The vicious circle of media use, exposure to light at ...

Journal of Physiology - Paris xxx (2017) xxx–xxx

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Journal of Physiology - Paris journal homepage: www.elsevier.com/locate/jphysparis

Review Paper

Disruption of adolescents’ circadian clock: The vicious circle of media use, exposure to light at night, sleep loss and risk behaviors Yvan Touitou a,⇑, David Touitou b, Alain Reinberg a a b

Unité de Chronobiologie, Fondation Ophtalmologique A. de Rothschild, 25 rue Manin, 75019 Paris, France UHSA – Groupe Hospitalier Paul Guiraud, 54, avenue de la République, 94806 Villejuif, France

a r t i c l e

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Article history: Received 24 October 2016 Received in revised form 12 April 2017 Accepted 5 May 2017 Available online xxxx Keywords: Electronic media use Light at night LEDs Clock disruption Melatonin Adolescent sleep Sleepiness Fatigue Chronotype Internet use Cellular phone Rhythm desynchronization Alcohol Smoking Binge drinking Substance abuse

a b s t r a c t Although sleep is a key element in adolescent development, teens are spending increasing amounts of time online with health risks related to excessive use of electronic media (computers, smartphones, tablets, consoles. . .) negatively associated with daytime functioning and sleep outcomes. Adolescent sleep becomes irregular, shortened and delayed in relation with later sleep onset and early waking time due to early school starting times on weekdays which results in rhythm desynchronization and sleep loss. In addition, exposure of adolescents to the numerous electronic devices prior to bedtime has become a great concern because LEDs emit much more blue light than white incandescent bulbs and compact fluorescent bulbs and have therefore a greater impact on the biological clock. A large number of adolescents move to evening chronotype and experience a misalignment between biological and social rhythms which, added to sleep loss, results in e.g. fatigue, daytime sleepiness, behavioral problems and poor academic achievement. This paper on adolescent circadian disruption will review the sensitivity of adolescents to light including LEDs with the effects on the circadian system, the crosstalk between the clock and the pineal gland, the role of melatonin, and the behavior of some adolescents (media use, alcohol consumption, binge drinking, smoking habits, stimulant use. . .). Lastly, some practical recommendations and perspectives are put forward. The permanent social jet lag resulting in clock misalignment experienced by a number of adolescents should be considered as a matter of public health. Ó 2017 Elsevier Ltd. All rights reserved.

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The circadian system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.1. From the internal clock to circadian rhythms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.2. From rhythm desynchronization to circadian disruption . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1.3. Assessment of rhythm synchronization/desynchronization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Physiology of melatonin from birth to adulthood . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.1. Fetus and infants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2.2. Children and adolescents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Light control of the circadian system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.1. Light effects on melatonin secretion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3.2. Sensitivity of adolescents to light. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Adolescent behavior: from media overuse to Internet addiction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.1. Electronic media overuse . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.2. Internet addiction or Internet gaming disorder. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4.3. Neural mechanisms of Internet addiction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Screens of electronic media and blue light impact . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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⇑ Corresponding author. E-mail address: [email protected] (Y. Touitou). http://dx.doi.org/10.1016/j.jphysparis.2017.05.001 0928-4257/Ó 2017 Elsevier Ltd. All rights reserved.

Please cite this article in press as: Touitou, Y., et al. Disruption of adolescents’ circadian clock: The vicious circle of media use, exposure to light at night, sleep loss and risk behaviors. J. Physiol. (2017), http://dx.doi.org/10.1016/j.jphysparis.2017.05.001

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Y. Touitou et al. / Journal of Physiology - Paris xxx (2017) xxx–xxx

5.1. Overuse of mobile phones and smartphones. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.2. Light-emitting diodes (LEDs) impact on clock functioning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5.3. Light at night impact on clock functioning and sleep . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6. Adolescent sleep deprivation, a matter of concern . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.1. Chronotype move to eveningness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.2. Health impacts of sleep deprivation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6.3. Recommendations on sleep hygiene . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7. Adolescent substance abuse . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.1. Alcohol consumption . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7.2. Binge drinking . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8. Cigarette smoking and e-cigarettes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8.1. Tobacco use . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8.2. Electronic cigarettes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8.3. Cannabis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9. Interventions on risk behaviors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Conflict of interest. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

The World Health Organization (WHO) defines adolescents as individuals in the 10–19 year age group, and youths as the 15–24 year age group. These two groups are considered to be young individuals, and they range from 10 to 24 years of age.

1. The circadian system

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humans and in experimental animals, both diurnal and nocturnal, with daily dark phase plasma concentrations three to ten times higher than during the light phase. This is related to a neuronal message that is initiated in the SCN when the neurons are no longer subjected to the effect of light. This results in an activation of the release of noradrenalin (NA) by the terminal nerves of the sympathetic system that act at the level of the beta-adrenergic receptors, thus activating the adenylate cyclase system and the key melatonin synthesizing enzyme N-acetyltransferase.

