Published Research - General Sleep and WED (RLS)

For everything and anything else not covered in the other WED/RLS sections.

Published Research - General Sleep and WED (RLS)

Postby ViewsAskew » Fri Apr 20, 2007 6:51 pm

Remember, go to the last page for the newest posts :). If you haven't been in this thread before, it's many pages long.
edited by Ann, 2012
___________________________________________________________________________________________________________________________________

I thought we had a thread for this, but I think it's in the Pharma section. So, I'll start one here for research about RLS but not related to drugs.

http://www.nyu.edu/socialwork/ip/archiv ... fe_10.html

This link will take you to a page with many links - all about quality of life. One of them is about RLS.

http://www.springerlink.com/content/t16 ... 92ba1&pi=6

The original was published last year - I remember them talking about it at the RLSF conference. But, it was interesting to see all the other studies here, too. It make me feel better, and worse, about the RLS. I know I'm not out of the norm, but it makes me sad that so many of us are affected so much by this.
Last edited by ViewsAskew on Sat Jan 10, 2009 9:42 pm, edited 1 time in total.
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Postby SquirmingSusan » Sat Apr 21, 2007 3:50 am

Yikes. So we're more affected physically and psychologically by RLS than people with Type 2 diabetes? :shock: No wonder this seems so difficult to live with.

Thanks for posting that, Ann.

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Postby ViewsAskew » Sat Jun 02, 2007 5:03 pm

Wow, this was fascinating. I seem to recall that we have talked about this in the past (awhile ago).

http://www.websciences.org/cftemplate/N ... D=20066131

Auditory startle reaction is disinhibited in idiopathic restless legs syndrome.
FRAUSCHER B, LOSCHER WN, HOGL B, POEWE W, KOFLER M.
Sleep 2007;30(4):489-93.
Department of Neurology, Innsbruck Medical University, Innsbruck, Austria

STUDY OBJECTIVES: Because the auditory startle reaction is abnormal in disorders with substantia nigra pathology, we hypothesized that auditory startle responses (ASRs) might also be altered in restless legs syndrome (RLS). DESIGN: Neurophysiologic study of the auditory startle reaction. SETTING: Neurology departments of a university hospital and an affiliated local hospital. PATIENTS AND PARTICIPANTS: Fifteen patients with idiopathic RLS (6 de novo, 9 untreated after a 7-day wash-out period of levodopa, mean duration of IRLS symptoms 21.2 +/- 17.9 years, mean RLS severity score 23.5 +/- 6.7) and 15 sex- and age-matched healthy controls were investigated. INTERVENTIONS: Not applicable. MEASUREMENTS AND RESULTS: ASRs were elicited by 8 high-intensity auditory stimuli differing randomly in tonal frequency and intensity. Reflex electromyographic activity was simultaneously recorded with surface electrodes from 8 facial, neck, arm, and leg muscles. In RLS patients, ASRs were significantly more frequent (541 of 960 possible responses; controls, 430 of 960), and ASR area under the curve was significantly larger (3812 +/- 450 microVms; controls, 1756 +/- 226 microVms). Analysis per body region revealed that ASRs were significantly more frequent in RLS patients than in controls in leg muscles (138/360 vs 55/360); ASR latencies to leg muscles were significantly shorter in RLS patients (129 +/- 6 ms vs 160 +/- 11 ms); ASR area under the curve was significantly larger in RLS patients in facial (7547 +/- 1326 mmicroVms vs 2982 +/- 448 microVms) and leg muscles (1373 +/- 308 microVms vs 541 +/- 193 microVms). CONCLUSIONS: Our data demonstrate disinhibition of reticulospinal pathways in RLS patients as compared to normal controls, likely originating from dysfunction rostral to the lower brainstem.
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Postby ViewsAskew » Sat Jun 02, 2007 5:11 pm

No worries, this one doesn't mean that RLSers have a higher risk of MS - but that as with many other disorders, RLS seems to tag along.

http://www.websciences.org/cftemplate/N ... D=20066104

High prevalence of restless legs syndrome in multiple sclerosis.
MANCONI M, FABBRINI M, BONANNI E, FILIPPI M, ROCCA M, MURRI L, FERINI-STRAMBI L.
Eur J Neurol 2007;14(5):534-9.
Sleep Disorders Center, Scientific Institute, University Ospedale San Raffaele, Milan, Italy. manconi.mauro@hsr.it

