Sei sulla pagina 1di 19

Adolescent Sleep Deprivation: Its Neurobiological Causes

and Its Impact on School Performance

Elizabeth A. Toledo

University of the Philippines Diliman

Psychology 160: Biopsychology

Ms. Eunice A. Liao

17 May 2016
From the increasing and excessive use of technology, to the need to work both day and

night shifts to earn enough money for the family, to the unbearable traffic that eats up a chunk of

commuters’ time, millions of people have been sleeping less and less hours every day. This lack

of sleep phenomenon has been gradually compromising the health of people worldwide.

Particularly in adolescents, research suggests that sleep deprivation has been undermining teen

health, affecting day-to-day functioning in a wide variety of ways. It is an alarming danger that

we should be understanding, addressing, and learning from.

Sleep is not a luxury but a necessity; it is a basic need. Most of people will sleep for

about 175,000 hours in our lifetimes (Pinel & Barnes, 2014, p. 366). This extraordinary amount

of time we devote on sleep implies how important it is to people’s well-being, even as vital as

the air we breathe and the food and water we eat and drink. Several researches, case studies, and

news about sleep deprivation clearly show that there are serious side effects from lack of sleep.

One famous case is the world record set by Peter Tripp, a famous DJ in New York who stayed

awake for 201 hours or 8.4 days. After 72 hours or 3 days, Tripp was reportedly becoming often

paranoid and confused, laughing hysterically without no reason, and hallucinating (Ingles-Arkell,

2014). Drowsiness and fatigue brought about by lack of sleep also cause more than 100,000

traffic accidents each year, as reported by the National Highway Traffic Safety Administration

(Carpenter, 2001). In extreme cases, there have even been several documented deaths about

excessive lack of sleep due to almost continuously playing of video games, ranging from 12

hours to 22 days (Hunt & Ng, 2015; Mccrum, 2015; Twomey, 2016).
These alarming consequences of sleep deprivation suggest how important sleep is. For

this reason, it is vital to research and study about the lack of sleep and its effects, especially on

adolescents. This research paper is a review of different literature and did not undergo

experimentation or surveys. It aims to explore on sleep deprivation by reviewing literature about

its causes and its effects, especially on adolescents. The researcher chose to narrow in on

adolescents because across postnatal development of human beings, adolescence is the period

wherein changes in the neural and cognitive, social and affect, and behavioral and sexual

development are most dramatic.

The focus of this research paper is on the neurobiological causes of sleep deprivation

among adolescents. Circadian timing system and homeostatic system changes, and alterations in

brain activity, structure and organization changes that result to sleep deprivation will be

explored. Psychosocial causes will be tackled but will not be thoroughly discussed. Another

focus of this report is the impact of sleep deprivation on the school performance of adolescents.

This is discussed by looking at the different affective, behavioral, and cognitive effects

associated with the neurobiological causes of sleep deprivation among adolescents. It should also

be noted that terms such as lack of sleep, insufficient sleep and sleep deprivation are used

interchangeably in this report. They are only used as generic terms and do not refer to specific

amount of sleep, rather to “less sleep than needed.”

According to Merriam-Webster Dictionary (2016), sleep is “the natural state of rest

during which your eyes are close and you become unconscious.” It is a widespread myth that

sleep is just a passive, dormant process. However, it is important to note that sleep is not just a
time when physical and mental activities shut down for a while. Rather, sleep is an active and

dynamic process, which involves several sleep stages.

The research on the stages of sleep started with the invention of the

electroencephalogram (EEG) by German researcher Hans Begrer in the late 1920’s. The

discovery that brain waves change - as evident in EEG activities - as wakefulness shifted into

sleep paved the way for rapid expansion of sleep study. Since 1953, several researchers have

studies about the different stages of sleep, naming Rapid Eye Movement (REM) and non-REM

stages of sleep and showing that sleep consists of several repeating sleep stages. By 1968, the

stages of sleep had become standardized (Mastin, 2013). ​During sleep, we usually pass through

five phases of sleep: stages 1, 2, 3, 4, which consist the ​non-REM sleep, and the ​REM s​ leep.

These stages progress in a cycle from stage 1 to REM sleep, then the cycle starts over again with

stage 1.