1.1. From the internal clock to circadian rhythms 1.2. From rhythm desynchronization to circadian disruption Circadian rhythms are dependent on an internal clock, a central brain pacemaker, located in the suprachiasmatic nucleus (SCN) of the anterior hypothalamus. On the one hand, the SCN serves as a central clock, synchronizing other clocks in peripheral tissues (e.g. liver, kidney, heart, retina, and others), and on the other hand it directly orchestrates circadian physiology (Richards and Gumz, 2012). The SCN generates circadian rhythms by means of a transcriptional-translational feedback loop. The molecular mechanism of the clock is present in every cell of the body. Clock genes (some examples in humans are CLOCK, CRY, PER, and BMAL1) comprise an autoregulatory transcriptional-translational feedback loop that cycles every 24 h (Hardin, 2000; Loros and Dunlap, 1991). The suprachiasmatic nucleus develops early in gestation, and circadian rhythms are present in the fetus and newborn (Kennaway et al., 1992; Serón-Ferré et al., 2001). The SCN is connected to the retina on the one hand, and to the pineal gland which secretes melatonin on the other hand. Intrinsically photosensitive retinal ganglion cells (ipRGCs) in the eye contain melanopsin that is expressed in a small subset of cells representing 1–2% of all retinal ganglion cells. Melanopsin is an OPN4-photoreceptor that is sensitive to blue light (i.e. wavelengths ranging from 460 to 480 nm) and that is fundamental for the functioning of the circadian system and for SCN entrainment. This system is called the non-image-forming system (NIF), as opposed to the classical visual system (based on rods and cones) that is responsible for image formation (Berson et al., 2002; Lucas, 2013). The light signal received by the retina is transmitted to the SCN by a retino-hypothalamic pathway, and then to the superior cervical ganglion by multisynaptic complexes, so as to end up at the pineal gland which secretes melatonin (5-methoxy-Nacetyltryptamine) derived from its precursor tryptophan. Pineal melatonin production exhibits a high-amplitude circadian rhythm that is reflected in plasma levels, with low levels during the day and high levels at night. This circadian pattern is comparable in

Under normal environmental conditions light is the major synchronizer (also called entraining agent or Zeitgeber) of the circadian system. Daily exposure to light maintains the 24 h cycle (i.e. the 24 h period) of the biological clock. Light thus synchronizes (or entrains, or adjusts) the endogenous period of the circadian system which is which is not exactly 24 h but close to 24.2 h. When light is absent, such as in constant darkness as documented in experimental protocols, the circadian rhythm of melatonin free-runs. This means that as it is no longer synchronized with the environmental light-dark cycle, it becomes out of phase with this environmental cycle (Reinberg and Touitou, 1996; Touitou et al., 2011, 2017). Desynchronization corresponds to a dissociation of the internal clock function from that of the local time and this results in a number of atypical symptoms such as, amongst others, persistent fatigue, poor appetite, sleep disorders that may lead to chronic insomnia, and mood disorders that can cause depression, although some desynchronized people do not experience any of these clinical signs (Reinberg and Ashkenazi, 2008; Reinberg et al., 2007, 2013; Touitou et al., 2011, 2017). When the circadian desynchronization becomes chronic, as may be observed under various circumstances like, amongst others, blindness, shift- and night-work, transmeridian flights, alcohol consumption, ingestion of specific medications, and also aging (e.g. Danel et al., 2001; Danel and Touitou, 2004; Touitou et al., 1981, 2011; Reiter et al., 2012; Gooley et al., 2011), it is often referred to as disruption of the circadian system (or chronodisruption). A particularly long-term exposure to artificial light at night (ALAN) is experienced by shift- and night-workers, and several health issues, mainly documented in nurses, can arise as a result of this chronodisruption, such as breast cancer (review in Costa and Haus, 2010; Touitou et al., 2017), cardiometabolic risks and obesity (Fonken et al., 2010; Wong et al., 2015; Reiter et al.,



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Fig. 1. Reproducibility of the circadian patterns of plasma melatonin (top) and cortisol (bottom), in young healthy men. Each subject participated in three 24-h sessions (S1, S2, S3): S2 took place two weeks after S1 and S3 four weeks after S2. The circadian rhythms of the two hormones are highly reproducible from a day to another. Both are useful circadian markers of the time structure. S1 (s), S2 (d), and S3 (▲). Each time point is the mean ± SEM of 31 subjects (from Selmaoui and Touitou, 2003).

2012) and cognitive impairments (Marquié et al., 2015). Inhibition of nocturnal secretion of melatonin, sleep deprivation, and clock disruption are three of the multiple mechanisms of action put forward to explain the deleterious effects of ALAN, and they are considered to be of primary importance (Touitou et al., 2017). Melatonin inhibition by ALAN results in the loss of the multiple biological effects of the hormone, such as free-radical scavenging activity, inhibition of aromatase activity, an anti-estrogenic effect by interaction with estrogen-receptors, inhibition of telomerase activity, perturbation of DNA repair and of the immune system, and oncostatic action by regulation of the metabolism of linoleic acid (Reiter et al., 2014; Touitou et al., 2017). Chronobiotics are substances that adjust the timing of internal biological rhythm and combat the circadian disruption. Amongst the substances potentially presenting chronobiotic properties, a consensus seems to be reached on the possible use of melatonin or its agonists to shift the phase of the human circadian clock,

but optimizing the dose, formulation and especially the time of administration require further studies (Herxheimer and Petrie, 2002; Touitou and Bogdan, 2007). 1.3. Assessment of rhythm synchronization/desynchronization Rhythm synchronization of an organism is assessed by marker rhythms. A marker rhythm is a physiological and rhythmic variable, for which the circadian pattern is highly reproducible on an individual basis and as a group phenomenon (Selmaoui and Touitou, 2003; Mailloux et al., 1999; Benstaali et al., 2001). A marker rhythm allows characterization of the timing of the endogenous rhythmic time structure, and it provides information on the synchronization (or desynchronization) of individuals (see Fig. 1). Circadian patterns of plasma melatonin, plasma cortisol, core body temperature, and motor activity (i.e. actigraphy) are the most frequent markers of rhythms that are used to assess the circadian


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Fig. 2. Salivary and urinary melatonin patterns of nine prepubertal healthy volunteer boys (10.8 ± 0. 11 years). Samples collected every 3 h during a 24-h span of time. Each value is the mean ± SEM. Correlation between salivary melatonin and urinary 6-sulphatoxymelatonin levels: linear regression analysis showed a positive relationship between melatonin and its urinary métabolite (R = +0.968, p < 0.001) (from Touitou et al., 2009). The grey zone corresponds to the dark phase.

