Snoring is very prevalent in our society, and is considered by most to be simply a cosmetic nuisance. The position health coverage takes in denying claims to treat snoring lends further support to this common consensus; at least for our patients. Unfortunately, in light of the mounting literature data which suggests that this is not the case, we have to ask ourselves, “Benign snoring  … How Benign is it?

Literature data suggests that Obstructive Sleep Apnea seems to progress from snoring. The vibration associated with snoring has been shown to lead to “nervous lesions”; muscle tissue atrophy and denervation. The degree of these changes has been shown to increase with increasing snore severity. Sensory neurons have also been shown to be affected by these vibrations. Studies have shown us that increasing severity of OSA is related to increase in “vibration & cold detection thresholds”; suggesting an impairment in the sensory neurons necessary to maintain airway patency.

When muscle tissue is altered by vibrations associated with snoring, the airway narrows making it more susceptible to collapse. When the pharyngeal sensory nerves become impaired from these same vibrations, the dilation reflex intended to prevent airway collapse also becomes impaired. It is particularly interesting that these “vibration caused lesions” become more prevalent in individuals that have increasing levels of disease from snoring to OSA.

Literature data also suggests that snoring and OSA may be important risk factors for Carotid Atherosclerosis and Stroke. A study of One hundred and ten volunteers that underwent full polysomnography, snoring quantification, and femoral and carotid artery ultrasound demonstrated this relationship. These subjects were categorized as mild, moderate or heavy snorers. The results showed that     prevalence of carotid atherosclerosis increased with increase in snoring severity. This was not the case for femoral atherosclerosis.

It was concluded that heavy snoring significantly increases the risk of carotid atherosclerosis and that this risk is independent of other risk factors including      measures of nocturnal hypoxia and OSA severity. These findings have substantial public health implications for the management of carotid atherosclerosis and the prevention of stroke.

Literature data clearly suggests that snoring is a precursor to OSA and that increasing severity levels of snoring is associated with increasing risk of Carotid Atherosclerosis and Stroke. Yet, snoring is commonly considered by many to be of cosmetic importance only.

In summary, increasing severity of snoring has been associated with changes in airway tissues, which impair upper airway function and to arterial changes which increase susceptibility to Stroke. The next time we are dealing with “Benign Snoring …” we need to ask ourselves; “How Benign is it?”

John Viviano DDS

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As oral appliance (OA) therapy gains ground as a viable sleep apnea solution, compliance concerns are being addressed by micro technology. But does that technology actually work?

A study published in the journal Thorax points toward the affirmative, with results indicating “the safety and feasibility of objective measurement of OA compliance.”

While OA therapy is reported to be efficacious for the treatment of SDB, data on compliance is usually limited to self-report. In the 3-month prospective clinical trial published in Thorax, researchers assessed the safety and feasibility of an objective measurement of compliance during OA therapy using an embedded micro sensor thermometer with “on-chip integrated readout electronics in 51 consecutive patients with an established diagnosis of sleep disordered breathing.”

No micro sensor-related adverse events were recorded, and no problems were encountered during the readout of the compliance data. The overall objective mean rate of OA use was 6.6±1.3 h per day with a regular OA users’ rate of 82% at the 3-month follow-up. Statistical analysis revealed no significant differences between objective and self-reported OA compliance data.

Measurement of the objective OA compliance allowed researchers to calculate the mean disease alleviation (MDA) as the product of objective compliance and therapeutic efficacy. MDA serves as a measure of the overall therapeutic effectiveness, and turned out to be 51.1%.

Researchers concluded: “Our findings suggest that objective measurement of OA compliance during SDB treatment is safe and feasible.” Click here for the full study.

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Lena Lavie, PhD, discusses the findings of her counter-intuitive study that continues to build momentum.

People who suffer from breathing disorders such as sleep apnea, are usually at higher risk for cardiovascular disease. However, a recent study from Technion-Israel Institute of Technology scientists suggests that some heart attack patients with these conditions may actually benefit from mild to moderate sleep-disordered breathing.

The study, entitled Endothelial Progenitor Cells in Acute Myocardial Infarction and Sleep-disordered Breathing appeared in the American Journal of Respiratory and Critical Care Medicine (vol 1. 187, no1). Click Here to Read Abstract.

Lena Lavie, PhD, along with researchers Slava Berger, PhD, Doron Aronson, PhD, and Peretz Lavie, PhD, essentially concluded that apnea and other types of sleep-disordered breathing can boost the numbers and functions of rare cells (endothelial progenitor cells or EPCs) that help to repair and build new blood vessels. They say the findings could help predict which patients are at a greater health risk after a heart attack, and may even suggest ways to rebuild damaged heart tissue.

