Monday, December 26, 2005

Gaboxadol for Insomnia

A novel agent, Gaboxadol is being developed for insomnia:
Gaboxadol significantly improved sleep initiation and maintenance while also increasing time spent in restorative slow-wave sleep in an acute phase II placebo-controlled trial, Stephen Deacon, Ph.D., reported at the annual meeting of the Associated Professional Sleep Societies.
Based upon these and other encouraging findings, gaboxadol—first in a novel class of sleep medications known as selective extrasynaptic γ-aminobutyric acid-A agonists, or SEGAs—is now in larger definitive phase III clinical trials, added Dr. Deacon, head of clinical development for sleep disorders at H. Lundbeck, Ltd., Milton Keynes, England.
The benzodiazepine receptor agonists, a class of drugs widely prescribed for insomnia, also target γ-aminobutyric acid (GABA) receptors; however, their action is confined to synaptic GABA receptors. The extrasynaptic GABA-A receptors modulated by gaboxadol are richly present in parts of the brain thought to be important in sleep regulation, he explained.

We are learning more about the GABA-A receptor every day. It will be interesting to see how Gaboxadol compares with the synaptic GABA-A agonists in efficacy and tolerability.

Sunday, December 25, 2005

Preschool Children are not Getting Enough Sleep

A recent study conducted by researchers at Bradley Hospital and Brown Medical School using actigraphy and sleep diaries finds that children under five years of age may suffer from sleep debt as much as older children and adults. The study conducted in the homes of 165 Rhode Island boys and girls between ages 1 and 5 for seven nights of sleep showed that on average children slept 8.7 hours a night and less than 9.5 in a 24-hour period when naps were included. Yet few nap: according to parent diaries, 82 percent no longer nap some or all days after 18 months of age. The amount of sleep found among pre-schoolers in the study contrasts with the 12 to 15 hours pediatric sleep experts recommend for these age groups. The 2005 NSF/Pampers® Baby-Dry™ survey of 1,003 children under 4 years old produced similar findings; on average, the amount of sleep children got each night in the NSF poll was 9.7 hours.
Another element of the Bradley Hospital/Brown Medical School study showed that family characteristics including socio-economic status (SES) significantly contributed to children’s sleep/wake patterns. In families that had lower educational achievement and lower occupational ratings, children were more likely to be out of bed earlier in the morning and spend less time in bed at night; however, these children also had less nighttime awakenings and more sleep efficiency.
"We were very surprised to find how little preschool aged children actually sleep at night," said Acebo. This concerns the authors and sleep experts because studies of school-aged children with poor sleep show lower physical and academic performance and higher rates of parent-reported behavior problems."

Reported by the National Sleep Foundation

Sunday, December 18, 2005

Why I ask patients about insurance status

An anonymous commenter on Kevin, MD wrote:
The first question out of the mouths of nearly all doctor's office staff is "What's your insurance?" I have lost track of how many doctors muse over what to do next and look at my chart murmuring, "What's your insurance?" Yes, they may be figuring out how to best work through the system of my particular insurer, but the net effect is thinking INSIDE the box. I have now taken to telling every doctor EVERY time I see them, "I don't care whether my plan pays for a particular course of action -- I want to know what YOU think is the best thing to do, regardless of cost, and then we'll decide what to do." I am looked at like I'm a Martian, because doctors don't think that way.
In sleep medicine, insurance status is crucial. Most sleep patients are going to need some type of sleep study to evaluate for sleep apnea. Insurance status is very important in properly carrying out and interpreting the sleep study. For example, if a person has Medicare, specific steps need to be taken in order to qualify the patient for the standard treatment of sleep apnea, CPAP. The sleep study pretty much has to be a full-night diagnostic study, rather than a split-night study. Like most insurance companies, Medicare requires an apnea-hypopnea index of at least 5 to qualify for CPAP. However, Medicare has a different definition of a hypopnea than other insurance companies. Medicare requires a 4% oxygen desaturation for hypopneas, most other agencies don't. Recently I had a young patient who I forgot to look up his insurance status before I wrote the orders of his sleep study. It turned out that he had Medicare due to a disability (there are a lot of non-elderly people with Medicare out there, you have to ask). The technician had to spend an additional 45 minutes rescoring the respiratory events to meet Medicare standards and I had to spend an additional 15 minutes reading the study again- Basically a wasted hour because I did not ask about insurance status.
Disclaimer: I have simplified Medicare requirements in the above discussion; it's actually more complicated, especially with the large number of dual-elgibles. This blog does not provide legal advice, you should consult an attorney if you plan on treating Medicare patients.

Wednesday, December 14, 2005

Sleep Boards Part 3

In response to my Dec 9 and 10 posts about the new sleep board examinations, a colleague of mine (and an old friend from residency days), Dr. Eric Clemons, writes (as always my comments will be in regular type, with quotes from Dr. Clemons in italics and color):
I had heard at one point Family Practice did not want to sponsor the ABIM exam as they are planning to offer their own certification to family practitioners. That would explain their reasoning. You are probably right about that.
I think it is unclear at this point what the new certification will mean. For academicians they will likely need this. For those in private practice I suspect the certification by the ABSM will be sufficient for most insurance companies for the foreseeable future and may make obtaining the new certification less of a necessity. I agree that in the short-term most insurance companies will continue to accept ABSM certification. However, I think that by the 2020's most insurance companies will stop accepting ABSM certification. (I plan to retire in the year 2039).
I was under the impression that all current diplomates of the ABSM who are MD's would be eligible to become certified through the practice pathway (and could sit for the first three exams). This would certainly help out your acquaintances and would keep anyone from losing their practices. My understanding was that the practice pathway was for those who did not complete an accredited sleep disorders fellowship. You still have to be board-certified in Internal Med, peds, psych, neuro, or ENT. The practice pathway just gives the candidate a flexible means of documenting sleep medicine experience. There is still a lot of confusion about the requirements for the new sleep boards, and I could be wrong.
Thanks for your comments, Eric

Sunday, December 11, 2005

New Long Term Data on Lunesta

The National Sleep Foundation reports:
A recent study conducted by Thomas Roth, PhD, a sleep researcher at the Henry Ford Hospital in Detroit, James K. Walsh, PhD, executive director and senior scientist at the Sleep Medicine and Research Center at St. Luke’s Hospital in St. Louis and fellow researchers investigated whether eszopiclone (Lunesta™) is effective for the long-term treatment of insomnia. Currently, the median duration of clinical trials evaluating the effectiveness of sleeping pills is one week. While a few studies have tested hypnotic agents for longer, Roth, Walsh and fellow researchers sought to find out how eszopiclone would treat insomnia over a year’s time. The first six months of the trial followed standard trial procedures – double-blind, placebo-controlled and randomized. The second six months the study was conducted "open-label," meaning the drug would be tested under conditions where both researchers and patients knew they were being treated with eszopiclone.
The study of 471 participants ages 21-64 found that eszopiclone was effective and well-tolerated for the length of the study. Researchers saw improvements in both six-month phases of the study, and they argue that the open-label phase was a valuable tool to assess the effectiveness of a medication in a real-life (or clinical) setting. Nevertheless, they note that they did not study what effects discontinuation of the medication would have upon these participants after the one-year trial. While the results of this study indicate that there is the potential for medication to treat chronic insomnia, more research on all areas of treatment for insomnia is necessary. Per the National Institute of Health’s state-of-the-science’s findings, "a substantial public and private research effort is warranted, including developing research tools and conducting longitudinal studies of randomized clinical trials."