time structure both in humans and in laboratory animals (Selmaoui and Touitou, 2003; Mailloux et al., 1999; Benstaali et al., 2001). The choice of a marker rhythm varies according to the aims of the research, e.g. white blood cells in cancer research, core body temperature in sports research, melatonin and cortisol in research dealing with shift work, although most often more than one rhythm marker is used to assess the rhythm synchronization of the subjects being studied. Although melatonin is commonly used as a phase marker in human adults, relatively little data are available regarding chronobiological aspects in children and

adolescents (Ehrenkranz et al., 1982; Attanasio et al., 1985; Ardura et al., 2003; Touitou et al., 2009). Saliva and urine collections provide a convenient, stress-free, non-invasive, and reliable technique for monitoring the biological rhythm of hormones. In prepubertal boys, we found a clear circadian rhythm for both salivary and urinary 6-sulphatoxy-melatonin (Fig. 2), with a higher level of secretion at night without any correlation with the body mass index (Touitou et al., 2009). For individuals of any age, the circadian pattern of melatonin is highly reproducible from day to day (Selmaoui and Touitou, 2003).



2. Physiology of melatonin from birth to adulthood 2.1. Fetus and infants The fetus is exposed to the melatonin rhythm of its mother, i.e. low concentrations during the day and high concentrations at night. During a normal pregnancy, the maternal melatonin level increases progressively until term, and it is readily transferred to the fetus, in which it plays important roles in brain formation and differentiation. In this regard, we have to underline that animal studies have supported a fetal neuroprotective role for melatonin when administered to the mother during pregnancy. Whether melatonin administration to the mother in humans, can reduce the risk of neurosensory disabilities and death, associated with fetal brain injury, for the preterm or term compromised fetus is still unknown (Cochrane library Wilkinson et al., 2016). The maternal melatonin provides the initial circadian signal to the fetus. Alteration of the maternal melatonin level has been associated with disruption of brain programming and consequent long-term effects (Serón-Ferré et al., 2012). Following birth, the secretion of melatonin is low until 2–3 months of age, at which time a circadian rhythmicity of the hormone becomes manifest. Concentrations of the hormone then increase progressively until 1 year of age in both preterm and term infants (Serón-Ferré et al., 2001). A recent study on 35 healthy Caucasian infants born at term and monitored from 6 to 18 weeks of age, showed a clear sequential pattern for the emergence of diurnal biological rhythms between 6 and 18 weeks of postnatal age: cortisol appeared first, at 8 weeks; then melatonin and maximum sleep efficiency at 9 weeks; followed by a mature deep body temperature around 11 weeks (Joseph et al., 2015). The authors postulated that ‘‘it is likely that this represents part of a maturation and adaption process as infants gain equilibrium with their external environment after birth”.

2.2. Children and adolescents Data published in the literature on melatonin secretion in young individuals are contradictory, with studies either reporting no effects (Cavallo, 1992; Ehrenkranz et al., 1982) or decreased nocturnal concentrations of the hormone in healthy children and adolescents at an advanced stage of puberty (Waldhauser et al., 1984; Salti et al., 2000). Cavallo (1993) pointed out that the difficulty with interpreting a number of studies dealing with melatonin in children and adolescents arises from methodological drawbacks, such as the use of single blood samples collected during the day or the night, failure to include temporal characteristics of melatonin secretion, lack of control of the actual duration and intensity of the light exposure, use of broad clinical features without hormonal markers to define puberty, varying sample sizes, and uncontrolled sleep-wake schedules (Cavallo, 1993). Whether melatonin has a role in the onset of puberty is still a matter of debate, and a regulatory role for melatonin has yet to be established in this regard. The relative contributions of age, gender, body mass index (BMI), and puberty stage (Tanner, 1962) on the salivary melatonin amplitude in 69 children and adolescents have been examined by Crowley et al. (2012) who were able to demonstrate a lower salivary melatonin amplitude decline during puberty: pre- and early pubertal youngsters exhibited higher melatonin amplitudes compared to the late- and post-pubertal youngsters. This decline in melatonin was similar for boys and girls, although overall the girls secreted more melatonin than did the boys. In this study, the Tanner stage and gender could explain the salivary melatonin

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amplitude decline during this developmental period, but age and BMI did not. By contrast, other studies did not find such a gender difference (Cavallo, 1992; Griefahn et al., 2003; Salti et al., 2000). With advanced age a decline in melatonin secretion has been reported in a number of studies regarding melatonin patterns in elderly humans (e.g. Touitou et al., 1981; Touitou, 2001; Iguchi et al., 1982; Zhao et al., 2002). 3. Light control of the circadian system Light is the major circadian synchronizer for humans, although non-photic time cues, such as meal times, physical activity and social interaction, also play a part in synchronization of the circadian system. Since the period of the internal clock in humans is not exactly 24 h but close to 24.2 h daily exposure to light allows maintain the 24 h cycle of the internal clock. 3.1. Light effects on melatonin secretion The effects of light on melatonin secretion depend on the time of day of the exposure, the intensity, the duration of the exposure, as well as its spectral properties. Exposure to light in the morning, i.e. within a few hours following the midpoint of melatonin secretion, results in a phase advance, with the peak of melatonin secretion occurring earlier than it would otherwise. On the other hand, when the exposure takes place at the end of the afternoon, i.e. within a few hours prior to the midpoint of melatonin secretion, the clock phase is delayed. An exposure between midnight and 4 am, i.e. at the normal time of peak melatonin secretion, results in a complete inhibition of secretion for the full duration of the exposure. These diverse effects that depend on the time of day can be converted into a phase response curve (PRC) of the effects of light (Moore-Ede et al., 1982) that can be used to treat desynchronized patients so as to reset the timing of their biological clocks when they are either phase-advanced or phase-delayed (Burke et al., 2013; Lewy, 2010; Zeitzer et al., 2014). Light blocks the release of NA by sympathetic terminal nerves of the pineal gland, and as result it neutralizes the activity of N-acetyltransferase (NAT), the key enzyme for synthesis of the hormone which results in a profound inhibition of melatonin synthesis [in Touitou et al., 1993]. Overall, melatonin is considered to be the hand of the clock since it transmits the dark signal to the whole organism. 3.2. Sensitivity of adolescents to light A study of the influence of light at night time on salivary melatonin inhibition in 13 Japanese children who were 9 years of age compared to their parents (average of 41 years of age) found that the percentage of melatonin inhibition by moderately bright light (i.e. 580 lux) in children was almost twice (88% inhibition) that in adults (46% inhibition), suggesting that melatonin is more sensitive to light at night time in children than in adults (Higuchi et al., 2014). Melatonin levels under domestic lighting conditions (i.e. standard room illumination of around 120–140 lux) was suppressed significantly more in children than in adults (51% vs. 26% inhibition, respectively). The pupil sizes in children were significantly larger than those in adults under both dim light and bright light, which might be a cause for greater melatonin suppression (Higuchi et al., 2014). These findings have been extended by a study of adolescent sensitivity to light by Crowley et al. (2015) who investigated the sensitivity of the circadian system to light (at 15, 150, and 500 lux) in 38 pre/midpubertal (i.e. 9.1–14.7 years of age) and 29 late/postpubertal (i.e. 11.5–15.9 years of age) adolescents. They found an increased sensitivity to evening light in


