FAA to Check Obese Pilots for Sleep Apnea
Posted by Frank Howard
WASHINGTON, Aug 17 (Reuters) - Severe sleep apnea raises the risk of dying early by 46 percent, U.S. researchers reported on Monday, but said people with milder sleep-breathing problems do not share that risk.
They said people with severe breathing disorders during sleep were more likely to die from a variety of causes than similar people without such sleep disorders. The risks are most obvious in men aged 40 to 70, Naresh Punjabi of Johns Hopkins University in Baltimore and colleagues found.
Sleep apnea is caused by a collapse of the upper airway during sleep. Strong snoring can be a symptom but what makes apnea different are numerous brief interruptions in breathing.
Sleep apnea is closely linked with obesity, high blood pressure, heart failure and stroke, but researchers have not been able to clearly quantify how much more likely it makes a person to die.
Punjabi's team studied 6,400 men and women for an average of eight years. Those who started with major sleep apnea were 46 percent more likely to die from any cause, regardless of age, sex, race, weight or smoking, they reported in the Public Library of Science journal PLoS Medicine.
Men aged 40 to 70 with severe sleep-disordered breathing were twice as likely to die from any cause as healthy men the same age, they reported in the study -- available online ">here
"Among men, 42.9 percent did not have sleep-disordered breathing, 33.2 percent had mild disease, 15.7 percent had moderate disease, and 8.2 percent had severe disease," they wrote.
They said about 25 percent of the women had mild sleep apnea, 8 percent had moderate disease and 3 percent had severely disordered breathing.
The researchers, funded by the National Heart, Lung, and Blood Institute of the National Institutes of Health, said people with milder sleep-breathing disorders were not more likely to die early.
The NHLBI estimates 12 million adult Americans have sleep apnea, but most are not diagnosed or treated. The National Sleep Foundation puts the number at 18 million.
"In severe sleep apnea a patient's airway is blocked while the patient suffers for 20 to 30 seconds and wakes up.
"When it becomes this frequent -- 30 times per hour -- about every two minutes it is severe sleep apnea and can become a problem," said Dr. David Rapoport of New York University, who worked on the study.
"The best treatment for sleep apnea is weight loss. However, the most successful treatment can be a nasal CPAP (continuous positive airway pressure) mask that applies pressure to help keep the airways of a patient open while they sleep, allowing normal breathing," he added in a statement.
"Another possible helpful treatment is surgery. That may include tonsil removal," said Rapoport. "A mouth guard that pulls a patient's mouth forward is another option."
A small Canadian company, Victhom Human Bionics Inc. (VHB.TO), has filed a patent on a new device to detect sleep apnea, which must usually be diagnosed in a sleep lab and Medtronic Inc. (MDT.N) makes sleep apnea devices. (Editing by Todd Eastham)
Sun, 16 Aug '09
In a recently-released final report concerning a Mesa Airlines flight operating as go! Airlines in Hawaii, it was determined that the pilot acting as captain of the aircraft and the first officer both inadvertently fell asleep in flight, causing the airplane to overshoot its destination by 26 miles. As part of the investigation it was determined that the captains' sleep schedule had been interrupted by previously undiagnosed obstructive sleep apnea (OSA).
According the information released by the NTSB, if a commercial pilot is diagnosed with OSA, the Federal Aviation Administration (FAA) 2006 Guide for Aviation Medical Examiners states that an aviation medical examiner (AME) must submit all pertinent medical information and current status report and include sleep study with a polysomnogram, use of medications and titration study [in which the optimal pressure for CPAP is identified] results. The guidance further notes that an initial special issuance of a medical certificate for the disorder requires an FAA decision. Subsequent issuance of a medical certificate may be authorized through the AME if the applicant provides a report performed in the last 90 days from the treating physician that describes the present treatment and its effectiveness in eliminating or reducing symptoms, including daytime sleepiness. A maintenance of wakefulness test is required if there is any question about compliance with or response to treatment, and the AME must defer the certification decision if the individual demonstrates sleep deficiency on a maintenance of wakefulness test, has developed an illness associated with OSA, or if there is doubt about compliance with or effectiveness of therapy. Treatment can only begin, however, after diagnosis, and there is evidence that certificated commercial pilots are significantly underdiagnosed.
