Obstructive sleep apnea is associated with low GABA and high glutamate in the insular cortex


The insular cortex is injured in obstructive sleep apnea (OSA) and responds inappropriately to autonomic challenges, suggesting neural reorganization. The objective of this study was to assess whether the neural changes might result from γ-aminobutyric acid (GABA) and glutamate alterations. We studied 14 OSA patients [mean age ± standard deviation (SD): 47.5 ± 10.5 years; nine male; apnea–hypopnea index (AHI): 29.5 ± 15.6 events h−1] and 22 healthy participants (47.5 ± 10.1 years; 11 male), using magnetic resonance spectroscopy to detect GABA and glutamate levels in insular cortices. We localized the cortices with anatomical scans, and measured neurochemical levels from anterior to mid-regions. Left and right anterior insular cortices showed lower GABA and higher glutamate in OSA versus healthy subjects [GABA left: OSA n = 6: 0.36 ± 0.10 (mean ± SD), healthy n = 5: 0.62 ± 0.18; < 0.05), right: OSA n = 11: 0.27 ± 0.09, healthy n = 14: 0.45 ± 0.16; < 0.05; glutamate left: OSA n = 6: 1.61 ± 0.32, healthy n = 8: 0.94 ± 0.34; < 0.05, right: OSA n = 14: 1.26 ± 0.28, healthy n = 19: 1.02 ± 0.28; < 0.05]. GABA and glutamate levels were correlated only within the healthy group in the left insula (r: −0.9, < 0.05). The altered anterior insular levels of GABA and glutamate may modify integration and projections to autonomic areas, contributing to the impaired cardiovascular regulation in OSA.


The insular cortex in obstructive sleep apnea (OSA) shows structural and functional alterations, which likely contribute to adverse autonomic and affective symptoms characteristic of the syndrome (Harperet al., 2003; Kumar et al., 2012; Macey et al., 2008). The altered functions include distorted insular functional magnetic resonance (fMRI) signals accompanying sympathetic nervous system challenges, and probably underlie the high sympathetic outflow in OSA, presumably contributing to the profuse sweating, cardiac arrhythmia and hypertension in the disorder. The insular injury in OSA also probably facilitates the development of depression and anxiety in the condition (Asghari et al., 2012; Kurthet al., 2010; Marin et al., 2012). Mechanisms underlying insular dysfunction in OSA are unclear, but understanding the nature of the brain alterations could provide insights into symptoms that persist even with treatment (Marin et al., 2012), as well as processes underlying partial or complete resolution with continuous positive airway pressure (CPAP) of other symptoms, such as high sympathetic tone (Fatoulehet al., 2015).

Structural brain alterations in OSA could arise from multiple pathologies. Reduced mean diffusivity, apparent in many OSA brain regions (Kumar et al., 2012), reflects an increase in barriers to intercellular water movement, which could arise from cell swelling due to inflammation or increased cell size due to glial activation. fMRI differences appear in the insular cortex during autonomic challenges (Harper et al., 2003). The processes underlining those differences could be elucidated by determining the levels of the neurotransmitters glutamate and γ-aminobutyric acid (GABA), which can now be measured non-invasively. Levels of these chemicals are sensitive to neural reorganization in response to injury, and can reflect different functional states (Arckens et al., 2000). High levels of glutamate, in particular, are associated with excitotoxicity, a probable mechanism of injury in some brain areas in OSA.

The objective of this study was to assess GABA and glutamate in the anterior insular cortex in OSA patients, relative to healthy subjects. The anterior mid-insula was selected, as that subregion preferentially serves autonomic roles (Macey et al., 2012). We hypothesized that, relative to healthy people, OSA patients would show elevated glutamate, based on the potential for hypoxia-induced excitotoxic conditions and altered GABA levels, based on impaired insular action.


We studied 14 OSA patients [mean age: 47.5 ± 10.5 years; nine male; mean apnea–hypopnea index (AHI): 29.5 ± 15.6 events h−1; SAO2 min: 83 ± 9%] and 22 healthy subjects (mean age: 47.5 ± 10.1 years; 11 male). Patients were diagnosed at the UCLA Sleep Disorders Center. No participants had a history of head trauma or disease, current mental illness, use of psychoactive medications, cancer or cardiac disease. Patients were untreated, apart from two who had a prior history of CPAP use. Healthy subjects were screened to exclude sleep disorders. Procedures were approved by the UCLA Institutional Review Board, and participants provided written informed consent.