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the pre/midpuberty group, with significantly more suppression of salivary melatonin at all tested light levels in these youngsters. This finding strongly suggests that the delayed circadian timing in older adolescents is not related to increased sensitivity to light at night. However, it remains to be determined whether the mechanisms of entrainment of the circadian system during puberty are affected (e.g. phase-advance or delay) by exposure to nocturnal light (Crowley et al., 2015). 4. Adolescent behavior: from media overuse to Internet addiction The effects on adolescent sleep (shortened and delayed) of electronic media use (television viewing, use of computers, internet and electronic gaming, use of mobile phones or smartphones) have been reported worldwide in several research papers. 4.1. Electronic media overuse Teens (>3 billion users) are spending increasing amounts of time online with benefits but also health risks related to excessive use resulting in Internet addiction, also called Internet Gaming disorder (or addiction), in some adolescent users. According to the 2013 Youth Risk Behavior Survey, 41.3% of adolescents in the United States spent on school days more than 3 h online not dedicated to school work (Kann et al. reported by Jorgenson et al., 2016). Large variations ranging from 0.2% up to 34% depending on the country have been reported in the prevalence rates of Internet Gaming Disorder (IGD) (Young, 2015). A model of intrinsic and extrinsic predictors (perception of risky events and flow, role of parents, media accessibility) of videogaming behavior and adolescent bedtimes showed that the amount of devices owned by an adolescent predicted gaming duration but not school night bedtimes. The key points that were identified to decrease the duration of gaming of adolescents, thus promoting earlier bedtimes, were flow and parental regulation of media (Smith et al., 2015, 2017). 4.2. Internet addiction or Internet gaming disorder Internet addiction or Internet gaming disorder is associated with several health issues such as sleep deprivation (later bedtimes and longer sleep latencies), negative association with daytime functioning (Pieters et al., 2014; Hale and Guan, 2015), mood alteration, depression, attention deficit hyperactivity disorder (ADHD), alcohol consumption, substance use disorders, and family conflicts (Young and Grella, 1998; Kuss and Lopez, 2016; Kaess et al., 2016; Chen and Gau, 2016). Furthermore, significant associations have been demonstrated in a longitudinal study between addictive use of the Internet at the age of 15 and heavy drinking and cigarette smoking at the age of 20 (Lee and Lee, 2017). This underlines the negative effects of addictive Internet use, one of the major issues with adolescents. Internet addiction has been included in the 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). While some authors supported this inclusion in the DSM-V, critical comments have been raised on e.g. the absence of an established definition, the lack of an agreed upon name among the several proposed ones such as «Internet addiction», «problematic Internet use», «compulsive Internet use», the confusion between addiction to Internet and addiction to a specific pursuit, the lack of consensus on symptomatology and assessment of problematic gaming, the social and political effects of declaring a social behavior as a disease. A rushed diagnosis may construct an addiction with potentially harmful effects on formerly healthy populations,

particularly adolescents, etc. (e.g. Weinstein et al., 2017; Aboujaoude, 2017; Aarseth et al., 2016; Kuss et al., 2016; Schou et al., 2016). 4.3. Neural mechanisms of Internet addiction The neural mechanisms underlying Internet Gaming Disorder resemble those of drug addiction. Functional Magnetic Resonance Imaging (fMRI) reported by Weinstein et al. (2017) showed changes in brain regions responsible for control of attention, impulse control, motor, sensory-motor coordination, and emotional regulation. The authors reported lower white matter density in brain regions involved in decision-making, behavioral inhibition and emotional regulation, and dopamine release similar in magnitude to those of drugs of abuse (Weinstein et al., 2017). More research is needed to clarify diagnostic criteria and optimal management and to answer the numerous concerns of researchers regarding the DSM proposal for Internet Gaming disorder 5. Screens of electronic media and blue light impact The American Academy of Pediatrics (2001) recommended that parents limit their children’s and adolescents’ exposure to screens to less than two hours per day. There is, however, a clear evidence that young people exceeds these less than 2 h recommendations irrespective of country of residence (Houghton et al., 2015). 5.1. Overuse of mobile phones and smartphones Adolescents are great users of mobile phones and smartphones with their several applications. A smartphone combines the features of a mobile phone with advanced other features like messaging, media player, video games, video camera, access to Internet. . .. American adolescents reported watching about 8 h of video per month on their smartphones, and 95% of adolescents reported using the internet, with 25% accessing the internet primarily through their mobiles (data of 2012 reported in Fobian et al., 2016). Smartphone overuse and smartphone gaming are a significant social issue and can be a sign of addiction (Liu et al., 2016), a recent concern that has resulted from the dramatic increase in worldwide smartphone use. The risk factors for smartphone addiction are female gender, girls being more prone to become addicted, Evening types, Internet use, alcohol use, and anxiety (Choi et al., 2015; Randler et al., 2016). In addition, excessive mobile phone or smartphone usage may lead to sleep disturbances with later bedtimes, shorter sleep duration, diurnal hypersomnolence, and headaches (Van den Bulck, 2003; Exelmans and Van den Bulck, 2017; Lemola et al., 2015; Pecor et al., 2016). 5.2. Light-emitting diodes (LEDs) impact on clock functioning The use of light-emitting diodes (LEDs) is increasing worldwide because they are long-lasting, have high energy efficiency, and are less expensive. LED bulbs (which are perceived by the users as being white) are in fact extremely enriched with a blue light component which makes them very active on the circadian clock. LEDs emit twice as much blue light as non-LED display screens, and they therefore have a greater impact on the biological clock and alertness than white incandescent bulbs and compact fluorescent bulbs. This blue light component is found in all electronic media such as computers, mobile phones, tablets, televisions, internet and electronic gaming consoles. Exposure of adolescents to these devices prior to bedtime is capable of acting on the clock, thus leading to a phase delay and