Reaction to studies in the medical world can be notoriously slow, and co-lead researcher Lena Lavie acknowledges that it is still too early to gauge the study’s impact.

“Usually, the impact of a study is built over time,” muses Lavie, a senior research fellow for The Lloyd Rigler Sleep Apnea Research Laboratory at Israel’s Technion Institute of Technology. “For instance, the seminal paper on ischemic preconditioning by Murry et al. published in 1986 [6] was scarcely cited for the first 4 years after its publication. Reviewers complimented our study and pointed to the possible implications toward sleep apnea patients. We also received several e-mails from colleagues in the field that congratulated us on the study.”

Lena Lavie, who also serves as a professor on The Ruth and Bruce Rappaport Faculty of Medicine, agreed to sit down with Sleep Diagnosis & Therapy to talk about the ground-breaking—and somewhat counterintuitive—results of the study.

When did you get the idea for your study?

Lena Lavie, PhD, senior research fellow at The Lloyd Rigler Sleep Apnea Research Laboratory, and a member of the The Ruth and Bruce Rappaport Faculty of Medicine, Technion Institute of Technology, Israel: Obstructive sleep apnea is strongly associated with increased cardiovascular morbidity and mortality, however not all sleep apnea patients develop cardiovascular consequences. The question is why?

The idea that sleep apnea may also activate protective mechanisms came up for the first time around 2002 when we acquired data on increased levels of stress proteins in sleep apnea patients [1]. These protective proteins are synthesized under various stresses, including intermittent decreases in blood oxygen levels, that are the hallmark of  sleep apnea. However, this notion crystalized in 2005 when we analyzed mortality data of sleep apnea patients and found out that in comparison with standard mortality data of the general population, the risk of mortality in sleep apnea patients declined with age [2].

Thus, in patients older than 50 the risk of mortality did not exceed that of the general population. Since these findings confirmed preliminary data we reported 10 years earlier, in 1995, we hypothesized that the syndrome may also activate protective mechanisms in some individuals (probably depending also on their genetic makeup). At that time we had evidence that sleep apnea is associated with increased levels of Vascular Endothelial Growth factor (VEGF), a protein responsible for angiogenesis [3] and that there are large inter-individual differences in VEGF levels in response to hypoxia [4]. This led us to hypothesize that the protective mechanisms may be related to enhanced cardiac collateralization [5].

Some summaries of your work concluded that sleep disorders could somehow “help” heart health. Is this an oversimplified conclusion? If so, how would you sum up your conclusions?

Yes, we believe that some of the health summaries are an oversimplification. We can conclude from our study that intermittent hypoxia in patients with mild to moderate sleep apnea syndrome, who suffered acute myocardial infarction (AMI), enhance the cardiac collateralization and repair of damaged tissue. This may confer protection and facilitate recovery from heart attack in some individuals. And the emphasis of our study is on “mild to moderate sleep apnea.”

What surprised you most about your study?

The great similarity between the impact of the nocturnal exposure to intermittent hypoxia because of the sleep apnea and the exposure to intermittent hypoxia in vitro, on the function of the EPCs was surprising. Even though the rate of the hypoxic events was widely different in the two conditions, the effects on cells’ activity was almost identical.

What did you expect to find when you started the study?

Our hypothesis was that intermittent hypoxia activates angiogenesis. This hypothesis was based on our earlier findings that vascular endothelial growth factor (VEGF), which is a growth factor promoting angiogenesis, was higher in OSA. Then, we reasoned that because EPCs are mobilized by hypoxia, we should find more EPCs in patients with sleep apnea than in patients without sleep apnea, and that potentially their EPCs should be more active.

What is the next logical follow-up study (if any) that should be done?

Our study raises many questions both with respect to treatment of patients suffering acute myocardial infraction and treatment of sleep apnea. First our study should be repeated in patients with severe sleep apnea, since as mentioned above the patients in our study had only mild and moderate syndrome.

Second, the same study should be repeated with women, because we studied only men. Third, the question if controlled exposure to intermittent hypoxia (by controlling intermittent hypoxia through breathing) of patients suffering from acute myocardial infarction (AMI) who do not have sleep apnea, can result in the same effects. This should be examined.

Fourth, the cellular measures obtained should be investigated with regard to endothelial function, left ventricular recovery etc., to determine if mild to moderate sleep apnea has measureable beneficial effects on cardiac functioning, as compared to patients without sleep apnea. Also, there should be a long-term follow-up of these patients to determine if these changes improve their prognosis. Fifth, since treatment with nasal continuous positive airway pressure (nCPAP) abolishes intermittent hypoxia in in sleep apnea, its effects on these measures should be studied as well.

