Abed H.S.,University of Adelaide |
Wittert G.A.,University of Adelaide |
Leong D.P.,University of Adelaide |
Shirazi M.G.,University of Adelaide |
And 10 more authors.
JAMA - Journal of the American Medical Association | Year: 2013
IMPORTANCE: Obesity is a risk factor for atrial fibrillation. Whether weight reduction and cardiometabolic risk factor management can reduce the burden of atrial fibrillation is not known. OBJECTIVE: To determine the effect of weight reduction and management of cardiometabolic risk factors on atrial fibrillation burden and cardiac structure. DESIGN, SETTING, AND PATIENTS: Single-center, partially blinded, randomized controlled study conducted between June 2010 and December 2011 in Adelaide, Australia, among overweight and obese ambulatory patients (N = 150) with symptomatic atrial fibrillation. Patients underwent a median of 15 months of follow-up. INTERVENTIONS: Patients were randomized to weight management (intervention) or general lifestyle advice (control). Both groups underwent intensive management of cardiometabolic risk factors. MAIN OUTCOMES AND MEASURES: The primary outcomes were Atrial Fibrillation Severity Scale scores: symptom burden and symptom severity. Scores were measured every 3 months from baseline to 15 months. Secondary outcomes performed at baseline and 12 months were total atrial fibrillation episodes and cumulative duration measured by 7-day Holter, echocardiographic left atrial area, and interventricular septal thickness. RESULTS: Of 248 patients screened, 150 were randomized (75 per group) and underwent follow-up. The intervention group showed a significantly greater reduction, compared with the control group, in weight (14.3 and 3.6 kg, respectively; P < .001) and in atrial fibrillation symptom burden scores (11.8 and 2.6 points, P < .001), symptom severity scores (8.4 and 1.7 points, P < .001), number of episodes (2.5 and no change, P = .01), and cumulative duration (692-minute decline and 419-minute increase, P = .002). Additionally, there was a reduction in interventricular septal thickness in the intervention and control groups (1.1 and 0.6 mm, P = .02) and left atrial area (3.5 and 1.9 cm2, P = .02). CONCLUSIONS AND RELEVANCE: In this study, weight reduction with intensive risk factor management resulted in a reduction in atrial fibrillation symptom burden and severity and in beneficial cardiac remodeling. These findings support therapy directed at weight and risk factors in the management of atrial fibrillation. TRIAL REGISTRATION: anzctr.org.au Identifier: ACTRN12610000497000. Copyright 2013 American Medical Association. All rights reserved. Source
Reynolds A.C.,University of South Australia |
Dorrian J.,University of South Australia |
Liu P.Y.,Harbor University of Los Angeles Medical Center |
van Dongen H.P.A.,Washington State University |
And 3 more authors.
PLoS ONE | Year: 2012
Background: Sleep restriction is associated with development of metabolic ill-health, and hormonal mechanisms may underlie these effects. The aim of this study was to determine the impact of short term sleep restriction on male health, particularly glucose metabolism, by examining adrenocorticotropic hormone (ACTH), cortisol, glucose, insulin, triglycerides, leptin, testosterone, and sex hormone binding globulin (SHBG). Methodology/Principal Findings: N = 14 healthy men (aged 27.4±3.8, BMI 23.5±2.9) underwent a laboratory-based sleep restriction protocol consisting of 2 baseline nights of 10 h time in bed (TIB) (B1, B2; 22:00-08:00), followed by 5 nights of 4 h TIB (SR1-SR5; 04:00-08:00) and a recovery night of 10 h TIB (R1; 22:00-08:00). Subjects were allowed to move freely inside the laboratory; no strenuous activity was permitted during the study. Food intake was controlled, with subjects consuming an average 2000 kcal/day. Blood was sampled through an indwelling catheter on B1 and SR5, at 09:00 (fasting) and then every 2 hours from 10:00-20:00. On SR5 relative to B1, glucose (F1,168 = 25.3, p<0.001) and insulin (F1,168 = 12.2, p<0.001) were increased, triglycerides (F1,168 = 7.5, p = 0.007) fell and there was no significant change in fasting homeostatic model assessment (HOMA) determined insulin resistance (F1,168 = 1.3, p = 0.18). Also, cortisol (F1,168 = 10.2, p = 0.002) and leptin (F1,168 = 10.7, p = 0.001) increased, sex hormone binding globulin (F1,167 = 12.1, p<0.001) fell and there were no significant changes in ACTH (F1,168 = 0.3, p = 0.59) or total testosterone (F1,168 = 2.8, p = 0.089). Conclusions/Significance: Sleep restriction impaired glucose, but improved lipid metabolism. This was associated with an increase in afternoon cortisol, without significant changes in ACTH, suggesting enhanced adrenal reactivity. Increased cortisol and reduced sex hormone binding globulin (SHBG) are both consistent with development of insulin resistance, although hepatic insulin resistance calculated from fasting HOMA did not change significantly. Short term sleep curtailment leads to changes in glucose metabolism and adrenal reactivity, which when experienced repeatedly may increase the risk for type 2 diabetes. © 2012 Reynolds et al. Source
Gottlieb D.J.,VA Boston Healthcare System |
Gottlieb D.J.,Harvard University |
Craig S.E.,Sleep Unit |
Lorenzi-Filho G.,University of Sao Paulo |
And 5 more authors.