I'll comment further on Lunesta when the actual study is published.

Reader Question about Xyrem

A reader (Dozy) asks: Can you talk a bit to how Xyrem is supposed to work? My understanding is it's entirely out of your system in 12 hours after taking it, so how would it help with Cataplexy for the other 12 hours? Xyrem is the only FDA approved treatment for Cataplexy, and has been approved recently for EDS as well. It is the only proven non-stimulant EDS medicine that I'm aware of for the treatment of EDS. For those PWN who have anxiety issues (like me), a non-stimulant approach is vital to functioning. Do you know if other non-stimulant meds are on the horizon?
As far as non-stimulants on the horizon, in 2006 a new version of Provigil, called Nuvigil, that contains only 1 of the 2 isomers (mirror images) of the molecule should be coming out. I think that researchers are also working on treatments that involve hypocretin.
No one is exactly sure how xyrem has its therapeutic effect in narcolepsy. It probably improves sleepiness in narcolepsy by consolidating nocturnal sleep and increasing slow wave sleep. It acts on multiple neurochemical systems. According to Principles and Practice of Sleep Medicine "Most studies to date indicate that the sedative-hypnotic effect is mediated through GABA-B agonist activity". It is also thought to act on the poorly understoon GHB receptor.
I don't know why it has an effect on cataplexy even after it is out of the blood stream- I can only guess that there is still some left in the brain or that it is having some long-lasting effect in the brain. Sorry I can't fully answer your question about xyrem (also known as sodium oxybate and gamma-hydroxybutyric acid)

Saturday, December 10, 2005

Reader Question about the new Sleep Boards

In response to my post about the new Sleep Board examinations, a reader asks "I guess the question is this: do these changes appear to serve any real purpose, or is it just another turf battle?If so, are there really any sleep specialists who need to protect their turf? The ones I know all have ponderous waiting lists."
There is a turf battle going on, but it is not among sleep specialists in private practice. This battle is within academic medicine; The American Board of Medical Specialties and The Accreditation Council for Graduate Medical Education are trying to consolidate their control. The American Board Medical Specialties is trying to eliminate any medical board/examination not under its direct control (such as the American Board of Sleep Medicine, which is an independent board). The Accreditation Council for Graduate Medical Education wants complete control of all residency and fellowship training in the US.
As a sleep specialist in private practice, I am upset that I will have to take the new sleep boards in several years; I am proud to currently be a diplomate of the American Board of Sleep Medicine.
In my earlier post, I mentioned that family practitioners would be inelgible for the new sleep boards. My understanding is that this was by choice of their board, and is not due to conflict with any of the other member boards of the American Board of Medical Specialties.
The American Board of Sleep Medicine is not innocent in all of this; the leadership of the board cooperated in its own destruction.
This post is a departure from the usual professional tone I try to maintain on this blog (I try to save my rants for Rebel Doctor). Please feel free to disagree in the commment section; I may republish some of the disagreements in a regular post.

Friday, December 09, 2005

New Sleep Board Examinations

The American Board of Internal Medicine announces an Added Qualifications Examination in Sleep Medicine. This examination will take the place of the exam offered by the American Board of Sleep Medicine.
The American Board of Internal Medicine, along with the American Board of Psychiatry and Neurology, the American Board of Pediatrics, and the American Board of Otolaryngology, was recently authorized by the American Board of Medical Specialties to offer an Added Qualifications Examination in Sleep Medicine. Representatives from all four Boards will be developing and setting standards for the new examination. ABIM has administrative responsibility for examination development, and the participating/sponsoring boards have responsibility for setting admission criteria for their own diplomates. The examination will be open to diplomates in internal medicine, pediatrics, neurology, psychiatry, or otolaryngology.
The first examination will be administered in fall 2007. Admission requirements for ABIM candidates are being finalized, and confirmed information about the requirements will be available by the fall of 2006.
The Training Pathway for ABIM candidates will require 12 months of satisfactorily completed sleep medicine fellowship training. Sleep medicine fellowship training undertaken July 1, 2009, and thereafter must be accredited by the Accreditation Council for Graduate Medical Education (ACGME). Sleep medicine training undertaken prior to July 1, 2009, must be conducted within a program affiliated with an ACGME-accredited internal medicine or pulmonary disease fellowship program. A Practice Pathway will be available for the first three examinations in 2007, 2009, and 2011. ABIM candidates who have not had formal sleep medicine fellowship training will be eligible to apply through this pathway by documenting certification by the American Board of Sleep Medicine (ABSM) or by documenting the equivalent of 12 months of full-time post-training experience providing clinical care in sleep medicine accumulated over a maximum period of five years prior to application for examination.

Under the old system, most doctors became sleep specialists by completing a residency in any speciality and then completing a fellowship (usually 1 year) in sleep medicine and then taking the examination offered by the American Board of Sleep Medicine.
Those of us who are diplomates of the American Board of Sleep Medicine are now going to have to pay a lot of money (probably $1000 to $2000) to take the new exams. Sleep specialists who are not boarded in psychiatry, pediatrics, neurology, internal medicine or ENT will be left out in the cold. I know several sleep specialists who are boarded in family practice and sleep medicine who will not be able to take the new boards.