The FAA does not provide guidance to AMEs describing risk factors for OSA, nor does the FAA routinely use medical information (such as height, weight, and blood pressure) collected during certification examinations to screen for the possible presence of the disorder. Furthermore, the Application for Airman Medical Certificate asks applicants about their history of over 20 specific conditions or symptoms but does not specifically ask about a history of OSA or the presence of symptoms, such as snoring or excessive daytime sleepiness, related to OSA.
Except for the FAA, every U.S. Federal agency that oversees passenger transportation either gathers or plans to gather subjective information specific to OSA from transportation operators. By contrast, the FAA is not yet formally considering such changes. Objective medical data already gathered by the FAA could be used to measure risk for OSA using existing consensus guidance on screening, but the most effective screening would require the FAA to gather additional information and develop additional guidance.
The NTSB concludes that efforts to identify and treat the disorder in commercial pilots could improve the safety of the traveling public. Therefore, the NTSB recommends that the FAA modify the Application for Airman Medical Certificate to elicit specific information about any previous diagnosis of OSA and about the presence of specific risk factors for that disorder. The NTSB further recommends that the FAA implement a program to identify pilots at high risk for OSA and require that those pilots provide evidence through the medical certification process of having been appropriately evaluated and, if treatment is needed, effectively treated for that disorder before being granted unrestricted medical certification. In addition, the NTSB recommends that the FAA develop and disseminate guidance for pilots, employers, and physicians regarding the identification and treatment of individuals at high risk of OSA, emphasizing that pilots who have OSA that is effectively treated are routinely approved for continued medical certification.
Restless Legs Syndrome (RLS) is a neurologic sensorimotor disorder that is characterized by an overwhelming urge to move the legs when they are at rest. The urge to move the legs is usually, but not always, accompanied by unpleasant sensations. It is less common but possible to have RLS symptoms in the arms, face, torso, and genital region. RLS symptoms occur during inactivity and they are temporarily relieved by movement or pressure. Symptoms of RLS are most severe in the evening and nighttime hours and can profoundly disrupt a patient's sleep and daily life.
RLS affects approximately 10% of adults in the U.S. Researchers believe that RLS is commonly unrecognized or misdiagnosed as insomnia or other neurological, muscular or orthopedic condition. RLS may also be confused with depression. According to the Restless Legs Syndrome Foundation, approximately 40% of people with RLS complain of symptoms that would indicate depression if assessed without knowledge or consideration of a sleep disorder.
RLS runs in families and may have a genetic component. In a recent study, the first RLS gene was discovered and was shown to account for approximately 50% of RLS cases. However, the researchers who identified the RLS gene cautioned that having it does not guarantee RLS. Rather, there are likely to be medical, environmental or other factors involved in translating RLS genetic susceptibility into RLS symptoms. Another recent RLS study also found that a genetic variant may account for about half of RLS cases and revealed an association between RLS and a gene for limb development, suggesting the possibility that RLS has components of a developmental disorder.
RLS also affects about 2% of children, according to a recent study of more than 10,000 families in the U.S. and U.K. The study also found a strong genetic component to RLS; more than 70% of children with RLS had at least one parent with the condition. There is also evidence suggesting that children with attention deficit hyperactivity disorder (ADHD) and a family history of RLS are at risk for more severe ADHD.
RLS affects both men and women and can start at any age. It may be confused with growing pains or restlessness when experienced by children. In addition, the severity of the disorder appears to increase with age. Older patients experience symptoms more frequently and for longer periods of time.
The exact cause of RLS is unknown but it has a primary form, not related to other disorders, and a secondary form related to an underlying condition such as kidney failure, pregnancy, or iron deficiency anemia. It may also be caused or made worse by certain medications. This is considered secondary RLS. When no other cause is found for RLS symptoms, it is considered a primary disorder. Primary RLS accounts for 40-60% of RLS diagnoses.