Sleep | Year: 2013
Sleep apnea is a common chronic disease that is associated with coronary heart disease, stroke, heart failure and mortality, although the ability of sleep apnea treatment to reduce cardiovascular morbidity and mortality has not been demonstrated. In contrast to patients seeking treatment in sleep disorders centers, as many as half of individuals with moderate to severe sleep apnea in the general population do not report excessive sleepiness; however, if treatment of sleep apnea were shown to reduce cardiovascular disease risk, this would provide a strong rationale for treatment of sleep apnea even in the absence of daytime sleepiness. This article summarizes the status of clinical trials evaluating the potential cardiovascular benefits of sleep apnea treatment and discusses the challenges of conducting such trials, and introduces the International Collaboration of Sleep Apnea Cardiovascular Trialists (INCOSACT), a clinical research collaboration formed to foster cardiovascular sleep research. Source
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.
Chai-Coetzer C.L.,Adelaide Institute for Sleep Health |
Chai-Coetzer C.L.,Flinders University |
Antic N.A.,Adelaide Institute for Sleep Health |
Antic N.A.,Flinders University |
And 12 more authors.
JAMA - Journal of the American Medical Association | Year: 2013
Importance: Due to increasing demand for sleep services, there has been growing interest in ambulatory models of care for patients with obstructive sleep apnea. With appropriate training and simplified management tools, primary care physicians are ideally positioned to take on a greater role in diagnosis and treatment. Objective: To compare the clinical efficacy and within-trial costs of a simplified model of diagnosis and care in primary care relative to that in specialist sleep centers. Design, Setting, and Patients: A randomized, controlled, noninferiority study involving 155 patients with obstructive sleep apnea that was treated at primary care practices (n=81) in metropolitan Adelaide, 3 rural regions of South Australia or at a university hospital sleep medicine center in Adelaide, Australia (n=74), between September 2008 and June 2010. Interventions: Primary care management of obstructive sleep apnea vs usual care in a specialist sleep center; both plans included continuous positive airway pressure, mandibular advancement splints, or conservative measures only. Main Outcome and Measures: The primary outcome was 6-month change in Epworth Sleepiness Scale (ESS) score, which ranges from 0 (no daytime sleepiness) to 24 points (high level of daytime sleepiness). The noninferiority margin was -2.0. Secondary outcomes included disease-specific and general quality of life measures, obstructive sleep apnea symptoms, adherence to using continuous positive airway pressure, patient satisfaction, and health care costs. Results: There were significant improvements in ESS scores from baseline to 6 months in both groups. In the primary care group, the mean baseline score of 12.8 decreased to 7.0 at 6 months (P < .001), and in the specialist group, the score decreased from a mean of 12.5 to 7.0 (P < .001). Primary care management was noninferior to specialist management with a mean change in ESS score of 5.8 vs 5.4 (adjusted difference, -0.13; lower bound of 1-sided 95% CI, -1.5; P = .43). There were no differences in secondary outcome measures between groups. Seventeen patients (21%) withdrew from the study in the primary care group vs 6 patients (8%) in the specialist group. Conclusions and Relevance: Among patients with obstructive sleep apnea, treatment under a primary care model compared with a specialist model did not result in worse sleepiness scores, suggesting that the 2 treatment modes may be comparable. Trial Registration: anzctr.org.au Identifier: ACTRN12608000514303. ©2013 American Medical Association. All rights reserved. Source