Adelaide Institute for Sleep Health
Adelaide Institute for Sleep Health
Simpson L.,University of Western Australia |
Simpson L.,Western Research Institute |
McArdle N.,Western Research Institute |
McArdle N.,Sir Charles Gairdner HospitalWA |
And 16 more authors.
Journal of Clinical Sleep Medicine | Year: 2015
Study Objectives: To investigate whether low levels of physical activity were associated with an increased occurrence of obstructive sleep apnea (OSA), OSA-related symptoms, and cardiometabolic risk. Methods: A case-control study design was used. OSA cases were patients referred to a sleep clinic for suspected OSA (n = 2,340). Controls comprised participants from the Busselton community (n = 1,931). Exercise and occupational activity were derived from questionnaire data. Associations were modelled using logistic and linear regression and adjusted for confounders. Results: In comparison with moderate exercise, the high, low, and nil exercise groups had an odds ratio (OR) for moderate-severe OSA of 0.6 (95% CI 0.5-0.8), 1.6 (95% CI 1.2-2.0), and 2.7 (95% CI 1.9-3.7), respectively. Relative to men in heavy activity occupations, men in medium, light and sedentary occupations had an OR for moderate-severe OSA of 1.7 (95% CI 1.1-2.5), 2.1 (95% CI 1.4-3.2), and 1.8 (95% CI 1.2-2.8), respectively. Relative to women in medium activity occupations, women in light and sedentary occupations had an OR for moderate-severe OSA of 4.2 (95% CI 2.6-7.2) and 3.5 (2.0-6.0). OSA patients who adequately exercised had lower: levels of doctor-diagnosed depression (p = 0.047); symptoms of fatigue (p < 0.0001); systolic (p = 0.015) and diastolic blood pressure (p = 0.015); and C-reactive protein (CRP) (p = 0.003). Conclusions: Low levels of physical activity were associated with moderate-severe OSA. Exercise in individuals with OSA is associated with lower levels of depression, fatigue, blood pressure and CRP.
Eastwood P.R.,Sir Charles Gairdner Hospital |
Eastwood P.R.,University of Western Australia |
Malhotra A.,Harvard University |
Palmer L.J.,University of Western Australia |
And 6 more authors.
Respirology | Year: 2010
Obstructive sleep apnoea (OSA) is a common disease, recognized as an independent risk factor for a range of clinical conditions, such as hypertension, stroke, depression and diabetes. Despite extensive research over the past two decades, the mechanistic links between OSA and other associated clinical conditions, including metabolic disorders and cardiovascular disease, remain unclear. Indeed, the pathogenesis of OSA itself remains incompletely understood. This review provides opinions from a number of leading experts on issues related to OSA and its pathogenesis, interaction with anaesthesia, metabolic consequences and comorbidities, cardiovascular disease, genetics, measurement and diagnosis, surgical treatment and pharmacotherapeutic targets. © 2010 Asian Pacific Society of Respirology.
MacKay S.G.,University of Wollongong |
Carney A.S.,Flinders Medical Center |
Carney A.S.,Flinders University |
Woods C.,Flinders Medical Center |
And 12 more authors.
Journal of Clinical Sleep Medicine | Year: 2013
Study Objectives: To investigate the surgical outcomes and efficacy of modified uvulopalatopharyngoplasty (mod UPPP) and Coblation channelling of the tongue (CCT) as a treatment for obstructive sleep apnea (OSA). Methods: Adult patients with simple snoring or obstructive sleep apnea were treated with combined modified UPPP, bilateral tonsillectomy, and CCT (N = 48). Full polysomnog-raphy was performed preoperatively and 3 months postop-eratively. Postoperative clinical assessment, sleep questionnaires, and patient demographics including body mass index were compared to preoperative data. All polysomnograms were re-scored to AASM recommended criteria by 2 sleep professionals. Results: The preoperative AHI (median and interquartile range) of 23.1 (10.4 to 36.6) was lowered to a postoperative AHI of 5.6 (1.9 to 10.4) (p < 0.05). The Epworth Sleepiness Scale score fell from 10.5 (5.5 to 13.5) to 5.0 (3.09 to 9.5) (p < 0.05). Morbidity of the surgery was low, with no long-term complications recorded. Conclusions: Modified UPPP combined with CCT is a highly efficacious intervention for OSA with minimal morbidity. It should be considered for individuals who fail or are intolerant of CPAP or other medical devices.