Recently, several research teams have taken a closer look at what might cause primary RLS. In particular, recent studies at Johns Hopkins and Pennsylvania State Colleges have found evidence for brain iron deficiency as a cause for primary RLS. This was first demonstrated in cerebrospinal fluid studies and more recently by the first-ever autopsy analysis of the brains of people with RLS. The autopsy studies reported that cells from the portion of the brain called the substantia nigra showed a deficit in one of the proteins that regulates iron status. However, this evidence suggests that the iron insufficiency in the brain of RLS patients comes directly from a failure of normal iron regulation. In terms of finding a cure, this is good news. The results of this study show that there is no brain damage in people with RLS and that drugs that target the problem of iron uptake may be one way to approach future developments of a treatment.
More than 80 percent of people with RLS also suffer from a condition know as periodic limb movement disorder (PLMD). Characteristics of PLMD include involuntary leg twitching or jerking movements during sleep that occur repeatedly throughout the night and result in disrupted sleep.
In addition to poor quality and short sleep at night, research has shown that people with RLS generally experience a reduced quality of life in the absence of treatment.
Symptoms include an urge to move the legs often associated with uncomfortable feeling in the legs (e.g. tingling, creepy, itching, pulling or aching) during periods of inactivity, including both sleep and wakefulness. Symptoms may also include involuntary jerking of the limbs that intensifies in the evening or at night and is relieved by movement. People with RLS tend to have difficulty falling or staying asleep and suffer from chronic sleep loss, leaving them with the cognitive and tired feelings that occur with sleep loss.
There is no specific diagnostic test for RLS. If you suspect you may have the disorder, talk to your doctor as soon as you can. If possible, bring a diary of your sleep as well as a record of the occurrence and severity of your symptoms with you. Your doctor will conduct tests to rule out factors that may be causing the symptoms such as pregnancy, iron deficiency and end-stage renal failure. You can expect that he or she will ask what time your symptoms occur, when they are most severe, what you were doing before the onset of symptoms, and how much time elapses before you are able to get to sleep due to your RLS. Your doctor will also need a record of your sleep quality and quantity during the time when symptoms appear and whether or not you experienced any pain along with the RLS symptoms.
Until recently, there were no FDA-approved drugs for the treatment of RLS. In May 2005, a drug called Requip® (ropinirole hydrochloride) that is commonly used to treat Parkinson disease was given FDA approval at lower doses for the treatment of moderate-to-severe primary RLS after patients in clinical trials enjoyed more and better quality sleep as early as one week after starting treatment. In 2006, a drug by the name of Mirapex® was also approved by the FDA for the treatment of moderate-to-severe primary RLS. In clinical trials of Mirapex® it was shown that lower doses (than used for Parkinson’s disease) improve RLS symptoms, sleep satisfaction, and quality of life. Both drugs may cause side effects such as nausea and dizziness and may cause patients to fall asleep without any warning, even while doing normal daily activities such as driving.
In addition to Requip® and Mirapex®, there are several drugs approved for other conditions that have been shown to alleviate RLS symptoms. They are:
Side effects may include daytime sleepiness (dopaminergic agonists and benzodiazepines), hallucinations and nausea (dopaminergic agents) or constipation and dependency (opiates). Before taking any medication, discuss the possibility of side effects with your doctor.
In 1996, Drs. Allen and Earley from Johns Hopkins University described a phenomenon called augmentation, in which RLS symptoms are more severe, spread to parts of the body other than the legs, and begin earlier in the evening as a result of taking dopaminergic agents to treat RLS symptoms. If augmentation occurs it can be managed with dose and medication adjustments.
