Attachment--and loss.

This chapter explores the ecology of human development, those forces in the person's environment that affect and influence development. Urie Bronfenbrenner's model of the human ecosystem guides the discussion, making connections between children in families and in communities and the larger society that surrounds them. The human ecosystem model is much like the study of the natural ecology, focusing on the interactions between subjects at various levels of the environment as they affect each other. The interaction between individual and environment forms the basis of an ecological approach to human development. This view sees the process of development as the expansion of the child's conception of the world and the child's ability to act on that world. Risks to development can come from both direct threats and the absence of opportunities for development. Sociocultural risk refers to the impoverishment in the child's world of essential experiences and relationships.

The Ecology of Human Development

Over more than a century of research has established the fact that sleep benefits the retention of memory. In this review we aim to comprehensively cover the field of "sleep and memory" research by providing a historical perspective on concepts and a discussion of more recent key findings. Whereas initial theories posed a passive role for sleep enhancing memories by protecting them from interfering stimuli, current theories highlight an active role for sleep in which memories undergo a process of system consolidation during sleep. Whereas older research concentrated on the role of rapid-eye-movement (REM) sleep, recent work has revealed the importance of slow-wave sleep (SWS) for memory consolidation and also enlightened some of the underlying electrophysiological, neurochemical, and genetic mechanisms, as well as developmental aspects in these processes. Specifically, newer findings characterize sleep as a brain state optimizing memory consolidation, in opposition to the waking brain being optimized for encoding of memories. Consolidation originates from reactivation of recently encoded neuronal memory representations, which occur during SWS and transform respective representations for integration into long-term memory. Ensuing REM sleep may stabilize transformed memories. While elaborated with respect to hippocampus-dependent memories, the concept of an active redistribution of memory representations from networks serving as temporary store into long-term stores might hold also for non-hippocampus-dependent memory, and even for nonneuronal, i.e., immunological memories, giving rise to the idea that the offline consolidation of memory during sleep represents a principle of long-term memory formation established in quite different physiological systems.

https://www.zora.uzh.ch/id/eprint/77770/1/physiol_rev_93.pdf

About sleep's role in memory

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Applied Missing Data Analysis

IN THE LAST FEW DECADES THERE HAS BEEN A SIGNIFICANT INCREASE IN THE PREVALENCE OF OBESITY WORLDWIDE AND THE WORLD HEALTH organization has declared it a global epidemic.1 Obesity in childhood is a cause of psychosocial problems including low self esteem,2 and frequently continues into adulthood3 where it is a cause of major morbidity and mortality including cardiovascular disease and type 2 diabetes. At the same time there has been a reduction in sleep time. National surveys in USA have shown a decline in self-reported sleep duration over the past 50 years by 1.5 to 2 hours.4 This sleep curtailment has been attributed to lifestyle changes.

Several studies have reported associations between duration of sleep (short as well as long) and ill-health, including relationships with self-reported well-being,5 morbidity and mortality,6–12 and with chronic conditions including type 2 diabetes, respiratory disorders, hypertension, and obesity.13–18 The associations between short duration of sleep and obesity, in particular, have stimulated a debate given the potential implications for children19,20 as well as adults.21,22 However, given the variety of studies and the large differences in the target populations, it is difficult to draw immediate conclusions on the consistency of the association, the direction of causality and the likely mechanisms involved. The aims of this article are to (i) systematically review published population-based studies, (ii) to carry out a meta-analysis to assess whether the evidence supports the presence of a relationship between short sleep duration and obesity at different ages, and (iii) to obtain a quantitative estimate of the risk in order to assess the consistency and potential public health relevance

