when we are awake, but it’s reduced by about 15%, since the glial cells have less fluid space to work with when the neurons expand.

This means that when we don’t get enough sleep, the glial cells aren’t as efficient at clearing the brain’s garbage. That may push certain degenerative brain disorders that are typical of later life to appear much earlier.

Both Nedergaard’s and Veasey’s work also hint at why older brains are more prone to developing Alzheimer’s, which is caused by a buildup of amyloid protein that isn’t cleared quickly enough.

“There is much less flow to clear away things in the aging brain,” says Nedergaard. “The garbage system picks up every three weeks instead of every week.” And like any growing pile of trash, the molecular garbage starts to affect nearby healthy cells, interfering with their ability to form and recall memories or plan even the simplest tasks.

The consequences of deprived sleep, says Dr. Mary Carskadon, professor of psychiatry and human behavior at Brown University, are “scary, really scary.”RIGHTSIZING YOUR SLEEP

All this isn’t actually so alarming, since there’s a simple fix that can stop this nerve die-off and slow the brain’s accelerated ride toward aging. What’s needed, says Carskadon, is a rebranding of sleep that strips away any hint of its being on the sidelines of our health.

As it is, sleep is so undervalued that getting by on fewer hours has become a badge of honor. Plus, we live in a culture that caters to the late-nighter, from 24-hour grocery stores to online shopping sites that never close. It’s no surprise, then, that more than half of American adults don’t get the recommended seven to nine hours of shut-eye every night.

Whether or not we can catch up on sleep–on the weekend, say–is a hotly debated topic among sleep researchers; the latest evidence suggests that while it isn’t ideal, it might help. When Liu, the UCLA sleep researcher and professor of medicine, brought chronically sleep-restricted people into the lab for a weekend of sleep during which they logged about 10 hours per night, they showed improvements in the ability of insulin to process blood sugar. That suggests that catch-up sleep may undo some but not all of the damage that sleep deprivation causes, which is encouraging given how many adults don’t get the hours they need each night. Still, Liu isn’t ready to endorse the habit of sleeping less and making up for it later. “It’s like telling people you only need to eat healthy during the weekends, but during the week you can eat whatever you like,” he says. “It’s not the right health message.”

Sleeping pills, while helpful for some, are not necessarily a silver bullet either. “A sleeping pill will target one area of the brain, but there’s never going to be a perfect sleeping pill, because you couldn’t really replicate the different chemicals moving in and out of different parts of the brain to go through the different stages of sleep,” says Dr. Nancy Collop, director of the Emory University Sleep Center. Still, for the 4% of Americans who rely on prescription sleep aids, the slumber they get with the help of a pill is better than not sleeping at all or getting interrupted sleep. At this point, it’s not clear whether the brain completes the same crucial housekeeping duties during medicated sleep as it does during natural sleep, and the long-term effects on the brain of relying on sleeping pills aren’t known either.

Making things trickier is the fact that we are unaware of the toll sleep deprivation takes on us. Studies consistently show that people who sleep less than eight hours a night don’t perform as well on concentration and memory tests but report feeling no deficits in their thinking skills. That just perpetuates the tendency to dismiss sleep and its critical role in everything from our mental faculties to our metabolic health.

The ideal is to reset the body’s natural sleep-wake cycle, a matter of training our bodies to sleep similar amounts every night and wake up at roughly the same time each day. An even better way to rediscover our natural cycle is to get as much exposure to natural light as possible during the day, while limiting how much indoor lighting, including from computer and television screens, we see at night. And of course, the best way to accomplish that is by making those seven to nine hours of sleep a must–not a luxury.

“I am now looking at and thinking of sleep as an ‘environmental exposure,'” says Brown University’s Carskadon–which means we should look at sleep similarly to how we view air-pollution exposure, secondhand smoke or toxins in our drinking water. If she and other researchers have their way, checking up on sleep would be a routine part of any physical exam, and doctors would ask about our sleep habits in the same way they query us about diet, stress, exercise, our sex life, our eyesight–you name it. And if we aren’t sleeping enough, they might prescribe a change, just as they would for any other bad health habit.

Some physicians are already taking the initiative, but no prescription works unless we actually take it. If our work schedule cuts into our sleep time, we need to make the sleep we get count by avoiding naps and exercising when we can during the day; feeling tired will get us to fall asleep sooner. If we need help dozing off, gentle exercises or yoga-type stretching can also help. Creating a sleep ritual can make sleep something we look forward to rather than something we feel obligated to do, so we’re more likely to get our allotted time instead of skipping it. A favorite book, a warm bath or other ways to get drowsy might prompt us to actually look forward to unwinding at the end of the day.