There are also a number of self-directed activities for managing the symptoms of RLS including walking, massaging the legs, stretching, hot or cold packs, vibration, and acupressure. Practicing relaxation techniques such as meditation or yoga have been known to alleviate symptoms. For many people, treating an underlying cause or effective pharmacological treatment of primary RLS and implementation of coping strategies provides relief from most symptoms. However, sometimes medications need to be changed over time or doses adjusted and regular consultation with a physician is recommended.
The following are some tips for coping with RLS:
There are also a number of RLS support groups around the country and they can help you learn new information about how others cope with RLS. For a list of such groups, go to www.rls.org or www.rlshelp.org.
2005 poll: 15% of the adult population responding to the NSF Sleep in America poll have symptoms of RLS a few nights a week or more, which could include unpleasant feelings in the legs such as creepy, drawly or tingling feelings, and 10% met the criteria for being at risk for RLS because – of those who experienced these symptoms -- such feelings were worse at night (146 persons).
Of those who have symptoms of RLS, 86% are also likely to have insomnia symptoms and sleep just 6.3 hours per weeknight, which is less than the mean for all respondents of 6.8 hours. Almost half (47%) of those experiencing RLS symptoms also take 30 minutes or more to fall asleep at night. Although 28% of all adults state that they missed work because of being too sleepy, 52% of those with RLS symptoms reported missing work or other events due to a sleep problem.
2002 poll: Even though 40% of adults polled rated their sleep as very good/excellent, just 20% of those with RLS symptoms reported the quality of their sleep this way. Also, of the total number of adults polled, 16% report experiencing RLS symptoms at least a few nights per week; however, just 4% have been diagnosed with the disorder. 32% of those with symptoms have used a sleep aid while 46% of those diagnosed used a sleep medication. Persons with RLS symptoms are more likely (60%) compared to the total (37%) to have daytime sleepiness a few days a month or more. Quality of life is affected by RLS symptoms. Those with these symptoms report being tired (35% vs. 20%), pessimistic (16% vs. 10%), prefer to be alone (34% vs. 22%), stressed (37% vs. 21%) and be angry (15% vs. 6%) during a typical day.
Reviewed by Richard P. Allen, Ph.D.and Merrill M. Mitler, Ph.D.
As with eating well, good sleep is a staple of optimal health.
While we may not often think about why we sleep, most of us acknowledge at some level that sleep makes us feel better. We feel more alert, more energetic, happier, and better able to function following a good night of sleep. However, the fact that sleep makes us feel better and that going without sleep makes us feel worse only begins to explain why sleep might be necessary. One way to think about the function of sleep is to compare it to another of our life-sustaining activities: eating. Hunger is a protective mechanism that has evolved to ensure that we consume the nutrients our bodies require to grow, repair tissues, and function properly. And although it is relatively easy to grasp the role that eating serves— given that it involves physically consuming the substances our bodies need—eating and sleeping are not as different as they might seem.
Both eating and sleeping are regulated by powerful internal drives. Going without food produces the uncomfortable sensation of hunger, while going without sleep makes us feel overwhelmingly sleepy. And just as eating relieves hunger and ensures that we obtain the nutrients we need, sleeping relieves sleepiness and ensures that we obtain the sleep we need. Still, the question remains: Why do we need sleep at all? Is there a single primary function of sleep, or does sleep serve many functions?
Scientists have explored the question of why we sleep from many different angles. They have examined, for example, what happens when humans or other animals are deprived of sleep. In other studies, they have looked at sleep patterns in a variety of organisms to see if similarities or differences among species might reveal something about sleep's functions. Yet, despite decades of research and many discoveries about other aspects of sleep, the question of why we sleep has been difficult to answer.
The lack of a clear answer to this challenging question does not mean that this research has been a waste of time. In fact, we now know much more about the function of sleep, and scientists have developed several promising theories to explain why we sleep. In light of the evidence they have gathered, it seems likely that no single theory will ever be proven correct. Instead, we may find that sleep is explained by two or more of these explanations. The hope is that by better understanding why we sleep, we will learn to respect sleep's functions more and enjoy the health benefits it affords. This essay outlines several current theories of why we sleep. To learn more about them, be sure to check out the "Bookshelf" feature at the end of this essay. There you'll find links to articles by researchers who are studying this fascinating question.
