A Longitudinal Study of Stress During Pregnancy, Children’s Sleep and Polygenic Risk for Poor Sleep in the General Pediatric Population

Early life stress is robustly associated with poor sleep across life. Preliminary studies suggest that these associations may begin already in utero. Here, we study the longitudinal associations of prenatal psychosocial stress with sleep across childhood, and assess whether prenatal stress interacts with genetic liability for poor sleep. The study is embedded in the Generation R population-based birth cohort. Caregivers reported on prenatal psychosocial stress (life events, contextual, parental or interpersonal stressors) and on children’s sleep at ages 2 months, 1.5, 2, 3 and 6 years. The study sample consisted of 4,930 children; polygenic risk scores for sleep traits were available in 2,063. Prenatal stress was consistently associated with more sleep problems across assessments. Effect sizes ranged from small (B = 0.21, 95%CI: 0.14;0.27) at 2 months to medium (B = 0.45, 95%CI: 0.38;0.53) at 2 years. Prenatal stress was moreover associated with shorter sleep duration at 2 months (Bhrs = -0.22, 95%CI: -0.32;-0.12) and at 2 years (Bhrs = -0.04, 95%CI -0.07; -0.001), but not at 3 years (Bhrs = 0.02, 95%CI: -0.02;0.06). Prenatal negative life events interacted with polygenic risk for insomnia to exacerbate sleep problems at 6 years (Binteraction = 0.07, 95%CI: 0.02;0.13). Psychosocial stress during pregnancy has negative associations with children’s sleep that persist across childhood, and are exacerbated by genetic liability for insomnia. Associations with sleep duration were more pronounced in infancy and seem to attenuate with age. These findings highlight the role of the prenatal environment for developing sleep regulation, and could inform early intervention programs targeting sleep in children from high-risk pregnancies.</p

Are some children genetically predisposed to poor sleep? A polygenic risk study in the general population

Background: Twin studies show moderate heritability of sleep traits: 40% for insomnia symptoms and 46% for sleep duration. Genome-wide association studies (GWAS) have identified genetic variants involved in insomnia and sleep duration in adults, but it is unknown whether these variants affect sleep during early development. We assessed whether polygenic risk scores for insomnia (PRS-I) and sleep duration (PRS-SD) affect sleep throughout early childhood to adolescence. Methods: We included 2,458 children of European ancestry (51% girls). Insomnia-related items of the Child Behavior Checklist were reported by mothers at child's age 1.5, 3, and 6 years. At 10–15 years, the Sleep Disturbance Scale for Children and actigraphy were assessed in a subsample (N = 975). Standardized PRS-I and PRS-SD (higher scores indicate genetic susceptibility for insomnia and longer sleep duration, respectively) were computed at multiple p-value thresholds based on largest GWAS to date. Results: Children with higher PRS-I had more insomnia-related sleep problems between 1.5 and 15 years (BPRS-I &lt; 0.001 =.09, 95% CI: 0.05; 0.14). PRS-SD was not associated with mother-reported sleep problems. A higher PRS-SD was in turn associated with longer actigraphically estimated sleep duration (BPRS-SD &lt; 5e08 =.05, 95% CI: 0.001; 0.09) and more wake after sleep onset (BPRS-SD &lt; 0.005 =.25, 95% CI: 0.04; 0.47) at 10–15 years, but these associations did not survive multiple testing correction. Conclusions: Children who are genetically predisposed to insomnia have more insomnia-like sleep problems, whereas those who are genetically predisposed to longer sleep have longer sleep duration, but are also more awake during the night in adolescence. This indicates that polygenic risk for sleep traits, based on GWAS in adults, affects sleep already in children.</p

Age-Related changes in thermoreception and thermoregulation

This chapter focuses on age-related changes in temperature sensitivity and thermoregulation in humans. Core temperature is the net result of heat production and heat loss. Deviations from the optimal temperature occur for two main reasons: physical activity generates heat and environmental heat or cold affects body temperature as well. These changes need to be sensed, processed, and counteracted if necessary. Thus, the thermoregulatory system can be conceptualized as containing three parts: thermosensitive afferent pathways, neuronal integration and control systems, and descending effector pathways altering heat gain or loss. The functional anatomy and physiological mechanisms of these compartments and their alterations with aging are covered in separate sections: thermoreception; thermogenesis, heat gain, and heat retention; heat loss and reduction of heat gain; and central thermoregulatory control including circadian rhythms. Further, humans need to regulate their body temperature to survive. Most of the deaths due to hypothermia or hyperthermia occur in elderly subjects. The reason the elderly especially are at such an increased risk of thermoregulatory deficit is not a new question, yet still important and not solved. Is it because their capability to sense temperature is compromised, because their thermoregulatory capacities are limited, or because their physiology is less tolerant to extreme temperatures? This discussion also describes what is known about the changes in thermoreception and thermoregulation with increasing age