Antic N.A.,Adelaide Institute for Sleep Health |
Antic N.A.,Flinders University |
Catcheside P.,Adelaide Institute for Sleep Health |
Catcheside P.,Flinders University |
And 8 more authors.
Sleep | Year: 2011
Study Objectives: The study aimed to document the neurobehavioral outcomes of patients referred to and treated by a sleep medicine service for moderate to severe obstructive sleep apnea (OSA). In particular, we aimed to establish the proportion of patients who, while appearing to have optimal continuous positive airway pressure (CPAP) adherence, did not normalize their daytime sleepiness or neurocognitive function after 3 months of CPAP therapy despite effective control of OSA. Design: Multicenter clinical-effectiveness study. Setting: Three academic sleep centers in Australia. Participants: Patients referred to a sleep medicine service with moderate to severe OSA (n = 174). Intervention: CPAP. Measurements and Results: Participants were assessed pretreatment and again after 3 months of CPAP therapy. At the beginning and at the conclusion of the trial, participants completed a day of testing that included measures of objective and subjective daytime sleepiness, neurocognitive function, and quality of life. In patients with symptomatic moderate to severe OSA (i.e., apnea-hypopnea index > 30/h), we found a treatment dose-response effect for CPAP in terms of Epworth Sleepiness Scale scores (P < 0.001). Several key indexes of neurobehavior (e.g., Functional Outcomes of Sleep Questionnaire, Epworth Sleepiness Scale) currently used to assess treatment response failed to normalize in a substantial group of patients after 3 months of CPAP treatment, even in those who were maximally compliant with treatment. Forty percent of patients in this trial had an abnormal Epworth Sleepiness Scale score at the conclusion of the trial. In addition, we showed no dose-response effect with the Maintenance of Wakefulness Test, raising doubts as to the clinical utility of the Maintenance of Wakefulness Test in assessing treatment response to CPAP in patients with OSA. Conclusions: Our study suggests that a greater percentage of patients achieve normal functioning with longer nightly CPAP duration of use, but a substantial proportion of patients will not normalize neurobehavioral responses despite seemingly adequate CPAP use. It is thus crucial to adequately assess patients after CPAP therapy and seek alternate etiologies and treatments for any residual abnormalities.
News Article | August 29, 2016
Millions of people in the United States suffer from obstructive sleep apnea, a condition that causes those afflicted to briefly stop breathing during sleep, sometimes several times at night. The disorder, which happens when the throat muscles relax during sleep and block the airway, has been linked to a range of health problems including high blood pressure, heart disease, stroke and type 2 diabetes. The standard treatment given to patients with the condition is continuous positive airway pressure (CPAP) therapy, which makes use of a machine. The CPAP machine works by pumping a stream of air through the nostril of the patient during sleep to keep the airway open. There are drawbacks with this therapy, one of which is non-compliance. Many people give up on using the machine because they find the air mask and hose uncomfortable. Some users bear with the discomfort because the therapy is believed to reduce potentially fatal health risks associated with the condition. A new study, however, challenges this idea. The Sleep Apnea Cardiovascular Endpoints (SAVE) study found that CPAP does not prevent heart attacks, strokes, hospitalizations or deaths in sleep apnea sufferers with existing cardiovascular disease. Craig Anderson, from the George Institute for Global Health in Sydney, and colleagues monitored sleep apnea patients with pre-existing vascular disease over a period of four years in 89 hospitals to determine if the use of the CPAP machine would prevent major cardiovascular events such as stroke and heart attack. Earlier studies suggest that CPAP has a positive impact on these health problems but the result of the study, which is by far the largest to look into the condition and involved 2,687 participants, revealed otherwise. The findings revealed that although the use of the CPAP machine reduces daytime sleepiness plaguing sleep apnea patients — reducing anxiety and depression and boosting mood and work productivity — the use of the CPAP machine does not appear to be helpful in reducing risk of heart attack and stroke in sleep apnea sufferers. In patients under the CPAP group, the rate of cardiovascular events was 17 percent, while the rate in the control group was 15.4 percent. "At the moment, we could not recommend, on the basis of our study findings, that CPAP be used for the prevention of cardiovascular disease in patients, particularly those who are asymptomatic from sleep apnea," said study lead Dr. Doug McEvoy from the Adelaide Institute for Sleep Health. The research was presented at a cardiology conference held in Rome, Italy on Sunday, Aug. 28 and published in the New England Journal of Medicine. © 2017 Tech Times, All rights reserved. Do not reproduce without permission.
