There is growing interest in examining dark personality traits, to better explain malevolent and self-serving behaviour patterns commonly observed in clinical and non-clinical settings. Recently, taxonomies of dark personalities have been developed, along with psychometric tools to measure and delineate between traits including psychopathy, Machiavellianism and narcissism. The extent to which these constructs are distinct or overlapping remains controversial. Psychophysiological research can improve understanding of biological mechanisms contributing to personality that may help to evaluate taxonomies. This study investigated diurnal variations (...) in salivary cortisol (on waking, cortisol awakening response, and at bedtime, over two days) and their relationship to personality traits (Short Dark Triad Scale and IPIP Mini), psychopathology (Depression, Anxiety and Stress Scale; DASS) and quality of life (WHOQOL-BREF) in a non-clinical sample (N=45, 26 females, 19 males, 18-59 years). Dark personality traits correlated with low bedtime cortisol, reduced sleep, depression and poorer quality of life. Hierarchical linear regressions analyses indicated that bedtime cortisol levels significantly accounted for variance in Psychopathy (F(1,39)=5.55, p=.02, R=.52, B=-1.81, 95% CI [-3.37-(-.26)], β=-.33, sr2=.10) and reduced sleep uniquely accounted for variance Machiavellianism (F(2,40)=5.99, p=.01, R=.48, B=1.01, 95% CI [.16-2.02], β=.34, sr2=.11). These data provide preliminary evidence that supports the cortisol hypoarousal hypothesis of Psychopathy and has identified a link between Machiavellianism, sleep-wake cycles, and chronotype. The hypoarousal hypothesis of Psychopathy contends that the hypothalamic-pituitary-adrenal axis is unresponsive to the stress of social engagement. Machiavellianism was predicted by longer days with evidence for an evening chronotype. These findings indicated that the Dark Triad traits have different underlying biological mechanisms that require further exploration. (shrink)

Sleep disturbances are common for children with attention-deficit/hyperactivity disorder (ADHD) and are of great clinical significance. Brain dopamine plays an important role for both ADHD symptoms and sleep-wake regulation. We therefore suggest that one basic aspect of integrative brain-behavior relationship such as the sleep-wake cycle may certainly be addressed in a dynamic developmental theory of ADHD.

This paper deals with new pharmacological and technological developments in the manipulation and curtailment of our sleep needs. While humans have used various methods throughout history to lengthen diurnal wakefulness, recent advances have been achieved in manipulating the architecture of the brain states involved in sleep. The progress suggests that we will gradually become able to drastically manipulate our natural sleep-wake cycle. Our goal here is to promote discussion on the desirability and acceptability of enhancing (...) our control over biological sleep, by illustrating various potential attendant ethical problems. We draw attention to the risks involved, possible conflicts of interests underlying the development of wake enhancement, and the potential impact on accountability for fatigue related errors. (shrink)

Consciousness can be studied only if subjective experience is documented and quantified, yet first-person accounts of the effects of brain injury on conscious experience are as rare as they are potentially useful. This report documents the alterations in waking, sleeping, and dreaming caused by a lateral medullary infarct. Total insomnia and the initial suppression of dreaming was followed by the gradual recovery of both functions. A visual hallucinosis during waking that was associated with the initial period of sleep and (...) dream suppression is described in detail. Since the changes in sleep and their recovery are comparable to results of animal experiments, it can be concluded that damage to the medullary brain stem causes extreme but short-lived alterations in conscious state and that substantial recovery occurs even though the damage to the brain stem endures. (shrink)

Unlike other organs that operate continuously, such as the heart and kidneys, many of the operations of the nervous system shut down during sleep. The evolutionarily conserved unconscious state of sleep that puts animals at risk from predators indicates that it is an indispensable integral part of systems operation. A reasonable expectation is that any hypothesis for the mechanism of the nervous system functions should be able to provide an explanation for sleep. In this regard, the semblance (...) hypothesis is examined. Postsynaptic membranes are continuously being depolarized by the quantally released neurotransmitter molecules arriving from their presynaptic terminals. In this context, an incidental lateral activation of the postsynaptic membrane is expected to induce a semblance (cellular hallucination of arrival of activity from its presynaptic terminal, which forms a unit for internal sensation) of the arrival of activity from its presynaptic terminal as a systems property. This restricts induction of semblance to a context of a very high ratio of the duration of the default state of neurotransmitter-induced postsynaptic depolarization to the total duration of incidental lateral activations of the postsynaptic membrane. This requirement spans within a time-bin of a few sleep-wake cycles. Since the duration of quantal release remains maximized, the above requirement can be achieved only by ceiling the total duration of incidental lateral activations of the postsynaptic membrane, which necessitates a state of sleep. (shrink)