Wednesday, December 07, 2005

Rozerem (ramelteon) Update

A reader (shrinkette) asks "I'm hearing a lot from Rozerem reps these days. I now have a Rozerem pen, a Rozerem mug, and some Rozerem notepads. What is your opinion of Rozerem? Thank you
I have prescribed Rozerem several times, but so far only one of the patients has come back for follow-up. She is taking it for primary insomnia, and seems to be doing well on it. She thinks it is comparable in efficacy to Ambien, which she has taken in the past.
Rozerem acts on 2 of the melatonin receptors (MT1 and MT2) while sparing the peripheral melatonin receptor MT3. Melatonin, which hits all 3 receptors, has the theroetical possibility of interfering with puberty/reproductive functioning because of its effect on MT3. MT1 and MT2 are located mainly in the brain, at the suprachiasmatic nucleus.
Melatonin itself is useful for shifting the biogical clock if given at the proper time. However, it is not a good drug for pure insomnia- it has only about 25 % effectiveness for primary insomnia. Why is Rozerem, a melatonin agonist, effective for insomnia while melatonin isn't?? Nobody knows for sure, but it may be because of increased bioavailabilty or because of its ratio of action at the 2 main melatonin receptors.
From what I've heard, Rozerem is a little less effective for insomnia than the benzodiazepines and the benzo agonists (Ambien, Lunesta, Sonata). But it has a good side effect profile and no risk of addiction. Psychiatrists need to be aware that Luvox (fluvoxamine) raises its levels to 50-70x's normal, and therefore Rozerem and luvox should not be prescribed together.
For more about Rozerem, see this site.
There is a lot we don't know about this novel agent for insomnia. But I can tell you one thing for sure: the Rozerem drug reps are giving out great pens. They are long, wide, and easy to write with.

Tuesday, December 06, 2005

Business All-Nighters

The New York Times has an article about business travelers who burn the midnight oil while away on business trips:
"A business trip is not about sleep," said Mr. Stevens, who spends the wee hours in his hotel's lobby or bar, mapping his strategy for the next day. "Nobody comes out of any business meeting and says, 'You did best today because you look freshest.' Clients couldn't care less if I am fresh as a daisy. They just want to know that when I or my team comes to the table, we've got a big idea."
Sleep deprivation eventually catches up with you:
On the other hand, he recalls the time he drifted off while walking down a street - and collided with a parking meter. On another occasion, the lead negotiator on his team fell asleep in midsentence.


A reader (Dozy) asks, Does Ambien affect sleep architecture? If so, how?
Ambien is a benzodiazepine agonist that binds to the alpha 1 subtype of the GABA-A receptor. It is therefore more selective then the benzodiazepines such as valium, ativan, and xanax.
The benzos (valium, etc) tend to increase stage 2 sleep while decreasing deep sleep (stage 3 and 4 ) and decreasing REM sleep. These effects are mild.
Ambien has minimal effects on sleep architecture. In many studies, its effect on sleep stages is no different than placebo. In at least one study, it increased deep (slow wave) sleep.
The brief answer to your question is that, in short-term studies, Ambien decreases sleep latency (time to fall asleep) and increases total sleep time with no significant effect on sleep architecture.

Sunday, December 04, 2005

Reader Questions about Sleep Medicine

For the next 10 days, I am asking for reader questions. Please leave any questions about sleep medicine in the comment section. I will try to answer as many of them as possible. I do not guarantee that I will answer all questions. I may rephrase questions to make it clear that I am not practicing medicine when I answer questions. For example, if someone asks "I have an AHI of 95, what would be the best treatment for me?" I might change that to "what are the best treatments for severe sleep apnea?" in my post. I will leave the original question in the comments section unchanged.

CPAP Supplies

One of my patients recommended that I look at this site, because of the great pictures of CPAP machines and CPAP supplies. (this is not an endorsement of, and not a recommendation to buy CPAP supplies from them).

More about Cardiovascular Disease and Sleep Apnea

On November 20th, I blogged about 2 recent articles in the New England Journal of Medicine. USNews and World Report has a pretty good discussion of these same 2 articles:
People with sleep apnea often don't realize they have it, since they don't remember waking up again and again, gasping for breath. Often, it's a bed partner who hears the choking and "industrial-strength snoring," says Klar Yaggi, a sleep specialist at Yale who led the study. He and his colleagues followed two groups of patients who were tested for sleep apnea (defined as stopping breathing five or more times per hour). Some had the condition; some didn't. During the 3½ years or so that they were studied, the people with sleep apnea were about twice as likely to have a stroke or die.
Another study in the same issue of the New England Journal looked at how well the continuous air treatment works for people with central sleep apnea, a different disorder altogether. In both forms of sleep apnea, you stop breathing periodically. But in central sleep apnea, the problem is not an obstructed airway but that the brain fails to send out the command to breathe. The disorder is usually caused by congestive heart failure, in which the heart doesn't pump as well as it should and fluid collects in the chest.
The treatment did help people with central sleep apnea in some ways: Their hearts worked better, they didn't stop breathing as often, they didn't have adrenaline surges, and they were able to exercise more.
"That's the good news," says Douglas Bradley, a pulmonologist at the University of Toronto and author of the article. "The bad news is that we didn't improve survival."


Another creation for the Somnus Sleep Clinic Website:

A polysomnogram (also know as a PSG) is an overnight sleep study. A PSG is useful in the diagnosis of several sleep disorders, especially obstructive sleep apnea.

Before the test begins, our technicians spend about 45 minutes applying the painless electrodes, sensors, and monitors to the patient.

EEG Electrodes on the scalp are used to monitor brainwaves. Electrodes are also applied to the chin to measure muscle tone and next to the eyes to monitor eye movements. These 3 sets of electrodes are used to determine stage and depth of sleep.

Electrodes are attached to the lower legs to monitor for the leg movements that characterize the disease Periodic Limb Movement Disorder.

To monitor breathing, airflow monitors are placed at the mouth and nose. The monitor at the nose is similar to an oxygen cannula. Belts are placed across the chest and abdomen to detect respiratory effort. These belts are useful in distinguishing between the 2 types of sleep apnea. An oximeter is placed on one finger to detect decreases in oxygen, which are common in obstructive sleep apnea.

Several electrodes are applied to the chest to monitor heart rate and rhythm.

Many patients ask if is possible to get up in the middle of the night during a PSG. It takes a technician only about a minute to help the patient wrap the wires around his neck and get out of bed. Then the patient can easily walk around

A PSG lasts about 8 hours. After the procedure is finished, it takes about 10 minutes to remove the electrodes and sensors. A shower with plenty of shampoo is necessary to remove the electrode gel from the hair!

Friday, December 02, 2005


Bedbugs are back.

The Basics of Narcolepsy

Here is something I have been working on for the Somnus Sleep Clinic website (which is why I wrote it in the 3rd person):

What is Narcolepsy?

Narcolepsy is a sleep disorder resulting in excessive daytime sleepiness. It is often associated with cataplexy. Cataplexy is characterized by sudden emotionally-induced loss of bilateral muscle tone. In many narcoleptics, laughter can provoke an episode of cataplexy. An episode of cataplexy lasts several seconds to several minutes, and often affects the knees, face, or neck.