Generally, there is a gradual increase in EEG voltage or amplitude and a decrease in EEG

frequency across the progression from stage 1 through stage 4. During the preparation to sleep,

alpha waves, which are bursts of 8- to 12-Hz EEG waves, begin to punctuate the low-voltage,

high-frequency waves of wakefulness. When fallen asleep, there is a sudden transition to stage 1

of sleep. At stage 1, sleep EEG is a low-voltage, high-frequency signal that is similar to, but is

slower than, that that of wakefulness. Our eyes move very slowly and muscle activity slows. At

stage 2, eye movements begin to stop and sleep EEG has a slightly higher amplitude and a lower

frequency, punctuated by two wave forms which are the ​K complexes, t​ he large negative wave

immediately followed by a single large positive wave, and the ​sleep spindles, t​ he 1- to 2-second

waxing and waning burst of 12- to 14-Hz waves​. At stage 3, the largest and slowest brain waves
with a frequency of 1 to 2 Hz called ​delta waves b​ egin to appear occasionally, interspersed with

smaller, faster waves. At stage 4, delta waves are predominant and almost exclusive. These four

stages are non-REM sleep stages, and stages 3 and 4 are often called slow-wave sleep (SWS)

(Pinel & Barnes, 2014, p. 367-368).

When switching into REM sleep, there is a low-amplitude, high-frequency sleep EEG.

Breathing becomes more rapid, irregular, and shallow. The eyes jerk rapidly in various

directions. There is a loss in core-muscle tone and muscles become temporarily paralyzed.

Cerebral activities such as blood flow, oxygen consumption, and neural firing, increase to

wakefulness levels in several brain structures. There is also a general increase in the variability

of autonomic nervous system activities; heart rate increases and blood pressure rises (American

Sleep Association, 2007).

Sleep deprivation and psychosocial factors

The several evidences of most adolescents’ chronical lack of sleep have raised questions,

one of which is about why most adolescents lack sleep. Researchers are curious about why there

seems to be a shift to a later sleeping times of adolescents.

For a variety of reasons, adolescents are particularly more prone to sleep deprivation.

school demands have directly or indirectly contributed to most adolescents’ lack of sleep. A

number of researches explored on how much impact school start times have on teenage students’

sleep cycle. These researches resulted in strikingly similar findings, such that students attending

school with a later or delayed start time were reported to have less daytime sleepiness, and better

attention, concentration and academic performance (Epstein et al., 1998 and Wolfson et al.,
2007). In addition, the pressure to stay awake to finish requirements for school also compel

students to drink more amounts of caffeine. Statistics show that adolescents are the fastest

growing group of caffeine users with an increase of 70% in the past 30 years (Temple, 2009).

Adolescents lack of sleep can be attributed to the advent of technology. Today’s

generation of adolescents have grown up in an electronic age. It is not anymore surprising that

researches have shown that exposure to electronic devices late at night has been associated with

lack of sleep. As reported by the National Sleep Foundation’s 2006 Sleep in America Poll, most

teenagers have in their bedrooms devices such as televisions, music players, video game

consoles, computers, and phones. These teenagers were also reported to engage in an average of

four electronic activities after nine o’clock in the evening (Owens, 2014). Aside from that the use

of electronics displaces sleep, another possible mechanism how electronics lead to adolescents’

lack of sleep is that the light produced by devices is said to disrupt circadian rhythms by

suppressing melatonin, a hormone that regulates sleep-wake cycles (Cain & Gradisar, 2010).

A number of other psychosocial and external factors have been largely attributed to sleep

deprivation among adolescents. However, in recent years, researchers have discovered that

biology also plays big a role in the changing sleep patterns of adolescents. Several researchers

argue that psychosocial factors cannot completely account for the sleep deprivation among


Sleep deprivation and the circadian timing and homeostatic systems

Adolescence is characterized by developments and maturation in psychological and

social aspects. There are changes in self-identity, independence, emotional regulation, and
affiliations with parents and friends (Schulenberg et al., 2004). In addition to these, there are also

physical and neurobiological changes among adolescence.

Researchers found that sleep deprivation particularly among adolescents is partly due to

pubertal alterations in the circadian timing system and the sleep-wake homeostatic system. The

changes in these two systems favor late timing of sleep among adolescents. In human beings, the

circadian timing system establishes and regulates normal sleep-wake cycles, while the

homeostatic system acts like a “sleep pressure” that increases the duration of wakefulness and

dissipates during sleep (Achermann, 2003; Hagenauer, Perryman, Lee & Carskadon, 2009;

Carskadon & Tarokh, 2014).