a slowing of melatonin secretion (Chang et al., 2015). This has become a great concern for researchers as the adverse effects have been pointed out in several studies (Cain and Gradisar, 2010). Their use at inappropriate times, e.g. in the evening before bedtime, results in an alteration of adolescent sleep that is shortened and delayed (Crowley, 2014). The effects of electronic media on sleep can be explained by the high level of use of a range of devices while their users are not aware of their deleterious effects on sleep, though the effects of pubertal development on adolescent sleep cannot be ruled out (Carskadon et al., 1993). In the United States, 74% of adolescents between the age of 15 and 17 have internet access at home (Van den Bulck, 2010; Weaver et al., 2010). In the same way, excessive mobile phone and internet usage may also lead to sleep disturbances (Calamaro et al., 2009; Pea et al., 2012; Van den Bulck, 2003; de Seze et al., 1999). 5.3. Light at night impact on clock functioning and sleep The concerns researchers have in regard to the exposure of adolescents to light at night, before bedtime, have been highlighted in a number of studies. Reading for 30 min before bedtime on an iPad which emits blue enriched light compared to reading a hardcopy book resulted in higher alertness and decreased sleepiness without any difference in sleep onset latency or time spent in the different sleep stages (Grønli et al., 2016). A field study revealed the negative impact of domestic lighting before the usual bedtime (Burgess and Molina, 2014). A randomized crossover study showed that a 5 h exposure to a white LED-backlit screen elicited a significant suppression of the evening rise in endogenous melatonin and subjective as well as objective sleepiness, and a higher level of alertness and concentration than in subjects working with a nonLED display screen (Cajochen et al., 2011). Another study reported that individuals using a tablet for a two hour period had lower melatonin levels than those using a tablet for two hours while wearing goggles that block blue light (Wood et al., 2013). A study comparing reading a printed book in reflected light versus reading a light-emitting eReader (LE-eBook) in the hours before bedtime found that the LE-eBook decreased subjective sleepiness, lengthened sleep latency, delayed the phase of the melatonin circadian rhythm, and impaired alertness the following morning (Chang et al., 2015). Blue light can also induce photoreceptor damage and may induce severe photochemical damage to the retina (Tosini et al., 2016). The study of retinal degeneration in albino and pigmented rats exposed to domestic levels of various LEDs (cold white, blue and green), showed that white LEDs induce more pronounced retinal degeneration than control fluorocompact lamps, and that pigmented rats are not protected from the deleterious effects of the LEDs. This study also found that exposure to LEDs induced breakdown of the external blood-retinal barrier (Krigel et al., 2016). 6. Adolescent sleep deprivation, a matter of concern The prevalence of sleep disorders in schoolchildren and adolescents in western countries ranges from 15% to around 50% depending on age, country and cultural habits, among other factors (Gradisar et al., 2011; Owens and Weiss, 2017). With age, adolescent bedtime is progressively more delayed both on weekdays and weekends, whereas morning rising time is later on weekends and earlier on weekdays (due to school attendance), resulting in a sleep debt on weekdays (Randler, 2008; Owens, 2010; Owens et al., 2014). The negative impact on sleep (both delayed and shortened) of inappropriate media use has been reported (Cain and Gradisar, 2010). Although the authors acknowledge that research in this area is correlational and not causal in nature, it remains,

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however, that the relationship between adolescent delayed sleep and the use of media at night, which has been reported in different countries over the world, rests a strong argument. Lastly, to reliably estimate adolescent sleep with its five related outcomes (bedtime, wake time, sleep onset latency, sleep duration, and wake after sleep onset), the recommendation has been done to document at least five weekday nights of sleep dairy entries (Short et al., 2017).

