Why sleep cause cardiovascular disease

Poor sleep is prospectively linked to all-cause and cardiovascular mortality. So why. Recently, Motivala from UCLA Semel Institute in USA found that sleep loss is associated with increase cytokines in sleep deprivation studies and in primary insomnia patients. He said bidirectional communication between the brain and the inmmune system is carried out through a complex network of autonomic nerves, endocrine hormones and cytokines. Disturbed sleep appears to perturb the functioning of this network and therefore contribute to elevations in inflammatory mediators linked to cardiovascular disease.

Sleep disorders in medical disease

Insomnia and hypersomnia are highly comorbid with medical conditions, such as chronic pain and diabetes, as well as with various cardiovascular, respiratory, gastrointestinal, urinary and neurological disorders. Restless legs syndrome and periodic leg movement syndrome have been associated with iron deficiency, kidney disease, diabetes, and neurological, autoimmune, cardiovascular and respiratory disorders. Rapid eye movement behaviour disorder has been described as an early manifestation of serious central nervous system diseases; thus, close neurological monitoring of patients referring with this complaint is indicated.

Therefore, identification and management of any sleep disorder in medical patients is important for optimizing the course and prognosis. Of equal importance is the search for undetected medical disorder in patients presenting with sleep disorders.

Psychological Flexibility is effective to treat Insomnia in Persons with Chronic Pain

Sleep disturbance is a common complaint in people with chronic pain, and is associated with a range of adverse outcomes including reports of greater pain and disability. Most of these people usually use pain killer to help them reduce insomnia. Recently, McCracken et al from King's college in UK found psychological flexibity, a process from acceptance and commitment therapy is helpful for the insomniac with chronic pain. They found the components of psychological flexibility, particularly acceptance of pain and values-based action is positive correlations with sleep quality. They said the psychological flexibity may be a new candidate to treat insomnia in persons with chronic pain.

Sleep and primary headaches

The relationship between sleep and primary headaches has been known for over a century, particularly for headaches occurring during the night or early morning. Migraine, tension-tyre headache, and cluster headache may cause sleep fragmentation, insomnia, and hypersomnia, causing considerable social and economical costs and several familial problems. By contrast, sleep disorders may themselves trigger headache attacks. Finally, headaches and sleep disorders can also be symptoms of other underlying pathologies. Despite this background, there is still no clarity about the mechanism that links these two entities and their interdependence remains to be defined. Patients with primary headache should undergo a careful assessment of sleep habits.

Placebo is effective to treat insomnia?

In clinical trial, sometime we may found placebo administration significantly decreased subjective sleep latency and increased subjective total sleep time. So is placebo effective to treat insomnia?

Recently, Ogawa et al from Kyoto University in Japan investigate the association between subjective sleep latency  fluctuation and the placebo response. They found higher fluctuation of subjective sleep latency was associated with a greater decrease in subjective sleep latency in placebo treatment. Multivariate analysis suggested that a wider standard deviation for daily subjective sleep latency and a higher weekly mean sSL were independent predictors of greater improvement in mean subjective sleep latency during the subsequent weeks of placebo treatment. Likewise, a wider standard deviation and lower mean of subjective total sleep time were independent predictors of greater improvement in mean subjective total sleep time  in the subsequent weeks.

So, placebo is effective to treat the insomniac with high fluctuation of subjective sleep latency and total sleep time.

cognitive-behaviour therapy for behavioural insomnia of school-aged children.

Chronic sleep problems can lead to the development of behavioural insomnia of Childhood - a sleep disorder involving problematic sleep-onset associations (i.e., parental presence), and resulting in impairments for children and family members.

Recently, Paine et al from Flinders University in Australia perform a controlled evaluation of cognitive-behaviour therapy (CBT) for behavioural insomnia. 42 children (M = 9.3 ± 1.9 yrs, range 7-13 yrs, 18f, 24m) were randomised to CBT (N = 21) or waitlist control (N = 21). CBT consisted of 6 sessions, and combined behavioural sleep medicine techniques (e.g., sleep restriction) with anxiety treatment techniques (e.g., cognitive restructuring). Compared to waitlist controls, children receiving CBT showed significant improvements in sleep latency, wake after sleep onset, and sleep efficiency (all p ≤ .003), but not total sleep time (p > .05). CBT was also associated with a reduction in problematic sleep associations (p ≤ .001), child-reported total and separation anxiety (both p ≤ .01), with all gains being maintained 6 months post-treatment.

This is the first controlled study to demonstrate that multi-component CBT can be effective for the sleep, insomnia, and anxiety symptoms of Behavioural Insomnia of Childhood in school-aged children.

Melatonin receptor agonists are new options for insomnia

The circadian nature of melatonin secretion, coupled with the localization of melatonin receptors to the suprachiasmatic nucleus, has led to numerous studies of the role of melatonin in modulation of the sleep-wake cycle and circadian rhythms in humans. Although much more needs to be understood about the various functions exerted by melatonin and its mechanisms of action, three therapeutic agents (ramelteon, prolonged-release melatonin, and agomelatine) are already in use, and melatonin receptor agonists are now appearing as new promising treatment options for sleep and circadian-rhythm related disorders.

Recently, Spadoni et al reviewed the medicinal chemistry strategies leading to MLT receptor agonists, and the evidence supporting therapeutic efficacy of compounds undergoing clinical evaluation.

A wide range of clinical trials demonstrated that ramelteon, prolonged-release melatonin and tasimelteon have sleep-promoting effects, providing an important treatment option for insomnia and transient insomnia, even if the improvements of sleep maintenance appear moderate.

Despite a large number of high affinity nonselective melatonin receptor agonists, only limited data on MT(1) or MT(2) subtype-selective compounds are available up to now. Administration of the MT(2)-selective agonist IIK7 to rats has proved to decrease NREM sleep onset latency, suggesting that MT(2) receptor subtype is involved in the acute sleep-promoting action of melatonin; rigorous clinical studies are needed to demonstrate this hypothesis. Further clinical candidates based on selective activation of MT(1) or MT(2) receptors are expected in coming years.