Neurotransmitters were measured with a magnetic resonance spectroscopy (MRS) method based on ‘two-dimensional’ MRS (Sarma et al., 2014; see Supporting information). Neurochemicals changes were measured using compressed sensing (CS)-based four-dimensional (4D) echo-planar J-resolved spectroscopic imaging (EP-JRESI). High-resolution T1-weighted scans were acquired for localization of insular cortex. Group differences in GABA and glutamate concentrations (ratios with respect to creatine) in the anterior to mid-insular cortex and adjacent tissue were assessed with t-tests. The relative concentrations of ‘Glx’, a combination of glutamate and glutamine indicative of glutamate levels, were also assessed, as Glx is a more robust MRS measure than glutamate.


Neurotransmitter concentrations were recorded successfully from subsets of the 22 healthy and 14 OSA subjects (Table 1; example spectra Fig. 1). Differences between OSA and healthy subjects emerged for GABA (Fig. 2a) and glutamate (Fig. 2b) in the right and left insulae. The left insula showed poorer data quality in more subjects than the right (right successful measures: 69% GABA, 92% glutamate; left successful measures: 31% GABA, 39% glutamate). Success rates were similar for the OSA and healthy groups. When the two OSA patients with a prior history of CPAP were excluded the mean differences were similar, and the significant differences between OSA and healthy subjects remained, with the exception of glutamate in the right insula. However, Glx showed significantly higher levels in OSA versus healthy subjects in the right and left insulae, with and without excluding the two previously treated subjects (Table 1). Correlations between GABA and glutamate were significant only in healthy subjects in the left insula (r: −0.90, P: 0.04; Table 2; Fig. 2c,d).

Table 1. Levels of GABA and glutamate in subsets of 14 OSA (12 never treated) and 22 healthy subjects
Left insula Right insula
OSA Healthy P OSA Healthy P
n Mean ± SD n Mean ± SD n Mean ± SD n Mean ± SD
  1. P, t-test for group differences; Glx, glutamate + glutamine; GABA, γ-aminobutyric acid; OSA, obstructive sleep apnea; SD, standard deviation.
GABA 6 0.36 ± 0.10 5 0.62 ± 0.18 0.03 11 0.27 ± 0.09 14 0.45 ± 0.16 < 0.01
Glutamate 6 1.61 ± 0.32 8 0.94 ± 0.34 < 0.01 14 1.26 ± 0.28 19 1.02 ± 0.28 0.02
Glx 6 1.92 ± 0.38 6 1.22 ± 0.44 0.01 14 1.75 ± 0.42 19 1.34 ± 0.42 0.01
Never treated OSA Never treated OSA
GABA 5 0.35 ± 0.10 (as above) 0.03 9 0.27 ± 0.10 (as above) < 0.01
Glutamate 5 1.50 ± 0.21 (as above) < 0.01 12 1.20 ± 0.25 (as above) 0.08
Glx 5 1.79 ± 0.18 (as above) 0.01 12 1.69 ± 0.43 (as above) 0.04

Left: example insula voxel is shown in red (15 mm3) overlaid an individual anatomical scan. Right: example two-dimensional magnetic resonance spectroscopy (2D-MRS) spectra from right insulae in obstructive sleep apnea (OSA) (56-year-old female) and control (53-year-old male) subjects, with resonances of various neurochemicals indicated (Cho, choline; Cr, creatine; mI, myo-inisotol; MM, other macromolecules; NAA, N-acetylaspartate; Tau, taurine).

Insular (a) gamma aminobutyric acid (GABA) and (b) glutamate levels in subsets of 14 obstructive sleep apnea (OSA) and 22 healthy subjects [mean ± standard error of the mean (SEM)]. Scatterplots of glutamate versus GABA for subjects with both measures in the left (c) and right (d) insular cortices.

Table 2. Correlation table in subjects with GABA and glutamate measures
Left insula Right insula
OSA Healthy OSA Healthy
n r P n r P n r P n r P
  1. P, correlation between γ-aminobutyric acid (GABA) and glutamate; OSA, obstructive sleep apnea.
Glutamate versus GABA 6 0.16 0.76 5 −0.90 0.04 11 −0.47 0.14 14 −0.04 0.90