Sleep is a fundamental property conserved across species. The homeostatic induction of sleep indicates the presence of a mechanism that is progressively activated by the awake state and that induces sleep. Several lines of evidence support that such function, namely, sleep need, lies in the neuronal assemblies rather than specific brain regions and circuits. However, the molecular mechanism underlying the dynamics of sleep need is still unclear. This review aims to summarize recent studies mainly in (...) rodents indicating that protein phosphorylation, especially at the synapses, could be the molecular entity associated with sleep need. Genetic studies in rodents have identified a set of kinases that promote sleep. The activity of sleep-promoting kinases appears to be elevated during the awake phase and in sleep deprivation. Furthermore, the proteomic analysis demonstrated that the phosphorylation status of synaptic protein is controlled by the sleep-wake cycle. Therefore, a plausible scenario may be that the awake-dependent activation of kinases modifies the phosphorylation status of synaptic proteins to promote sleep. We also discuss the possible importance of multisite phosphorylation on macromolecular protein complexes to achieve the slow dynamics and physiological functions of sleep in mammals. (shrink)

A new working hypothesis of sleep-wake cycle mechanisms is proposed, based on ontogeny and functional/anatomic compression of two stochastic neuronal models of information coding that complement each other in a key/lock fashion: the axonal arbor patterns (AAP – “hardware”) and the neuronal spike interval inequality patterns (SIIP – “software”). [Hobson et al.; Nielsen; Revonsuo; Solms; Vertes & Eastman].

Although we are beginning to understand the neuronal and biochemical nature of sleep regulation, questions remain about how sleep is homeostatically regulated. Beyond its importance in basic physiology, understanding sleep may also shed light on psychiatric and neurodevelopmental disorders. Recent genetic studies in mammals revealed several non-secretory proteins that determine sleep duration. Interestingly, genes identified in these studies are closely related to psychiatric and neurodevelopmental disorders, suggesting that the sleep-wake cycle shares some common (...) mechanisms with these disorders. Here we review recent sleep studies, including reverse and forward genetic studies, from the perspectives of sleep duration and homeostasis. We then introduce a recent hypothesis for mammalian sleep in which the fast and slow Ca2+-dependent hyperpolarization pathways are pivotal in generating the SWS firing pattern and regulating sleep homeostasis, respectively. Finally, we propose that these intracellular pathways are potential therapeutic targets for achieving depolarization/hyperpolarization balance in psychiatric and neurodevelopmental disorders. How animals implement sleep homeostasis is a great mystery. Here, we review recent studies with highlighting the hypothesis that the slow Ca2+-dependent hyperpolarization pathway regulates sleep homeostasis via modifying the fast pathway; the activity of CaMKIIα/β increases during wakefulness, which triggers sleep by phosphorylating the components in the fast pathway. (shrink)

Recent longitudinal observations show that human menstrual cycles, sleep‐wake cycles and manic‐depressive cycles can become synchronized with lunar cycles, but do so in uniquely complex and heterogeneous ways that are unlikely to have been detected by past studies. Past studies’ negative results have given rise to a scientific consensus that human biology and behavior are unaffected by lunar cycles. The recent observations show that synchrony can be temporary, and can occur with more than one type of lunar (...) class='Hi'>cycle, more than one phase of a lunar cycle and more than one resonant frequency of a lunar cycle. Given the variability of human responses to lunar cycles, aggregate analyses used in almost all previous studies would likely have cancelled out individuals’ responses and led to false negative results. In light of these observations, the question of lunar influence should be investigated further, with longitudinal observations and case‐by‐case analyses of individuals’ data. (shrink)