How is Narcolepsy Diagnosed?

After a history and physical by a sleep physician, further sleep testing is usually required to make a diagnosis of narcolepsy. The key test in the diagnosis of narcolepsy is the multiple sleep latency test (MSLT). This test involves a series of 4-5 nap opportunities during the day. By measuring brain wave activity (EEG), this test measures how long it takes a person to fall asleep, and if a person enters REM sleep (dream sleep) during a nap. During the MSLT, narcoleptics will typically fall asleep within 5 to 8 minutes and enter into REM sleep during at least 2 of the naps. The MSLT can be a difficult test to properly administer and interpret; significant experience on the part of the sleep physician and technical staff is necessary. For more technical information about the proper administration of the MSLT, please see Dr. Rack’s recent comments in The American Journal of Psychiatry (

What Causes Narcolepsy?

Recent research suggests that narcolepsy is an autoimmune disorder. More specifically, narcolepsy is thought to be caused by autoimmune destruction of hypocretin neurons in the hypothalamus (the hypothalamus is an area at the base of the brain important in the regulation of sleep and wakefulness).

How is Narcolepsy Treated?

Sleepiness is usually treated with stimulants (such as Ritalin) or Provigil. Many antidepressants help with cataplexy. Xyrem is helpful for both sleepiness and cataplexy. Behavioral methods, especially brief naps, are also useful in the treatment of narcolepsy.

Where can I find out more information?

Dr. Rack has written extensively about narcolepsy and its treatment in his blog, sleepdoctor ( Much of this information is located at

Wednesday, November 30, 2005

New Indication for Xyrem

The National Sleep Foundation reports:
The Food and Drug Administration’s (FDA) latest drug approval may provide significant symptom relief for narcolepsy patients. Researchers found that Xyrem® (sodium oxybate), a medication approved for treatment of cataplexy (the loss of muscle tone in narcolepsy patients) in 2002, abated symptoms of excessive daytime sleepiness in 4- and 8-week clinical trials. Participants reported a significant improvement in quality of life and the medication was generally well-tolerated. Researchers tested three doses of the drug – 4.5g, 6g, or 9g in divided doses (one at bedtime and the other 2.5 to 4 hours later) in the randomized, double-blind, placebo-controlled trial and found improvement in narcolepsy patients’ reports of excessive sleepiness for the individuals taking the 6g and 9g doses.
Narcolepsy is a neurological disorder caused by the brain’s inability to regulate sleep-wake cycles normally, and its prevalence in the developed world is approximately the same as Parkinson’s disease and multiple sclerosis. Researchers are hopeful that sodium oxybate will provide relief for the disabling effects of excessive daytime sleepiness in narcolepsy patients.

Xyrem has been approved for several years for cataplexy. I have tried to prescribe it several times, but patients find it too inconvenient and don't want to try it. It has to be ordered from a central pharmacy (Another name for Xyrem is gamma-hydroxybutyrate, the "date rape" drug). Also, the patient has to awaken in the middle of the night to take the 2nd dose. From the data I've seen, it is no more effective than the tricyclic antidepressants for cataplexy. And it has the nasty side effect of enuresis (bedwetting).
Its effect on sleepiness is mild- less than the stimulants and provigil. It is thought to decrease sleepiness by improving nocturnal sleep. It consolidates sleep and increases slow wave sleep.
Xyrem may be worth a try in narcoleptics who are having trouble tolerating the traditional medications (stimulants, provigil, antidepressants) used for the symptoms of narcolepsy.

Friday, November 25, 2005

New Sleep Billing Codes

Does anyone have any experience with the new ICD-9 billing codes for sleep, especially the codes for obstructive sleep apnea (OSA)??
780.53-0 used to be the code for OSA. Now there are 2 main codes for OSA:
780.53 (hypersomnia with sleep apnea, unspecified) and 327.23 (obstructive sleep apnea).
What I have been doing is using 780.53 for suspected cases of OSA, and 327.23 for confirmed cases. For upper airway resistance syndrome, I usually code 780.53. Does anyone know if this is correct?? Does anyone have any references?? I bought my copy of The International Classification of Sleep Disorders-2nd edition this summer, before the new ICD-9 codes were available. Have ICD-9 codes been added to the International Classification of Sleep Disorders yet?

Sunday, November 20, 2005

Cardiovascular Disease and Sleep Apnea

The Nov 10 issue of the New England Journal of Medicine had several interesting articles about sleep apnea.

Obstructive sleep apnea (OSA) is a risk factor for the development of hypertension. Increasing evidence also links OSA to ischemic heart disease and stroke. Yaggi HK and colleagues (N Engl J Med 2005;353:2034-41), in an observational cohort study, found that OSA significantly increases the risk of stroke or death from any cause. This increase in risk is independent of other risk factors, including hypertension.

Both obstructive and central sleep apnea are common in patients with CHF; central sleep apnea is present in up to 40% of patients with chronic heart failure. Bradley TD et al. (N Engl J Med 2005;353:2025-33) randomly assigned 258 patients with CHF and central sleep apnea to receive either CPAP or no CPAP. CPAP decreased apnea, increased the injection fraction, and improved nocturnal oxygenation, but did not increase survival.

Nasal CPAP is the standard treatment for OSA; other treatment modalities include oral appliances and ENT surgery. The first step in the management of central sleep apnea associated with heart failure is optimization of cardiac functioning. Other possible treatments include CPAP, BiPAP, supplemental oxygen, and theophylline.

Tuesday, November 15, 2005

Adolescent Insomnia

The New York Times reports that the use of medication to treat insomnia in adolescents is increasing:
In 2004, more than 180,000 people under age 20 in the United States - most of them 10 or older took sleep medications, according to estimates released last month by Medco Health Solutions, a large managed-care company.
Although that represents only about one child in 500, Medco found that usage was up by 85 percent since 2000.
The numbers reported by Medco were somewhat mysterious: the company's report did not indicate why the pills were prescribed for the patients under 18, or which pills were prescribed for them.
That makes some doctors worry that the large increase may reflect a certain amount of unnecessary prescribing.