News Article | January 21, 2016
I wake up in darkness, and reach over the edge of my mattress, like I have every morning for the past two weeks. I feel around the inky void until I grab hold of a sleek white headset. It looks like a pair of snowboarding goggles, but without the lenses. I tap the “on” button, and the headset glows with a bright blue-green light. I slip the device on my head and let my eyes adjust to the light—which is now shining straight into my eyes—and groggily stumble to the bathroom. The light obscures my vision, and so I stumble over a boot along the way. When I look in the mirror, I can’t help thinking that, in terms of sci-fi cred, I look more SkyMall than Darth Maul. This has been my new morning routine—a slightly strange, and kind of silly, but earnest (I swear) attempt to reset my body’s internal clock so that I can go to bed earlier and wake up earlier the next day. You see, I’m a chronic night owl, often to my detriment; I often can’t get to bed before midnight without a little help. Recently, that’s meant taking melatonin supplements, a naturally occurring hormone believed to induce sleep in mammals. When I wake up for work, I’m tired as hell. The device on my face is called the Re-Timer. It was created by Leon Lack, a clinical psychologist at the Adelaide Institute for Sleep Health in Australia. The Re-Timer is supposed to re-adjust the wearer’s circadian rhythms—the 24 hour cycle of chemicals like melatonin and other physiological cues that together determine when you go to sleep and wake up—by shining bright blue and green light into the wearer's eyes. Researchers believe that light plays the largest role in regulating circadian rhythms related to sleep, and so the idea is that the Re-Timer tricks your brain into thinking it needs to go to sleep earlier or later by mimicking the conditions it’s used to in the natural world—sunlight at daybreak, for example. It’s basically a SAD lamp that you wear on your face, and retails for $299 USD. “We have a biological clock, and the master clock is in the brain, in the suprachiasmatic nucleus,” which is part of the hypothalamus said Julie Carrier, a professor of psychology at the University of Montreal’s Center for Advanced Research in Sleep Medicine. “There are other clocks in the body, we know that, but the master one is in the hypothalamus. And it’s a good thing we have these circadian rhythms, because it allows mammals and humans to do the correct action at the same time. For human beings, it’s good to be asleep at night, because we don’t see much.” The suprachiasmatic nucleus, or SCN, as it turns out, is connected to your eyes via photoreceptor cells that are sensitive to short wavelength blue and green light, Carrier told me. These cells are used to receiving cues from natural sunlight and communicating them to the SCN, but they’ll also respond to artificial light. The idea is that, by wearing a device like the Re-Timer, your circadian rhythms will respond in kind. “Bright light can be used to shift the timing of the body clock. There’s been a lot of research to show that, and ours was actually some of the earliest work in that area,” Lack said over a Skype conversation. “One of my students wrote his PhD in 1990 and showed that a single pulse of four hours of bright light at high intensity had the effect to earlier delay the body clock or shift it earlier, depending on when the light exposure occurred.” The Re-Timer is apparently based on this and other academic research spanning the past 25 years, and has a handful of peer-reviewed papers to back it up (most of them co-authored by Lack himself). To get to sleep earlier and wake up earlier (my goal), you’re supposed to wear the Re-Timer for up to an hour, within a half hour of your normal wake time. According to the company, you should see results after three or four days. The results after this period of time will likely be a change of 20 or 30 minutes in your sleep schedule, Lack said, because the light is less intense than what you see in a lab. However, if the glasses are worn for much longer, those changes could stretch to a couple hours. You’re probably wondering by now: how did it go for me? The most I can say is that results were promising, but inconclusive. I began wearing the glasses on a Sunday. After several days—occasionally cheating by wearing them later than the recommended half hour after waking up, if I was running late to work—I really couldn’t tell if anything was different. If I felt a little more energetic one morning, was it really because of a pricey device? As far as I could tell, I was inconveniencing myself without much benefit. At least my coworkers got a show, since wearing the Re-Timer to work quickly turned my desk into a zoo exhibit, and I was the main attraction: a dude with ominous green lights shining into his eyes. But then, something strange happened. On Sunday night, exactly a week after I started wearing the glasses, I was overcome by tiredness at 9:30 PM (about three hours shy of my normal bedtime) and went to sleep. I woke up at 5 AM. I initially wrote this off as coincidence, because I’d partied a little too hard over the weekend and not slept much. But on Monday and Tuesday, the phenomenon repeated itself. Was it because of the Re-Timer, or because I was catching up on sleep lost over a couple of weekend nights? I’m not sure I can say for certain—although, my experience somewhat mimics what Lack found in a 2007 paper published in Sleep and Biological Rhythms. In that study, subjects that received two hours of blue light after waking up for a week straight were able to shift their wake up time back by nearly three hours. However, after the study ended, the change didn’t stick. Coey gets her shine on. Photo: Raf Katigbak I also learned that going to bed at a reasonable hour just isn’t my style. I’m a night owl and I think I like it. But the science behind bright light therapy is solid, Carrier assured me, and according to her, it works. “[These products] are for sure legitimate,” Carrier said. “For most people, they are a good purchase, and they can be very useful during winter. But light outside will also be sufficient to achieve some of the effect that you want.” In the summer, for example, the same effect could likely be achieved by going outside for a run in the morning, Carrier said—or, hell, just standing outside your door and looking around. Whether you shell out for a fancy piece of tech to hack your body’s rhythms or go the all-natural route will probably depend on what season it is, and how you feel about looking like an extra from a low-rent Blade Runner remake. As for me, it really does seem like light, even from an LED, has some sort of tangible effect on your body—but that I already knew. I think I'll just stick with the sun, thanks.