/pdf/meta-analysis-of-short-sleep-duration-and-obesity-in-490mql6je2.pdf

Meta-Analysis of Short Sleep Duration and Obesity in Children and Adults

Objective. The main purpose of the present study was to calculate percentile curves for total sleep duration per 24 hours, for nighttime and for daytime sleep duration from early infancy to late adolescence to illustrate the developmental course and age-specific variability of these variables among subjects. Methods. A total of 493 subjects from the Zurich Longitudinal Studies were followed using structured sleep-related questionnaires at 1, 3, 6, 9, 12, 18, and 24 months after birth and then at annual intervals until 16 years of age. Gaussian percentiles for ages 3 months to 16 years were calculated for total sleep duration (time in bed) and nighttime and daytime sleep duration. The mean sleep duration for ages 1 to 16 years was estimated by generalized additive models based on the loess smoother; a cohort effect also had to be included. The standard deviation (SD) was estimated from the loess smoothed absolute residuals from the mean curve. For ages 3, 6, and 9 months, an alternative approach with a simple model linear in age was used. For age 1 month, empirical percentiles were calculated. Results. Total sleep duration decreased from an average of 14.2 hours (SD: 1.9 hours) at 6 months of age to an average of 8.1 hours (SD: 0.8 hours) at 16 years of age. The variance showed the same declining trend: the interquartile range at 6 months after birth was 2.5 hours, whereas at 16 years of age, it was only 1.0 hours. Total sleep duration decreased across the studied cohorts (1974–1993) because of increasingly later bedtime but unchanged wake time across decades. Consolidation of nocturnal sleep occurred during the first 12 months after birth with a decreasing trend of daytime sleep. This resulted in a small increase of nighttime sleep duration by 1 year of age (mean 11.0 ± 1.1 hours at 1 month to 11.7 ± 1.0 hours at 1 year of age). The most prominent decline in napping habits occurred between 1.5 years of age (96.4% of all children) and 4 years of age (35.4%). Conclusions. Percentile curves provide valuable information on developmental course and age-specific variability of sleep duration for the health care professional who deals with sleep problems in pediatric practice.

Sleep duration from infancy to adolescence: reference values and generational trends.

Adolescent development is accompanied by profound changes in the timing and amounts of sleep and wakefulness. Many aspects of these changes result from altered psychosocial and life-style circumstances that accompany adolescence. The maturation of biological processes regulating sleep/wake systems, however, may be strongly related to the sleep timing and amount during adolescence-either as "compelling" or "permissive" factors. The two-process model of sleep regulation posits a fundamental sleep-wake homeostatic process (process S) working in concert with the circadian biological timing system (process C) as the primary intrinsic regulatory factors. How do these systems change during adolescence? We present data from adolescent participants examining EEG markers of sleep homeostasis to evaluate whether process S shows maturational changes permissive of altered sleep patterns across puberty. Our data indicate that certain aspects of the homeostatic system are unchanged from late childhood to young adulthood, while other features change in a manner that is permissive of later bedtimes in older adolescents. We also show alterations of the circadian timing system indicating a possible circadian substrate for later adolescent sleep timing. The circadian parameters we have assessed include phase, period, melatonin secretory pattern, light sensitivity, and phase relationships, all of which show evidence of changes during pubertal development with potential to alter sleep patterns substantially. However the changes are mediated-whether through process S, process C, or by a combination-many adolescents have too little sleep at the wrong circadian phase. This pattern is associated with increased risks for excessive sleepiness, difficulty with mood regulation, impaired academic performance, learning difficulties, school tardiness and absenteeism, and accidents and injuries.

Regulation of Adolescent Sleep: Implications for Behavior

Pediatricians provide a major source of knowledge for parents about children's behavior and development, although their advice is largely based on their own cultural values and beliefs in interaction with their personal and clinical experience. This review presents cross-cultural aspects of children's sleep behavior in industrialized and complex modern societies and provides a basis for understanding dimensions and mechanisms of cultural differences. We submit that it is the interaction between culture and biology that establishes behavioral and developmental norms and expectations regarding normal and problematic children's sleep. Pediatricians need to recognize the cultural environment in which children live and be knowledgeable about how cultural beliefs and values of both families and physicians interact with the needs and biological characteristics of individual children.

Children's sleep: an interplay between culture and biology.

STUDY OBJECTIVES: 

To examine the effects of total sleep deprivation on adolescent sleep and the sleep electroencephalogram (EEG) and to study aspects of sleep homeostasis.