The anterior insular cortex in OSA shows low GABA and high glutamate, conditions which would modify neural patterns within the structure. GABA normally acts as an inhibitory neurotransmitter, while glutamate is normally excitatory to neural processes. The influences of the insular cortices are complex, with both inhibitory and excitatory influences on hypothalamic, cingulate and frontal cortical structures, among others. On a simplistic level, the combination of a reduction in the inhibitory GABA and increase in the excitatory glutamate could reflect a more active state overall; however, the complexity of the insular projections to multiple structures precludes such an exclusive generalization (Kurth et al., 2010). For excitatory projections, enhanced glutamate could enhance insular influences, and the normal inhibition over hypothalamic structures could be reduced by the lower GABA levels, leading potentially to the exaggerated sympathetic tone in the condition. The altered neurotransmitter levels could also modify cingulate and hippocampal projections influencing mood, such as depression and anxiety, both of which are common in OSA. Low GABA in the insula has been associated with high levels of anxiety (Rosso et al., 2014), and levels appear to be associated with processing of interoceptive stimuli, a function linked with depressive mechanisms (Wiebking et al., 2014). The structures involved in anxiety and depression include the anterior cingulate, recipient of fibres from the cingulum and insular cortices. High glutamate has been found in these limbic areas in bipolar disorder (Soeiro-De-Souza et al., 2015). The hypoxia exposure during apneic events probably leads to excessive excitation of the insular connecting fibres, and such excitotoxic processes are facilitated by glutamate. It is unknown whether the altered neurotransmitter levels revert to normal with CPAP treatment, but such knowledge would assist the selection of interventions and the determination of whether regional GABA and glutamate levels could be useful biomarkers of local neural tissue state in OSA.

The findings of reduced GABA and higher glutamate build upon an earlier demonstration of alterations in the anterior insular cortex in OSA, including changes in structure, function and metabolite levels. The insula shows impaired responses to autonomic challenges in OSA, especially during periods of sympathetic activity increases (Harper et al., 2003). Resting state functional patterns also differ from heathy subjects when those patterns are correlated with other regions (Zhang et al., 2015). Changes in water diffusivity reflect structural changes arising probably from glial activation or inflammation due to hypoxia, and damage to neurones or axons and myelin (Kumar et al., 2012; Macey et al., 2008). Increased myo-inositol in the left insula of OSA patients is also consistent with glial alterations (Yadavet al., 2014). Increased glutamate levels may arise directly from astrocyte activation, as astrocytic glutamate is an energy source for neurones (Pellerin and Magistretti, 1994); if metabolism is altered by OSA in the insular cortex, glutamate from astrocytes may increase to compensate. The combined chemical, functional and structural findings confirm injury and reorganization of the insula in OSA, which probably contribute to clinical symptoms in the condition (Asghari et al., 2012; Kurth et al., 2010; Macey et al., 2013; Marin et al., 2012).

The high glutamate may reflect damaging excitotoxic processes arising from intermittent hypoxia (Jagadapillai et al., 2014). Only 5 h of intermittent hypoxia simulating OSA effects can lead to cellular death (Pae et al., 2005); thus, similar processes are probably operating in people with OSA. However, the high glutamate measured here was in whole tissue, and does not necessarily correspond to concentrations in extracellular fluid, where the neurochemical is key for excitotoxicity.

Interventions complementary to CPAP that influence neurotransmitter levels may help to normalize brain function in OSA. Both GABA and glutamate can be manipulated directly with pharmacological approaches and indirectly with behavioural changes. The measurements presented here could serve as a biomarker of any intervention targeting these brain chemicals.

Measurements were successful in 58% of instances, with the remainder not meeting quality criteria, especially in the left insula. Because OSA and healthy measurements were affected similarly, the low data quality is due probably to technical rather than biological reasons (e.g. poor shimming). The resolution of the MRS voxels was limited (example in Fig. 1), so the measures did not cover the entire anterior to mid-portion of the structure, and included adjacent tissue; the subregion studied will have varied slightly between subjects.

In conclusion, the anterior to mid-insular cortex shows lower GABA and higher glutamate levels in OSA compared with healthy subjects. These alterations probably reflect a functional neural reorganization that contributes to the autonomic and psychological symptoms in OSA, such as high sympathetic tone and refractory hypertension, and anxiety, depression and cognitive difficulties. High glutamate would facilitate excitotoxic processes. The altered neurotransmitter levels provide a biomarker of regional functional status of the OSA brain, and will allow insights into the neurological effects of treatment with CPAP or other interventions.

