Nonpsychologically distressed, normally sleeping, obese men had low cortisol secretion. The cortisol secretion was slightly activated by SA and returned to low by CPAP use. The low cortisol secretion in obesity through its inferred hyposecretion of hypothalamic CRH might predispose the obese to sleep apnea.

Sleep loss has been associated with increased sleepiness, decreased performance, elevations in inflammatory cytokines, and insulin resistance. Daytime napping has been promoted as a countermeasure to sleep loss. To assess the effects of a 2-h midafternoon nap following a night of sleep loss on postnap sleepiness, performance, cortisol, and IL-6, 41 young healthy individuals (20 men, 21 women) participated in a 7-day sleep deprivation experiment (4 consecutive nights followed by a night of sleep loss and 2 recovery nights). One-half of the subjects were randomly assigned to take a midafternoon nap (1400-1600) the day following the night of total sleep loss. Serial 24-h blood sampling, multiple sleep latency test (MSLT), subjective levels of sleepiness, and psychomotor vigilance task (PVT) were completed on the fourth (predeprivation) and sixth days (postdeprivation). During the nap, subjects had a significant drop in cortisol and IL-6 levels (P < 0.05). After the nap they experienced significantly less sleepiness (MSLT and subjective, P < 0.05) and a smaller improvement on the PVT (P < 0.1). At that time, they had a significant transient increase in their cortisol levels (P < 0.05). In contrast, the levels of IL-6 tended to remain decreased for approximately 8 h (P = 0.1). We conclude that a 2-h midafternoon nap improves alertness, and to a lesser degree performance, and reverses the effects of one night of sleep loss on cortisol and IL-6. The redistribution of cortisol secretion and the prolonged suppression of IL-6 secretion are beneficial, as they improve alertness and performance.

E xcessive daytime sleepiness (EDS) is very common in modern societies. In the general population, the prevalence of EDS is estimated to range between 5% and 20%. [1][2][3][4][5][6][7][8][9] EDS and fatigue are the most common complaints of patients referred to the sleep disorders clinic. 10,11 Moreover, they are potential risk factors for cardiovascular disease and mortality, 12,13 are associated with a negative perception of general health and quality of life, 14,15 and raise major public safety concerns. 16 EDS is commonly assumed to be primarily the result of disturbed or inadequate sleep. Sleep deprivation and sleep apnea are known predictors of EDS. However, in previous studies, the association between EDS and sleep apnea has been found to be significant but rather modest. Two large studies in general population samples demonstrated that, among patients with sleep apnea, approximately 20% to 40% reported EDS. 17,18 On the other hand, it has been found that conditions highly comorbid with sleep apnea, such as obesity, are associated with EDS independent of sleep apnea. [19][20][21] Furthermore, large population-based epidemiologic studies have shown that the presence of EDS is strongly associated with depression, obesity, and diabetes. [7][8][9] More recently, physical activity has been suggested as a novel significant factor for sleepiness in the general population after controlling for body mass index (BMI), apnea, age, and other covariates. 8,9 Studies in sleep apneics have found that sleep fragmentation, nocturnal hypoxemia, depression, and age are independent predictors of daytime sleepiness in this group. [22][23][24][25] However, to our knowledge, no studies have investigated the effect of exercise on daytime sleepiness in patients with sleep apnea.The aim of this study was to determine the association between EDS and lack of regular exercise quantified by a standardized questionnaire, as well as depression and severity of apnea, in a large clinical sample of patients with sleep apnea.

Objectives: The aim of our study was to examine the association between ABCB1 polymorphisms G2677T/A (rs2032582) and C3435T (rs1045642) and common CYP2D6 variants, with the response to antipsychotic treatment of psychotic patients, in a naturalistic setting, in Greece.Methods: One hundred patients suffering from schizophrenia and other psychotic disorders were included in the study. Dosages were normalized to chlorpromazine equivalents. Response following 1 month of treatment was assessed as either a continuous variable, using the distribution of the corrected Positive and Negative Syndrome Scale percent change, or as a dichotomous variable defined as the number of patients scoring ≥30% from the corrected baseline Positive and Negative Syndrome Scale score. Genotyping was achieved with established polymerase chain reaction-restriction fragment length polymorphism methods.Results: With response treated as a continuous variable, the homozygous recessive rs2032582 genotypes (TT) who were simultaneously carriers of a loss-of-function CYP2D6 allele (*4 or *5) responded significantly worse than the rest of the patients. Comparison of genotype frequencies revealed a statistically significant association of the above combination. No significant association between chlorpromazine equivalents and the tested genotypes was detected. Conclusion:We have detected a possible interaction between ABCB1 and CYP2D6 in affecting response of psychotic patients to drug treatment, in a naturalistic setting.