It's a fairly good article, but I disagree with one of the statements made by a sleep specialist in the article:
"The last thing we want to suggest is that it's O.K. to throw a medication at something without understanding the problem," said Dr. Judith Owens, the director of the Pediatric Sleep Disorders Clinic at Hasbro Children's Hospital, in Providence, R.I. "Insomnia is a symptom, not a disorder. It's like pain. You're not going to give a patient pain medication without figuring out what's causing the pain."
At least in adults, considering insomnia to be just a symptom is outdated. To quote from the new book Cognitive Behavioral Treatment of Insomnia (Perlis ML et al, 2005), "In the early 1980's...there was perhaps no rallying cry as popular as 'insomnia is a symptom, not a disorder'....After more than two decades of sleep research...Insomnia is once again considered a distinct nosological entity." The "NIH State of the Science Conference Statement on Manifestations and Management of Chronic Insomnia in Adults Statement" moves away from the concept of 'secondary insomnia'. It uses the term 'comorbid insomnia'. For example, in the case of depression associated with insomnia, it is often impossible to tell if depression is causing the insomnia, or if insomnia is causing the depression. According to the conference statement, "the limited understanding of mechanistic pathways in chronic insomnia precludes drawing firm conclusions about the nature of these associations or direction of causality."

Saturday, November 12, 2005

Sleep in Animals

The NY Times has a nice article about how scientists are studying sleep in animals in order to better understand the mysteries of human sleep:
It has been almost 600 million years since human ancestors diverged from those of flies. As those ancestors evolved, their sleep evolved as well. Human sleep, for example, features not only slow-wave sleep, but bouts of sleep when the eyes make rapid movements and when we dream. Rapid eye movement, or REM sleep, as it is known, generally comes later in the night, after periods of intense slow-wave sleep.
Other mammals also experience a mix of REM and non-REM sleep, as do birds. Sleep researchers would like to know whether this pattern existed in the common ancestors of birds and mammals, reptilian animals that lived 310 million years ago. It is also possible that birds and mammals independently evolved this sleep pattern, just as birds and bats independently evolved wings.
Answering that question may help scientists understand why REM sleep exists. Scientists have long debated its function, suggesting that it may play important roles in memory or learning. In the Oct. 27 issue of Nature, Jerome Siegel, a sleep expert at the University of California, Los Angeles, argues that REM does not play a vital physiological role like slow-wave sleep. He points out that brain injuries and even medications like antidepressants can drastically reduce REM without any apparent ill effect.
"People who don't have REM sleep are remarkably normal," Dr. Siegel said. "There's no evidence for any intellectual or emotional problems."
So why do mammals and birds have REM sleep at all? "The best answer I can come up with is that it's there to prepare you for waking," Dr. Siegel said. "When the important work of sleep is done, REM sleep just makes you as alert as you can be while you're asleep."

Circadiana blogged about this topic on Nov 1st.

Tuesday, October 25, 2005

Brief Update

I have left the University of Mississippi Medical Center. Somnus Sleep Clinic will be opening in several weeks.

Tuesday, August 30, 2005

Restless Leg Syndrome

Below is a collumn about restless leg syndrome that I wrote for the newsletter of the Mississippi Psychiatric Association newsletter:
It’s summer and time for vacation! Although the time spent at the vacation destination is usually pleasant, long car and airplane trips can be tedious. For those with restless leg syndrome, these trips can be pure misery.
Restless leg syndrome (RLS) is characterized by an urge to move the legs, usually accompanied by disagreeable/uncomfortable leg sensations. These sensations, often described as "creeping" or "crawling," are typically perceived in the calves, but can also involve other parts of the lower extremities, and in more severe cases, can involve the upper extremities. RLS is worse in the evening/night and in sedentary situations such as long car rides. The symptoms often interfere with sleep. Vigorous movement improves RLS symptoms. Response to a dopaminergic drug is considered to be supportive of the diagnosis.
Approximately 10% of the population has at least mild, intermittent symptoms of RLS; about 3% of the population has moderate to severe symptoms.
RLS can be idiopathic, familial (often inherited in an autosomal dominant pattern), or secondary. Common secondary causes of RLS include iron deficiency, pregnancy, uremia, and neuropathy. RLS has also been reported to occur in association with folate, B12, and magnesium deficiencies. Many psychiatric medications, including dopamine antagonists, serotonergic antidepressants, and lithium, can unmask or worsen RLS. Wellbutrin, however, does not worsen RLS. Wellbutrin, due to its dopaminergic properties, has been speculated to improve RLS, but data is lacking.
RLS is diagnosed based on history; polysomnography is not necessary or indicated for diagnosis, though in most cases periodic leg movements occur during sleep. The differential diagnosis includes nocturnal leg cramps, neuropathy, akathisia, and vascular disease. The most important lab test to check in someone with restless leg syndrome is a ferritin level. Iron supplementation should be administered to keep the ferritin level above 50.
RLS is commonly treated with dopaminergic agents. Requip (ropinirole) is the first and only FDA-approved medication for the treatment of moderate-to-severe primary RLS. Mirapex (pramipexole) is also commonly used. Ergot-derived medications, such as pergolide, should be avoided due to the risk of cardiac valvuopathy. Sinemet can be used for short-term treatment or to confirm the diagnosis, but has a higher risk of augmentation than the other dopaminergic medications. Augmentation is the shifting of symptoms to several hours earlier than was typical before pharmacologic intervention. Other medications used to treat RLS include benzodiazepines, opioids, and gabapentin.
RLS is a common, unpleasant condition that can be unmasked or worsened by many psychiatric medications. Its prevalence in the psychiatric population is probably higher than in the general population. In cases in which the diagnosis is uncertain or in which the psychiatrist feels uncomfortable treating RLS, referral to a sleep specialist or a neurologist is indicated

Tuesday, August 23, 2005

Missouri Medicaid Cuts CPAP coverage

From the National Sleep Foundation:
Effective September 1, 2005, Missouri Medicaid will no longer cover many kinds of durable medical equipment (DME), including positive airway pressure (PAP or CPAP) devices which are the mainstay of treatment for obstructive sleep apnea.
NSF Chairman,
Barbara Phillips, MD, MSPH, explained, "This is a dangerous public health decision, not just for the 1 in 20 Missourians who have sleep apnea, but also for those on the roads and in the cars with them." Sleep apnea causes adverse or worsens many health problems, including hypertension, cardiovascular disease, diabetes, cognitive impairment and cerebrovascular accidents. CPAP treatment is effective in reversing these consequences. More important for all Missourians, however, is the fact that untreated sleep apnea results in automobile crashes; the risk of this is normalized with CPAP treatment. Budgetary limitations are a sad fact of life, but it's important to know that the cost of care of patients with sleep apnea goes down after CPAP treatment is initiated. The decision to eliminate coverage of DME passed by the Missouri State Legislature in Senate Bill 539 endangers the health of all Missourians, and will likely cost more money in the long run if enacted. Sleep Health Advocates are urged to contact their legislators if they are Missourians ( as well as the Missouri Medicaid Offices.
Learn more here.