Evan’s book is in many ways an exercise in remapping. The first is suggested by the book’s title. Waking, Dreaming, Being challenges existing ways of mapping the conceptual relationship between conscious states across the sleep-wake cycle. The idea that waking and dreaming are not discrete states but can interpenetrate each other—that, to use Evan’s words, they “aren’t opposed but flow into and out of [one] an other” —is a central theme running through the book. If Evan is (...) correct, then the taxonomy of conscious states that underlies large parts of contemporary philosophy of mind and cognitive neuroscience has to be redrawn. As Evan tells us in the introduction, the book’s organizing principle... (shrink)

Consciousness undergoes dramatic and stereotyped changes in parallel with changes in brain state over the sleep‐wake cycle. No change is more striking or more informative than that which differentiates waking and REM sleep dreaming. For example, dreaming is characterized by internally generated perceptions, by false beliefs, by cognitive impairments, by emotional intensification, and by amnesia. When they occur in waking, these formal state features characterize what is called mental illness. Because the underlying changes in brain state (...) are well described, it is possible to create a model which links the formal features of the mental state to changes in brain physiology and chemistry. The resulting synthesis of conscious state phenomenology and brain neurophysiology provides a solid foundation for mind‐body integration in both normal and abnormal conditions. (shrink)

The crying curve across early infancy may reflect the developing interaction between circadian and homeostatic processes of sleep-wake regulation. Excessive crying may be interpreted as a misalignment of the two processes. On the basis of the proposed mechanism, excessive crying may be an honest signal of need, namely, to elicit parental resources to modulate the behavioral state.

Circadian rhythms in the sleep/wake cycle, along with a range of physiological measures, are severely disrupted in individuals with major depressive disorder (MDD). Moreover, several central circadian genes have been implicated as potential genetic factors underlying the illness through candidate gene studies and some genome wide association studies. However, investigations into the molecular underpinnings of circadian disturbances in the human brain have been quite challenging. In their recent publication, Li and colleagues have used a novel approach to (...) determine the rhythmic patterns of circadian gene expression in several regions of the human brain, and how these patterns are disrupted in MDD. Their findings demonstrate that in healthy subjects, several brain regions outside the suprachiasmatic nucleus (the master clock) exhibit diurnal gene expression patterns that are disrupted in the brains of MDD subjects. These findings will provide the foundation for future studies of gene‐specific drug targets, and biomarkers for the disease. (shrink)

AimWhite matter changes in individuals at ultra-high risk for psychosis (UHR) may be involved in the transition to psychosis. Sleep-wake disturbances commonly precede the first psychotic episode and predict development of psychosis. We examined associations between white matter microstructure and sleep-wake disturbances in UHR individuals compared to healthy controls (HC), as well as explored the confounding effect of medication, substance use, and level of psychopathology.MethodsSixty-four UHR individuals and 35 HC underwent clinical interviews and diffusion weighted imaging. (...) Group differences on global and callosal mean fractional anisotropy (FA) was tested using general linear modeling. Sleep-wake disturbances were evaluated using the subjective measures disturbed sleep index (DSI) and disturbed awakening index (AWI) from the Karolinska Sleep Questionnaire, supported by objective sleep measures from one-night actigraphy. The primary analyses comprised partial correlation analyses between global FA/callosal FA and sleep-wake measures. Secondary analyses investigated multivariate patterns of covariance between measures of sleep-wake disturbances and FA in 48 white matter regions of interest using partial least square correlations.ResultsUltra-high risk for psychosis individuals displayed lower global FA (F = 14.56, p < 0.001) and lower callosal FA (F = 11.34, p = 0.001) compared to HC. Subjective sleep-wake disturbances were significantly higher among the UHR individuals (DSI: F = 27.59, p < 0.001, AWI: F = 36.42, p < 0.001). Lower callosal FA was correlated with increased wake after sleep onset (r = −0.34, p = 0.011) and increased sleep fragmentation index (r = −0.31, p = 0.019) in UHR individuals. Multivariate analyses identified a pattern of covariance in regional FA which were associated with DSI and AWI in UHR individuals (p = 0.028), but not in HC. Substance use, sleep medication and antipsychotic medication did not significantly confound these associations. The association with objective sleep-wake measures was sustained when controlling for level of depressive and UHR symptoms, but symptom level confounded the covariation between FA and subjective sleep-wake measures in the multivariate analyses.ConclusionCompromised callosal microstructure in UHR individuals was related to objectively observed disruptions in sleep-wake functioning. Lower FA in ventrally located regions was associated with subjectively measured sleep-wake disturbances and was partly explained by psychopathology. These findings call for further investigation of sleep disturbances as a potential treatment target. (shrink)