The circadian timing system is controlled by the body’s “biological clock,” called the

suprachiasmatic nucleus ​(SCN), which rests in the hypothalamus. Signals from the SCN travel

to different brain structures, including the pineal gland, which responds to signals induced by

light, by switching off production of melatonin. The increase in melatonin level when darkness

falls makes people feel drowsy and sleepy (American Sleep Association, 2007). In adolescents,

however, growing evidence supports that light sensitivity of the circadian timing system is

altered during adolescence. Adolescents have a higher light sensitivity, having an advance phase

response to light exposure in the morning and an exaggerated delayed phase response to light

exposure in the evening (Crowley, 2009; Hagenauer, Perryman, Lee, & Carskadon, 2009).

The homeostatic system is said to be the sleep drive of human beings. One research on

adolescent homeostatic system showed that when compared to younger adolescents, older

adolescents are slower to fall asleep at critical times, after 14.5, 16.5, and 18.5 hours awake
(Taylor, Jenni, Acebo, & Carskadon, 2005). Another research showed that the buildup of sleep

drive is slower in older adolescents than young adolescents. This sleep drive was modeled as an

accumulation of slow wave activity (SWA), a marker of homeostatic system in response to sleep

deprivation (Jenni, Achermann, & Carskadon, 2009).

These researches suggest that a developmental change in adolescents’ circadian timing

system and homeostatic system may provide physiologically mediated “excuse” for later

sleeping times during adolescence.

Sleep deprivation and the brain activity, structure, and organization

Aside from the altered sleep-wake regulating systems of the body, several researchers

found that there are changes in the EEG of adolescents. Several analysis of sleep EEG have

provided a detailed description of the changes in sleep among adolescents, with emphasis on

alterations in the characteristics of delta waves or slow waves. These alterations in the

characteristics of delta waves include a dramatic decrease in SWA (Feinberg et al. 2006;

Gaudreau et al. 2001; Jenni and Carskadon 2004) among adolescents. Feinberg and his

colleagues (2006) also reported that the amplitude of slow waves increases until pre-puberty, and

then shows a marked decrease during adolescence. EEG studies also show a 50% reduction of

deep sleep, particularly stage 4 sleep, in adolescence (​Dustman, Shearer, & Emmerson, 1999)​.

These findings suggest that because the adolescent brains have a slow wave or delta wave

activity, which is a major EEG characteristic of sleep stages 3 and 4, they physiologically have a

greater chance of getting less (deep) sleep.

Aside from these changes in slow wave or delta wave, there have also been converging

evidences from EEG, functional magnetic resonance imaging (fMRI), and postmortem studies

which show changes in the adolescent brain structure and organization. Adolescence is

associated with a changing balance between maturing limbic systems and later-maturing frontal

executive functions (Giedd, 2008), an ongoing myelination of neuronal axons, with an increase

in white matter (Courchesne et al. 2000; Reiss et al. 1996; Sowell et al. 2004), and a rapid

decline in the volume of cortical gray matter, which include brain regions involved in muscle

control, sensory perception, speech, memory, self-control, and decision-making (Giedd 2004;

Sowell et al. 2002; Steen et al. 1997). If this decrease gray matter volume reductions are partly

accounted for by decreases in synaptic density, it may be related to the EEG changes previously

discussed. This hypothesis was confirmed, such that curvilinear decrease in gray matter volume

of the frontal and parietal lobes were matched by similar curvilinear decrease in EEG amplitude

of the said regions, supporting the relationship between anatomical brain changes and EEG

changes (Whitford et al., 2006).

These researches suggest that because the adolescent brains are not yet fully developed

and still undergo dramatic changes, they are more susceptible to the neurological consequences

of sleep deprivation, especially in the frontal and parietal lobes.

Sleep deprivation effects and their impact on school performance

Along with the neurobiological etiology of sleep deprivation among adolescents are its

affective, behavioral, and cognitive effects. Whitford and colleagues (2006) showed that

decrease in gray matter volume in frontal and parietal lobes were matched by a similar decrease
in EEG amplitude. Thus, it suggests that while these two brain structures are possible causes of

sleep deprivation, they are also the most affected areas when adolescents experience sleep


The frontal lobe is considered to be the emotional control center and the home to

personality (Kolb & Wishaw, 1990). It is also involved in problem solving, memory, language,

impulse control, decision making, social behavior, and motor function (Levin et. al., 1987). On

the other hand, the parietal lobe is involved in sensation and perception, and concerned with

integrating sensory input, primarily with the visual system (Kandel, Schwartz & Jessel, 1991).