Tuesday, July 26, 2005

A New Medication for Insomnia

Rozerem (ramelteon), a new hypnotic medication that is "indicated for the treatment of insomnia characterized by difficulty with sleep onset," was approved by the U.S. Food and Drug Administration (FDA) last Friday (July 22). Because of its unique characteristics, ramelteon is considered to be the first of a new class of sleep aids.
In clinical trials conducted with 4,200 patients, most with chronic insomnia, researchers for Takeda Pharmaceuticals North America were able to demonstrate that ramelteon reduced the time to fall asleep and resulted in a modest increase in total sleep time of patients, but did not decrease nocturnal awakenings, a significant factor for persons whose insomnia causes them to have frequent or prolonged awakenings during the night. 472 patients took ramelteon nightly for one year. After cessation, ramelteon did not cause “rebound insomnia,” a worsening of symptoms that can occur after treatment is halted.
Unlike other prescription sleep aids, ramelteon is thought to work by selectively affecting melatonin receptors (neurons) in the suprachiasmatic nucleus, a part of the brain that functions to regulate times for sleep and times for optimal alertness or wakefulness. This contrasts with other hypnotic medications that work by binding to GABA receptors, which reduce central nervous system (CNS) activity.
Other studies found no evidence that ramelteon has a potential for abuse or dependence. As a result, ramelteon has not been designated as a scheduled substance by the U.S. Drug Enforcement Administration (DEA), the first prescription sleep aid to not be controlled. Additionally, the FDA will allow physicians to prescribe ramelteon for long-term use in adults.
Like other medications, ramelteon does come with precautions. Its use should be preceded by a thorough health evaluation and consideration of alternatives. Labeling information should be read and discussed with a physician or pharmacist to learn about drug interactions and side effects. To date, the effectiveness of ramelteon has not been studied in patients with severe sleep apnea or COPD, nor was it compared in clinical trials to cognitive behavioral therapy, a non-pharmacological treatment method that was identified by a recent National Institutes of Health "State of the Science" panel as effective for treatment of chronic insomnia. Ramelteon is not recommended for use during pregnancy, during nursing or for pediatric use.

From the National Sleep Foundation
As the first non-addictive, non-controlled hypnotic approved by the FDA, Ramelteon should be a popular drug.

Tuesday, June 28, 2005

The Future of Sleep Medicine

It is an exciting time for the field of sleep medicine. ICSD-2, the 2nd edition of the International Classification of Sleep Disorders, was introduced at the 19th Annual Meeting of the Associated Professional Sleep Societies. In many ways the ICSD-2 is a big improvement over the original ICSD. For example, there are now separate criteria for adult and pediatric obstructive sleep apnea- this is important since adult and pediatric OSA usually have different etiologies (adenotonsilar hypertrophy in kids and obesity/craniofacial abnormalities in adults). Unfortunately, where to draw the line between children and adults is unclear, though most sleep specialists draw it at puberty.
Another development in sleep medicine is a revision of the R+K scoring manual. There was a lot of debate about the proposed revisions at the 19th Annual Meeting. The new manual should be available in late 2006. The committee revising R+K hopes to simplify the criteria for the ending and beginning of REM sleep. Stage 3+4 will probably be combined into one stage. The scoring of periodic limb movements may be revised. Unfortunately, no one is able to agree on what exactly a "hypopnea" is; and there is little consensus about what if any degree of saturation should be required to score a hypopnea. The lack of a standard definition of a hypopnea limits research into Obstructive sleep apnea, it would be easier to compare studies if there was a standard definition.

Friday, June 17, 2005

I am going on vacation

I am leaving tomorrow morning for the 19th Annual Meeting of the Associated Professional Sleep Societies.
I will be getting back late on June 23rd. I don't know if I will have internet access at the meeting. Blogging will be light until the 24th.

Sleep Medicine is now an Official Subspecialty

Sleep medicine gained approval from the American Board of Medical Specialties as an official subspecialty for physicians practicing psychiatry, neurology, internal medicine, and pediatrics in March. This development is expected to further delivery of care to millions of individuals with sleep disorders and foster research and education in the field, said Michael Sateia, M.D., president of the American Academy of Sleep Medicine. Sateia, a professor of psychiatry, directs sleep medicine at Dartmouth Medical School.
The Accreditation Council for Graduate Medical Education (ACGME) approved program requirements for sleep medicine fellowship training programs in psychiatry, neurology, internal medicine, otolaryngology, and pediatrics in 2004. Information and application forms for ACGME-approved sleep medicine fellowships are posted online at <>.
From Psychiatric News

Thursday, June 16, 2005

Sleep Fellowship

As of yesterday, I am the new program director of the University of Mississippi Medical Center Sleep Disorders Fellowship. I will be using this blog as the official web site of the fellowship, and will be posting the sleep conference schedule on it, as well as tips for passing the sleep boards. The Sleep Fellowship accepts 1 full time fellow per year; requirements include board elgibility in neurology, psychiatry, internal medicine, pediatrics, or otolaryngology. If any physicians have a question about the fellowship or sleep medicine in general, they can post a comment or e-mail me at An application for the 2006/2007 academic year can be requested by e-mailing me your (snail-mail) address.

Sunday, May 22, 2005

Reader Questions

A reader asks about/speculates that there "might be one form of “ADD” that is simply a phenotype of ADD but that is actually caused by narcolepsy and the patient's attempt to compensate for it. This might explain why modafinil has been occasionally known to improve ADD symptoms - the reasons to engage inthe ADD behavior are abolished by the absence of sleepiness."
The new edition of Principles and Practice of Pediatric Sleep Medicine has a good chapter on "Attention Deficit, Hyperactivity, and Sleep Disorders." Conditions such as obstructive sleep apnea that present with sleepiness in adults often present with inattention and hyperactivity in children. From Principles and Practice: "...increasing evidence suggests that a variety of childhood sleep disorders are associated with inattention, hyperactivity, and cognitive impairment that could have significantly adverse effects on such important outcomes as development and school performance."
Obstructive sleep apnea and restless legs syndrome are the 2 sleep disorders that have the most evidence linking them to ADHD symptoms.
As far as narcolepsy, Principles and Practice of Pediatric Sleep Medicine mentions that "Children with narcolepsy often have problems with inattention and hyperactivity that may improve upon treatment" and "Adults who have been diagnosed with narcolepsy frequently give a history of 'attention deficit disorder' in childhood."
I have never used Modafinil (Provigil) to treat ADHD, but a quick Medline search suggests that it is effective for ADHD symptoms.
Inattention and hyperactivity can be symptoms of psychiatric disorders (including ADHD) and can be symptoms of sleep disorders. Multiple studies have linked inattention and hyperactivity to sleep disorders in children, but research is lacking in adults. However, I think it is quite possible for inattention to be a symptom of a sleep disorder in an adult.

