The Annoying Thing You're Doing In Bed That Might Be A Total Turn-Off

The Huffington Post  |  By Sarah Klein

Posted: 02/14/2015 8:46 am EST Updated: 02/15/2015 9:59 pm EST

If there's one thing we think it's safe to say is almost always a bummer in the bedroom, it's snoring.

According to a new survey from the American Academy of Dental Sleep Medicine (AADSM), 39 percent of American adults agree: When the opposite sex snores, it's a turn-off.

Luckily for the snorers among us, it's not a total deal-breaker -- 83 percent of the 1,009 people surveyed by telephone said they had had a snoring bed partner, but only 26 percent said all that log sawing made them angry or annoyed and just 9 percent said snoring has had a negative impact on a romantic relationship.

"Because it can be embarrassing, snoring can often be the elephant in the room when it comes to addressing relationship frustrations and health concerns," Kathleen Bennett, DDS, president of the AADSM, said in a statement. "But it's important that your significant other is made aware of their snoring -- and the effects it has on you, your relationship and their personal health -- so they can begin taking steps to remedy it."

Long thought to be simply an annoyance to a bed partner and not much more, snoring is now understood to carry some pretty substantial health risks. "When you are snoring, you're spending too much energy to breathe," Dr. M. Safwan Badr, past president of the American Academy of Sleep Medicine, previously told HuffPost. "Snoring is like fever for a general internist -- it tells you somethig is going on, but it doesn't tell you what."

Snoring could be a sign of sleep apnea or other sleep-disordered breathing, which has been linked to increased risk of hearing loss, osteoporosis, depression and more. Understandably, 43 percent of the AADSM survey respondents said they worried about the health of their snoring bed partners.

Sleep apnea is typically treated with continuous positive airway pressure, or CPAP, which is delivered by a bedside machine that can be, let's just say, a little cumbersome. The AADSM advocates for another option called oral appliance therapy, or OAT, a mouthguard-like device that, while not exactly sexy, may at least be a little sexier.

For snorers who don't have sleep apnea, experts recommend sleeping on your side, avoiding alcohol too close to bedtime and shedding excess weight. Your bed partner will thank you for the Valentine's Day gift of a quieter night's rest.

http://www.huffingtonpost.com/2015/02/14/snoring-turn-off_n_6679120.html#slide=start

Notes from Dr. Norman Blumenstock

Breathing problems or a chronic lack of sleep early in life may double the risk that a child will be obese by age 15, according to research published Thursday in The Journal of Pediatrics.

December 11, 201410:54 AM ET

ALISON BRUZEK

Sleep tight — and quietly, please.

ImageZoo/Corbis

A solid night's sleep does more than recharge a growing brain — it may also help keep a growing body lean.

Breathing problems or a chronic lack of sleep early in life may double the risk that a child will be obese by age 15, according to research published Thursday in The Journal of Pediatrics.

Childhood obesity has been linked before with the number of hours a kid sleeps each night. But other early problems with nighttime breathing — like snoring, or the more serious sleep apnea — also seem to be predictive of significant weight gain among children, according to the research.

It's the first study to look at both sleep duration and breathing problems as separate risk factors for obesity, says Karen Bonuck, professor of family and social medicine at the Albert Einstein College of Medicine of Yeshiva University and lead author.

"Sleep problems need to be thought of as a composite," she tells Shots. "It's not just sleep duration, sleep hygiene, sleep-disordered breathing. We need to think about healthy sleep overall, and we need to think about it early."

To examine sleep habits and how they might predict a child's body mass index, Bonuck and her colleagues used the Avon Longitudinal Study of Parents and Children, which tracked 1,900 children in England for 15 years.

The mothers surveyed were asked how long their children typically slept at ages 18 months, 2.5 years, about 5 years, 6 years and 7 years. They also reported any sleeping problems like snoring, apnea or mouth breathing between the ages of 6 months and about 7 years old. Finally, the survey collected the height and weight of the children at ages 7 years, 10 years and 15 years.

They found that children who had multiple sleeping problems were twice as likely to be obese by age 7, 10 or 15 years, compared with those who had no problems. At age 15, 9.7 percent of teens with no sleep problems were obese, compared with 18.3 percent of those with multiple sleep problems.

