Journal of Physiology - Paris 110 (2016) 467–479

Contents lists available at ScienceDirect

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

a r t i c l e i n f o a b s t r a c t

Article history: Although sleep is a key element in adolescent development, teens are spending increasing amounts of
Received 24 October 2016 time online with health risks related to excessive use of electronic media (computers, smartphones,
Received in revised form 12 April 2017 tablets, consoles. . .) negatively associated with daytime functioning and sleep outcomes. Adolescent
Accepted 5 May 2017
sleep becomes irregular, shortened and delayed in relation with later sleep onset and early waking time
Available online 12 May 2017
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
Keywords:
great concern because LEDs emit much more blue light than white incandescent bulbs and compact flu-
Electronic media use
Light at night
orescent bulbs and have therefore a greater impact on the biological clock. A large number of adolescents
LEDs move to evening chronotype and experience a misalignment between biological and social rhythms
Clock disruption which, added to sleep loss, results in e.g. fatigue, daytime sleepiness, behavioral problems and poor aca-
Melatonin demic achievement. This paper on adolescent circadian disruption will review the sensitivity of adoles-
Adolescent sleep cents to light including LEDs with the effects on the circadian system, the crosstalk between the clock and
Sleepiness the pineal gland, the role of melatonin, and the behavior of some adolescents (media use, alcohol con-
Fatigue sumption, binge drinking, smoking habits, stimulant use. . .). Lastly, some practical recommendations
Chronotype
and perspectives are put forward. The permanent social jet lag resulting in clock misalignment experi-
Internet use
enced by a number of adolescents should be considered as a matter of public health.
Cellular phone
Rhythm desynchronization Ó 2017 Elsevier Ltd. All rights reserved.
Alcohol
Smoking
Binge drinking
Substance abuse

Contents

1. The circadian system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 468

1.1. From the internal clock to circadian rhythms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 468
1.2. From rhythm desynchronization to circadian disruption . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 468
1.3. Assessment of rhythm synchronization/desynchronization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 469
2. Physiology of melatonin from birth to adulthood . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 471
2.1. Fetus and infants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 471
2.2. Children and adolescents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 471
3. Light control of the circadian system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 471
3.1. Light effects on melatonin secretion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 471
3.2. Sensitivity of adolescents to light. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 471
4. Adolescent behavior: from media overuse to Internet addiction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 472
4.1. Electronic media overuse . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 472
4.2. Internet addiction or Internet gaming disorder. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 472
4.3. Neural mechanisms of Internet addiction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 472
5. Screens of electronic media and blue light impact . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 472

⇑ Corresponding author.
E-mail address: yvan.touitou@chronobiology.fr (Y. Touitou).

http://dx.doi.org/10.1016/j.jphysparis.2017.05.001
0928-4257/Ó 2017 Elsevier Ltd. All rights reserved.
468 Y. Touitou et al. / Journal of Physiology - Paris 110 (2016) 467–479

5.1. Overuse of mobile phones and smartphones. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 472

5.2. Light-emitting diodes (LEDs) impact on clock functioning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 472
5.3. Light at night impact on clock functioning and sleep . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 473
6. Adolescent sleep deprivation, a matter of concern . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 473
6.1. Chronotype move to eveningness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 473
6.2. Health impacts of sleep deprivation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 474
6.3. Recommendations on sleep hygiene . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 474
7. Adolescent substance abuse . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 474
7.1. Alcohol consumption . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 474
7.2. Binge drinking . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 475
8. Cigarette smoking and e-cigarettes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 475
8.1. Tobacco use . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 475
8.2. Electronic cigarettes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 475
8.3. Cannabis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 475
9. Interventions on risk behaviors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 476
10. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 476
Conflict of interest. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 476
Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 476
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 476

humans and in experimental animals, both diurnal and nocturnal,

with daily dark phase plasma concentrations three to ten times
The World Health Organization (WHO) defines adolescents as
higher than during the light phase. This is related to a neuronal
individuals in the 10–19 year age group, and youths as the
message that is initiated in the SCN when the neurons are no
15–24 year age group. These two groups are considered to be
longer subjected to the effect of light. This results in an activation
young individuals, and they range from 10 to 24 years of age.
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
1. The circadian system
key melatonin synthesizing enzyme N-acetyltransferase.

1.1. From the internal clock to circadian rhythms

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 mecha-
nism of the clock is present in every cell of the body. Clock genes
(some examples in humans are CLOCK, CRY, PER, and BMAL1) com-
prise 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. Intrinsi-
cally photosensitive retinal ganglion cells (ipRGCs) in the eye con-
tain 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 supe-
rior cervical ganglion by multisynaptic complexes, so as to end up
at the pineal gland which secretes melatonin (5-methoxy-N-
acetyltryptamine) 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
1.2. From rhythm desynchronization to circadian disruption
Under normal environmental conditions light is the major syn-
chronizer (also called entraining agent or Zeitgeber) of the circa-
dian 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 num-
ber of atypical symptoms such as, amongst others, persistent fati-
gue, 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 clini-
cal 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 chronodisrup-
tion). 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.,
 Y. Touitou et al. / Journal of Physiology - Paris 110 (2016) 467–479 469

