Sustained polyphasic sleep restriction abolishes human growth hormone release.

STUDY OBJECTIVES: Voluntary sleep restriction is a common phenomenon in industrialized societies aiming to increase time spent awake and thus productivity. We explored how restricting sleep to a radically polyphasic schedule affects neural, cognitive, and endocrine characteristics. METHODS: Ten young healthy participants were restricted to one 20-minute nap opportunity at the end of every 4 hours (i.e. six sleep episodes per 24 hours) without any extended core sleep window, which resulted in a cumulative sleep amount of just 2 hours per day (i.e. ~20 minutes per bout). RESULTS: All but one participant terminated this schedule during the first month. The remaining participant (a 25-year-old male) succeeded in adhering to a polyphasic schedule for five out of the eight planned weeks. Cognitive and psychiatric measures showed modest changes during polyphasic as compared to monophasic sleep, while in-blood cortisol or melatonin release patterns and amounts were apparently unaltered. In contrast, growth hormone release was almost entirely abolished (>95% decrease), with the residual release showing a considerably changed polyphasic secretional pattern. CONCLUSIONS: Even though the study was initiated by volunteers with exceptional intrinsic motivation and commitment, none of them could tolerate the intended 8 weeks of the polyphasic schedule. Considering the decreased vigilance, abolished growth hormone release, and neurophysiological sleep changes observed, it is doubtful that radically polyphasic sleep schedules can subserve the different functions of sleep to a sufficient degree.

The BclI polymorphism of the glucocorticoid receptor gene is associated with emotional memory performance in healthy individuals.

Glucocorticoids, stress hormones released from the adrenal cortex, are important players in the regulation of emotional memory. Specifically, in animals and in humans, glucocorticoids enhance memory consolidation of emotionally arousing experiences, but impair memory retrieval. These glucocorticoid actions are partly mediated by glucocorticoid receptors in the hippocampus, amygdala and prefrontal cortex, key brain regions for emotional memory. In a recent study in patients who underwent cardiac surgery, the BclI polymorphism of the glucocorticoid receptor gene (NR3C1) was associated with traumatic memories and posttraumatic stress disorder symptoms after intensive care therapy. Based on this finding, we investigated if the BclI polymorphism is also associated with emotional memory in healthy young subjects (N=841). We used a picture-learning task consisting of learning and recalling neutral and emotional photographs on two consecutive days. The BclI variant was associated with short-delay recall of emotional pictures on both days, with GG carriers showing increased emotional memory performance as compared to GC and CC carriers. We did not detect a genotype-dependent difference in recall performance for neutral pictures. These findings suggest that the Bcll polymorphism contributes to inter-individual differences in emotional memory also in healthy humans.

A 3-day estrogen treatment improves prefrontal cortex-dependent cognitive function in postmenopausal women.

Estrogen secretion in young women follows a cyclic pattern characterized by a pronounced surge in estrogen around ovulation. The way in which this estrogen peak affects cognitive functioning is unclear. Short-term estrogen treatment for a few days mimicking normal pre-menopausal estrogen dynamics substantially enhanced cognitive functions in ovariectomized animals. Here, we provide evidence that inducing a single estrogen peak in postmenopausal women improves their cognitive abilities. Healthy women (51-64 yrs, n=14) received either 100 microg estrogen transdermally for 3 days or placebo in a double-blind within-subject design. The treatment caused a temporary rise in serum estrogen levels roughly comparable to the mid-cyclic changes in estrogen in young women. At the end of the treatment, the women completed two types of tests involving primarily hippocampus-dependent functions of memory retention or prefrontal cortex-dependent functions. Results revealed a clear beneficial effect of estrogen on tasks mainly involving the prefrontal cortex: performance on a digit-ordering task (p<0.05) and on a task requiring short-term memory of event sequences in an unfamiliar story (p<0.01) were improved, and susceptibility to interference in the Stroop test (p<0.05) was diminished after estrogen. On the other hand, estrogen did not affect hippocampus-dependent retention of a story, with delayed recall tested after 30 min or 1 week, although immediate recall was improved by estrogen. We conclude that in postmenopausal women, a transient increase in plasma estrogen concentration acutely improves prefrontal cortex-dependent cognitive functions, whereas hippocampus-dependent memory retention is less affected. Our results encourage future studies to investigate whether repeated induction of short-lasting estrogen peaks could enhance cognitive efficacy of hormonal replacement therapy.