Sleep Prevention Research Articles

Evaluation of the Prevalence of Sleep Disorder Among Patients with Type 2 Diabetes Mellitus Referring to Ghaem Hospital from 2016 to 2017.

Diabetes is the most common metabolic disease in primary health care. The prevalence and severity of diabetes can be influenced through lifestyle modification. This study was aimed to identify the prevalence of sleep disorders as a modifiable lifestyle factor among diabetic patients. This cross-sectional study was conducted on 190 patients with type 2 diabetes mellitus who referred to the Internal Medicine Clinic of the Ghaem Hospital, Mashhad, Iran from 2016 to 2017. A demographic questionnaire and the Pittsburgh Sleep Quality Assessment questionnaire (with sleep disorder defined as scores higher than 5) was filled for each subject. Blood tests including haemoglobin A1 C (Hb A1C), fasting blood sugar (FBS) and 2 hour post prandial glucose as well as the assessment of blood pressure and body mass index (BMI) were performed for all patients. Data were analysed using the statistical package for social sciences (SPSS) version 16. Age of the patients (with male to female ratio being 71/119s) was 56.31 ± 7.37 years. BMI of more than 25 kg/m2was observed in 145 (76.3%) of patients. Mean Pittsburgh Sleep Quality Assessment score was 7.48 ± 4.11. Fifty-one (26.8%) patients were good sleepers and 139 (73.2%) were poor sleepers. There was a significant relationship between sleep disorder and age (p=0.019) and female gender (p=0.017), but no other variables which included level of education, occupation, HbA1 C, FBS, 2-hour post prandial glucose, systolic and diastolic blood pressure. Sleep disorders are common among type 2 diabetic patients especially women. It is recommended that sleep disorders should be screened in diabetic patients. Treatment and prevention of sleep disorders through sleep hygiene education including recommendation to have normal nocturnal sleep should be focused by practitioners in type 2 diabetic patients, especially women. Appropriate measures should be taken to manage sleep disorders by weight control in this population.

Sleep deprivation decreases neuronal excitability and responsiveness in rats both in vivo and ex vivo

Sleep deprivation has severe consequences for higher nervous functions. Its effects on neuronal excitability may be one of the most important factors underlying functional deterioration caused by sleep loss. In the present work, excitability changes were studied using two complementary in vivo and ex vivo models. Auditory evoked potentials were recorded from freely-moving animals in vivo. Amplitude of evoked responses showed a near-continuous decrease during deprivation. Prevention of sleep also reduced synaptic efficacy ex vivo, measured from brain slices derived from rats that underwent sleep deprivation. While seizure susceptibility was not affected significantly by sleep deprivation in these preparations, the pattern of spontaneous seizure activity was altered. If seizures developed, they lasted longer and tended to contain more spikes in slices obtained from sleep-deprived than from control rats. Current-source density analysis revealed that location and sequence of activation of local cortical networks recruited by seizures did not change by sleep deprivation. Moderate differences seen in the amplitude of individual sinks and sources might be explained by smaller net transmembrane currents as a consequence of decreased excitability. These findings contradict the widely accepted conception of synaptic homeostasis suggesting gradual increase of excitability during wakefulness. Our results also indicate that decreased neuronal excitability caused by sleep deprivation is preserved in slices prepared from rats immediately after deprivation. This observation might mean new opportunities to explore the effects of sleep deprivation in ex vivo preparations that allow a wider range of experimental manipulations and more sophisticated methods of analysis than in vivo preparations.

Sleep-associated fall in glucose disposal and hepatic glucose output in normal humans. Putative signaling mechanism linking peripheral and hepatic events.

Values reported for basal hepatic glucose production and glucose utilization do not reflect metabolic changes occurring during sleep. To determine the effect of sleep with its associated lowered metabolic rate and thermogenesis on glucose kinetics and gluconeogenic substrate availability, 11 normal volunteers underwent an overnight study in which [3-3H]glucose was infused. Despite decreased insulin secretion, a fall in hepatic glucose output was observed with sleep that was synchronous with a reduction in glucose utilization and lipolysis (decreased plasma glycerol and free fatty acids). When activity was increased, these parameters rose toward previously reported basal levels. Prevention of sleep in 6 additional subjects attenuated the fall in glucose utilization and production as well as the fall in glycerol and free fatty acids despite similar insulin and counterregulatory hormone profiles. We suggest that sleep-associated metabolic changes produce a peripheral signal(s) that modulates hepatic glucose production in humans.

Attempts to modify the sleep patterns of the rat

Attempts were made to modify the sleep patterns of rats by three extensive behavior control procedures: restriction of activity from weaning for three months; prevention of sleep during a set six hr period per day by water wheel enforced movement for 30 days; shock contingently associated with the onset of sleep during a set and well cued six hr period per day for ten days. Little or no modification of any enduring character was found when compared with control conditions. The data suggest a strong inherent control of the sleep response in the rat.