Despite the fact that multiple sclerosis (MS) patients often include leg restlessness as a sensory symptom, MS is not mentioned amongst symptomatic restless legs syndrome (RLS) forms. The aim of this study was to estimate RLS prevalence in a large population of MS patients, comparing clinical and MRI findings between patients with and without RLS. Each of the 156 MS patients (100 females, 56 males, mean age 40.7 +/- 10.4) enrolled in a prospective study underwent a medical history interview, a neurological examination with the assessment of the Expanded Disability Status Scale (EDSS), and a structured questionnaire to verify the presence and features of RLS. Conventional brain-spinal MRIs of 99 subjects were also evaluated and compared between patients with and without RLS. Fifty-one subjects (32.7%) (mean age 43.8 +/- 12.8) met the criteria for RLS. In a few patients (8.5%), the RLS preceded clinical MS onset, whilst in the remaining cases the RLS was followed by or was simultaneous with clinical MS onset. Comparing the RLS group with the group without RLS, no significant differences were found in MS duration, gender, and referred sleep habits. The primary progressive MS course was more represented in the RLS group, which also showed a higher EDSS score. RLS is a very common finding in MS patients and should be considered amongst the symptomatic RLS forms. RLS is also associated with higher disability.
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Postby ViewsAskew » Sat Jun 09, 2007 6:24 pm

The next time you see anything about how RLS is overblown, refer them to this very new study. It was designed to find out just that. . .


http://www.neurology.org/cgi/content/ab ... 64/11/1920

More interesting, is that this was published in 2005. It may even have been part of the larger REST study that was done.
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Postby cornelia » Wed Jul 18, 2007 5:55 pm

Hope for the future!

Gene linked to restless leg syndromeArticle from: ReutersFont size: Decrease Increase Email article: Email Print article: Print By Gene Emery in Boston

July 19, 2007 02:59am
TWO studies released today offer new evidence that inheritance plays a role in restless leg syndrome, an uncomfortable and sometimes painful feeling in the legs that can wreak havoc with sleep.

Researchers reporting in the journal Nature Genetics say they have found three pieces of the human genetic code that are linked to RLS, giving more scientific backing to a condition sometimes derided as normal restlessness.

About three per cent of the population is affected with RLS so badly that they have trouble sleeping.
About 10 per cent reportedly experience some degree of symptoms, which usually appear when a person is in bed or sitting quietly and can sometimes be temporarily relieved by moving the legs or getting up and walking.

Julianne Winkelman of the Max Planck Institute of Psychiatry in Munich, and her colleagues, said three genes seem to account for up to 74 per cent of the cases, based on studies of people in Germany and Canada.

In a related study, published online by the New England Journal of Medicine, a team led by Hreinn Stefansson of deCODE Genetics Inc. in Reykjavik, Iceland, found that the periodic leg movements that occur during the night in most patients with RLS seems to be linked one of the three identified in the Nature Genetics article.

Both research teams pinpointed the same gene independently.

The Stefansson team found from genetic testing of people in Iceland and North America that the gene accounts for about half of the cases of people whose legs move two or three times per minute during sleep and complain of RLS.

“And that's a conservative estimate,” said David Rye of Emory University School of Medicine in Atlanta, who worked on the Stefansson study.

However many doctors believe that most people who experience periodic limb movements during sleep do not have RLS.

Growing older, antidepressant medicines and other sleep disorders can cause the movements as well.

Biological basis

RLS has been the subject of skepticism from people who regard it as little more than a modern-day diagnosis for old fashioned “ants in the pants” restlessness.

This attitude has gained some popularity after the condition was heavily promoted in “talk to your doctor” advertisements by GlaxoSmithKline , which is marketing the Parkinson's disease drug Requip as an RLS treatment.

“We now have concrete evidence that RLS is an authentic disorder with recognisable features and an underlying biological basis,” said Mr Rye.

He said the new finding was derived from genetic studies from French Canadians, Germans, Central Europeans, Icelanders and Americans, “so I don't think it's a frivolous result”.

In a Journal commentary, Dr John Winkelman of Brigham and Women's Hospital in Boston said the gene may not be one for RLS per se, but for its worst symptom - the leg movements that disturb sleep.