6.1. Chronotype move to eveningness Human people differ in their time of circadian preference or chronotype, that is the preferred timing for sleep and activity (Adan et al., 2012). Chronotype can be measured by using comprehensive questionnaires such as the morningness–eveningness questionnaire of Horne and Östberg (1976). Preference for early wake up hours and morning alertness characterize Morning types (MT) subjects (called larks), whereas Evening types (ET) subjects (called owls) prefer later bedtimes and rise times and feel at their best in the evening. Environmental factors (photoperiod, temperature. . .), social factors (courses timing at schools and universities, parental control of adolescent sleep, life style. . .), and genetic factors (Hu et al., 2014) may play a role in the circadian preference. Morningness-eveningness changes significantly during the lifespan, from eveningness in adolescence towards morningness in young adults. In a cross-sectional study based on 26,214 German male and female participants covering the full spectrum of age from very young children until early adulthood (between 0 and 30 years; mean age: 14.68 ± 6.04) the authors showed a strong turn to eveningness at the age of 9 years, and a peak of eveningness around the age of 16 years followed by a return to morningness (Randler et al., 2017). Different data have been, however, published in the literature on this matter (Borisenkov et al., 2010; Roenneberg et al., 2004; review in Randler et al., 2017). The breaking point for the turn towards morningness is 17.2 years in boys and 15.7 in girls. The Center for Disease Control and Prevention (CDC) recommends at least 10 h of daily sleep for school-age children and 7– 8 h of sleep per night for adults. Although adolescents need about 9–9.25 h sleep per night (with, however, large interindividual variation) most of them sleep 7–8 h, resulting in a sleep debt of approximately 2 h per night, which accumulates throughout the week (Wolfson and Carskadon, 1998; Wolfson et al., 2007). This decrease in sleep time is linked to a delayed bedtime with a move of a large number of adolescents around the world to eveningness resulting in a cumulative sleep debt with fatigue, behavioral problems and poor academic achievement (see below). Due to early school starting times, evening-type adolescents experience a greater misalignment between biological and social rhythms: they sleep less on school days, their quality of life related to health is worse, they report more school-related problem, and they achieve lower grades (Carissimi et al., 2016). Recent studies have estimated the prevalence of delayed sleep phase (including DSPD) as 3.4–8.4% among high school students (Saxvig et al., 2012; Sivertsen et al., 2015; Danielsson et al., 2016). Evening orientation is thus associated with a worse academic performance, both in school pupils and university students though such relationship changes over time, being weaker in university students (Tonetti et al., 2015a,b) whereas Morningness has been described as a significant predictor of earlier sleep time, quality of sleep, and hygiene (Vollmer et al., 2017). At the end of adolescence, morningness scores tend to increase with age (Roenneberg et al., 2004). In addition, inadequate sleep may play a role in cardiometabolic risk and obesity at a later age for children and adolescents (Golley et al., 2013; Miller et al., 2015; Quist et al., 2015).


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Table 1 Preventive interventions on sleep and adolescent behavior. According to the item the main actors are presented (parental-based, school- or community-based, and peerbased) though it is evident that the intervention of any of the actors is suitable for each of these items when educational programs are involved. Preventive interventions

Involved partners

Bedroom at night Quiet environment Appropriate temperature Low light exposure No electronic media No television No LEDs No mobile phone Education

Parents, Family, School

Bedtime No cognitive stimulations No emotional stimulations No exposure to bright light No caffeine intake No smoking Education

Parents

All of the partners

Parents, school & peers Parents, school & peers All of the partners

Prevention and education Setting of bedtimes Prevention of substance abuse Moving school start times later Education

Parents Parents, school & peers Policymakers All of the partners

Promotion of sleep hygiene Reduction of computer use Reduction of any screen use Regular bedtime and wake up Regular meal timing Regular practice of physical activities Exposure to light during daytime No caffeine intake No late-night activities No evening light Education

Parents, school & peers Parents Parents Parents Parents Parents, school & peers Parents Parents, school & peers Parents Parents All of the partners

Partners of prevention program School-based Community-based Family-based Computer-based Policymakers Medical doctors School nurses Mass media campaigns

Parents & school Policymakers Education Education Policymakers & associations

Gooding et al., 2016; Gradisar et al., 2011). Fatigue is a frequent complaint of adolescents, that is often related to an excess of recreational (sports, artistic activities. . .), or school work activities, but also to the overuse, even at night, of computers. Late bedtimes, especially after 11:30 PM, have been reported to result in poor sleep, poor school performance, poor motivation with an increased relative risk (RR) for depressive symptoms, and various health hazards e.g. type 2 diabetes, unhealthy diet, smoking, etc. (Merikanto et al., 2013). Psychophysiological variables (e.g. reaction time, eye–hand skill, letters cancellation test, random number addition test, performance test, and logical reasoning) have been measured to better understand rhythmic processes in adolescents and getting potential benefits from the use of these findings in the school environment (Guerin et al., 1991; Onyper et al., 2012). These studies showed that children are tired when they come to school in the morning (for example, 08:30 in France, earlier in the US) then, they gradually increase their learning and attention capacity with two peaks, one in the morning around 10:00–11:00 h, and the other one in the early afternoon around 15:00–16:00 h (Guerin et al., 1991; Touitou and Bégué, 2010). 6.3. Recommendations on sleep hygiene A number of basic recommendations on sleep hygiene including bedroom characteristics and adolescent behaviors (Owens, 2010; Touitou and Bégué, 2010; Bartel et al., 2015) are reported in Table 1. The parental setting of bedtime is considered by adolescents as the main factor determining their bedtime on school nights, resulting in earlier bedtimes, more sleep, less fatigue and improvement of daytime wakefulness (Gangwisch et al., 2010; Short et al., 2013). Parental setting of bedtimes is thus efficient, even if it decreases with age and is no longer accepted by the teens at the age of 17 (Randler and Bilger, 2009). Moving school start times later was found to increase sleep duration and decrease fatigue and daytime sleepiness in an American study (Owens, 2010). Last, adolescents and parents should be educated by medical doctors and school nurses on the key role of sleep in adolescent well being and quality of life. 7. Adolescent substance abuse

6.2. Health impacts of sleep deprivation Recent reports indicate that nearly 30% of American adults report getting an average of 6 h or less of sleep per night, and only 31% of high school students report getting at least 8 h of sleep on an average school night (CDC, 2003). Sleep deprivation impacts strongly on adolescent physical and mental health, as indicated by a large number of disturbances that have been related to a delayed bedtime that result in sleep debt: persistent fatigue, daytime sleepiness, poor appetite, memory deficits, decreased levels of attention and alertness that underlie a doubling in the risk of traffic accidents, impaired concentration and performance, behavioral issues, decreased socialization resulting in poor motivation and poor school attendance, poor academic achievement levels, anxiety, irritability and mood disorders, depression and even suicidal thoughts, drug and substance abuse (e.g. alcohol consumption, caffeine and illicit drug use), increased metabolic risk and BMI, drowsy driving while tired and motor vehicle accidents, and reduced work performances (O’Brien, 2009; James et al., 2011; Saxvig et al., 2012; Touitou, 2013; Crowley et al., 2014; Owens and Weiss, 2017; Fischer et al., 2015; Short and Louca, 2015;