DESIGN: Subjects were studied during baseline and recovery sleep after 36 hours of wakefulness.

SETTING: Four-bed sleep research laboratory.

PARTICIPANTS: Seven prepubertal or early pubertal children (pubertal stage Tanner 1 or 2 = Tanner 1/2; mean age 11.9 years, SD +/- 0.8, 2 boys) and 6 mature adolescents (Tanner 5; 14.2 years, +/- 1.4, 2 boys).

INTERVENTIONS: Thirty-six hours of sleep deprivation.

MEASUREMENTS: All-night polysomnography was performed. EEG power spectra (C3/A2) were calculated using a Fast Fourier transform routine.

RESULTS: 

In both groups, sleep latency was shorter, sleep efficiency was higher, non-rapid eye movement (NREM) sleep stage 4 was increased, and waking after sleep onset was reduced in recovery relative to baseline sleep. Spectral power of the NREM sleep EEG was enhanced after sleep deprivation in the low-frequency range (1.6-3.6 Hz in Tanner 1/2; 0.8-6.0 Hz in Tanner 5) and reduced in the sigma range (11-15 Hz). Sleep deprivation resulted in a stronger increase of slow-wave activity (EEG power 0.6-4.6 Hz, marker for sleep homeostatic pressure) in Tanner 5 (39% above baseline) than in Tanner 1/2 adolescents (18% above baseline). Sleep homeostasis was modeled according to the two-process model of sleep regulation. The build-up of homeostatic sleep pressure during wakefulness was slower in Tanner 5 adolescents (time constant of exponential saturating function 15.4 +/- 2.5 hours) compared with Tanner 1/2 children (8.9 +/- 1.2 hours). In contrast, the decline of the homeostatic process was similar in both groups.

CONCLUSION: 

Maturational changes of homeostatic sleep regulation are permissive of the sleep phase delay in the course of adolescence.

/pdf/homeostatic-sleep-regulation-in-adolescents-4wtrtjb1az.pdf

Homeostatic sleep regulation in adolescents.

OBJECTIVES: To describe sleep-wake patterns in kindergarten children by measures derived from questionnaire, diary, and actigraphy and to report rates of agreement between methods according to Bland and Altman. DESIGN: Cross-sectional study, data from 7 nights of actigraph recordings and sleep diary and from a questionnaire. SETTING: Children studied in their homes. PARTICIPANTS: Fifty children, aged 4 to 7 years. MAIN OUTCOME MEASURES: Sleep start, sleep end, assumed sleep, actual sleep time, and nocturnal wake time derived from different methods. RESULTS: Differences between actigraphy and diary were +/- 28 minutes for sleep start, +/- 24 minutes for sleep end, and +/- 32 minutes for assumed sleep, indicating satisfactory agreement between methods, whereas for actual sleep time and nocturnal wake time, agreement rates were not sufficient (+/- 106 minutes and +/- 55 minutes, respectively). Agreement rates between actigraphy and questionnaire as well as between diary and questionnaire were insufficient for all variables. Sex and age of children and socioeconomic status did not influence the differences between methods for all variables. CONCLUSIONS: Actigraphy and diary may be interchangeably used for the assessment of sleep start, sleep end, and assumed sleep but not for nocturnal wake times. The diary is a cost-effective and valid source of information about children's sleep-schedule times, while actigraphy may provide additional information about nocturnal wake times or may be used if parents are unable to report in detail. It is insufficient to collect information by a questionnaire or an interview asking about children's normal sleep patterns.

https://jamanetwork.com/journals/jamapediatrics/articlepdf/379365/poa80005_350_358.pdf

Oskar G. Jenni

Papers

Sleep duration from infancy to adolescence: reference values and generational trends.

Regulation of Adolescent Sleep: Implications for Behavior

Children's sleep: an interplay between culture and biology.

Homeostatic sleep regulation in adolescents.

Agreement rates between actigraphy, diary, and questionnaire for children's sleep patterns.