Do your findings point to a reconsideration of sleep therapy in some cases? If so, what cases might those be?

Our findings are particularly relevant to the treatment of asymptomatic elderly patients with mild to moderate sleep apnea. Given the fact that approximately 60% of the people older than 65 have at least 15 respiratory events per hour of sleep, which is considered to be moderate sleep apnea, and that most of them are asymptomatic, our findings may suggest that a decision if to treat an elderly with mild-moderate sleep apnea should be based on the existence of symptoms.

What has been the reaction to your study? 

It is too early to say what the reactions to the study are. Usually the impact of a study is built overtime. For instance, the seminal paper on ischemic preconditioning by Murry et al. published in 1986 [6] was scarcely cited for the first 4 years after its publication. The immediate reaction was an editorial that accompanied our paper. The reviewers complemented our study and pointed to the possible implications toward sleep apnea patients. We also received many e-mails from colleagues in the field that congratulated us on the study.

What are your current research efforts?

Generally, our research interests are focused on the functions of various blood cells and how these functions are affected by hypoxia and intermittent hypoxia. Thus far, besides EPCs we have studied endothelial cells that are lining the blood vessels, monocytes, and their development into foam cells which induce atherosclerosis, platelets and their pro-thrombotic effects—neutrophils and lymphocytes—all of which were shown to be activated and to promote inflammatory sequelae in sleep apnea patients as well as in response to intermittent hypoxia in vitro.

How do you think sleep medicine will evolve over the next few years?

Sleep medicine is presently undergoing a major change. In the area of sleep apnea, emphasis is shifting from diagnosis to treatment, and there is a major effort to find an alternative treatment to nCPAP. I believe that this process will continue and that in the next 10 to 15 years sleep apnea will be handled by general practitioners. As sleep apnea is the flagship of sleep medicine, this may have major negative effects on the future of sleep medicine.

About Lena Lavie, PhD

Lena Lavie obtained her PhD from the Department of Biology in the Technion Israel Institute of Technology, and did her post-doctoral training in the department of Biological Chemistry at Harvard Medical School, Boston. She is currently a senior research fellow, an associate professor, and the head of the Lloyd Rigler Sleep Apnea Research Laboratory in the Ruth and Bruce Rappaport Faculty of Medicine at Israel’s Technion Institute of Technology.

References

1.         Lavie, L., Obstructive sleep apnoea syndrome–an oxidative stress disorder. Sleep Med Rev, 2003. 7(1): p. 35-51.

2.         Lavie, P., L. Lavie, and P. Herer, All-cause mortality in males with sleep apnoea syndrome: declining mortality rates with age. Eur Respir J, 2005. 25(3): p. 514-20.

3.         Lavie, L., et al., Plasma vascular endothelial growth factor in sleep apnea syndrome: effects of nasal continuous positive air pressure treatment. Am J Respir Crit Care Med, 2002. 165(12): p. 1624-8.

4.         Schultz, A., et al., Interindividual heterogeneity in the hypoxic regulation of VEGF: significance for the development of the coronary artery collateral circulation. Circulation, 1999. 100(5): p. 547-52.

5.         Lavie, L. and P. Lavie, Ischemic preconditioning as a possible explanation for the age decline relative mortality in sleep apnea. Med Hypotheses, 2006. 66(6): p. 1069-73.

6.         Murry, C.E., R.B. Jennings, and K.A. Reimer, Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation, 1986. 74(5): p. 1124-36.

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With an eye-catching headline that labels home sleep testing as “controversial,” Kentucky’s Courier-Journal once again shines a light on obstructive sleep apnea. Physicians deemed “skeptical” of home sleep testing are quoted throughout.

“We order some at-home tests…But unfortunately, a lot of that is driven by insurance,” says Dr. Subin Jain, a partner at Louisville Pulmonary Care and director of the Baptist Health Louisville Sleep Disorders Center. “It’s increasingly difficult to have studies done in the lab. The amount of data (from a home study) is significantly less than what you’d get in the lab.”

The article goes on to document insurance company efforts to steer patients toward home testing for financial reasons, noting that home sleep tests cost about $200 to $400, compared with lab tests that “can range from $600 in a free-standing sleep center to around $1,300 in a hospital.”

Home study proponents in the article bring up the fact that home tests can be especially helpful for patients who live far from sleep centers, or who are intimidated by laboratory settings. Reporter Laura Ungar also references a widely reported June 2012 study in the journal Sleep, which concluded that home testing was “not inferior in terms of acceptance, adherence, time to treatment and functional improvements.”

