Summary The aim of this study was to investigate long‐term trends in insomnia symptoms, tiredness and school performance among Finnish adolescents. A time–series from 1984 to 2011 was analysed from two large‐scale survey studies, the Finnish School Health Promotion Study and the Health Behavior in School‐Aged Children study. A total of 1 136 583 adolescents aged 11–18 years answered a standardized questionnaire assessing frequency of insomnia symptoms, tiredness and school performance. A clear approximately twofold increasing trend in insomnia symptoms and tiredness was found from the mid‐1990s to the end of the 2000s. The increase was evident in all participating age groups and in both genders. After 2008, the increase seems to have stopped. Insomnia symptoms and tiredness were associated with lower school performance and they were more prevalent among girls (11.9 and 18.4%) compared to boys (6.9 and 9.0%, respectively). Unexpectedly, we also observed an increasingly widening gap in school performance between normally vigilant and chronically tired pupils. The underlying causes of these phenomena are unknown, but may concern changes in the broader society. The observed recent increasing trend in adolescents’ sleep problems is worrisome: poor sleep quality has also been suggested to associate with clinical or subclinical mood or anxiety disorders and behavioural problems and predispose to sleep and psychiatric disorders later in life. Our results justify further studies and call for serious attention to be paid to adolescent's sleep in the Finnish educational system and society at large.

Here we report the first and most robust evidence about how sleep habits are associated with regional brain grey matter volumes and school grade average in early adolescence. Shorter time in bed during weekdays, and later weekend sleeping hours correlate with smaller brain grey matter volumes in frontal, anterior cingulate, and precuneus cortex regions. Poor school grade average associates with later weekend bedtime and smaller grey matter volumes in medial brain regions. The medial prefrontal - anterior cingulate cortex appears most tightly related to the adolescents’ variations in sleep habits, as its volume correlates inversely with both weekend bedtime and wake up time, and also with poor school performance. These findings suggest that sleep habits, notably during the weekends, have an alarming link with both the structure of the adolescent brain and school performance, and thus highlight the need for informed interventions.

Sleep saves energy, but can brain energy depletion induce sleep? We used 2,4-dinitrophenol (DNP), a molecule which prevents the synthesis of ATP, to induce local energy depletion in the basal forebrain of rats. Three-hour DNP infusions induced elevations in extracellular concentrations of lactate, pyruvate and adenosine, as well as increases in non-REM sleep during the following night. Sleep was not affected when DNP was administered to adjacent brain areas, although the metabolic changes were similar. The amount and the timing of the increase in non-REM sleep, as well as in the concentrations of lactate, pyruvate and adenosine with 0.5-1.0 mM DNP infusion, were comparable to those induced by 3 h of sleep deprivation. Here we show that energy depletion in localized brain areas can generate sleep. The energy depletion model of sleep induction could be applied to in vitro research into the cellular mechanisms of prolonged wakefulness.

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Depression and disturbed sleep are intimately and bidirectionally related. During adolescence, the incidence of both insomnia and major depression increases simultaneously, in a gender-specific manner. The majority of depressed adolescents suffer from different types of subjective sleep complaints. Despite these complaints, the results from polysomnographic studies in depressed adolescents remain inconsistent. In general, similar features to those seen among adults with depressive disorder (e.g. abnormalities in rapid eye movement sleep and difficulties in sleep onset) have been reported, but expressed to a lesser degree. The inconsistency in findings may be linked with maturational factors, factors related to the stage of illness and greater heterogeneity in the clinical spectrum of depression among adolescents. The exact neurobiological mechanisms by which sleep alterations and depression are linked during adolescence are not fully understood. Aberrations in brain maturation, expressed at different levels of organization, for example gene expression, neurotransmitter and hormone metabolism, and activity of neuronal networks have been suggested. The circadian systems may change in adolescent depression beyond that observed during healthy adolescent development (i.e. beyond the typical circadian shift towards eveningness). A number of therapeutic approaches to alleviate sleep disruption associated with depression have been proposed, but research on the efficacy of these interventions in adolescents is lacking. Knowledge of the neurobiological links between sleep and depression during adolescence could lead to new insights into effective prevention and treatment of depression.

Objective sleep measures differed significantly between the young and postmenopausal groups. These differences may be more because of the physiology of ageing than the rapid changes across the menopause, since similar sleep characteristics were already present in the premenopausal women. The increase in sleep complaints after menopause was not associated with sleepiness or disturbances in objective sleep quality, mood or cognitive performance.

Proton magnetic resonance spectroscopy (1H-MRS) allows in vivo assessment of the metabolism related to human brain functions. Visual, auditory, tactile, and motor stimuli induce a temporary increase in the brain lactate level, which may act as a rapid source of energy for the activated neurons. The authors studied the metabolism of the frontal lobes during cognitive stimulation and measured local lactate levels with standard 1H-MRS, after localizing the activated area by functional MRI. Lactate levels were monitored while the subjects either silently listed numbers (baseline) or performed a silent word-generation task (stimulus-activation). The cognitive stimulus-activation produced a 50% increase in the brain lactate level in the left inferior frontal gyrus. The results show that metabolic imaging of neuronal activity related to cognition is possible using 1H-MRS.

Summary Both aging and sleep deprivation disturb the functions of the frontal lobes. Deficits in brain energy metabolism have been reported in these conditions. Neurons use not only glucose but also lactate as their energy substrate. The physiological response to elevated neuronal activity is a transient increase in lactate concentrations in the stimulated area. We have previously shown that cognitive stimulation increases brain lactate. To study the effect of prolonged wakefulness on the lactate response we designed an experiment to assess brain lactate levels during a 40‐h sleep deprivation period in young (19–24 years old; n = 13) and in aged (60–68 years old; n = 12) healthy female volunteers. Brain lactate levels were assessed with proton MR‐spectroscopy (1H MRS) during the performance of a silent word generation task. The 1H MRS voxel location was individually selected, using functional magnetic resonance imaging, to cover the activated area in the left frontal lobe. The degree of sleepiness was verified using vigilance tests and self‐rating scales. In the young alert subjects, the silent word generation test induced a 40% increase in lactate, but during the prolonged wakefulness period this response disappeared. In the aged subjects, the lactate response could not be detected even in the alert state. We propose that the absence of the lactate response may be a sign of malfunctioning of normal brain energy metabolism. The behavioral effects of prolonged wakefulness and aging may arise from this dysfunction.