Jordan A.S.,University of Melbourne |
Jordan A.S.,Institute for Breathing and Sleep |
Cori J.M.,University of Melbourne |
Cori J.M.,Institute for Breathing and Sleep |
And 11 more authors.
Sleep | Year: 2015
Study Objectives: To compare changes in end-tidal CO2, genioglossus muscle activity and upper airway resistance following tone-induced arousal and the return to sleep in healthy individuals with small and large ventilatory responses to arousal.Design: Observational study.Setting: Two sleep physiology laboratories.Patients or Participants: 35 men and 25 women with no medical or sleep disorders.Interventions: Auditory tones to induce 3-s to 15-s cortical arousals from sleep.Measurements and Results: During arousal from sleep, subjects with large ventilatory responses to arousal had higher ventilation (by analytical design) and tidal volume, and more marked reductions in the partial pressure of end-tidal CO2 compared to subjects with small ventilatory responses to arousal. However, following the return to sleep, ventilation, genioglossus muscle activity, and upper airway resistance did not differ between high and low ventilatory response groups (Breath 1 on return to sleep: ventilation 6.7 ± 0.4 and 5.5 ± 0.3 L/min, peak genioglossus activity 3.4% ± 1.0% and 4.8% ± 1.0% maximum, upper airway resistance 4.7 ± 0.7 and 5.5 ± 1.0 cm H2O/L/s, respectively). Furthermore, dilator muscle activity did not fall below the pre-arousal sleeping level and upper airway resistance did not rise above the pre-arousal sleeping level in either group for 10 breaths following the return to sleep.Conclusions: Regardless of the magnitude of the ventilatory response to arousal from sleep and subsequent reduction in PETCO2, healthy individuals did not develop reduced dilator muscle activity nor increased upper airway resistance, indicative of partial airway collapse, on the return to sleep. These findings challenge the commonly stated notion that arousals predispose to upper airway obstruction.
PubMed | Adelaide Institute for Sleep Health, University of Zürich, University College Dublin, Rochester College and 3 more.
Type: | Journal: Nature reviews. Disease primers | Year: 2016
Obstructive sleep apnoea syndrome (OSAS) is a common clinical condition in which the throat narrows or collapses repeatedly during sleep, causing obstructive sleep apnoea events. The syndrome is particularly prevalent in middle-aged and older adults. The mechanism by which the upper airway collapses is not fully understood but is multifactorial and includes obesity, craniofacial changes, alteration in upper airway muscle function, pharyngeal neuropathy and fluid shift towards the neck. The direct consequences of the collapse are intermittent hypoxia and hypercapnia, recurrent arousals and increase in respiratory efforts, leading to secondary sympathetic activation, oxidative stress and systemic inflammation. Excessive daytime sleepiness is a burden for the majority of patients. OSAS is also associated with cardiovascular co-morbidities, including hypertension, arrhythmias, stroke, coronary heart disease, atherosclerosis and overall increased cardiovascular mortality, as well as metabolic dysfunction. Whether treating sleep apnoea can fully reverse its chronic consequences remains to be established in adequately designed studies. Continuous positive airway pressure (CPAP) is the primary treatment modality in patients with severe OSAS, whereas oral appliances are also widely used in mild to moderate forms. Finally, combining different treatment modalities such as CPAP and weight control is beneficial, but need to be evaluated in randomized controlled trials. For an illustrated summary of this Primer, visit: http://go.nature.com/Lwc6te.