Increase In Total Sleep Research Articles

Infant growth and tolerance with a formula based on novel native demineralized whey: A randomized double-blind pilot study.

The aim of the study was to evaluate the effects on infant growth and tolerance of a Test infant formula based on a novel whey extraction and demineralization process, compared to a Standard formula and a breastfed reference arm. Healthy term infants (n = 61) aged up to 21 days were randomized to Test or Control formula. A breastfed group (n = 39) served as a reference. Growth, tolerance, adverse events, and sleep were evaluated every month until 6 months of age. Plasma amino-acid concentrations at 3 months of age were measured in a subgroup population. Growth curves of all infants globally agreed with World Health Organization standards across the 6-month period study. Regarding tolerance, no difference between the formula-fed groups was observed on daily number of crying episodes, intensity or time to onset of regurgitations, and stool frequency or consistency, except at 5 months with infants in the Control group having more watery stools. Plasma concentration of some amino acids differed between the groups, especially tryptophan concentration which was higher in infants fed with the Test formula. In parallel, total sleep duration was longer in these infants at 2, 3, and 5 months of age, corresponding to an increase in daytime sleep. Test formula supported an adequate infant growth from birth to 6 months of age and was well-tolerated by all infants. An increase in total sleep at several months was also observed with the Test formula.

Infant sleep and anxiety disorders in early childhood: Findings from an Australian pregnancy cohort study

AbstractEmphasis on continuous infant sleep overnight may be driven by parental concern of risk to child mental health outcomes. The Mercy Pregnancy and Emotional Wellbeing Study (MPEWS) examined whether infant sleep at 6 and 12 months postpartum predicts anxiety disorders at 2–4 years, and whether this is moderated by maternal depression, active physical comforting (APC) or maternal cognitions about infant sleep. Data included 349 women and infants. Infant sleep was measured using the Brief Infant Sleep Questionnaire and child anxiety disorders by the Preschool Age Psychiatric Assessment. The risk of developing generalised anxiety or social phobia disorders at 3–4 years was reduced by 42% (p = 0.001) and 31% (p = 0.001), respectively, for a one standard deviation increase in total sleep at 12 months. No other infant sleep outcomes were associated. Maternal depression, APC and cognitions about infant sleep did not significantly moderate these relationships. Focus may need to be on total infant sleep, rather than when sleep is achieved.Highlights To assess whether infant sleep outcomes (i.e., frequency of nocturnal wakes; nocturnal wakefulness and total sleep per day) at 6 and 12 months predict early childhood anxiety disorders at 3–4 years of age. Maternally reported infant sleep outcomes were not associated with the risk of developing early childhood anxiety disorders at 3–4 years. It may be total infant sleep, irrespective of when sleep occurs or night waking and, independently, active physical comforting that requires further investigation.

Mutation of the Drosophila melanogaster serotonin transporter dSERT impacts sleep, courtship, and feeding behaviors.

The Serotonin Transporter (SERT) regulates extracellular serotonin levels and is the target of most current drugs used to treat depression. The mechanisms by which inhibition of SERT activity influences behavior are poorly understood. To address this question in the model organism Drosophila melanogaster, we developed new loss of function mutations in Drosophila SERT (dSERT). Previous studies in both flies and mammals have implicated serotonin as an important neuromodulator of sleep, and our newly generated dSERT mutants show an increase in total sleep and altered sleep architecture that is mimicked by feeding the SSRI citalopram. Differences in daytime versus nighttime sleep architecture as well as genetic rescue experiments unexpectedly suggest that distinct serotonergic circuits may modulate daytime versus nighttime sleep. dSERT mutants also show defects in copulation and food intake, akin to the clinical side effects of SSRIs and consistent with the pleomorphic influence of serotonin on the behavior of D. melanogaster. Starvation did not overcome the sleep drive in the mutants and in male dSERT mutants, the drive to mate also failed to overcome sleep drive. dSERT may be used to further explore the mechanisms by which serotonin regulates sleep and its interplay with other complex behaviors.

Book Review: Schizophrenia, Sleep, and Acupuncture

Peggy Bosch, Maurits van den Noort. 348 pages Hogrefe & Huber Publishers 2008 Hardcover, £31.00 978-0-88937-355-8 Schizophrenia is a complicated mental illness, which I feel is best left to the psychiatrists. Patients hate the side effects of medication. I don’t treat patients with schizophrenia with acupuncture: would this book change my mind? A large collection of international experts have been drawn together to give their views on the diagnosis and medical treatment of the condition with a dedicated chapter on neuroimaging, which concludes only that schizophrenia is associated with frontal and temporal brain dysfunction. One quarter of the book is taken up with scientific discussion of the disease, which is covered well, but you have to ask yourself whether you would prefer to read this in a conventional medical textbook rather than a book on acupuncture. The next two chapters look at sleep disturbance because “insomnia is associated with almost all psychiatric disorders” and a poor quality of life. An increase in total sleep with anti-psychotic medication, with an increase in REM (rapid eye movement) sleep …