Corrie (I don't quite understand the last paragraph though)
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Postby ViewsAskew » Fri Jul 20, 2007 6:05 pm

And, another variant of that research.

http://content.nejm.org/cgi/content/full/NEJMe078129v1

This is from the New England Journal of Medicine:

Today, 350 years after its first description, the restless legs syndrome (RLS) is strangely controversial. Experts and patients alike describe RLS both as a miserably impairing disorder and as "the most common disorder you have never heard of." Critics do not regard RLS as a disorder at all but, rather, as the fabrication of an omnivorous pharmaceutical industry. RLS is a waking sensorimotor disturbance with features of both neurologic and sleep disorders. Those afflicted describe an intensely uncomfortable, overwhelming urge to move the legs (often accompanied by dysesthesias), predominantly in the evening or at night, that is present at rest and relieved only temporarily by movement. These leg sensations dramatically disturb sleep, and impairment in quality of life is common.1

Once asleep, the majority of (but not all) patients with RLS have periodic limb movements in sleep, which was originally called "nocturnal myoclonus." These movements consist of recurrent (every 20 to 30 seconds), involuntary dorsiflexion of the foot and lower leg, with each movement lasting about 2 to 5 seconds. Such movements can be recorded in the home with simple surface monitors on the leg. Roughly one quarter of such limb movements are associated with arousal from sleep, as seen on electroencephalography, and all are followed by large elevations in systolic (20 to 25 mm Hg) and diastolic (10 to 15 mm Hg) blood pressure.2 However, the vast majority of persons with periodic limb movements in sleep do not have waking symptoms of RLS. Such movements are common without RLS, with increased age, in patients who are taking antidepressant medications and in those with certain neurologic and sleep disorders (e.g., narcolepsy and rapid-eye-movement sleep behavior disorder). Outside of RLS, the clinical significance of periodic limb movements in sleep remains uncertain, though concern exists regarding the effects of the movements on sleep quality and cardiovascular functioning.3

Some of the earliest descriptions of RLS recognized its strongly familial nature. Recent linkage studies have shown a number of susceptibility loci for familial RLS.4 However, until now, no gene has been identified. For this reason, the report by Stefansson et al.5 in this issue of the Journal showing an association between a sequence variant in chromosome 6p and periodic limb movements in sleep in distinct Icelandic and American cohorts of subjects with RLS and their families, as well as controls, is exciting and important. The simultaneously published report by Winkelmann et al.6 showing an association between RLS and the same sequence variant, as well as two additional single-nucleotide polymorphisms (SNPs), in German and Canadian cohorts with RLS makes this finding even more secure.

Inspection of the data provided by Stefansson et al., however, shows that this sequence variant does not appear to be a gene for RLS but, rather, for periodic limb movements in sleep. The investigators observed the highest odds ratio in subjects with periodic limb movements in sleep without RLS. As this group became increasingly diluted with subjects with RLS, the association with the SNP became less and less apparent. Although a significant association with the SNP was still present in the entire group with RLS (with and without periodic limb movements), it disappeared completely in subjects with RLS without periodic limb movements in sleep. Since Winkelmann et al.6 did not report on periodic limb movements in sleep in their study, it is unclear whether the other sequence variants they found are truly for RLS, for periodic limb movements in sleep, or for some other RLS marker.

What is the advantage of knowing the genetic basis for periodic limb movements in sleep? These movements may serve as a heritable biologic marker, or endophenotype, for RLS. Disorders with a complex phenotype and heritability, such as RLS, are increasingly being dissected into their component parts with the use of endophenotypes. Endophenotypes are relatively simple, stable biologic phenomena that can be measured objectively and are genetically determined. To function as an endophenotype, a marker must be present both in affected patients with the disorder and in unaffected family members. In theory, although the disorder itself will usually result from a mixture of multiple genetic and nongenetic abnormalities, the endophenotype, as a simpler biologic phenomenon, will have a more straightforward genetic and pathophysiological basis. This method has been constructively applied to a number of disorders, such as hemochromatosis (with serum iron as the endophenotype), the long-QT syndrome (QT prolongation), and familial adenomatous polyposis coli (intestinal polyps).7