Given what scientists are learning about how much the body–and especially the brain–needs a solid and consistent amount of sleep, in-the-know doctors aren’t waiting for more studies to prove what we as a species know intuitively: that cheating ourselves of sleep is depriving us from taking advantage of one of nature’s most powerful drugs.

“We now know that there is a lasting price to pay for sleep loss,” says Veasey. “We used to think that if you don’t sleep enough, you can sleep more and you’ll be fine tomorrow. We now know if you push the system enough, that’s simply not true.”
–WITH REPORTING BY MANDY OAKLANDER AND ALEXANDRA SIFFERLIN/NEW YORK CITY

Notes from Dr. Norman Blumenstock
Dr Oz  understands the importance of of optimal sleep.

Please check out the video.

http://www.doctoroz.com/episode/dr-oz-nationwide-sleep-clinic-sleep-breakthroughs-uncovered

Notes from Dr. Norman Blumenstock

Excessive snoring might seem like a relatively harmless issue, but more evidence shows that sleep apnea can cause serious health issues to your brain.

Kathleen Lees k.lees@scienceworldreport.com

First Posted: Sep 10, 2014 06:16 PM EDT

More than 18 million Americans are estimated to have sleep apnea, a breathing disorder that disrupts air flow and can result in a poor night's rest. (Photo : Reuters)

Excessive snoring might seem like a relatively harmless issue, but more evidence shows that sleep apnea can cause serious health issues to your brain.

Recent findings published in the journal PLOS ONE show that blood flow in the brain can actually damage related tissues presented by this health issue.

"We know there is injury to the brain from sleep apnea, and we also know that the heart has problems pumping blood to the body, and potentially also to the brain," said lead study author Paul Macey, associate dean for Information Technology andInnovations at the UCLA School of Nursing, in a news release. "By using this method, we were able to show changes in the amount of oxygenated blood across the whole brain, which could be one cause of the damage we see in people with sleep apnea."

For the study, researchers measured blood flow in the brain by using a non-invasive MRI procedure: the global blood volume and oxygen dependent (BOLD) signal. This method is usually used to observe brain activity. Because previous research showed that poor regulation of blood in the brain might be a problem for people with sleep apnea, the researchers used the whole-brain BOLD signal to look at blood flow in individuals with and without obstructive sleep apnea (OSA).

In the study, researchers measured men and women both with and without the issue that had their BOLD signals measured during three physical tasks while they were awake, according to the release: 

• The Valsalva maneuver: participants forcefully breathe out through a very small tube, which raises the pressure in the chest.
• A hand-grip challenge: participants squeeze hard with their hand.
• A cold pressor challenge: A participants's right foot is put in icy water for a minute.

"When we looked at the results, we didn't see much difference between the participants with and without OSA in the Valsalva maneuver," said Macey. "But for the hand-grip and cold-pressor challenges, people with OSA saw a much weaker brain blood flow response."

"This study brings us closer to understanding what causes the problems in the brain of people with sleep apnea," concluded Macey.

With future studies, researchers hope to determine better treatments for certain types of obstructive sleep apnea and how to reverse related health issues. 

Events: September 8-14, 2014 is Idiopathic Hypersomnia Awareness Week

Notes from Dr. Norman Blumenstock

An overnight sleep study is necessary to diagnosis the cause of your excessive daytime sleepines. It could be caused by obstructive sleep apnea, idiopathic hypersomnia or Upper Airway Resistance Syndrome (UARS). 

08 September 2014

Events: September 8-14, 2014 is Idiopathic Hypersomnia Awareness Week

From the Hypersomnia Foundation website:

"Hypersomnia is a debilitating neurological disorder where patients lose their cognitive ability, sleep excessively, yet still crave sleep above all else. ...This means they often struggle to work, operate a vehicle or live independently. In fact, often just waking up is an ordeal in and of itself with even sonic boom alarms, the help of family and powerful stimulants not being enough. While the onset of symptoms is generally in early adulthood it routinely takes up to a decade for new patients to be formally diagnosed…"

The founder of SHC was diagnosed with Idiopathic Hypersomnia (IH) several years ago after finding herself faceplanting into her laptop during engaging teleconferences with clients. At some point, the daytime sleepiness was so severe that she was afraid to drive more than an hour at a time without having to stop to nap. She finally realized that "being a working mother" was not a reasonable explanation for her otherwise unreasonable symptoms. She participated in both an overnight polysomnogram and a daytime multiple sleep latency test (MSLT) to uncover the source of her excesses daytime sleepiness. It turned out to be a combination of IH and Upper Airway Resistance Syndrome (UARS). Treating both conditions has made all the difference in the world. She can drive safely, manage online meetings with maximal alertness and get through the day without taking added naps, which impose on her already busy schedule.

If you feel excessively sleepy, day in and day out, and you want your energy and your hours back (!), please consult your physician about potential causes.