With these functions of the two lobes, it is not surprising that several researches show that sleep

deprivation affect sleepiness and mood (Lo et al., 2016), attention, verbal learning (Drummond

et al, 2000), memory acquisition and retention (Chee & Chuah, 2007; Yoo et al., 2007), and

emotional memories and emotional processing (Sterpenich et al., 2007; Yoo et al., 2007).

Sleep restricted adolescents have been consistently found to be more sleepy and moody.

In their study, Lo and colleagues (2016) found that sleep deprived adolescents (in the

experimental group of their study) demonstrated increased sleepiness and decrease in positive

mood, and that subjective sleepiness did not return to baseline level even after two recovery

nights. Meanwhile, other adolescents (in the control group of their study) maintained baseline

levels of subjective sleepiness and mood the entire day. Other studies supported this claim and

revealed that shorter duration of sleep is associated with high levels of subjective sleepiness

(Wolfson & Carskadon, 1998) and elevated negative affect ratings (Talbot et al., 2010). Because

of sleep deprivation, students tend to sleep during class hours, thus missing class lectures.
In relation to decreased mood, the effects of sleep deprivation in the consolidation of

emotional memories and in emotional processing have been studies through fMRI, and these

studies found that sleep deprivation lead to deterioration in the recollection of neutral and

positive memories, but not of negative memories. Sterpenich and colleagues (2007) found that

recollecting of negative memories (but not positive memories) when sleep deprived lead to

eliciting of larger responses in the amygdala and occipital area. In addition, Yoo and colleagues

(2007) also demonstrated using an emotional stimulus viewing task, that there is enhanced neural

responses to negative stimuli in the amygdala. Thus, students’ negative mood and their tendency

to remember negative memories instead of positive ones, may also affect their relationship with

their classmates and teachers, and also their motivation and attitude toward school work.

Attention also appears to be particularly sensitive to sleep loss. Sleep deprivation affects

attention, such that the lack of sleep result in poor attention. Several fMRI studies on tasks

involving attention and memory have investigated the effects of sleep deprivation on functioning

and the evidences from these fMRI studies are congruent to the effects of sleep deprivation on

decreased neural activity observed in PET studies. Drummond and colleagues (1999),

particularly, found decreased activation in several brain regions such as the frontal lobe

(prefrontal cortex and premotor cortex) and parietal lobe. In school, attention is absolutely

important. It is vital for different aspects of learning and memory storage. Encoding information

and recalling memory both require attention, thus attention is crucial for a student’s school

performance (DNA Learning Center, n.d.).

Sleep deprivation also impairs visual short-term memory, limiting its capacity, as evident

in fMRI scans. Chee and Chuah (2007) used fMRI and manipulated perceptual or memory load
in visual tasks. They found that the tasks showed reductions in parietal activation and declines in

behavioral performance after sleep deprivation. The lack of sleep reduced the linear relationship

between memory load and parietal activation. In addition, Yoo and colleagues (2007) also found

that sleep deprivation produced a significant decrease in hippocampal activity during encoding of

episodic memory, resulting in bad retention of memories. This finding suggest that lack of sleep

compromises both behavioral and neural capacity for encoding new experiences to memory,

which is essential in school for learning.

Interestingly, in contrast to the previously discussed increase in sleepiness and declines in

positive mood, attention, and memory acquisition and retention, some studies found that verbal

learning is better after sleep deprivation. For instance, Drummond and colleagues (2000)

reported an increase in the activation of the prefrontal cortex and parietal lobe during a

performance of a verbal learning task after 35 hours of sleep deprivation. This increased

activation in the prefrontal cortex and parietal lobe was associated with better verbal memory

performance on the task. However, they also found that the greater activation in the said brain

regions only happened when the task was complex and involved difficult words. It is also

important to note that the task only demanded for rote learning and there was no comprehension

and understanding needed. This is not particularly helpful in school, because in most, if not all,

lessons, comprehension and understanding is crucial in learning.