Although we are beginning to understand the neurocognitive processes that underlie the emergence of dreaming, what accounts for the bizarre phenomenology of dreams remains debated. I address this question by comparing dreaming with waking mind wandering and challenging previous accounts that utilize bizarreness to mark a sharp divide between conscious experiences in waking and sleeping. Instead, I propose that bizarreness is a common, non-deficient feature of spontaneous offline simulations occurring across the sleep-wake cycle and can be tied (...) to the specific characteristics of spontaneous thought as being dynamic, unconstrained, (hyper)associative and highly variable in content. Rather than misrepresenting waking reality, bizarreness can be employed to investigate the very building blocks of spontaneous cognition. The absence of bizarreness in thought processes is imposed by automatic and deliberate cognitive constraints. By contrast, thought and memory processes operating on their own without such constraints are inherently marked by different degrees and types of bizarreness. (shrink)

It would be unwise to dismiss the possibility of human brain organoids developing sentience. However, scepticism about this idea is appropriate when considering current organoids. It is a point of consensus that a brainstem-dead human is not sentient, and current organoids lack a functioning brainstem. There are nonetheless troubling early warning signs, suggesting organoid research may create forms of sentience in the near future. To err on the side of caution, researchers with very different views about the neural basis of (...) sentience should unite behind the “brainstem rule”: if a neural organoid develops or innervates a functioning brainstem that registers and prioritizes its needs, regulates arousal, and leads to sleep-wake cycles, then it is a sentience candidate. If organoid research leads to the creation of sentience candidates, a moratorium or indefinite ban on the creation of the relevant type of organoid may be appropriate. A different way forward, more consistent with existing approaches to animal research, would be to require ethical review and harm-benefit analysis for all research on sentience candidates. (shrink)

The power of the application of bioinformatics across multiple publicly available transcriptomic data sets was explored. Using 19 human and mouse circadian transcriptomic data sets, we found that NR1D1 and NR1D2 which encode heme‐responsive nuclear receptors are the most rhythmic transcripts across sleep conditions and tissues suggesting that they are at the core of circadian rhythm generation. Analyzes of human transcriptomic data show that a core set of transcripts related to processes including immune function, glucocorticoid signalling, and lipid metabolism (...) is rhythmically expressed independently of the sleep‐wake cycle. We also identify key transcripts associated with transcription and translation that are disrupted by sleep manipulations, and through network analysis identify putative mechanisms underlying the adverse health outcomes associated with sleep disruption, such as diabetes and cancer. Comparative bioinformatics applied to existing and future data sets will be a powerful tool for the identification of core circadian‐ and sleep‐dependent molecules. (shrink)

Evidence of reflective awareness and metacognitive monitoring during REM sleep dreaming poses a significant challenge to the commonly held view of dream cognition as necessarily deficient relative to waking cognition. To date, dream metacognition has not received the theoretical or experimental attention it deserves. As a result, discussions of dream cognition have been underrepresented in theoretical accounts of consciousness. This paper argues for using a converging measures approach to investigate the range and limits of cognition and metacognition across the (...) sleep–wakefulness cycle. The paradigm developed by LaBerge and his colleagues to study "lucid-control" dreaming offers one such framework for relating phenomenological, cognitive, and physiological measures. In a lucid-control dream, the dreamer is both aware that the experimental context is a dream and has the ability to intentionally regulate aspects of the dream . Subjects can make patterns of deliberate eye movements to signal from the dream and thus index significant events such as the time of lucidity onset and the completion of previously agreed-upon tasks in the dream. Lucid dreaming and other examples of reflective awareness during dreaming have important implications for models of human cognition. The existence of these phenomena raises fundamental questions about current assumptions regarding "state" constraints on consciousness and cognition. (shrink)