Effects of light and temperature on sleep in adults and elderly

From the very beginning of evolution on, virtually all life forms have developed in an environment where light intensity and temperature cycled at a rate of about 24h. It is therefore not surprising that rhythms of about 24h, i.e., circadian, are integrated in all processes of life, including gene expression, the biochemical processes in a cell, the complex physiology of an organism, its behavior and cognition. A complex system comprising central autonomous oscillators and peripheral slaved damped oscillators is responsible for this circadian modulation of our bodily functions, and is described in detail in other parts of this Encyclopedia. Sleep is one of the states that is under control of the body clock system; sleep is most likely to occur within a specified phase range of the circadian cycle. Homeostasis is the second important factor involved in sleep regulation; the need for sleep increases with the duration of wakefulness. The circadian and homeostatic regulatory systems interact to concertedly regulate the timing of sleep and wakefulness. With increasing age, cracks may start to appear in the functionality of this complex interacting system. For human sleep, this can result in a decreased ability to maintain uninterrupted sleep during the night and an increased probability for napping during the day. Sleep complaints indeed increase with age and are among the most disturbing subjectively judged consequences of getting older. At present, satisfactory pharmacological interventions to improve the sleep–wake rhythm on a daily basis are lacking. The present paper addresses the question whether the human sleep-wake rhythm is still sensitive to its evolutionary oldest environmental modulators or “Zeitgebers”: light and temperature. The focus moreover is on their capacity to support the sleep–wake rhythm of elderly people on a daily basis

The large-scale functional connectivity correlates of consciousness and arousal during the healthy and pathological human sleep cycle

Advances in neuroimaging have greatly improved our understanding of human sleep from a systems neuroscience perspective. However, cognition and awareness are reduced during sleep, hindering the applicability of standard task-based paradigms. Methods recently developed to study spontaneous brain activity fluctuations have proven useful to overcome this limitation. In this review, we focus on the concept of functional connectivity (FC, i.e. statistical covariance between brain activity signals) and its application to functional magnetic resonance imaging (fMRI) data acquired during sleep. We discuss how FC analyses of endogenous brain activity during sleep have contributed towards revealing the large-scale neural networks associated with arousal and conscious awareness. We argue that the neuroimaging of deep sleep can be used to evaluate the predictions of theories of consciousness; at the same time, we highlight some apparent limitations of deep sleep as an experimental model of unconsciousness. In resting state fMRI experiments, the onset of sleep can be regarded as the object of interest but also as an undesirable confound. We discuss a series of articles contributing towards the disambiguation of wakefulness from sleep on the basis of fMRI-derived dynamic FC, and then outline a plan for the development of more general and data-driven sleep classifiers. To complement our review of studies investigating the brain systems of arousal and consciousness during healthy sleep, we then turn to pathological and abnormal sleep patterns. We review the current literature on sleep deprivation studies and sleep disorders, adopting the critical stance that lack of independent vigilance monitoring during fMRI experiments is liable for false positives related to atypical sleep propensity in clinical and sleep-deprived populations. Finally, we discuss multimodal neuroimaging as a promising future direction to achieve a better understanding of the large-scale FC of the brain during sleep and its relationship to mechanisms at the cellular level.Fil: Tagliazucchi, Enzo Rodolfo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Física de Buenos Aires. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Física de Buenos Aires; ArgentinaFil: van Someren, Eus J.W.. Netherlands Institute For Neuroscience Nin - Knaw; Países Bajo

A clinical interpretation of shame regulation in maladaptive perfectionism

Maladaptive perfectionism, a transdiagnostic personality trait, is associated with depression. Shame has been associated with depressive disorders and to negatively impact its treatment. Interestingly, maladaptive perfectionism and maladaptive shame regulation strategies might be both expressions of an internalizing personality style. We applied forward and backward stepwise linear regression modeling to explain maladaptive perfectionism by association of shame coping styles in a highly powered cross-sectional study of 1436 participants. Maladaptive perfectionism was shown to have significant positive associations with the two internalizing coping styles attacking the self, and withdrawing, and negative associations with adaptive coping. Furthermore, a significant positive interaction effect was shown for the two internalizing coping styles. Our research shows that participants who adopt maladaptive perfectionism, internalize the pain of shame. Clinically, this is especially relevant during treatment: the patterns of maladaptive perfectionism must come into the open, the client feels exposed and, consistent with his shame regulation style, shame grows. Our research might account for the negative responsiveness of perfectionism to brief therapies for depression: there may not be enough focus on and time for working through the evoked shame

Insomnia and personality—a network approach

Studies on personality traits and insomnia have remained inconclusive about which traits show the most direct associations with insomnia severity. It has moreover hardly been explored how traits relate to specific characteristics of insomnia. We here used network analysis in a large sample (N = 2089) to obtain an integrated view on the associations of personality traits with both overall insomnia severity and different insomnia characteristics, while distinguishing direct from indirect associations. We first estimated a network describing the associations among the five factor model personality traits and overall insomnia severity. Overall insomnia severity was associated with neuroticism, agreeableness, and openness. Subsequently, we estimated a separate network describing the associations among the personality traits and each of the seven individual items of the Insomnia Severity Index. This revealed relatively separate clusters of daytime and nocturnal insomnia complaints, that both contributed to dissatisfaction with sleep, and were both most directly associated with neuroticism and conscientiousness. The approach revealed the strongest direct associations between personality traits and the severity of different insomnia characteristics and overall insomnia severity. Differentiating them from indirect associations identified the targets for improving Cognitive Behavioral Therapy for insomnia with the highest probability of effectively changing the network of associated complaints