In addition, children who slept less than 10 hours per night at ages 5 and 6 years were more likely to be obese at age 15.

While the study could only confirm an association, not causality, it makes sense that children who don't get enough solid sleep are tired, and may eat more, sleep scientists say. "Some of this actually might be related to certain hormones that regulate appetite," says Dr. Rakesh Bhattacharjee, a pediatric sleep medicine specialist at the University of Chicago Medicine Comer Children's Hospital.

Another theory holds that poor sleep quality or short duration may cause stress on the body that leads to inflammation.

Though many questions about sleep's effects and mechanisms remain, all agree it's important, especially in growing children, Bonuck says. Newborns should get around 16 to 18 hours per day, according to the Centers for Disease Control and Prevention, and preschoolers 11 to 12 hours.

Parents should look for early signals, Bonuck says. Noisy or halted breathing at night could mean something serious is amiss. "Watch your child," she says. "Does she or he snore more than three times a week?"

The American Academy of Pediatrics recommends that all children who snore regularly be screened for sleep apnea — partly because it's easier to prevent childhood obesity than to treat it. "As Benjamin Franklin once said, 'An ounce of prevention is worth a pound of cure,' " Bonuck says. "Pun intended."

Evidence Mounts for Poor Sleep/Pediatric Obesity Connection

Sleep-related breathing problems and chronic lack of sleep may each double the risk of a child becoming obese by age 15, according to new research from Albert Einstein College of Medicine of Yeshiva University. The good news is that both sleep problems can be corrected. The study, which followed nearly 2,000 children for 15 years, published online in The Journal of Pediatrics.

“In recent years, lack of sleep has become a well-recognized risk for childhood obesity,” said Karen Bonuck, Ph.D., professor of family and social medicine and of obstetrics & gynecology and women’s health at Einstein and lead author on the paper. “Sleep-disordered breathing, or SDB, which includes snoring and sleep apnea, is also a risk factor for obesity but receives less attention. These two risk factors had not been tracked together in children over time to determine their potential for independently influencing weight gain. Our study aimed to fill in that gap.”

Dr. Bonuck and her colleagues used data collected on 1,899 children by the Avon Longitudinal Study of Parents and Children (ALSPAC) based in Avon, England. ALSPAC collected parent questionnaire data on both child sleep duration and SDB symptoms from birth through 6.75 years and child BMI data from research ALSPAC clinics.

Sleep-disordered breathing

The researchers found that children with the most severe SDB had the greatest risk for obesity. Those children who fell into the “worst case” SDB category were twice as likely to become obese by 7, 10 and 15 years of age, compared to the asymptomatic group. Children considered “worst case” scored highest for SDB symptoms of snoring, sleep apnea or mouth-breathing.

Children whose SDB peaked later, around 5 to 6 years old, fared better but still had a 60 to 80 percent increased risk of becoming obese. Overall, one-fourth of children in this population-based cohort had an increased statistical risk of obesity that arose from SDB symptoms experienced earlier in life.  Obesity was defined as BMI greater than the 95^th percentile for age and gender, according to the International Obesity Task Force.

Sleep duration

With respect to sleep duration, children with the shortest sleep time at approximately 5 and 6 years of age had a 60 to 100 percent increased risk of being obese at 15 years. Children with short sleep duration at other ages saw no significant increase in risk. (In this study, children with short sleep duration were those who, in any given age group, slept less than 90 percent of their peers. For those aged 5 and 6 years old, this was 10.5 hours a night or less.)

Interestingly, SDB and lack of sleep were equally strong risk factors for obesity, but their effects were independent of each other. The researchers looked for associations between short-sleep-duration children and SDB children across all age groups included in the study but did not find clustering, i.e., there was little evidence that children with one risk factor were more likely to also be affected by the other.  The study did not analyze whether children affected by both of the sleep-related risk factors were at greater risk for obesity than were children who had just one risk factor.

Can Sleep Apnea Predict a Heart Attack?

By Eric Cohen, MD Published Sep 8, 2014

Many of the patients I see who complain about sleep issues have some level of obstructive sleep apnea (OSA). In fact, as many one in five adults have at least a mild form of sleep apnea. People with obstructive sleep apnea are also more likely to have hypertension, high blood pressure, and cardiovascular disease.