New, Low-Cost Screening Process for Obstructive Sleep Apnea

Measuring the oxygen desaturation index (ODI) with overnight pulse oximetry is an effective, low-cost way to screen for obstructive sleep apnea (OSA), a new study published in the Journal of Clinical Sleep Medicine suggests.
OSA is often underrecognized in hospitalized patients and associated with significant morbidity and mortality, according to researchers from Thomas Jefferson University and Hospitals, in Philadelphia.
“Sleep disordered breathing is associated with cardiovascular complications and sudden death,” said lead study author Sunil Sharma, MD, FAASM, associate professor of pulmonary medicine in the Sidney Kimmel Medical College at Thomas Jefferson University, in a press release.
The researchers conducted a prospective study with 754 patients to test the efficacy of this screening for identifying OSA in patients admitted to a tertiary care hospital. The patients were admitted between February 2013 and February 2014.
Obese patients (body mass index >30 kg/m2) were automatically screened for OSA—being overweight is a risk factor for OSA—using the STOP (snoring, tiredness during daytime, observed apnea, high blood pressure) questionnaire. Patients with positive results were advised to have a follow-up evaluation, which included an overnight polysomnography.
The optimal screening cutoff for OSA was ODI greater than or equal to 10 events per hour (Matthews correlation coefficient, 0.36; 95% CI, 0.24-0.47). The researchers found that 129 of the 149 patients who underwent polysomnography were shown to have OSA.
“The results showed that our screening process identified sleep disordered breathing in 87% of patients who followed up with a polysomnography,” said Dr. Sharma. “We confirmed the high prevalence of undetected sleep-disordered breathing among hospitalized patients and also validated a low-cost protocol to detect it.”
The authors noted a significant increase in the number of hospitalized patients recommended to undergo polysomnography after implementing this screening process.
“This study should be of great interest to hospitals looking at ways to reduce complications,” said Dr. Sharma. “Recent data suggests that for inpatients with cardiovascular disorders, early diagnosis and intervention for sleep apnea may lead to reduced readmission rates.”

Sleep Apnea Linked to Depression in Men

Obstructive sleep apnea (OSA) is associated with an increased risk of depression in men, a large Australian study found.

Among 1,875 men ages 35 to 83 who were assessed for depression at two time points about 5 years apart in the Men Androgen Inflammation Lifestyle Environment & Stress Study (MAILES), previously undiagnosed severe OSA was associated with depression (OR 2.1, 95% CI 1.1-4, P<0.05), reported Carol J. Lang, PhD, of the University of Adelaide, at theannual meeting of the American Thoracic Society here.

This statistical significance remained even after adjustment for age, waist circumference, smoking, relationship status, financial difficulties, erectile dysfunction, and nocturia, she noted.

“Depression is highly prevalent in OSA, reaching 39% in clinic studies. However, few population-based studies have been done and results have been mixed,” Lang said.

In one longitudinal study that included 1,400 men and women, a dose-dependent association between a sleep-related breathing disorder and depression was seen, with a 2.6-fold increased risk of depression and a moderate or severe sleep-related breathing disorder.

A cardinal symptom of OSA is excessive daytime sleepiness, although not all affected patients report this problem. It’s unclear whether daytime sleepiness is associated with depression in OSA, and in the longitudinal study, sleepiness was not found to be an explanatory factor for the observed relationship between the sleep-related breathing disorder and depression.

Further complicating this relationship was the finding in another study that residual sleepiness persisting after continuous positive airway pressure treatment was linked with refractory depression.

In an attempt to clarify the association of OSA and depression, in 2010 Lang and colleagues conducted telephone interviews asking men if they had ever been diagnosed with sleep apnea with a sleep study, and those answering in the negative were invited to participate. A total of 857 men then underwent at-home polysomnography testing.

Depression was assessed using the Center for Epidemiologic Studies Depression Scale/Beck’s Depression Inventory, and daytime sleepiness was evaluated according to the Epworth Sleepiness Scale.

OSA was defined as an apnea-hypopnea index higher than 10. Mild-to-moderate OSA was an index score of 10 to 29, and severe was 30 or higher.

Logistic regression analysis determined that, along with severe OSA, daytime sleepiness was associated with depression (OR 1.1, 95% CI 1-1.2, P<0.05).

Then, in a model that included both previously undiagnosed OSA and excessive daytime sleepiness, individuals with both had 4.2 times greater odds of depression than those with neither, and 3.5 times greater likelihood of depression than those with either alone.

“The message is that clinicians need to be aware of these risks and assess for the other if one is present,” Lang said.

The precise mechanisms underlying the link between these conditions are uncertain, but may involve low oxygen levels, arterial inflammatory responses, and neurologic changes in the brain, she said.

The press conference moderator, Mihaela Teodorescu, MD, of the department of pulmonary and critical care at the University of Wisconsin in Madison, agreed that this is an important clinical issue.