Many unhealthy behaviors like internet addiction (see above), alcohol consumption, smoking, illicit drug use . . . begin during adolescence and lead often to adulthood disorders. They are a major public health issue with increased morbidity and mortality. Beside the effects on adolescent health and well-being, substance abuse has a major impact on families. Several factors can enhance the risk for initiating or continuing substance abuse e.g. socioeconomic status, lack of support or involvement from parents, low levels of academic achievement, low self-image or selfesteem, and predisposition toward drug addiction (Das et al., 2016). 7.1. Alcohol consumption Changes in sleep and circadian misalignment that occur during adolescence may impair reward-related brain dysfunction by disrupting reward mechanisms, and thus increase the risk of alcohol use disorders (Hasler and Clark, 2013; Hasler et al., 2014). This results in severe daytime sleepiness, diminished reaction time and performance that have been found with alcohol consumption of adolescents before bedtime (Walsh et al., 1991; Popovici and French, 2013). In this respect, we have to underline that alcohol by itself is able to desynchronize the circadian system (Danel and



Touitou, 2004; Danel et al., 2001; Reinberg et al., 2010), even at moderate doses (Reinberg and Touitou, 1996). In adolescent girls the alteration of the circadian time structure with oral contraceptives (Reinberg et al., 1996) may have a cumulative effect with alcohol. As a result, adolescents who consume alcohol to promote sleep suffer more traffic accidents and accidents at home (Walsh et al., 1991). Regular alcohol use, binge drinking and other risk-taking behaviors (smoking, substance use. . .) emerge in adolescence. Young age of drinking onset is associated with increased risk for lifetime violence, fights and injuries associated with alcohol use (Mair et al., 2013) and development of alcohol dependence (Cheng et al., 2016) in interaction with sleep problems in adolescent boys (Comasco et al., 2010). Besides, in late adolescence less REM, and more stage 2 sleep have been reported with alcohol consumption (Chan et al., 2013). Furthermore, alcohol use is associated with dependence in adulthood, but also with more mental health and social harms. High alcohol consumption in late adolescence continues into adulthood, is associated with alcohol issues including dependence, and the likelihood of developing a substance use disorder later in life (McCambridge et al., 2011). The adolescent brain, especially the hippocampus, may be particularly vulnerable to the effects of alcohol (Welch et al., 2013), thus predisposing the adolescent to mental health and neurocognitive problems which can persist into adulthood (Hanson et al., 2011; Welch et al., 2013).

7.2. Binge drinking Adolescent binge drinking (i.e. consumption of five or more drinks in a row) is an increasingly common behavior among teenagers over the world that induces long-lasting neurobehavioral alterations in adulthood. Binge drinking peaks between the ages of 18 and 25 years. Around one-third of college students report heavy episodic drinking at least once in the past 2 weeks i.e. 4–5 or more drinks in one sitting (Merrill and Carey, 2016). The percentage of students who reported being drunk 10 times or more in the last year differed according to the country, e.g. 8% in the United States and 40% in Denmark (Andersson et al., 2002; Crews et al., 2016). The Clock genes PER2, BMAL1 and other clock gene variants have been found to be associated with alcohol consumption and abuse (Partonen, 2015). Alcohol binge drinking could alter human development with, however, variations in genetics, peer groups, family structure, early life experiences, and the emergence of psychopathology that confound studies. Experimental data arising from the Neurobiology of Adolescent Drinking in Adulthood (NADIA) Consortium support the hypothesis that adolescent binge drinking leads to long-lasting changes in the adult brain that increase risks of adult psychopathology, particularly for alcohol dependence (Crews et al., 2016). Adolescents are less sensitive to ethanol sedative-motor responses that most likely contribute to binge drinking and blackouts. This means that they have a low sensitivity to alcohol-induced motor incoordination and sedative responses that can promote, with other associated factors, extreme binge drinking and elevated blood alcohol levels (Popovici and French, 2013). The personality profile of binge drinking in students i.e. anxious personality in women and impulsive personality in men should be interesting to take in account in studies dealing with prevention and treatment (Adan et al., 2016). The harmful effects of exposure to alcohol marketing should be underlined. Young people who have greater exposure to alcohol marketing appear to be more likely subsequently to initiate alcohol use and engage in binge and hazardous drinking (Jernigan et al., 2017).

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8. Cigarette smoking and e-cigarettes Tobacco use is prevalent among adolescents. Nicotine exposure results in deficits in working memory and attention, increases anxiety and impulsivity and affects adolescent development. In addition, experimental studies suggest that nicotine has a priming effect that increases addiction liability for other drugs (England et al., 2017). 8.1. Tobacco use Tobacco use is started and established primarily during childhood and adolescence which is an age of increased nicotine addiction risk. Approximately 5 million middle and high school American students were current tobacco users in 2015 (Singh et al., 2016). The large number of adolescents who start smoking early in life and continue throughout adulthood is an important concern. Almost 90% of adults who smoke began at or before 18 years of age. The most established predictors of initiation and maintenance of smoking during adolescence are social and environmental factors, such as friend smoking, peer and parental smoking, exposure to tobacco advertising. Flavours in tobacco products are substances intentionally added to increase the attractiveness of the product to adolescents and young adults interested in initiating tobacco use or experimenting with different products due to the availability of different flavours (Huang et al., 2016). The World Health Organization Framework Convention on Tobacco Control guidelines (2012) recommended restrictions or bans on flavours in tobacco products and recognised that «masking tobacco smoke harshness with flavours contributes to promoting and sustaining tobacco use» and that «there is no justification for permitting the use of ingredients, such as flavouring agents, which help make tobacco products attractive». 8.2. Electronic cigarettes Electronic nicotine delivery systems (ENDS) or electronic cigarettes (e-cigarettes) are handheld battery-operated devices that vaporize a solution the user then inhales. They contain nicotine (some are free of nicotine), chemicals and flavours (chocolate, cinnamon . . .) that attract adolescents. E-cigarettes are subject to considerable public health debate. While they are supported by some authors as safer than conventional cigarettes and as potentially valuable in helping quitting or reducing smoking (Bullen et al., 2013), others, by contrast, raise their potential health issues (Clacy and Babineau, 2016; Peterson and Hecht, 2017). Furthermore, e-cigarettes may be used as a gateway to traditional cigarette use by non-smokers, and during early adolescence, youth using e-cigarettes are more likely to smoke traditional cigarettes compared to youth not using e-cigarette (Lanza et al., 2017). 8.3. Cannabis E-cigarettes can be used to vaporize cannabis, although use rates among adolescents are not yet precisely known (Morean et al., 2015, 2017). About three-fourths of American adolescents did not think there was great risk in using cannabis (Hughes et al., 2016). The practice of mixing tobacco with marijuana by Australian aboriginal youth, and the resultant coalition of dependencies, will likely presage according to the authors a rise in pulmonary and central nervous system pathology over the coming decades (Iede et al., 2016). Furthermore, a review of the current literature points out a strong association between early, frequent,