Now, as a result of the latest research, when we test for sleep apnea we also examine and focus on the state of a person’s heart.

The link between sleep apnea and cardiovascular disease has been studied for several years. In 2013 it was announced that this link even includes the possibility of heart attacks related to obstructive sleep apnea. The head of a long-term study, Apoor Gami, MD, a cardiac electrophysiologist at Midwest Heart Specialists-Advocate Medical Group in Elmhurst, Ill., notes, “The presence and severity of sleep apnea are associated with a significantly increased risk of sudden cardiac death.”

There are a number of causes behind this association. Sleep apnea can cause you to stop breathing several times a night. When this happens, your blood oxygen levels go down, which can cause your heart rhythm to flutter. This is a heart complication that also occurs at the time of sudden cardiac death.

The problem is huge. In the United States alone, more than 450,000 deaths are caused each year by sudden cardiac death. 

These figures illustrate why anyone presenting with symptoms such as loud snoring, daytime fatigue, waking with a sore throat, hypertension, high blood pressure or cardiovascular disease should be tested for sleep apnea. One positive from the study on sleep apnea, and recognizing the link between sleep apnea and heart problems, is we have found that improving obstructive sleep apnea may dramatically improve the health of your heart. The longer your symptoms go untreated, however, the higher your chance for heart disease, stroke, or cardiac arrest.

The good news is there are ways to improve your sleep without surgery. Here are six recommendation I give to my patients who want to improve the quality of their sleep:

1. Avoid caffeine in the evenings.
2. Avoid excessive alcohol consumption: Too much alcohol can affect a person’s sleep.
3. Create a regimen of regular physical activity.
4. Arrange your bedroom into a calming, sleep-inducing environment.
5. Establish a pre-sleep routine (bath, herbal tea, reading a book, etc.).
6. Keep a consistent sleep cycle; this helps your internal clock stay regulated.

If you’re over 60, obese, and constantly tired or fatigued, make sure you are tested for sleep apnea. Older women especially should be tested for sleep apnea, and your doctor should also be evaluating you for signs of heart disease. Tests can show weak spots, and if caught early, this could save lives. Now, as we know more about the connection between sleep apnea and the heart, doctors can get more accurate results regarding any sleep troubles you may be experiencing.

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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13 Struggles Of Sleeping With A Snorer

Notes from Dr. Norman Blumenstock
Sleeping with a heavy snorer and just dealing with it is no way to live.

Eh, sleep is overrated, anyway.posted on Aug. 22, 2014, at 7:29 p.m.

1. You will do everything you can to try and fall asleep before them.

Sleeping pills, alcohol, going to bed an hour earlier, etc. You’ve tried it all in order to try to beat them to the punch.

2. But even if you do, their intense snoring will wake you up, anyway.

They can’t be doing it on purpose, right?

3. Good luck falling asleep if they fall asleep first.

It’s like sleeping with the Inception “BRAHM!” on a constant loop next to you.

4. You will constantly nudge them throughout the night to stop, all to no avail.

Sometimes more than a nudge is needed, not that it will work any better.

5. It’s even worse if they do turn on their stomach or side AND STILL SNORE.

#Thereisnohope

6. And let’s not even discuss when they fall asleep drunk or after taking medication, because then nothing will wake them up.

It’s like sleeping next to a dead body. A snoring, heavy breathing, dead body.

7. You’ve learned that pillows, earplugs, and white noise machines do nothing to cancel out the snores.

The only that seems to work is, well… Any suggestions?

8. You’ve also bought the snorer those nasal strips, herbal remedies, etc., but none of which have worked.

Not that that will stop you from searching for a solution.

9. Knowing they have to get up early, you’ve struggled with not waking in order to let them sleep.

truggled, in that you inevitably wake them because you need sleep, too.

10. Sleeping in another room? LOL you can still hear them.

“Nowhere to run to baby, nowhere to hide…”

11. When said snorer denies that they are, indeed, a snorer.

Who else do you think I’m talking to? The ghost of Jacob Marley?

12. OR, when they turn the tables and claim that YOU keep THEM up.

Oh, I rustle in my sleep and that bothers you? TRY SLEEPING NEXT TO A FREIGHT TRAIN!

13. Finally, the awful feeling when they don’t snore for a minute and you think they’ve stopped, only to…