The use of periodic limb movements in sleep as an endophenotype for RLS may present a number of valuable opportunities and insights. From a genetic perspective, it might assist with linkage to other relevant susceptibility genes so that polygenic interactions can be discerned. From a diagnostic perspective, the use of periodic limb movements in sleep may improve diagnostic accuracy and provide a more homogeneous RLS phenotype for epidemiology, physiology, genotyping, and treatment studies. RLS has a number of clinical mimics (e.g., peripheral neuropathy and nocturnal leg cramps), and its diagnosis with the use of questionnaires is fraught with difficulty. The study by Stefansson et al. provides some insight into this problem since their questionnaire had a false positive rate of 25% and a similar false negative rate, as compared with an expert clinical interview.

In addition, RLS may have a number of subtypes, some with and some without periodic limb movements in sleep. For instance, many, but not all, patients with RLS have an excellent response to dopaminergic therapy, which also nearly eliminates periodic limb movements in sleep.8 The subtyping of patients with RLS may predict treatment responses to these agents. Finally, patients with end-stage renal failure who have periodic limb movements in sleep are at increased risk of death,9 and such movements may also contribute to the observed elevated risk of cardiovascular disease in patients with RLS.10 Use of the endophenotype for periodic limb movements, or even of the sequence variant itself, may allow stratification of these risks in patients with RLS or other conditions marked by such movements.

The association between the SNP and reduced serum ferritin indexes is an important feature of the study by Stefansson et al. Multiple studies that used magnetic resonance imaging scans, analysis of cerebrospinal fluid, transcranial ultrasonography, and analysis of autopsy specimens11 showed that patients with RLS had a reduction in iron in the central nervous system. Iron levels in the brain may thus reflect an independent endophenotype for RLS or may be a causative factor for RLS or periodic limb movements in sleep.

The demonstration of a strong association between a sequence variant and periodic limb movements in sleep and, to a lesser extent, RLS does not validate RLS as a "genuine" disorder. Many physiological features that vary in the otherwise normal population (e.g., baldness, height, and eye color) have genetic bases. The legitimacy of RLS as a bona fide disorder is provided by the clinically apparent and well-documented sleep disturbance and distress of the roughly 3% of the adult population with frequent and bothersome RLS symptoms. The genetic finding reported by Stefansson et al. offers hope to patients with periodic limb movements in sleep and RLS that the syndrome's pathophysiology will be understood and that such knowledge will lead to additional effective and durable treatments.

Dr. Winkelman reports receiving research support and consulting fees from Boehringer Ingelheim, GlaxoSmithKline, and Schwarz Pharma and lecture fees from Boehringer Ingelheim and GlaxoSmithKline. No other potential conflict of interest relevant to this article was reported.


Source Information

From the Division of Sleep Medicine, Brigham and Women's Hospital, and Harvard Medical School — both in Boston.

This article (10.1056/NEJMe078129) was published at www.nejm.org on July 18, 2007. It will appear in the August 16 issue of the Journal.

References


Allen RP, Walters AS, Montplaisir J, et al. Restless legs syndrome prevalence and impact: REST general population study. Arch Intern Med 2005;165:1286-1292. [Free Full Text]
Pennestri MH, Montplaisir J, Colombo R, Lavigne G, Lanfranchi PA. Nocturnal blood pressure changes in patients with restless legs syndrome. Neurology 2007;68:1213-1218. [Free Full Text]
Hornyak M, Feige B, Riemann D, Voderholzer U. Periodic leg movements in sleep and periodic limb movement disorder: prevalence, clinical significance and treatment. Sleep Med Rev 2006;10:169-177. [CrossRef][ISI][Medline]
Winkelmann J, Polo O, Provini F, et al. Genetics of restless legs syndrome (RLS): state-of-the-art and future directions. Mov Disord (in press).
Stefansson H, Rye DB, Hicks A, et al. A genetic risk factor for periodic limb movements in sleep. N Engl J Med 2007;357. DOI: 10.1056/NEJMoa072743.
Winkelmann J, Schormair B, Lichtner P, et al. Genome-wide association study of restless legs syndrome identifies common variants in three genomic regions. Nat Genet (in press).
Braff DL, Freedman R, Schork NJ, Gottesman II. Deconstructing schizophrenia: an overview of the use of endophenotypes in order to understand a complex disorder. Schizophr Bull 2007;33:21-32. [Free Full Text]
Hening WA. Current guidelines and standards of practice for restless legs syndrome. Am J Med 2007;120:Suppl 1:S22-S27. [CrossRef][ISI][Medline]
Benz RL, Pressman MR, Hovick ET, Peterson DD. Potential novel predictors of mortality in end-stage renal disease patients with sleep disorders. Am J Kidney Dis 2000;35:1052-1060. [ISI][Medline]
Winkelman JW, Shahar E, Sharief I, Gottlieb DJ. Association of restless legs syndrome and cardiovascular disease in the Sleep Heart Health Study. Neurology (in press).
Allen RP, Earley CJ. The role of iron in restless legs syndrome. Mov Disord (in press).
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Postby ViewsAskew » Fri Jul 20, 2007 6:10 pm