Sleep-inducing effects of adenosine microinjections into the medial preoptic area are blocked by flumazenil

Microinjection of a wide range of sedative agents, including triazolam, pentobarbital, ethanol and adenosine, into the medial preoptic area has been shown to increase sleep, suggesting that it is an important (though not necessarily the only) anatomic site mediating hypnotic effects of these compounds. The mechanism by which adenosine increases sleep at this site is not clear, but one possibility is that this is related to its effects on the GABA A-benzodiazepine receptor complex. In order to assess this possibility, this paper describes the administration of adenosine, alone and in combination with the benzodiazepine receptor blocker flumazenil, into the MPA. It was found that 12.5 and 25 nM of adenosine significantly reduced sleep latency and increased total sleep time. The sleep-inducing effect was blocked by flumazenil. Flumazenil caused a modest increase in total sleep, and prevented the increase in total sleep induced by the higher dose of adenosine. These data suggest that at least one aspect of the hypnotic properties of adenosine is mediated by a direct or indirect action on the GABA A-benzodiazepine receptor complex.

The effects of delta-sleep-inducing peptide (DSIP) on wakefulness and sleep patterns in the cat

The effect of a single injection of synthetic delta-sleep-inducing peptide (DSIP, 7 nmol/kg) into the lateral ventricle of 10 cats was investigated by monitoring the sleep-wake cycle during an 8 h period. A significant decrease in sleep latency and a significant increase in total sleep and in total slow wave sleep (SWS) was found following DSIP administration. The increase in sleep resulted exclusively from a significant increase in deep slow wave sleep (S 2), while light slow wave sleep (S 1) was significantly decreased. Neither the total amount of REM sleep, nor hourly values of REM sleep were affected by DSIP application. Additional measures of REM sleep, like REM sleep latency, mean episode number and mean episode length were not different from those found in control conditions. DSIP was immediately effective since the amount of S 2 increased to more than 50% in the first postinjection hour and the difference from the control value was highly significant. The increase in S 2 was maintained over 7 h, and disappeared by the eighth hour. The increase in S 2 was caused by a prolongation of S 2 episodes and not by their more frequent occurrence. The results obtained suggest a sleep-facilitating property of DSIP.

The effect of sleep deprivation on sleep in rats with suprachiasmatic lesions

The effect of 24-h sleep deprivation on sleep was investigated in rats whose circadian rest-activity rhythms were extensively disrupted by bilateral lesions of the suprachiasmatic nuclei (SCN). Sleep deprivation caused an increase in total sleep, REM sleep and the slow wave sleep fraction of non-REM sleep. It is concluded that the homeostatic component of sleep regulation is morphologically and functionally distinct from the circadian component.

The delta-sleep inducing peptide (DSIP) increases duration of sleep in rats

The synthetic delta-sleep-inducing nonapeptide (DSIP) was injected intravenously to free-moving rats (30, 40 and 80 nmol/kg). In EEG tests combined with electro-oculography (EOG) and electromyography (EMG), a significant increase in total sleep, chiefly slow wave (NREM) sleep, occurred 1–4.5 h after injection.

Effects of loxapine on the sleep of chronic schizophrenics

The sleep patterns of four male chronic schizophrenic patients were monitored throughout the various phases of a 1-year therapeutic trial with loxapine succinate, a newly developed neuroleptic. Compared with the initial drug-free baseline, the early drug period was characterized by an increase in REM percentage, REM density, and REM activity. During the drug maintenance period, the increase in REM phasic events was accompanied by an increase in total sleep. Severe insomnia was noted during the initial period of drug withdrawal. The absence of time lag between changes in drug administration schedule and the associated alterations in sleep patterns was in contrast with the time latency of the therapeutic response. This neuroleptic on sleep and on psychopathology are mediated by different mechanisms.

Effects of five to seven days of sleep deprivation produced by electrical stimulation of the midbrain reticular formation

Most methods of sleep deprivation either induce stress or fail to totally eliminate sleep. In this study, sleep deprivation was produced by electrical stimulation of the midbrain reticular formation. Seven cats were prepared for chronic recordings: Four animals received continuous stimulation, and five were stimulated intermittently. Electrographic data were collected continuously during 5–7 days of stimulation and for 48 hr thereafter. Behavioral and electrographic correlates of sleep were abolished by both methods of stimulation for 3 days. Although stimulation continued, behavioral signs of sleep appeared along with electrographic evidence of brief epochs of slow-wave sleep. Maintenance of wakefulness beyond 3 days became increasingly difficult and required frequent changes in the stimulus values. After the cessation of stimulation, there was a significant increase in total sleep in both groups for 48 hr, primarily at the expense of the drowsy state. The termination of continuous stimulation resulted in an initial rebound in slow-wave sleep and a later rebound in rapid eye movement (REM) sleep. The cessation of intermittent stimulation resulted in a large REM sleep rebound followed by a modest rebound in slow-wave sleep. These results, corroborated by data from previous studies, show that total sleep deprivation is attained by continuous stimulation; whereas REM deprivation is the main effect of intermittent stimulation.