The New England Comparative Effectiveness Public Advisory Council, which considers benefits and value of medical innovations, also voted in January that home sleep testing was “functionally equivalent” to lab tests for diagnosing sleep apnea in appropriate patients.

Read full article.

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Nightmares and unhealthy beliefs about sleep may increase the risk of suicide in people who are depressed, a new study suggests.

“Nightmares and Dysfunctional Beliefs about Sleep Mediate the Effect of Insomnia Symptoms on Suicidal Ideation” is published in the Journal of Clinical Sleep Medicine.

Read Abstract.

The findings reaffirm earlier research linking sleep problems to an increased risk of suicide, and suggest which symptoms doctors might want to target with treatment to reduce that risk, the researchers said.

Unhealthy beliefs about sleep can take several forms: for example, the thought that a poor night’s sleep will disturb sleep for the whole week, or that sleep loss will have dire and irreversible consequences. Such ideas carry an atmosphere of hopelessness, an emotion researchers know is connected to suicide risk.

Nightmares and unhealthy beliefs about sleep may increase the risk of suicide in people who are depressed, a new study suggests.

The findings reaffirm earlier research linking sleep problemsto an increased risk of suicide, and suggest which symptoms doctors might want to target with treatment to reduce that risk, the researchers said.

Unhealthy beliefs about sleep can take several forms: for example, the thought that a poor night’s sleep will disturb sleep for the whole week, or that sleep loss will have dire and irreversible consequences. Such ideas carry an atmosphere of hopelessness, an emotion researchers know is connected to suicide risk.

“Insomniacan lead to a very specific type of hopelessness, and hopelessness by itself is a powerful predictor of suicide,” said study researcher Dr. W. Vaughn McCall, chair of the Department of Psychiatry and Health Behavior at Georgia Health Sciences University in Augusta.

While the factors that contribute to suicide risk are not the same for everyone, “For some patients, I think sleep problems are part of the [symptom] profile,” McCall said.

During the study, McCall and colleagues surveyed 50 depressed people ages 20 to 84, some of whom were in the hospital. Nearly every patient was taking some type of psychiatric medication, and 56 percent had attempted suicide at least once.

The study participants were surveyed to assess their degree of insomnia and suicidal thinking, as well as whether they experienced nightmares or unhealthy beliefs about sleep.

The study found a link between insomnia and suicidal thinking: The more severe a person’s insomnia was, the more likely he or she was to express suicidal thoughts and desires. However, when the researches took into account whether or not individuals experienced frequent nightmares or unhealthy beliefs about sleep, the link disappeared. This indicates the two factors —nightmares and unhealthy beliefs about sleep —play a role in the link.

Earlier studies have found that people with insomnia are up to twice as likely to commit suicide as people who don’t have such difficulties sleeping. A 2011 study in teens found that those who had sleep problems at ages 12 to 14 were 2.5 times more likely to have suicidal thoughts in their late teen years.

Depending on the person, insomnia could be a cause or an effect of depression, McCall said. Insomnia may exacerbate depression because people feel they cannot find relief or escape from their condition, even at night, he said.

“People become pretty discouraged and demoralized living with insomnia night and after night,” McCall said.

The new study, along with previous work, suggests that people with insomnia should be evaluated for mental illness, including depression and suicide risk, McCall said.

Treating nightmares or unhealthy beliefs about sleep with psychotherapy or, perhaps, medication may reduce the risk of suicide, but future studies will be needed to investigate this. McCall plans to conduct more research to see if treating insomnia with sleep medication can reduce the risk of suicide.

SOURCE: My Health News Daily

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WASHINGTON, DC – In the wake of massive Medicare reimbursement cuts across several sectors of DME (including a 47% cut to CPAP), staff members for several House Representatives held a closed-door meeting with CMS officials earlier this week.

Reports drifting in to the National Association of Independent Medical Equipment Suppliers (NAIMES) indicate that House staffers were “very angry, and frustrated to the point of walking out.” Wayne Stanfield, founder of NAIMES, reports that one health legislative aid expressed “anger and irritation at CMS’ lack of response to almost any questions asked.”

On average, DME suppliers took a 45% reimbursement hit across eight product categories. In the realm of sleep, a full-face mask used with PAP device will now garner a $99 single payment amount (SPA). Click here for the full list of SPAs affecting sleep-related equipment. Click here for the official CMS press release/announcement.