OK, what interested me about this so much is that it really suggests that we take away the distinction between RLS and PLMD.

OK, but what about the huge percentage of people with PLMD that are A)not bothered by it and B) do not have RLS? Haven't we been told that something like 85% of us with RLS have PLMD, but only 25% of those with PLMD have RLS?

Hmmm.

I wonder what the difference is between PLMD in RLSers and non-RLSers - for example, do all RLSers with PLMD have impaired sleep? Is anyone comparing sleep study results to see if those with RLS have something slightly different happening?

Oh, well. I'm just full of questions this morning and no answers. . .
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Postby ViewsAskew » Tue Jul 24, 2007 5:34 pm

Another facsinating study - the temps in this are really high (to me), as our external temp is more like 76-78 in the summer when we sleep. I'd love to find a way to get more slow-wave sleep, though. I wish I could read the whole thing to find out if this applies at lower temps. . .

http://www.websciences.org/cftemplate/N ... D=20066338

Influence on human sleep patterns of lowering and delaying the minimum core body temperature by slow changes in the thermal environment.
TOGO F, AIZAWA S, ARAI J, YOSHIKAWA S, ISHIWATA T, SHEPHARD RJ, AOYAGI Y.
Sleep 2007;30(6):797-802.
Exercise Sciences Research Group, Tokyo Metropolitan Institute of Gerontology, Itabashi, Tokyo, Japan


STUDY OBJECTIVES: We hypothesized that appropriate changes in thermal environment would enhance the quality of sleep. DESIGN/SETTING: Controlled laboratory study. PARTICIPANTS: Healthy young men (n = 7, mean age 26 years). INTERVENTIONS: Nocturnal sleep structures in semi-nude subjects were compared between a condition where an ambient temperature (Ta) of 29.5 degree C was maintained throughout the night (constant Ta), and a second condition (dynamic Ta) where Ta changed slowly within the thermoneutral range (from 27.5 C to 29.5 degree C). MEASUREMENTS AND RESULTS: Statistically significant (P < 0.05) results included a lower and a later occurrence of minimum core body temperature (Tc), and a longer duration of slow-wave (stages 3+4) sleep in dynamic versus constant T. However, total sleep time, sleep efficiency, the total durations of light (stages 1+2) and rapid eye movement sleep, and the latencies to sleep onset, slow-wave sleep, and rapid eye movement sleep did not differ between conditions. CONCLUSIONS: Lowering the minimum and delaying the nadir of nocturnal Tc increases slow-wave sleep (probably by an increase of dry heat loss); use of this tactic might improve the overall quality of sleep.
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Postby ViewsAskew » Tue Jul 24, 2007 5:47 pm

For those of us with PLMS - this is another interesting study (I guess most of them are interesting, aren't they?). This fascinates me because it shows that events are happening in the body up to 6 seconds PRIOR to the movement - so, what is causing that???? Is the movement somehow in response to that event?

http://www.websciences.org/cftemplate/N ... D=20066384

The significance of the sympathetic nervous system in the pathophysiology of periodic leg movements in sleep.
GUGGISBERG AG, HESS CW, MATHIS J.
Sleep 2007;30(6):755-66.
Center of Sleep Medicine, Department of Neurology, University of Berne, Inselspital, Bern, Switzerland. aguggis@gmail.com