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 for-
ward to explain the deleterious effects of ALAN, and they are con-
sidered 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 vari-
able, 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 mar-
ker rhythm allows characterization of the timing of the endoge-
nous 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
470 Y. Touitou et al. / Journal of Physiology - Paris 110 (2016) 467–479

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 collec-
tions 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 sali-
vary 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).
 Y. Touitou et al. / Journal of Physiology - Paris 110 (2016) 467–479
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 trans-
ferred to the fetus, in which it plays important roles in brain for-
mation 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 preg-
nancy. 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 pro-
cess 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 diffi-
culty 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
471
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 circa-
dian 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 secre-
tion, results in a phase advance, with the peak of melatonin secre-
tion 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 desyn-
chronized 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-acetyl-
transferase (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 mela-
tonin 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 sensi-
tive 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 sup-
pressed significantly more in children than in adults (51% vs. 26%
inhibition, respectively). The pupil sizes in children were signifi-
cantly 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) ado-
lescents. They found an increased sensitivity to evening light in
472 Y. Touitou et al. / Journal of Physiology - Paris 110 (2016) 467–479
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 mech-
anisms 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 elec-
tronic 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 dis-
order (or addiction), in some adolescent users. According to the
2013 Youth Risk Behavior Survey, 41.3% of adolescents in the Uni-
ted 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 video-
gaming behavior and adolescent bedtimes showed that the
amount of devices owned by an adolescent predicted gaming dura-
tion but not school night bedtimes. The key points that were iden-
tified 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 alter-
ation, 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 pro-
posed 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 dis-
ease. A rushed diagnosis may construct an addiction with poten-
tially 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 emo-
tional 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 magni-
tude to those of drugs of abuse (Weinstein et al., 2017). More
research is needed to clarify diagnostic criteria and optimal man-
agement 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 fea-
tures of a mobile phone with advanced other features like messag-
ing, 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 signifi-
cant 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 addic-
tion 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 dura-
tion, 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 com-
ponent 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 alert-
ness 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 elec-
tronic 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
 Y. Touitou et al. / Journal of Physiology - Paris 110 (2016) 467–479
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 ado-
lescents 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 nega-
tive 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 signif-
icant 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 non-
LED 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, length-
ened 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 reti-
nal degeneration than control fluorocompact lamps, and that pig-
mented rats are not protected from the deleterious effects of the
LEDs. This study also found that exposure to LEDs induced break-
down 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 adoles-
cents in western countries ranges from 15% to around 50% depend-
ing on age, country and cultural habits, among other factors
(Gradisar et al., 2011; Owens and Weiss, 2017). With age, adoles-
cent 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 short-
ened) 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,
473
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 reli-
ably estimate adolescent sleep with its five related outcomes (bed-
time, wake time, sleep onset latency, sleep duration, and wake
after sleep onset), the recommendation has been done to docu-
ment 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 compre-
hensive 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, tempera-
ture. . .), social factors (courses timing at schools and universities,
parental control of adolescent sleep, life style. . .), and genetic fac-
tors (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 break-
ing 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) recom-
mends 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 vari-
ation) 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 prob-
lems 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 adoles-
cence, morningness scores tend to increase with age (Roenneberg
et al., 2004). In addition, inadequate sleep may play a role in car-
diometabolic risk and obesity at a later age for children and adoles-
cents (Golley et al., 2013; Miller et al., 2015; Quist et al., 2015).
474 Y. Touitou et al. / Journal of Physiology - Paris 110 (2016) 467–479