Arctic Fox at rest.
One of the earliest theories of sleep, sometimes called the adaptive or evolutionary theory, suggests that inactivity at night is an adaptation that served a survival function by keeping organisms out of harm’s way at times when they would be particularly vulnerable. The theory suggests that animals that were able to stay still and quiet during these periods of vulnerability had an advantage over other animals that remained active. These animals did not have accidents during activities in the dark, for example, and were not killed by predators. Through natural selection, this behavioral strategy presumably evolved to become what we now recognize as sleep. A simple counter-argument to this theory is that it is always safer to remain conscious in order to be able to react to an emergency (even if lying still in the dark at night). Thus, there does not seem to be any advantage of being unconscious and asleep if safety is paramount.
Although it may be less apparent to people living in societies in which food sources are plentiful, one of the strongest factors in natural selection is competition for and effective utilization of energy resources. The energy conservation theory suggests that the primary function of sleep is to reduce an individual’s energy demand and expenditure during part of the day or night, especially at times when it is least efficient to search for food.
Lions conserving energy after a meal.
Research has shown that energy metabolism is significantly reduced during sleep (by as much as 10 percent in humans and even more in other species). For example, both body temperature and caloric demand decrease during sleep, as compared to wakefulness. Such evidence supports the proposition that one of the primary functions of sleep is to help organisms conserve their energy resources. Many scientists consider this theory to be related to, and part of, the inactivity theory.
Another explanation for why we sleep is based on the long-held belief that sleep in some way serves to "restore" what is lost in the body while we are awake. Sleep provides an opportunity for the body to repair and rejuvenate itself. In recent years, these ideas have gained support from empirical evidence collected in human and animal studies. The most striking of these is that animals deprived entirely of sleep lose all immune function and die in just a matter of weeks. This is further supported by findings that many of the major restorative functions in the body like muscle growth, tissue repair, protein synthesis, and growth hormone release occur mostly, or in some cases only, during sleep. Other rejuvenating aspects of sleep are specific to the brain andcognitive function. For example, while we are awake, neurons in the brain produce adenosine, a by-product of the cells' activities. The build-up of adenosine in the brain is thought to be one factor that leads to our perception of being tired. (Incidentally, this feeling is counteracted by the use of caffeine, which blocks the actions of adenosine in the brain and keeps us alert.) Scientists think that this build-up of adenosine during wakefulness may promote the "drive to sleep." As long as we are awake, adenosine accumulates and remains high. During sleep, the body has a chance to clear adenosine from the system, and, as a result, we feel more alert when we wake.
PET scan showing brain activity in a 20-year-old.
One of the most recent and compelling explanations for why we sleep is based on findings that sleep is correlated to changes in the structure and organization of the brain. This phenomenon, known as brain plasticity, is not entirely understood, but its connection to sleep has several critical implications. It is becoming clear, for example, that sleep plays a critical role in brain development in infants and young children. Infants spend about 13 to 14 hours per day sleeping, and about half of that time is spent in REM sleep, the stage in which most dreams occur. A link between sleep and brain plasticity is becoming clear in adults as well. This is seen in the effect that sleep and sleep deprivation have on people's ability to learn and perform a variety of tasks.
This theory and the role of sleep in learning are covered in greater detail in Sleep, Learning, and Memory.
Although these theories remain unproven, science has made tremendous strides in discovering what happens during sleep and what mechanisms in the body control the cycles of sleep and wakefulness that help define our lives. While this research does not directly answer the question, "Why do we sleep?" it does set the stage for putting that question in a new context and generating new knowledge about this essential part of life. For more about why we sleep, watch the video Why Sleep Matters and explore Consequences of Insufficient Sleep.
This content was last reviewed on December 18, 2007
A resource from the Division of Sleep Medicine at Harvard Medical School
Produced in partnership with WGBH Educational Foundation