STUDY OBJECTIVES: Periodic leg movements in sleep (PLMS) are frequently accompanied by arousals and autonomic activation, but the pathophysiologic significance of these manifestations is unclear. DESIGN: Changes in heart rate variability (HRV), HRV spectra, and electroencephalogram (EEG) spectra associated with idiopathic PLMS were compared with changes associated with isolated leg movements and respiratory-related leg movements during sleep. Furthermore, correlations between electromyographic activity, HRV changes, and EEG changes were assessed. SETTING: Sleep laboratory. PATIENTS: Whole-night polysomnographic studies of 24 subjects fulfilling the criteria of either periodic leg movements disorder (n = 8), obstructive sleep apnea syndrome (n = 7), or normal polysomnography (n = 9) were used. MEASUREMENTS AND RESULTS: Spectral HRV changes started before all EEG changes and up to 6 seconds before the onset of all types of leg movements. An initial weak autonomic activation was followed by a sympathetic activation, an increase of EEG delta activity, and finally a progression to increased higher-frequency EEG rhythms. After movement onset, HRV indicated a vagal activation, and, the EEG, a decrease in spindle activity. Sympathetic activation, as measured by HRV spectra, was greater for PLMS than for all other movement types. In EEG, gamma synchronization began 1 to 2 seconds earlier for isolated leg movements and respiratory-related leg movements than for PLMS. Significant correlations were found between autonomic activations and electromyographic activity, as well as between autonomic activations and EEG delta activity, but not between higher-frequency EEG rhythms and EMG activity or HRV changes. CONCLUSIONS: These results suggest a primary role of the sympathetic nervous system in the generation of PLMS.
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Postby SquirmingSusan » Tue Jul 24, 2007 5:52 pm

OK, for those of you who can't do the math in your head, like me, I found a temperature converter on line.

27.5C = 81.5F
29.5C = 85.1F
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Postby ViewsAskew » Tue Aug 21, 2007 4:05 am

This is an interesting study. . .it showed that people with RLS had poorer sleep than people without, (yeah, like that is news???). But, I'm not sure if it's saying that this is for people with RLS that do not have PLMs, too, or for all of us. I'd like to see what it is for those without PLMs - if their sleep is worse, that really does change how I think about RLS...

http://www.immunesupport.com/library/sh ... fm/ID/8252
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Postby cornelia » Tue Aug 21, 2007 9:15 am

I'm not sure what they mean exactly too, Ann.

But my own opinion (and experience) is that RLS (without PLMS) goes on during sleep. It must be. But I'm not quite sure what the experts think about this.
When I had my first sleep study done on no meds it showed no PLMS. But I always woke up so very, very tired that I couldn't go to work. So my sleep was poor, while I slept 6 to 7 hours, only waking up once generally.

What exactly would change your opinion?

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Lack of sleep - heart disease

Postby ViewsAskew » Tue Sep 25, 2007 5:57 am

Well, this sounds like something that anyone who doesn't get RLS should understand. For a long time I have not told people I have RLS - I say I have a movement disorder. I will now modify that - I have a movement disorder that prevents me from getting a full night's sleep.

http://health.yahoo.com/news/179663

From Reuters, 9/24/07

People who do not get enough sleep are more than twice as likely to die of heart disease, according to a large British study released on Monday.

Although the reasons are unclear, researchers said lack of sleep appeared to be linked to increased blood pressure, which is known to raise the risk of heart attacks and stroke.

A 17-year analysis of 10,000 government workers showed those who cut their sleeping from seven hours a night to five or less faced a 1.7-fold increased risk in mortality from all causes and more than double the risk of cardiovascular death.

The findings highlight a danger in busy modern lifestyles, Francesco Cappuccio, professor of cardiovascular medicine at the University of Warwick's medical school, told the annual conference of the British Sleep Society in Cambridge.

&quot;A third of the population of the UK and over 40 percent in the U.S. regularly sleep less than five hours a night, so it is not a trivial problem,&quot; he said in a telephone interview.

&quot;The current pressures in society to cut out sleep, in order to squeeze in more, may not be a good idea -- particularly if you go below five hours.&quot;

Previous research has highlighted the potential health risks of shift work and disrupted sleep. But the study by Cappuccio and colleagues, which was supported by British government and U.S. funding, is the first to link duration of sleep and mortality rates.