Clinical and experimental evidence suggests that hippocampal damage causes more severe disruption of episodic memories if those memories were encoded in the recent rather than the more distant past. This decrease in sensitivity to damage over time might reflect the formation of multiple traces within the hippocampus itself, or the formation of additional associative links in entorhinal and association cortices. Physiological evidence also supports a two-stage model of the encoding process in which the initial encoding occurs during active waking and (...) deeper consolidation occurs via the formation of additional memory traces during quiet waking or slow-wave sleep. In this article I will describe the changes in cholinergic tone within the hippocampus in different stages of the sleep-wake cycle and will propose that these changes modulate different stages of memory formation. In particular, I will suggest that the high levels of acetylcholine that are present during active waking might set the appropriate dynamics for encoding new information in the hippocampus, by partially suppressing excitatory feedback connections and so facilitating encoding without interference from previously stored information. By contrast, the lower levels of acetylcholine that are present during quiet waking and slow-wave sleep might release this suppression and thereby allow a stronger spread of activity within the hippocampus itself and from the hippocampus to the entorhinal cortex, thus facilitating the process of consolidation of separate memory traces. (shrink)

Sleep is phenomenologically rich, teeming with different kinds of conscious thought and experience. Dreaming is the most prominent example, but there is more to conscious experience in sleep than dreaming. Especially in non‐rapid eye movement sleep, conscious experience, sometimes dreamful, sometimes dreamless, also alternates with a loss of consciousness. Yet while dreaming has become established as a topic for interdisciplinary consciousness science and empirically informed philosophy of mind, the same is not true of other kinds of (...) class='Hi'>sleep‐related experience, nor is it true of sleep itself. I argue that this is a mistake. Conscious experience in sleep is more diverse than dreaming and we need to explain its different forms as well as the alternation between conscious and unconscious sleep states. We also need to ask how different kinds of sleep‐related experience relate to foundational issues about sleep and wakefulness as well as sleep stages. I survey recent findings and theoretical developments from sleep and dream research to show how the traditional view of sleep and its relation to wakefulness and consciousness is flawed. I then suggest that by refining our frameworks of sleep‐related experiences and sleep staging in tandem, we can work toward a better view. As we are only beginning to understand the diversity of consciousness in sleep, an important aim is programmatic: We need a philosophy of sleep and of consciousness in sleep, not just a philosophy of dreaming, and a future theory of sleep needs to integrate phenomenological considerations with neuroscientific and behavioral evidence. Working toward such a theory will radically transform our understanding of sleep, wakefulness, and our conscious minds. (shrink)

Metaphysics relies on the presupposition of the non-being of the world: since the world has once not existed it is necessary to postulate a cause for its existence, i.e. an extrinsic principle to explain the absolute beginning of the causal series of all things that constitute the world. After the critique of theologizing metaphysics by authors like Kant, Hegel and Nietzsche, the notion of an absolute beginning still persists though in a field in which it often goes as such unnoticed, (...) while it factually enjoys wide acceptance, namely in epistemology. It sounds as a truism that knowledge begins: personal inexistence (birth-death cycle) and the phenomenon of unconsciousness (sleep-wake cycle) seem to endorse the obviousness of that statement. Now, to link the beginning of the phenomenal series of subjective acts of knowledge with the existence of an external world that causes the specific content of our temporary cognitive acts relies, however, on two presuppositions, namely on the thesis of a complete non-being or nothingness of knowledge and, intrinsically related to this first presupposition, on the thesis of an absolute beginning of cognitive activity. If knowledge begins from its own nothingness, there must be a cause that is external to the totality of acts of knowledge, a cause that it doesn´t belong to the series of cognitive acts and, therefore, that it is not caused by any of them: this uncaused cause of contentful knowledge is supposed to be the real world external to the knowing subject. In my paper I make explicit the relation between realist-empiricist approachs to epistemology and the double presupposition of the nothingness and absolute beginning of knowledge, I explain the difficulties implied by these two presuppositions and, finally, I propose as a plausible solution to those difficulties some key theoretical claims of absolute idealism. (shrink)