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and heavy adolescent cannabis exposure and impaired cognition and persistent, adverse neuropsychiatric outcomes in adulthood, though it remains to demonstrate that cannabis consumption alone is sufficient to cause these deficits in adolescents (Levine et al., 2017). Lastly, cannabis use during adolescence increases the risk of developing a psychiatric disorder in adulthood, including anxiety, depression, and schizophrenia, though genetic factors and environmental factors cannot be ruled out (Renard et al., 2014). 9. Interventions on risk behaviors The reasons why children and adolescents are getting less sleep are critical as they may result in research and recommendations on how to prevent their circadian disruption and sleep loss. Adolescence is a critical period of development with longlasting implications for health and well-being. Engagement in risk behaviors such as tobacco, alcohol, cannabis and other illicit drug use has multiple negative health consequences, including respiratory problems, violence, injury, sexual risk behavior, poorer educational attainment, psychosis, mental illness, risk of dependence, morbidity and mortality later in life (see above). Peer interventions have a role to play in preventing tobacco, alcohol and possibly also cannabis use during adolescence. The inclusion of peers in public health interventions would have benefits in preventing harmful behaviors during adolescence (MacArthur et al., 2016; Das et al., 2016). The effectiveness of interventions to prevent tobacco, alcohol, and drug use among adolescents has been reported in an overview where the authors report that school-based prevention programs, family-based intensive interventions, and mass media campaigns over long period of time are effective in reducing smoking (Das et al., 2016). There is, however, moderate-quality evidence that family-based interventions prevent children and adolescents from starting to smoke (Thomas et al., 2016). With regard to alcohol use, school-based alcohol interventions have been associated with reduced frequency of drinking, while family-based interventions have a small but persistent effect on alcohol misuse among adolescents (Das et al., 2016). For drug abuse, school-based interventions based on a combination of social competence and social influence approaches have shown protective effects against cannabis and drug use, including combined substance abuse (Das et al., 2016). The evaluation of programmes of prevention strategies (n = 288; 436,180 students; elementary school, early adolescence, middle and late adolescence) on smoking, alcohol and drug use allowed to underline that the prevention depended upon the age group : elementary schoolchildren benefitted from enhancing personal competencies, targeting social norms was beneficial for early adolescents, and substance use prevention increased during late adolescence (Onrust et al., 2016). 10. Conclusion We are living in the digital age. Children and adolescents use everyday, even at night, all kinds of consoles and screens. These devices have been shown to have harmful effects on sleep, and on circadian physiology. This behavior results in sleep deprivation and impacts strongly on adolescent mental, social and physical health. Light at night, before bedtime, both in the living areas and in the adolescents’ and children’s bedrooms should therefore be reduced and controlled, as this affords the most straightforward way to minimize the deleterious effects of such exposure, and reduce circadian clock misalignment. Any type of tablet (e.g. iPads, computers, smartphones, etc.) emitting blue-enriched light that blocks the secretion of melatonin

and that delays the phase of the circadian clock results in a rhythm desynchronization that in the long run results in disruption of the circadian time structure. Technical progress in regard to the design of LED devices might also be able to yield such an outcome. With this in mind, manufacturers should be aware of the health impacts on the young (and others!) of self-luminous devices, and they should find ways to control the level of emission of harmful blue light so as to prevent disruption of the internal clock and its numerous adverse health effects. Lastly, wearing blue-blocker glasses may be useful in adolescents as a countermeasure for alerting effects and melatonin suppression induced by light exposure through LED screens and potentially impede the negative effects of exposure to light at night on the circadian system (Van der Lely et al., 2015). A sleep education program based on a checklist of sleeppromoting behaviors on daytime sleepiness in adolescents, as recently proposed by a Japanese team, could improve sleeppromoting behavior and sleep patterns (Tamura and Tanaka, 2016). A knowledge-to-action framework to assess the strengths and weaknesses of such kinds of programs and to identify strategies that can be used to enhance the translation of empirical evidence in pediatric sleep to effective action has been proposed (Gruber, 2016). On schooldays and during the weekend, parental control may have a moderating effect on the relationship between bedtime and media use (Pieters et al., 2014). Unhealthy adolescent behaviors lead often to adulthood disorders. Further research is needed to evaluate the effectiveness of specific intervention components with standardized interventions and outcome measures. Various delivery platforms, including digital platforms and policy initiative, may improve substance abuse outcomes among adolescents. Further research is needed to better understand the risk behaviors of adolescents and the way to better combat them (Patton et al., 2016). Lastly, the permanent social jet lag experienced by a number of adolescents should be considered as a matter of public health.

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