Synthesis, Conclusion, Recommendation

For a long time, external or psychosocial factors are mostly the reasons people pinpoint

as to why people, specifically adolescents, experience sleep deprivation. However, in the recent
years, several researches provide neurobiological evidences that explain why adolescents seem to

have a later sleeping time, thus leading to sleep deprivation.

Adolescence is the period wherein changes in the neural and cognitive, social and affect,

and behavioral and sexual development are most dramatic. Pubertal alterations in the circadian

timing system and the sleep-wake homeostatic system lead to changes in adolescents’ sleeping

habits. Adolescents are more sensitive to light, thus just little exposure to light increases

melatonin levels. In addition, sleep drive is also slower in adolescents. Aside from these changes

in the systems related to sleep, adolescents also undergo developmental changes in brain activity,

structure and organization. As evident in EEG, adolescence is characterized by dramatic decrease

in SWA and in slow wave amplitude, thus leading to 50% reduction of deep sleep, particularly

stage 4 sleep. In addition, the decrease in gray matter of the frontal and parietal lobes were

matched by similar decrease in EEG amplitude of the said regions, supporting the relationship

between anatomical brain changes and EEG changes.

Along with these neurobiological etiology of sleep deprivation among adolescents are its

affective, behavioral, and cognitive effects. Several researches show that sleep deprivation lead

to increased sleepiness, enhanced negative emotional processing leading to negative mood,

reduced attention, and deteriorated memory acquisition and retention. All these consequences of

sleep deprivation among adolescents affect school performance in a wide variety of ways, such

as decelerating or slowing down learning and ruining relationships with classmates and mentors.

These researches on the neurobiological causes of sleep deprivation among adolescents

suggest that developmental changes in the circadian timing system and homeostatic system and
the brain activity, structure and organization, may provide physiologically mediated “excuse” for

later sleeping times during adolescence. It seems like adolescents are “pre-programmed” to sleep

late and thus experience sleep deprivation. With these developmental changes that we cannot

avoid and change, what can we do to prevent or even get rid of sleep deprivation?

Several researches found that in some places, a later school start time lead to reported less

sleepiness and increased academic performance. ​Delayed school start times in Massachusetts

resulted in longer sleep times, improved academic performance, and reduced tardiness (Wolfson

et al., 2005) and in Minnesota, Colorado, and Wyoming public schools, starting school at 8:30am

or later allowed for more than 60% of students to obtain at least eight hours of sleep per school

night. Additional results included improved academic performance, reduced tardiness, and

improved performance on state and national achievement tests (Wahlstrom et al., 2014). Also,

based on the literature about adolescents’ increase sensitivity to light, it is suggested that

minimizing exposure to gadgets late at night should be done to help in reducing later sleeping

time and sleep deprivation.

Just because there are evidences that show that adolescence pubertal and developmental

changes contribute to sleep deprivation, it does not mean that we cannot do our part in keeping

ourselves healthy, by sleeping at the right times and with enough hours.
Achermann, P. (2003). Mathematical models of sleep regulation. ​Frontiers in Bioscience,​ ​8(​ 1-3),

s683. doi:10.2741/1064

American Sleep Association. (2007, May). What is Sleep? Retrieved from

Cain, N., & Gradisar, M. (2010). Electronic media use and sleep in school-aged children and

adolescents: A review. ​Sleep Medicine​, ​11​(8), 735-742. doi:10.1016/j.sleep.2010.02.006

Carskadon, M. A., & Tarokh, L. (2014). Developmental changes in sleep biology and potential

effects on adolescent behavior and caffeine use. ​Nutr Rev​, ​72​, 60-64.


Carpenter, S. (2001). Sleep deprivation may be undermining teen health. ​Monitor on Psychology​,

32​(9), 42. doi:10.1037/e303952004-037

Chee, M. W., & Chuah, Y. M. (2007). Functional neuroimaging and behavioral correlates of

capacity decline in visual short-term memory after sleep deprivation. ​Proceedings of the

National Academy of Sciences,​ ​104(​ 22), 9487-9492. doi:10.1073/pnas.0610712104

Crowley, S. J. (2009). ​Weekend recovery sleep in adolescents: can it occur without a circadian

phase delay? (Doctoral dissertation). Retrieved from ProQuest Dissertations and Theses


DNA Learning Center. (n.d.). ​Attention and Memory​ [Video file]. Retrieved from
Drummond, S. P., Brown, G. G., Gillin, J. C., Stricker, J. L., Wong, E. C., & Buxton, R. B.