“Sleep apnea leads to more refractory depression and patients get more treatment, including with benzodiazepines, which can aggravate and further contribute to depression,” she said.

Urgent Adenotonsillectomy in Kids Results in Good Outcome

Patients who require urgent tonsillectomy without or with adenoidectomy (TA) tend to be younger, have elevated obstructive apnea-hypopnea indices, and more persistent desaturations below 80% than children who receive timely TA. Their desaturations also tend to be unresponsive to supplemental oxygen. After surgery, approximately half of children who receive urgent TA will no longer require supplemental oxygen because of a dramatic improvement in gas exchange.

Conan Liang, BA, from the University of Colorado School of Medicine in Aurora, and colleagues published the results of their retrospective medical record review online January 2 in JAMA Otolaryngology–Head & Neck Surgery. They report that at their institution, pediatric patients who receive urgent TA (n = 35) resemble those who meet hospital admission criteria for bronchiolitis. In particular, the decision to perform urgent TA was typically (85% of the time) based on persistent desaturation below 80% despite receipt at least 0.5 L of oxygen.

Patients receiving urgent TA had an average age of 3.8±2.1 years compared to the 6.6±4.2 years seen in the control group. Patients in the urgent TA group had average apnea-hypopnea indices of 39.4 events per hour.

TA is considered a relatively safe procedure with a low incidence of postoperative complications. Results from the current study are consistent with this, and the authors report that 94% of patients had a favorable postoperative course. The authors acknowledge, however, that that their hospital had a low (26%) follow-up rate for postoperative polysomnography.

The authors did not find an increased number of pulmonary comorbidities in the urgent TA cohort compared with the control cohort. This finding led the authors to suggest that children in the urgent TA group may have had subclinical findings that predisposed them to developing hypoxemia.

Urgent vs Timely TA
As more polysomnographies are performed, an increasing number of children are likely to be diagnosed with severe obstructive sleep apnea (OSA) with gas exchange abnormalities. The severity of OSA is correlated with adenotonsillar hypertrophy, and so, not surprisingly, TA is commonly performed in response to sleep-related breathing disorders.

OSA is now understood, however, to be a chronic as opposed to an acute condition, suggesting that it may not require urgent treatment. The study underscores that there are no clearly defined indications for urgent TA in the pediatric population.

7 Ways To Stop Your Snoring

Before you resort to sleeping in separate beds, try these at-home remedies for snoring. 

7 Ways To Stop Your Snoring

Forget about the monster under your bed. If you have a partner who snores, you’re dealing with a monster in your bed — and it’s often a near-nightly showdown. In a new National Sleep Foundation survey, 40 percent of Americans admitted to snoring a few nights per week (or more).

And the ones who are suffering aren’t usually the folks sawing logs. “The most common side effect of snoring is waking up other people, whether in the same bed or the next bedroom, depending on how loud it is,” says Eric Kezirian, MD, a professor of otolaryngology at the University of Southern California, who specializes in the treatment of snoring.

In fact, people with a snoring significant other tend to lose an hour of sleep per night, according to Craig Schwimmer, MD, founder of The Snoring Center. Perhaps as a result, “couples in snoring relationships report lower marital satisfaction scores, they have less sex, and they often resort to sleeping apart,” he tells Yahoo Health.

That’s why snoring is considered a social issue more so than a medical one, although in some cases, it does indicate a more serious problem: obstructive sleep apnea. “When we go to sleep at night, the muscles in the throat relax, and as we breathe in and out, this relaxed tissue tends to vibrate,” explains Schwimmer. If that tissue simply vibrates — and nothing more — you’ll probably just bother your bedmate. But if that tissue closes as it vibrates, blocking your airway, you may have obstructive sleep apnea. “Snoring and sleep apnea are really just different points on a continuum,” says Schwimmer.

Obstructive sleep apnea, of course, requires serious medical intervention. But simple snoring can often be treated with these at-home remedies:

Adjust your position

If you’re a chronic snorer, back isn’t best. “Most people snore more on the back than they do on the side, and more on the side than they do on the stomach,” says Schwimmer. It can be tough to switch your preferred sleeping position, so sleep doctors often suggest this trick to encourage people to stay on their side: Sew a pocket on the back of a T-shirt between the shoulder blades, and slip two tennis balls inside.

“When people sleep on their side, their shoulder can get sore. So they roll on their back,” says Kezirian. “The tennis balls aren’t very comfortable, so they end up rolling to their other side.”