The study looked at sleep patterns of participants aged 35-55 years at two points in their lives -- 1985-88 and 1992-93 -- and then tracked their mortality rates until 2004.

The results were adjusted to take account of other possible risk factors such as initial age, sex, smoking and alcohol consumption, body mass index, blood pressure and cholesterol.

The correlation with cardiovascular risk in those who slept less in the 1990s than in the 1980s was clear but, curiously, there was also a higher mortality rate in people who increased their sleeping to more than nine hours.

In this case, however, there was no cardiovascular link and Cappuccio said it was possible that longer sleeping could be related to other health problems such as depression or cancer-related fatigue.

&quot;In terms of prevention, our findings indicate that consistently sleeping around seven hours per night is optimal for health,&quot; he said.
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Why one of the "warning" signs of RLS is overweigh

Postby ViewsAskew » Wed Oct 17, 2007 4:22 pm

http://news.yahoo.com/s/hsn/20071017/hl ... overeating

This new research may explain why a seemingly disproportionate number of RLSers have trouble with weight gain.

WEDNESDAY, Oct. 17 (HealthDay News) -- Chronic overeaters may have their DNA to blame, research suggests.

Scientists from the University at Buffalo say people with genetically lower levels of dopamine, a brain chemical that helps make eating and other behaviors more rewarding, may be driven to consume more food.

"We weren't studying obesity, per se, but motivation to eat. We wanted to understand how the brain regulates motivation to eat," explained study co-author Jennifer Temple, a research assistant professor of pediatrics.

Reporting in the October issue of Behavioral Neuroscience, Temple's team looked at genes associated with differences in brain activity, in particular the influence of a genetic variation linked to a lower number of dopamine D2 receptors on cells. About half the population has this variation, called the Taq1A1 allele.

According to the researchers, people with fewer of the dopamine receptors need to take in more of a rewarding substance -- such as food or drugs -- to get an effect that other people get with less.

Investigating further, the Buffalo team studied 29 obese and 45 non-obese men and women, aged 18 to 40. The researchers took DNA samples from inside each person's cheek to see if they carried the Taq1A1 variation.

"They came to the lab twice," Temple said. "The first visit, we gave them a large portion of six snack foods and told them it was a taste test. They rated the food on taste characteristics. We left the food in the room while they were completing the rating." Participants were told they could eat as much as they wanted, and the researchers took note of their intake.

On the second visit, the researchers evaluated each participant's motivation to eat. To earn a food reward, each person had to click a computer mouse 20 times. "To get more food, they had to click 40 times," Temple said. "We were looking to see how hard they were willing to work for food." The participants could choose food or the chance to read a newspaper as a reward.

"The combination of being very motivated to get food and having the genotype made people eat the most," Temple said. "We had people very high in motivation to get food who didn't have the genotype," she added, but those people still "ate less than people who were both motivated and had the [Taq1A1] genotype."

The bottom line: "A combination of [having] this genotype with being very motivated to consume food or with being obese seems to make people more prone to overeat," Temple said.

The study results do not imply that your genes doom you to obesity, however. "People who had the genotype were heavier, but there were certainly people who had the genotype who were not obese," Temple stressed.

While other research has turned up similar findings, Temple said her team looked at behaviors associated with the genotype. "Others have found that differences in the density of dopamine are associated with obesity," she noted.

In their future work, the team will use brain scans to reveal more about the relationship between the genotype and the drive toward eating.

Eventually, Temple said, the dopamine system may become a target for weight-loss therapies. For instance, drugs that affect the dopamine system, such as drugs now used for attention deficit hyperactivity disorder (ADHD), might help with weight-loss efforts, she theorized.

Another expert, Dr. Samuel Klein, director of the Center for Human Nutrition at Washington University School of Medicine in St. Louis, said the study "addresses an important and relatively overlooked area in obesity -- the contribution of reward addiction in the regulation of food intake."

Dr. Julio Licinio, professor and chairman of psychiatry and behavioral sciences at the University of Miami Miller School of Medicine, agreed. "This really is like another piece of the puzzle, showing there is a genetic component and that those with this genotype are likely to have different weights because of the food reinforcement."

Licinio published similar research last year, in which he found that people with a particular genotype for a receptor for the brain chemical serotonin were more likely to eat red meat than those who lacked it.
Ann - Take what you need, leave the rest

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