Based on genetic and biochemical advances on the molecular mechanism of circadian rhythms, a computational model for the mammalian circadian clock is used to examine the dynamical bases of circadian‐clock‐related physiological disorders in humans. Entrainment by the light–dark cycle with a phase advance or a phase delay is associated with the Familial advanced sleep phase syndrome (FASPS) or the Delayed sleep phase syndrome (DSPS), respectively. Lack of entrainment corresponding to the occurrence of quasiperiodic oscillations with or without (...) phase jump can be associated with the non‐24 h sleep–wake syndrome. In the close vicinity of the entrainment domain, the model uncovers the possibility of infradian oscillations of very long period. Perturbation in the form of chronic jet lag, as used in mice, prevents entrainment of the circadian clock and results in chaotic or quasiperiodic oscillations. It is important to clarify the conditions for entrainment and for its failure because dysfunctions of the circadian clock may lead to physiological disorders, which pertain not only to the sleep–wake cycle but also to mood and cancer. BioEssays 30:590–600, 2008. © 2008 Wiley Periodicals, Inc. (shrink)

Emotions are complex reactions that allow individuals to cope with significant positive and negative events. Research on emotion was pioneered by Darwin’s (1871) work on emotional expressions in humans and animals. But Darwin was concerned mainly with facial and bodily expressions of significance for humans, citing mainly examples from mammals (e.g., apes, dogs, and cats). In birds, emotional expressions are less evident for a human observer, so a different approach is needed. Understanding avian emotions will provide key evolutionary information on (...) the evolution of related behaviors and brain circuitry. Birds and mammals are thought to have evolved from different groups of Mesozoic reptiles, theropod dinosaurs and therapsids, respectively, and therefore their common ancestor is likely to be a basal reptile living about 300 million years ago, during the Carboniferous or Permian. Yet, birds and mammals exhibit extensive convergence in terms of relative brain size, high levels of activity, sleep/wakefulness cycles, endothermy, and social behavior, among others. This article focuses on two basic emotions with negative valence: fear and frustration. Fear is related to the anticipation of dangerous or threatening stimuli (e.g., predators or aggressive conspecifics). Frustration is related to unexpected reward omissions or devaluations (e.g., loss of food or sexual resources). These results have implications for an understanding of the conditions that promote fear and frustration, and for the evolution of supporting brain circuitry. (shrink)

Disorders of consciousness (DOC) are a family of related neurological syndromes characterized by deficits of varying degrees of wakefulness (e.g., sleep–wake cycles and arousal) or awareness (e.g., reacting to stimuli, interacting with the environment). Although coma rarely persists for more than a few weeks, some patients remain in a subsequent vegetative state or a minimally conscious state for months or years. Caring for patients with DOC raises ethical questions, but the perspectives of healthcare providers on these questions remain (...) poorly documented. We conducted a qualitative study involving healthcare providers with different backgrounds. Semistructured interviews were used to explore attitudes toward ethical issues. We found that contextual (e.g., time, resource allocation) and relational aspects (e.g., communication process, families) shaped how ethical challenges surfaced and were managed. We call for greater awareness of contextual, institutional and social aspects and focus on these issues in training programs. (shrink)

Dramatic modern advances in emergency and resuscitation medicine, starting perhaps with the development of effective mechanical ventilators in the mid-20th century, have created a large class of persons who in earlier times would almost certainly have died, but who can now go on existing, suspended at least temporarily in a state somewhere between death and the conscious life they formerly pursued. A very wide range of brain injuries lead first to coma, in which the patient shows no sign of conscious (...) awareness, or even of wakefulness, in which eye openings and closings indicate the presence of a sleep/wake cycle unconsciously mediated by structures in the brain stem. Following emergence from coma, which may take days to months or more if it happens at all, patients typically show signs of wakefulness without conscious awareness – they are then in a so-called vegetative state (VS). For many this state becomes permanent, but some go on to a more recently described condition called the minimally conscious state (MCS), in which signs of conscious awareness can be detected by careful neurological examination (see Laureys & Tononi, 2009, chapter 14). A very few such persons ultimately progress to more or less full recovery, but another and particularly horrifying possible outcome is the “locked-in” state, in which a patient is fully conscious but has extremely little or no capacity for voluntary motor action. A famous modern example is that of Jean-Dominique Bauby, author of The Diving Bell and the Butterfly, who suffered a stroke to his upper brainstem and awakened 20 days later to find himself fully conscious but capable only of blinking his left eye. A tiny fraction of surgical patients find themselves in similarly terrifying conditions caused by the combination of muscle relaxants with insufficient levels of anesthetic agents (Kelly et al., 2007, p. 387 n. 18). (shrink)