Not extreme enough? Try the Night Shift Sleep Positioner, a device you wear around your neck that vibrates when you roll onto your back, increasing in intensity until you shift to your side. “I wore it one night, and it drove me crazy,” says W. Christopher Winter, MD, director of Charlottesville Neurology and Sleep Medicine. “But it worked. After a few days of that, you would not be sleeping on your back.”

Play with pillows

For some people, the tennis ball trick works — but only because it keeps them up all night. If you simply can’t sleep with sports equipment attached to your PJs, try resting a body pillow between your legs, which helps align your spine and makes side sleeping more comfortable. Or wedge a C-shaped pregnancy pillow behind your back, suggests Winter.

If you still can’t adjust to lying on your side, lie on your back, but prop up your head and shoulders. “You want to make a little incline — a wedge — with a couple pillows,” says Kezirian. “It’s not just lifting up your head.” Try placing one underneath your shoulders to elevate your chest, then another two under your head. That may help keep the back of your throat open.

Avoid alcohol before bed

It’s not just your inhibitions that loosen up when you’re drinking. “Alcohol preferentially relaxes the muscles in the throat, so everybody’s snoring is worse after a couple drinks,” says Schwimmer. Plus, since you’re more sedated after drinking, your snoring is less likely to stir you awake, leaving your bedmate to suffer longer. “Most wives will tell you, ‘When Walter goes out drinking with his buddies, he’s going to snore like crazy. I don’t even sleep in the bed with him that night,’” says Winter. The simple fix: Stop your imbibing within four hours of bedtime.

Open your nose

Sometimes, snoring isn’t due to flapping muscles in your throat — it may simply be a problem of clogged or narrow nasal passages. If they’re consistently congested, a saltwater nasal spray may be the only fix you need. “When you brush your teeth in the morning and at night, put a spray or two in either side of your nose,” says Kezirian. Not only will that keep your nostrils clear, it will also maintain the moisture in your nose, preventing the dryness and irritation that can promote snoring.

Another way to keep your nasal passages open: Breathe Right strips. “If your airway is collapsing in the back of your throat, putting a sticker across your nose is not really going to help,” says Winter. But if narrow nasal passages are the problem (or if they’re chronically clogged due to allergies), the sticky strips could make a big difference.

Try this test to see if these strips might be the right remedy for you: While looking into a mirror, inhale deeply through your nose, and see if the sides of your nose collapse. If your nostrils cave in, you probably have narrow nasal passages, so the strips could do the trick, says Kezirian.

Control your acid reflux

What’s happening in your esophagus may not seem relevant to the noises you make at night, but acid reflux can actually play a major role in snoring. When stomach acid coats your throat, it creates inflammation, says Schwimmer. “The tissue is swollen, so that narrows the airway,” he says. “Swollen tissue is more vibratory.” To tame your reflux, stop eating two to three hours before bedtime, and if that doesn’t work, try taking Tums or Rolaids before bed.

Be a mouth breather

People who snore often sound like a choo-choo train while they snooze. “They’re puffing up their cheeks, and exhaling against a closed mouth,” which can lead to snoring, says Winter. ProVent stickers turn your nostrils into a one-way valve, allowing you to breath in, but not out, through your nose. “That creates extra pressure in the back of your airway and holds it open,” he explains. In other words, the stickers force you to exhale through your mouth. “They’re really for sleep apnea, but I have patients who say that they help with their snoring,” says Winter.

Belt it out

Here’s motivation to turn your morning commute into a concert: In a 2013 British study, people who did singing exercises — a series of simple, repetitive noises put to music — for 20 minutes a day showed a significant reduction in snoring after three months. But you don’t necessarily have to do the specific exercises in the study — just belting it out may have a benefit. “There are a lot of muscles in your upper airway that don’t get used a tremendous amount,” says Winter. By singing, you may strengthen and tone those muscles, which could potentially reduce your snoring, he says.