Monday, May 02, 2005

Grand Rounds 32

Grand Rounds 32, A Day in the Life of a Medical Student, is up at MudFud.
This carnival celebrates every aspect of medicine, from the student,to the surgeon and the patient on the table.

Sunday, May 01, 2005

Narcolepsy 3

Part 1, Part 2
This is 3rd in a series about narcolepsy.
In the last 5-6 years there has been a revolution in our understanding of narcolepsy. In 1999 hypocretin (orexin) was discovered. Most cases of human narcolepsy are due to a loss of hypocretin cells in the lateral hypothalamus, which results in very low levels of hypocretin in the cerebrospinal fluid. In contrast, narcolepsy in animal models (e.g. Doberman pinschers) is usually due to dysfunction of the hypocretin receptors.
Hypocretin neurons project to multiple areas in the brainstem and hypothalamus involved in the regulation of the alternation of sleep/wake and REM/non-REM cycles. There are 2 main theories about the function of hypocretin: 1) hypocretin promotes wakefulness and 2) hypocretin promotes stability of sleep/wake/REM/non-REM states. These 2 theories are not mutually exclusive.
Thus narcolepsy, a hypocretin deficient state, can be thought of as 1) a disorder of excessive daytime sleepiness in which a person has irresistable episodes of sleep and/or 2) a disorder of unstable sleep/wake/REM/non-REM states in which daytime wakefulness is interrupted by periods of sleep and nighttime sleep is frequently restless and fragmented (intrusion of wakefulness). Cataplexy can be explained in this model as a mixture of REM sleep and wakefulness- cataplexy is the intrusion of the muscle atonia (decreased/absent muscle tone) of REM sleep into wakefulness.
Hypocretin is also involved in appetite, feeding and metabolism. This is an area I know very little about, so I won't mention it further.
That's it for now. I know I've been promising to talk more about Xyrem- I'll try to do this in part 4.

Tuesday, April 26, 2005

Sleeping on the job

From a Fox News story about Michael Jackson's attorneys:
Oxman had come to the case as Randy Jackson's lawyer from previous domestic skirmishes within the Jackson family. But he had no experience in criminal defense matters, and often slept through crucial sessions in Jackson's child molestation case.
Not enough info in the story to determine if he has a sleep disorder.

Thursday, April 14, 2005

Insomnia Increases Falls in the Elderly

According to this report from the National Sleep Foundation, insomnia increases the risk for falls in the elderly:
Falling is a significant cause of health problems and injury among older adults. According to the Centers for Disease Control, in 2001, more than 1.6 million seniors were treated in emergency departments for fall-related injuries and nearly 388,000 were hospitalized. The problem is even worse among nursing home residents where as many as 75% of residents fall annually, twice the rate of seniors living in the community. Despite prevalent sleep problems experienced by many nursing home residents, use of sleeping pills has been contraindicated due to a concern that their use might contribute to falls. A recent study in Journal of the American Geriatrics Society shows that contrary to common beliefs, it may not be sleeping medication but rather insomnia that increases nursing home residents' risk of falling. The study included more than 34,000 Michigan nursing home residents over age 65. Participants who had untreated insomnia at the start of the study were 90% more likely to fall in the next six months compared with those who did not have insomnia. In contrast, those who were taking hypnotic drugs to treat their insomnia at the start were only 29% more likely to fall. Alon Avidan, MD, MPH, first author of the study, explained, "Our findings suggest that people whose insomnia is effectively treated are less likely to fall than untreated insomniacs."

Wednesday, April 13, 2005

More about Narcolepsy

As I mentioned in the April 11 post about narcolepsy, the two main symptoms of narcolepsy are sleepiness and cataplexy. The sleepiness is usually treated with stimulants or Modafinil. Treatment improves the sleepiness, but it usually does not entirely go away.
The stimulants, but not modafinil, also slightly reduce cataplexy.
Cataplexy is " a sudden weakness of the muscles of the body, especially the legs but also the face and neck, that is brought on by strong emotion, especially laughing. " Cataplexy can be very effectively treated by the antidepressants that increase brain levels of norepinephrine, including venlafaxine (effexor), protryptiline (vivactil) and fluoxetine (prozac). (although prozac is a selective serotonin reuptake inhibitor, it has a metabolite that increases norepinephrine).
Xyrem is a novel treatment for cataplexy. Xyrem is gamma hydroxybutyrate (one of the "date rape"/club drugs). It improves night-time sleep, reduces cataplexy, and mildly improves daytime sleepiness. It is FDA approved for the treatment of cataplexy.
From the National Sleep Foundation: This medication is usually administered in two doses, at bedtime and 4 hours later. It produces consolidation of sleep and improvement of disturbed nocturnal sleep characteristic of narcolepsy. This improvement may contribute to decreased daytime drowsiness and diminished cataplexy (Broughton and Mamelak, 1980; Scharf et al.,1985). The dosing makes it very inconvenient to take. Also, because of its history as a date rape drug, it must be ordered from a central pharmacy and mailed to the patient.
In my opinion, Xyrem is faily worthless drug. Cataplexy is usually fairly easy to control with antidepressants. For disturbed night-time sleep in narcolepsy, I prefer to use a hypnotic such as Ambien rather than Xyrem. The only reason to prescribe xyrem, in my opinion, is if someone can not tolerate antidepressants
In my next post about narcolepsy, I will more about how xyrem works, and will also discuss the reconceptualization of narcolepsy from a disorder of sleepiness to a disorder of instability of the sleep/wake systems.

