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Sleep Medicine

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In what may be the largest study of sleep problems among individuals with multiple sclerosis (MS), researchers at UC Davis have found that widely undiagnosed sleep disorders may be at the root of the most common and disabling symptom of the disease: fatigue. Study paticipant reports of sleep disorder frequency, sleep patterns and complaints of excessive daytime sleepiness suggest that sleep problems may be a hidden epidemic in the MS population.

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A sleep-promoting circuit located deep in the primitive brainstem has revealed how we fall into deep sleep. Discovered by researchers at Harvard School of Medicine and the University of Buffalo School of Medicine and Biomedical Sciences, this is only the second "sleep node" identified in the mammalian brain whose activity appears to be both necessary and sufficient to produce deep sleep.  Using designer genes, researchers were able to 'turn on' specific neurons in the brainstem that result in deep sleep.

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Insomnia can cause chronic inflammation, which can lead to weight gain, hypertension, diabetes, heart disease, and earlier death. This study finds that curing the insomnia reduces the inflammation and hopefully reduces disease. It also found the best way to cure lack of sleep is through the use of a common psychotherapy treatment - cognitive behavioural therapy.

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Getting enough sleep is important to people of any age, but it is especially so for teenagers, with insufficient sleep possibly being linked to obesity as an adult.

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A study is shining new light on a sleep disorder called “sleep drunkenness.” The disorder may be as prevalent as affecting one in every seven people. Sleep drunkenness disorder involves confusion or inappropriate behaviour, such as answering the phone instead of turning off the alarm, during or following arousals from sleep, either during the first part of the night or in the morning. An episode, often triggered by a forced awakening, may even cause violent behaviour during sleep or amnesia of the episode.

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Ever wondered about the effects of binge sleeping? Are naps bad or how long should you nap for? For all these myths debunked follow the link

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Link between obstructive sleep apnea and increased bone resorption in men

A recent Japanese study is first evidence of a link between obstructive sleep apnoea (OSA) and abnormal bone metabolism, due to the effects of hypoxia, microinflammation and oxidative stress.

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Obstructive sleep apnea (OSA) is a prevalent disorder and should be considered a systemic illness.

Studies have shown that the pro-inflammatory cytokines interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNFalpha) are elevated in patients with OSA independently of obesity and that visceral fat.

OSA in obese patients is now considered manifestations of the Metabolic Syndrome, include:

  • obesity without OSA is associated with daytime sleepiness;
  • PCOS and diabetes type 2 are independently associated with EDS after controlling for SDB, obesity, and age;
  • increased prevalence of OSA in post-menopausal women, with hormonal replacement therapy associated with a significantly reduced risk for OSA;
  • lack of effect of continuous positive airway pressure (CPAP) in obese patients with apnea on hypercytokinemia and insulin resistance indices; and
  • the prevalence of the metabolic syndrome in the US population from the Third National Health and Nutrition Examination Survey (1988-1994) parallels the prevalence of symptomatic OSA in general random samples. Finally, the beneficial effect of a cytokine antagonist on EDS in obese, male apneics and that of exercise on SDB in a general random sample, supports the hypothesis that cytokines and insulin resistance are mediators of EDS and sleep apnea in humans.

 Hypoxia, micro-inflammation and oxidative stress are also known to affect bone metabolism.

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Model for mediation of effects of E on osteoclast formation and function by cytokines in bone marrow microenvironment.

The bone metabolic abnormalities in patients with OSA were studied, specifically the serum/ urinary levels of bone resorption markers and their attenuation following CPAP therapy in subjects with OSA.

The study was a cross-sectional and prospective study and was conducted in 50 consecutive male subjects visiting a sleep clinic and 15 age-matched control subjects without OSA. Plasma concentrations of IL-1β, IL-6, TNF-alfa, 3-nitrotyrosine, osteocalcin, bone-specific alkaline phosphatase (BAP), and urinary concentrations of cross-linked C-terminal telopeptide of type I collagen (CTX) were examined before and after 3 months' CPAP in subjects with OSA.

 The results showed that the plasma levels of the cytokines as well as the urinary CTX levels were higher in subjects with severe OSA than in those with mild OSA or control subjects. Significant decrease of the urinary excretion of CTX (before: 211±107 vs. after: 128±59 μg/mmol/creatinine; p<0.01) as well as of the plasma levels of the cytokines was observed following 3 months' CPAP.

Overall this study found that increased OSA severity correlates with the serum/ urinary levels of bone resorption markers and there is reversal following CPAP in subjects with OSA.

More information on Bone Metabolism

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