The study of sleep and wakefulness can inform debates about the nature of consciousness. We argue that sleep and wakefulness fall along a multidimensional continuum and that inconsistencies and paradoxes with the accounts put forth by Merker et al. and Tononi can be understood in terms of a pervasive false dichotomy between these two states.

Recent studies have highlighted the relevance of sleep for procrastination at work. Procrastination at work is defined as the irrational delay of the initiation or completion of work-related activities. In line with recent studies, we offer a self-regulation perspective on procrastination. We argue that procrastination is an outcome of depleted self-regulatory resources and that the restoration of self-regulatory resources during high-quality sleep at night would prevent procrastination.AimsIn an attempt to further develop this line of research, the current study (...) aimed to achieve a broader understanding of the relevance of sleep and circadian rhythm for procrastination. Therefore, we explored the effect of sleep quality on procrastination for different chronotypes. We also considered the shift to daylight saving time as a phenomenon that aggravates circadian misalignment and thereby later chronotypes' dependence on high-quality sleep. Specifically, we hypothesized that compared to employees with an earlier chronotype, employees with a later chronotype are more dependent on good sleep at night to prevent procrastination the next day. This effect would be especially pronounced after the shift to daylight saving time.MethodsFor this repeated-measures study, participants were 101 full-time employees. They completed a general questionnaire and day-specific questionnaires on the Monday before and the Monday following the shift to daylight saving time.ResultsThe multilevel analyses showed that employees procrastinated less on days following nights during which they slept better and that later chronotypes experienced more procrastination than earlier chronotypes. Our findings also supported the hypothesis that the relationship between sleep quality and procrastination is stronger for later chronotypes compared to earlier chronotypes on the Monday following the shift to daylight saving time. In other words, the lower the sleep quality of later chronotypes during the previous night, the more they procrastinated on the Monday following the shift to daylight saving time.DiscussionOur findings further corroborate the existing findings on the relevance of sleep and chronotype for well-being and performance at work. (shrink)

Postnatal parent-infant physiological regulatory effects described in the previous paper (Part I) are viewed here as being biologically contiguous with events that occur prenatally, preparing and sensitizing the fetus to the average microenvironment into which the infant is expected, based on its evolutionary past, to be born. Following McKenna (1986), evidence (some of which is circumstantial) is presented concerning fetal hearing and fetal amniotic liquid breathing as they are affected both by maternal cardiovascular blood flow sounds in the uterus and (...) by fluctuating maternal blood sugar levels. These data are linked in turn to the infant’s postulated postnatal responsivity to parental sensory cues, including auditory and vestibular respiratory cues that may assist infants as they “learn” to breathe and, for some, to resist a SIDS event. Data on the respiratory and vocalizing behavior of normal and hearing-impaired persons are used to show that not all forms of human breathing are innate; some forms develop with experience. These data reveal how human infants learn, for example, to coordinate higher and lower brain respiratory nuclei in the context of learning initially to cry with intent and purpose and later to speak. Voluntary, cortex-based breathing emerges at the same time that infants are most likely to die from SIDS, between 2 and 4 months of age. This switch between voluntary and involuntary breathing during both sleep (while dreaming) and wake cycles, which depends on the integration of higher cortical and lower brain stem nuclei, is complex and is possibly the basis of the human species’ unique susceptibility to SIDS—a syndrome as yet unrecognized in other species. These human infant vulnerabilities, including delayed maturity, can explain in part why natural selection ought to favor increased infant sensitivity to parental sensory cues provided by a caregiver—stimuli available in the evolving parental care environment that included parent-infant co-sleeping for more than 4–5 million years of human evolution. (shrink)