Since providers who won contracts have already been contacted via e-mail, sleep physicians and sleep labs with long-standing referral relationships can now check to see if their DME company will still be serving Medicare CPAP patients. Providers have until Feb 13, 2013, to decide whether or not to accept the contract and the rate.

DME providers continue to fight competitive bidding in hopes of replacing it with an industry-favored market pricing program (MPP). Advocates at the American Association for Homecare plan to push the replacement measure as part of a debt ceiling package, or a budget continuing resolution, that Congress will discuss in May.

“Several House staff members plan to request meetings with CMS and representatives from their states joining them,” added Stanfield. “The reports from the meeting held yesterday exceeded industry expectation for the lack of substantive answers.”

Source: Greg Thompson, Staff writer

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DME providers in 91 major metropolitan areas received unwelcome news this week in the form of a 47% Medicare reimbursement cut to the CPAP single payment amount (SPA). The cut comes courtesy of competitive bidding, a nationwide program mandated by the Medicare Modernization Act of 2007, and administered by CMS.

A full-face mask used with PAP device will now garner a $99 SPA. Click here for the full list of SPAs affecting sleep-related equipment. Click here for the official CMS press release/announcement.

While providers reportedly began receiving competitive bidding contract offers from CMS as early as yesterday (1/31), a full list of contracted suppliers will not be released until spring 2013. New SPAs for CPAP and related accessories will officially go into effect by spring 2013.

By law, CMS can extend competitive bidding rates nationwide, and many advocates expect that to happen. Self dispensing sleep labs, and/or physicians who sell CPAP equipment, are also subject to competitive bidding and its new rate structure.

Home care providers throughout the country swiftly criticized the round two rates. “The sky really is falling,” said Michael Hamilon, executive director, Alabama Durable Medical Equipment Association. “Those rates are unsustainable, and most of the equipment can only be provided by buying the cheapest piece of junk on the market and offering really poor service.”

“The existing program is not fair to the millions of patients who depend on these services for life itself,” added Joel D. Marx, chairman of AAHomecare, and a DME provider in Cleveland. “They will lose access and quality. They will suffer unfairly due to the tragic misguided implementation of a deeply flawed program.”

DME providers continue to fight competitive bidding in hopes of replacing it with an industry-favored market pricing program (MPP). Advocates at the American Association for Homecare plan to push the replacement measure as part of a debt ceiling package that Congress will discuss in May.

On the same day as CMS released the new SPAs, the American Academy of Sleep Medicine publicized a new “spring course” that offered clinical and practical guidelines for providing DME. The course is aimed at physicians and support staff. “As long as they need to go through the same competitive bidding program as the HME industry is currently going through,” said Helen Kent, RRT, CEO of Progressive Medial, Carlsbad, Calif, “I say go for it.”

As for the new competitive bidding rates, Kent shares the frustration of many providers. “With a cut of 47% to CPAP/Bi-Level, I can’t even afford to grandfather in the Medicare patients that I am currently servicing,” she said. “Looks like CMS will be able to get rid of lots of mom and pops in this industry. Who is next?”

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Scientists have known for decades that the ability to remember newly learned information declines with age, but it was not clear why. A new study may provide part of the answer.

The report suggests that structural brain changes occurring naturally over time interfere with sleep quality, which in turn blunts the ability to store memories for the long term.

“Sleep-dependent memory triage: evolving generalization through selective processing” is published in the journal Nature Neuroscience.

Read Abstract

The connection between poor sleep, memory loss and brain deterioration as we grow older has been elusive. But for the first time, scientists at the University of California, Berkeley, have found a link between these hallmark maladies of old age. Their discovery opens the door to boosting the quality of sleep in elderly people to improve memory.

UC Berkeley neuroscientists have found that the slow brain waves generated during the deep, restorative sleep we typically experience in youth play a key role in transporting memories from the hippocampus – which provides short-term storage for memories – to the prefrontal cortex’s longer term “hard drive.”

However, in older adults, memories may be getting stuck in the hippocampus due to the poor quality of deep ‘slow wave’ sleep, and are then overwritten by new memories, the findings suggest.

“What we have discovered is a dysfunctional pathway that helps explain the relationship between brain deterioration, sleep disruption and memory loss as we get older – and with that, a potentially new treatment avenue,” said sleep researcher Matthew Walker, an associate professor of psychology and neuroscience at UC Berkeley and senior author of the study to be published this Sunday, Jan. 27, in the journal Nature Neuroscience.

The findings shed new light on some of the forgetfulness common to the elderly that includes difficulty remembering people’s names.

Poor Sleep – Memory Loss – Brain Deterioration View Video Here

SOURCE: UC Berkeley NewsCentere

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