Table 1 Gooding et al., 2016; Gradisar et al., 2011). Fatigue is a frequent

Preventive interventions on sleep and adolescent behavior. According to the item the complaint of adolescents, that is often related to an excess of recre-
main actors are presented (parental-based, school- or community-based, and peer-
based) though it is evident that the intervention of any of the actors is suitable for
ational (sports, artistic activities. . .), or school work activities, but
each of these items when educational programs are involved. also to the overuse, even at night, of computers. Late bedtimes,
especially after 11:30 PM, have been reported to result in poor
Preventive interventions Involved partners
sleep, poor school performance, poor motivation with an increased
Bedroom at night Parents, Family, School relative risk (RR) for depressive symptoms, and various health haz-
Quiet environment
Appropriate temperature
ards e.g. type 2 diabetes, unhealthy diet, smoking, etc. (Merikanto
Low light exposure et al., 2013).
No electronic media Psychophysiological variables (e.g. reaction time, eye–hand
No television skill, letters cancellation test, random number addition test, perfor-
No LEDs
mance test, and logical reasoning) have been measured to better
No mobile phone
Education All of the partners understand rhythmic processes in adolescents and getting poten-
tial benefits from the use of these findings in the school environ-
Bedtime Parents
No cognitive stimulations ment (Guerin et al., 1991; Onyper et al., 2012). These studies
No emotional stimulations showed that children are tired when they come to school in the
No exposure to bright light morning (for example, 08:30 in France, earlier in the US) then, they
No caffeine intake Parents, school & peers gradually increase their learning and attention capacity with two
No smoking Parents, school & peers
peaks, one in the morning around 10:00–11:00 h, and the other
Education All of the partners
one in the early afternoon around 15:00–16:00 h (Guerin et al.,
Prevention and education
Setting of bedtimes Parents
1991; Touitou and Bégué, 2010).
Prevention of substance abuse Parents, school & peers
Moving school start times later Policymakers 6.3. Recommendations on sleep hygiene
Education All of the partners
Promotion of sleep hygiene Parents, school & peers A number of basic recommendations on sleep hygiene including
Reduction of computer use Parents
Reduction of any screen use Parents
bedroom characteristics and adolescent behaviors (Owens, 2010;
Regular bedtime and wake up Parents Touitou and Bégué, 2010; Bartel et al., 2015) are reported in Table 1.
Regular meal timing Parents The parental setting of bedtime is considered by adolescents as the
Regular practice of physical activities Parents, school & peers main factor determining their bedtime on school nights, resulting
Exposure to light during daytime Parents
in earlier bedtimes, more sleep, less fatigue and improvement of
No caffeine intake Parents, school & peers
No late-night activities Parents daytime wakefulness (Gangwisch et al., 2010; Short et al., 2013).
No evening light Parents Parental setting of bedtimes is thus efficient, even if it decreases
Education All of the partners with age and is no longer accepted by the teens at the age of 17
Partners of prevention program (Randler and Bilger, 2009). Moving school start times later was
School-based found to increase sleep duration and decrease fatigue and daytime
Community-based sleepiness in an American study (Owens, 2010). Last, adolescents
Family-based
Computer-based Parents & school
and parents should be educated by medical doctors and school
Policymakers Policymakers nurses on the key role of sleep in adolescent well being and quality
Medical doctors Education of life.
School nurses Education
Mass media campaigns Policymakers & associations
7. Adolescent substance abuse

Many unhealthy behaviors like internet addiction (see above),

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, day-
time 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, behav-
ioral issues, decreased socialization resulting in poor motivation
and poor school attendance, poor academic achievement levels,
anxiety, irritability and mood disorders, depression and even suici-
dal 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;
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. socio-
economic status, lack of support or involvement from parents,
low levels of academic achievement, low self-image or self-
esteem, 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 dis-
rupting 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
 Y. Touitou et al. / Journal of Physiology - Paris 110 (2016) 467–479
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 contracep-
tives (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 behav-
iors (smoking, substance use. . .) emerge in adolescence. Young age
of drinking onset is associated with increased risk for lifetime vio-
lence, 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 contin-
ues into adulthood, is associated with alcohol issues including
dependence, and the likelihood of developing a substance use dis-
order later in life (McCambridge et al., 2011).
The adolescent brain, especially the hippocampus, may be par-
ticularly vulnerable to the effects of alcohol (Welch et al., 2013),
thus predisposing the adolescent to mental health and neuro-
cognitive 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 teen-
agers 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 per-
centage of students who reported being drunk 10 times or more
in the last year differed according to the country, e.g. 8% in the Uni-
ted 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 con-
found 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 psy-
chopathology, 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 per-
sonality 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).
475
8. Cigarette smoking and e-cigarettes
Tobacco use is prevalent among adolescents. Nicotine exposure
results in deficits in working memory and attention, increases anx-
iety and impulsivity and affects adolescent development. In addi-
tion, 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 child-
hood 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 differ-
ent 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 nico-
tine (some are free of nicotine), chemicals and flavours (choco-
late, cinnamon . . .) that attract adolescents. E-cigarettes are
subject to considerable public health debate. While they are sup-
ported 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 tra-
ditional cigarette use by non-smokers, and during early adoles-
cence, 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 depen-
dencies, will likely presage according to the authors a rise in pul-
monary and central nervous system pathology over the coming
decades (Iede et al., 2016). Furthermore, a review of the current lit-
erature points out a strong association between early, frequent,
476 Y. Touitou et al. / Journal of Physiology - Paris 110 (2016) 467–479
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 environ-
mental 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 long-
lasting 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 respira-
tory problems, violence, injury, sexual risk behavior, poorer educa-
tional 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 bene-
fits in preventing harmful behaviors during adolescence
(MacArthur et al., 2016; Das et al., 2016). The effectiveness of inter-
ventions to prevent tobacco, alcohol, and drug use among adoles-
cents 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, how-
ever, 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 combi-
nation 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 per-
sonal 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 alert-
ing 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 sleep-
promoting behaviors on daytime sleepiness in adolescents, as
recently proposed by a Japanese team, could improve sleep-
promoting 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 strate-
gies that can be used to enhance the translation of empirical evi-
dence 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 disor-
ders. Further research is needed to evaluate the effectiveness of
specific intervention components with standardized interventions
and outcome measures. Various delivery platforms, including dig-
ital 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.
Conflict of interest
The authors report no conflict of interest.
Acknowledgments
The help of the Thérèse Tremel Pontremoli donation for
Chronobiologic Reseach at The Fondation Adolphe de Rothschild,
Paris, is acknowledged.
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