Tuesday, April 12, 2005

Dreaming and Schizophrenia

I just read an interesting article from the Neuroscience Education Institute comparing schizophrenia to the dream state.
In both REM (dream) sleep and in wakefulness in schizophrenia, the dorsolateral prefrontal cortex is relatively deactivated. This may be why the dreams of normal subjects and the delusions of schizophrenics seem real. In normal wakefulness, the dorsolateral prefrontal cortex is fully engaged.
"Dreams are brief madness and madness a long dream"
-Arthur Schopenhauer

Monday, April 11, 2005


Shrinkette ( recently forwarded me a question about narcolepsy from another blogger. I am posting some info about narcolepsy from the National Sleep Foundation (in italics) along with my comments:
What is narcolepsy?
Narcolepsy is a chronic (long-lasting) neurological (affecting the brain or nerves) disorder that involves your body's central nervous system. The central nervous system is the "highway" of nerves that carries messages from your brain to other parts of your body. For people with narcolepsy, the messages about when to sleep and when to be awake sometimes hit roadblocks or detours and arrive in the wrong place at the wrong time. This is why someone who has narcolepsy, not managed by medications, may fall asleep while eating dinner or engaged in social activities - or at times when he or she wants to be awake.
The major symptoms of narcolepsy are:
Excessive daytime sleepiness is usually the first symptom to appear, and often the most troubling. It is an overwhelming and recurring need to sleep at times when you want to be awake. In addition to sleepiness, key symptoms of narcolepsy can include regular episodes of:
cataplexy - a sudden loss of muscle control ranging from slight weakness (head droop, facial sagging, jaw drop, slurred speech, buckling of knees) to total collapse. It is commonly triggered by intense emotion (laughter, anger, surprise, fear) or strenuous athletic activity. Most persons with narcolepsy have some degree of cataplexy.
sleep paralysis - being unable to talk or move for a brief period when falling asleep or waking up. Many persons with narcolepsy suffer short-lasting partial or complete sleep paralysis.
hypnagogic hallucinations - vivid and often scary dreams and sounds reported when falling asleep. People without narcolepsy may experience hypnagogic hallucinations and sleep paralysis as well.
automatic behavior - familiar, routine or boring tasks performed without full awareness or later memory of them.

Cataplexy is one of the main symptoms that a sleep specialist looks for in diagnosing narcolepsy- this symptom is specific to narcolepsy. Unfortunately, it can take up to 10 years after sleepiness first occurs for cataplexy to develop. Excessive daytime sleepiness is common to a wide variety of sleep disorders, including obstructive sleep apnea.
The diagnosis of narcolepsy:
In addition to a medical history and physician examination, a diagnosis is made from polysomnogram tests in an overnight sleep laboratory to measure brain waves and body movements as well as nerve and muscle function. A diagnosis also includes the results of the Multiple Sleep Latency Test (MSLT), which measures the time it takes to fall asleep and to go into deep sleep while taking several naps over a period of time.
The major medications for sleepiness are the stimulants and Modafinil. Cylert is not used anymore due to liver toxicity:
Common stimulants include: dextroamphetamine sulfate (DexedrineTM), methylphenidate hydrochloride (RitalinTM), and pemoline (CylertTM). Methamphetamine hydrochloride (DesoxynTM) is prescribed less frequently for narcolepsy.
Some of the most common side effects of stimulants are headache, irritability, nervousness, insomnia, irregular heart beat, and mood changes.
A wake-promoting drug, modafinil (ProvigilTM) was approved by the U.S. Food and Drug Administration (FDA) in 1999 for use in treating the excessive daytime sleepiness associated with narcolepsy. It does not act as a stimulant for other body systems and studies have shown that modafinil is effective in improving alertness with few side effects and low abuse potential.

Modafinil is less effective than the stimulants. It is often better tolerated, though it can cause headaches. Modafinil interacts with birth control pills and decreases their efficacy.
Antidepressants are usually used to treat cataplexy:
Several classes of antidepressants are prescribed to treat cataplexy, hypnagogic hallucinations and sleep paralysis. One class, multicyclics, includes imipramine (TofranilTM), desimpramine (NorpraminTM), clomipramine (AnafranilTM), and protriptyline (VivactilTM). Another class are selective serotonin re-uptake inhibitors (SSRIs). These include fluoxetine (ProzacTM), paroxetine (PaxilTM), and sertraline (ZoloftTM).
The multicyclics (tricyclics) can have cardiac side effects, including fast heart rate and heart arrhythmias. They can also cause dry mouth and constipation. They are more effective, in my opinion, than the SSRI's for cataplexy. The only SSRI that has been well studied for cataplexy is Prozac. The tricyclics increase norepinephrine and serotonin levels. The SSRI's increase serotonin levels; Prozac also has a norepinephrine-increasing metabolite. Norepinephrine-increasing effects are thought to be necessary for treatment of cataplexy. I am not aware of evidence that the serotonin selective reuptake inhibitors (other than prozac) are effective for cataplexy (I'd be interested in hearing any comments on this).
Xyrem is a relatively new drug for cataplexy; it also decreases sleepiness:
Sodium oxybate (XyremTM) is the first and only FDA-approved medication for the treatment of cataplexy associated with narcolepsy. It produces consolidation of sleep and improvement of disturbed nighttime sleep characteristic of narcolepsy. It is sedating and should only be used at night. Xyrem is a Schedule III controlled drug substance with abuse potential that is available by prescription.
That's it about narcolepsy today; more later.

Saturday, March 19, 2005

Today's Sleep Tip

Don't eat or drink too much too close to bedtime. Heavy meals will make you less comfortable and cause you to wake during the night. Restrict fluids close to bedtime to prevent nighttime awakenings to use the bathroom.

from the National Sleep Foundation

Thursday, March 17, 2005

The fattest generation

The New York times reports on the childhood obesity epidemic. The supersizing of America may save Social Security, but will be devastating for Medicare:

For the first time in two centuries, the current generation of children in America may have shorter life expectancies than their parents, according to a new report, which contends that the rapid rise in childhood obesity, if left unchecked, could shorten life spans by as much as five years.
The report, to be published Thursday in The New England Journal of Medicine, says the prevalence and severity of obesity is so great, especially in children, that the associated diseases and complications - Type 2 diabetes, heart disease, kidney failure, cancer - are likely to strike people at younger and younger ages.
The report comes at a time when the country is embroiled in a debate over Social Security. While the report's authors say they started their research long before the current debate, they write that "the U.S. population may be inadvertently saving Social Security by becoming more obese" and dying sooner, but that "this 'benefit' will occur at the expense of the economy in the form of lost productivity before citizens reach retirement and large increases in Medicare costs associated with obesity and its complications."

Heaven and Hell

The difference between paradise and hell: you can always sleep in paradise, never in hell.

from bookofjoe, quoting Man, the Insomniac Animal — by E. M. Cioran

Monday, March 07, 2005

A New Casualty in the War against Obesity

The war against obesity is having unintended consequences:
Most girls thought that being slim would make them more popular, claimed the research in the British Journal of Developmental Psychology. They would also have no hesitation in dieting if they gained weight. The study was conducted among five- to eight-year-olds in South Australia, but experts said last night that British children felt "paranoid" about their weight - partly because of the Government's anti-obesity message.
"We want people who are overweight to do something about it. We don't want to terrorise youngsters."
The UK Eating Disorders Association said it was known that children as young as eight had been diagnosed with eating disorders and there may have been instances in younger children.

Monday, February 07, 2005

Coming Soon

Sleepdoctor is coming in March 2005.