Sleep apnea is defined as pause/brief cessation in breathing while sleeping.It is not uncommon in children.A good comfortable sleep is necessary for proper growth and functioning of brain.The most common cause of sleep apnea in children is obstructive sleep apnea(OSA) caused by adenotonsillar hypertrophy in which adenoid and tonsils are unduely enlarged causing obstruction in the airway more while sleeping leading to sleep apnea. Obesity is a predisposing factor.According to Philips survey 2009 ,14% Indians are suffering from this disorder.
The chief symptom of OSA is snoring which is seen in 15-20 % of children without having this disease ,so in majority of cases it goes unrecognised.If your child have any of these symptoms,look for OSA
Restless night sleep
Excessive day time sleepiness
Hyperactivity with /without aggressive or violent behaviour
Poor attention span
Subnormal academic performance
Low stamina at sports
Poor growth
Abnormal behaviour
The diagnostic test for this disorder is POLYSOMNOGRAPHY(PSG),which is available at very few centres in India.Sleep medicine is a new branch in India.In PSG the child has to be admiited in hospital and by a device his/her ,breathing,heart rate , rhythm,and brain activities are recorded while the child is sleeping.It costs nearly 15000 INR in Indian private set up.
In most of the cases ,weight reduction and operative removal of adenoid and tonsils are curative.

Unaddressed OSA may lead to early development of these but not limited to these:
Diabetes Mallitus

Respiratory disorders in children by DR DK JHA's photo.

Respiratory disorders in children by DR DK JHA's photo.

Suspect OSA in patients with unexplained daytime sleepiness

Adult patients who are excessively sleepy during the day for no apparent reason should be targeted for assessment of obstructive sleep apnea (OSA) using a sleep study, a new guideline from the American College of Physicians (ACP) recommends.

Sleep study records patients’ brain activity, eye movements, heart rate, and blood pressure during sleep to diagnose OSA and determine disease severity.

In patients whom OSA is suspected, the guideline recommends full-night, in-laboratory polysomnography (PSG) to establish the diagnosis. This test requires specialized facilities, is expensive and demands that patients spend the night under observation in a foreign environment, but yields the most accurate diagnostic information. [Ann Intern Med 2014;161:210-220]

Home-based portable sleep monitors may be used as an alternative in patients without comorbid conditions or when PSG is not available, although these can yield substantially different scores on the apnea-hypopnea index (AHI), which accounts for the number of pauses in breathing per hour of sleep.

Daytime sleepiness (hypersomnia) is a clinically relevant symptom of OSA, but clinicians should also include in their assessment other symptoms such as fatigue, insomnia and snoring, and risk factors such as obesity, said the guideline authors.

Clinicians are not advised to assess OSA in the absence of daytime sleepiness or treat patients with low AHI scores as evidence suggests neither improves clinical outcomes. Of note, portable monitoring in patients with chronic lung disease, congestive heart failure, neurologic disorders and other major comorbidities is also not recommended as very few studies included these patients. There is also little evidence for pre-operative screening for OSA and its effect on surgical outcomes.

The guideline, which is based on reviews of peer-reviewed studies published from 1996 to May 2013, is developed to provide clinicians with guidance on diagnosing OSA. For guidance on treatment, clinicians could refer to the ACP guideline on the management of OSA.

“Obstructive sleep apnea is a serious health condition that is associated with cardiovascular disease, hypertension, cognitive impairment, and type 2 diabetes,” said ACP president Dr. David Fleming. “It is important to diagnose individuals with unexplained daytime sleepiness so that they can get the proper treatment.”

Snoring mothers-to-be linked to low birth weight babies.

Experts say snoring may be a sign of breathing problems that could deprive an unborn baby of oxygen

A newborn baby. Scientists found that women who snored both before and during pregnancy were more likely to have smaller babies and elective C-sections. Photograph: Christopher Furlong/Getty Images

Mothers-to-be who snore are more likely to give birth to smaller babies, a study has found. Snoring during pregnancy was also linked to higher rates of Caesarean delivery.

Experts said snoring may be a sign of breathing problems that could deprive an unborn baby of oxygen.

Previous research has shown women who start to snore during pregnancy are at risk from high blood pressure and the potentially dangerous pregnancy condition pre-eclampsia.

More than a third of the 1,673 pregnant women recruited for the US study reported habitual snoring.

Scientists found women who snored in their sleep three or more nights a week had a higher risk of poor delivery outcomes, including smaller babies and Caesarean births.

Chronic snorers, who snored both before and during pregnancy, were two-thirds more likely to have a baby whose weight was in the bottom 10%.

They were also more than twice as likely to need an elective Caesarean delivery, or C-section, compared with non-snorers.

Dr Louise O’Brien, from the University of Michigan’s Sleep Disorders Centre, said: “There has been great interest in the implications of snoring during pregnancy and how it affects maternal health but there is little data on how it may impact the health of the baby.

“We’ve found that chronic snoring is associated with both smaller babies and C-sections, even after we accounted for other risk factors. This suggests that we have a window of opportunity to screen pregnant women for breathing problems during sleep that may put them at risk of poor delivery outcomes.”

