Introduction: Sleep is critical to human physiological function, cognitive performance, and emotional regulation. Healthcare personnel, especially physicians, are chronically exposed to long working hours, which are o...Introduction: Sleep is critical to human physiological function, cognitive performance, and emotional regulation. Healthcare personnel, especially physicians, are chronically exposed to long working hours, which are often accompanied by decreased sleep time. Clinical evidence indicates that these conditions affect their cognitive function and professional practice, but researchers in the field have not sufficiently explored the possible effects of reductions in sleep time on social cognition. Objective: The aim of this is to further explore the effects of sleep restriction among medical residents, the specific impairments in social cognition that it produces, and the effects of a sleep hygiene orientation on those impairments. Method: There were 124 medical residents (50 males, 74 females) who completed a daily sleep/work log, a battery of sleep tests/questionnaires, and neuropsychological evaluations. The participants then received a short course (8 hours) on basic concepts of sleep hygiene and sleep psychoeducation. Once the course was completed, participants filled out the questionnaires again. Results: The results indicate that sleep disturbances in medical residents were associated with severe neurocognitive and social cognition impairments. After the sleep hygiene intervention, neuropsychological function and sleep parameters improved, awareness increased, and social cognition performance significantly improved. Conclusion: Using sleep psychoeducation and sleep hygiene intervention in medical residents is a simple strategy to mitigate the effects of sleep restriction.展开更多
Plasma testosterone levels display circadian variation, peaking during sleep, and reaching a nadir in the late afternoon, with a superimposed ultradian rhythm with pulses every 90 min reflecting the underlying rhythm ...Plasma testosterone levels display circadian variation, peaking during sleep, and reaching a nadir in the late afternoon, with a superimposed ultradian rhythm with pulses every 90 min reflecting the underlying rhythm of pulsatile luteinizing hormone （LH） secretion. The increase in testosterone is sleep, rather than circadian rhythm, dependent and requires at least 3h of sleep with a normal architecture. Various disorders of sleep including abnormalities of sleep quality, duration, circadian rhythm disruption, and sleep-disordered breathing may result in a reduction in testosterone levels. The evidence, to support a direct effect of sleep restriction or circadian rhythm disruption on testosterone independent of an effect on sex hormone binding globulin （SHBG）, or the presence of comorbid conditions, is equivocal and on balance seems tenuous. Obstructive sleep apnea （OSA） appears to have no direct effect on testosterone, after adjusting for age and obesity. However, a possible indirect causal process may exist mediated by the effect of OSA on obesity. Treatment of moderate to severe OSA with continuous positive airway pressure （CPAP） does not reliably increase testosterone levels in most studies. In contrast, a reduction in weight does so predictably and linearly in proportion to the amount of weight lost. Apart from a very transient deleterious effect, testosterone treatment does not adversely affect OSA. The data on the effect of sleep quality on testosterone may depend on whether testosterone is given as replacement, in supratherapeutic doses, or in the context abuse. Experimental data suggest that testosterone may modulate individual vulnerability to subjective symptoms of sleep restriction. Low testosterone may affect overall sleep quality which is improved by replacement doses. Large doses of exogenous testosterone and anabolic/androgenic steroid abuse are associated with abnormalities of sleep duration and architecture.展开更多
文摘Introduction: Sleep is critical to human physiological function, cognitive performance, and emotional regulation. Healthcare personnel, especially physicians, are chronically exposed to long working hours, which are often accompanied by decreased sleep time. Clinical evidence indicates that these conditions affect their cognitive function and professional practice, but researchers in the field have not sufficiently explored the possible effects of reductions in sleep time on social cognition. Objective: The aim of this is to further explore the effects of sleep restriction among medical residents, the specific impairments in social cognition that it produces, and the effects of a sleep hygiene orientation on those impairments. Method: There were 124 medical residents (50 males, 74 females) who completed a daily sleep/work log, a battery of sleep tests/questionnaires, and neuropsychological evaluations. The participants then received a short course (8 hours) on basic concepts of sleep hygiene and sleep psychoeducation. Once the course was completed, participants filled out the questionnaires again. Results: The results indicate that sleep disturbances in medical residents were associated with severe neurocognitive and social cognition impairments. After the sleep hygiene intervention, neuropsychological function and sleep parameters improved, awareness increased, and social cognition performance significantly improved. Conclusion: Using sleep psychoeducation and sleep hygiene intervention in medical residents is a simple strategy to mitigate the effects of sleep restriction.
文摘Plasma testosterone levels display circadian variation, peaking during sleep, and reaching a nadir in the late afternoon, with a superimposed ultradian rhythm with pulses every 90 min reflecting the underlying rhythm of pulsatile luteinizing hormone （LH） secretion. The increase in testosterone is sleep, rather than circadian rhythm, dependent and requires at least 3h of sleep with a normal architecture. Various disorders of sleep including abnormalities of sleep quality, duration, circadian rhythm disruption, and sleep-disordered breathing may result in a reduction in testosterone levels. The evidence, to support a direct effect of sleep restriction or circadian rhythm disruption on testosterone independent of an effect on sex hormone binding globulin （SHBG）, or the presence of comorbid conditions, is equivocal and on balance seems tenuous. Obstructive sleep apnea （OSA） appears to have no direct effect on testosterone, after adjusting for age and obesity. However, a possible indirect causal process may exist mediated by the effect of OSA on obesity. Treatment of moderate to severe OSA with continuous positive airway pressure （CPAP） does not reliably increase testosterone levels in most studies. In contrast, a reduction in weight does so predictably and linearly in proportion to the amount of weight lost. Apart from a very transient deleterious effect, testosterone treatment does not adversely affect OSA. The data on the effect of sleep quality on testosterone may depend on whether testosterone is given as replacement, in supratherapeutic doses, or in the context abuse. Experimental data suggest that testosterone may modulate individual vulnerability to subjective symptoms of sleep restriction. Low testosterone may affect overall sleep quality which is improved by replacement doses. Large doses of exogenous testosterone and anabolic/androgenic steroid abuse are associated with abnormalities of sleep duration and architecture.