Women who snored both before and during pregnancy were more likely to have smaller babies and elective C-sections, the researches found. Those who started snoring only during pregnancy had a higher risk of both elective and emergency Caesareans, but not of smaller babies.

Snoring is a key sign of obstructive sleep apnoea, which results in the airway becoming partially blocked, said the researchers, whose findings appear in the journal Sleep.

This can reduce blood oxygen levels during the night and is associated with serious health problems, including high blood pressure and heart attacks.

Sleep apnoea can be treated with CPAP (continuous positive airway pressure), which involves wearing a machine during sleep to keep the airways open.

Dr O’Brien added: “If we can identify risks during pregnancy that can be treated, such as obstructive sleep apnoea, we can reduce the incidence of small babies, C-sections and possibly NICU (neo-natal intensive care unit) admission that not only improve long-term health benefits for newborns but also help keep costs down.”

Morbidity and mortality in children with obstructive sleep apnoea: a controlled national study.


Background Little is known about the diagnostic patterns of obstructive sleep apnoea (OSA) in children. A study was undertaken to evaluate morbidity and mortality in childhood OSA.

Methods 2998 patients aged 0–19 years with a diagnosis of OSA were identified from the Danish National Patient Registry. For each patient we randomly selected four citizens matched for age, sex and socioeconomic status, thus providing 11 974 controls.

Results Patients with OSA had greater morbidity at least 3 years before their diagnosis. The most common contacts with the health system arose from infections (OR 1.19, 95% CI 1.01 to 1.40); endocrine, nutritional and metabolic diseases (OR 1.30, 95% CI 0.94 to 1.80); nervous conditions (OR 2.12, 95% CI 1.65 to 2.73); eye conditions (OR 1.43, 95% CI 1.07 to 1.90); ear, nose and throat (ENT) diseases (OR 1.61, 95% CI 1.33 to 1.94); respiratory system diseases (OR 1.78, 95% CI 1.60 to 1.98); gastrointestinal diseases (OR 1.34, 95% CI 1.09 to 1.66); skin conditions (OR 1.32, 95% CI 1.02 to 1.71); congenital malformations (OR 1.56, 95% CI 1.31 to 1.85); abnormal clinical or laboratory findings (OR 1.21, 95% CI 1.06 to 1.39); and other factors influencing health status (OR 1.29, 95% CI 1.16 to 1.43). After diagnosis, OSA was associated with incidences of endocrine, nutritional and metabolic diseases (OR 1.78, 95% CI 1.29 to 2.45), nervous conditions (OR 3.16, 95% CI 2.58 to 3.89), ENT diseases (OR 1.45, 95% CI 1.14 to 1.84), respiratory system diseases (OR 1.94, 95% CI 1.70 to 2.22), skin conditions (OR 1.42, 95% CI 1.06 to 1.89), musculoskeletal diseases (OR 1.29, 95% CI 1.01 to 1.64), congenital malformations (OR 1.83, 95% CI 1.51 to 2.22), abnormal clinical or laboratory findings (OR 1.16, 95% CI 1.06 to 1.27) and other factors influencing health status (OR 1.35, 95% CI 1.20 to 1.51). The 5-year death rate was 70 per 10 000 for patients and 11 per 10 000 for controls. The HR for cases compared with controls was 6.58 (95% CI 3.39 to 12.79; p<0.001).

Conclusions Children with OSA have significant morbidities several years before and after their diagnosis.

Source: Thorax

Obstructive sleep apnoea and type 2 diabetes mellitus: a bidirectional association.

Obstructive sleep apnoea and type 2 diabetes are common medical disorders that have important clinical, epidemiological, and public health implications. Research done in the past two decades indicates that obstructive sleep apnoea, through the effects of intermittent hypoxaemia and sleep fragmentation, could contribute independently to the development of insulin resistance, glucose intolerance, and type 2 diabetes. Conversely, type 2 diabetes might increase predisposition to, or accelerate progression of, obstructive and central sleep apnoea, possibly through the development of peripheral neuropathy and abnormalities of ventilatory and upper airway neural control. Although more research is needed to clarify the mechanisms underlying the bidirectional association between the two disorders, their frequent coexistence should prompt all health-care professionals to embrace clinical practices that include screening of a patient presenting with one disorder for the other. Early identification of obstructive sleep apnoea in patients with metabolic dysfunction, including type 2 diabetes, and assessment for metabolic abnormalities in those with obstructive sleep apnoea could reduce cardiovascular disease risk and improve the quality of life of patients with these chronic diseases.

Source: lancet