(2000). Altered brain response to verbal learning following sleep deprivation.

Nature​, ​403​(6770), 655-657. Retrieved from

Dustman, R., Shearer, D., & Emmerson, R. (1999). Life-span changes in EEG spectral

amplitude, amplitude variability and mean frequency. ​Clinical Neurophysiology,​ ​110(​ 8),

1399-1409. doi:10.1016/s1388-2457(99)00102-9

Giedd, J. N. (2008). The Teen Brain: Insights from Neuroimaging. ​Journal of Adolescent Health,​

42​(4), 335-343. doi:10.1016/j.jadohealth.2008.01.007

Hagenauer, M., Perryman, J., Lee, T., & Carskadon, M. (2009). Adolescent Changes in the

Homeostatic and Circadian Regulation of Sleep. ​Developmental Neuroscience,​ ​31(​ 4),

276-284. doi:10.1159/000216538

Hunt, K., & Ng, N. (2015, February 19). Man dies in Taiwan after 3-day online gaming

binge.​CNN.​ Retrieved from


Inglis-Arkell, E. (2014, March 24). The Sleep Deprivation Publicity Stunt That Drove One Man

Crazy. Retrieved from


Jenni, O. G., Achermann, P., & Carskadon, M. A. (2009). Homeostatic sleep regulation in
adolescents. ​Journal of Sleep,​ ​31(​ 4), 276–284. doi:10.1159/000216538

Kandel, E. R., Schwartz, J. H., & Jessell, T. M. (2000). ​Principles of neural science​ (4th ed.).

Retrieved from

Kolb, B., & Milner, B. (1981). Performance of complex arm and facial movements after focal

brain lesions. ​Neuropsychologia​, ​19​(4), 491-503. doi:10.1016/0028-3932(81)90016-6

Levin, H. S., Amparo, E., Eisenberg, H. M., Williams, D. H., High, W. M., McArdle, C. B., &

Weiner, R. L. (1987). Magnetic resonance imaging and computerized tomography in

relation to the neurobehavioral sequelae of mild and moderate head injuries. ​Journal of

Neurosurgery​, ​66​(5), 706-713. doi:10.3171/jns.1987.66.5.0706

Lo, J. C., Ong, J. L., Leong, R. L., Gooley, J. J., & Chee, M. W. (2016). Cognitive Performance,

Sleepiness, and Mood in Partially Sleep Deprived Adolescents: The Need for Sleep

Study. ​SLEEP,​ ​39(​ 03), 687-698. doi:10.5665/sleep.5552

Mastin, L. (2013). How Sleep Works. Retrieved from

Mccrum, K. (2015, September 3). Tragic teen gamer dies after 'playing computer for 22 days in a

row'. ​Mirror.​ Retrieved from


Merriam Webster Dictionary. (2016). Sleep. In ​Merriam Webster Dictionary.​ Retrieved from

Owens, J. (2014). Insufficient Sleep in Adolescents and Young Adults: An Update on Causes
and Consequences. ​PEDIATRICS​, ​134​(3), e921-e932. doi:10.1542/peds.2014-1696

Pinel, J. P., & Barnes, S. J. (2014). Sleep, Dreaming, and Circadian Rhythms. In ​Introduction to

biopsychology​ (9th ed., pp. 366-389). England: Pearson Education Limited.

Sterpenich, V., Albouy, G., Boly, M., Vandewalle, G., Darsaud, A., Balteau, E., … Maquet, P.

(2007). Sleep-Related Hippocampo-Cortical Interplay during Emotional Memory

Recollection. ​PLoS Biology,​ ​5(​ 11), e282. doi:10.1371/journal.pbio.0050282

Taylor, D. J., Jenni, O. G., Acebo, C., & Carskadon, M. A. (2005). Sleep tendency during

extended wakefulness: insights into adolescent sleep regulation and behavior. ​Journal of

Sleep Research,​ ​14(​ 3), 239-244. doi:10.1111/j.1365-2869.2005.00467.x

Temple, J. L. (2009). Caffeine use in children: What we know, what we have left to learn, and

why we should worry. ​Neuroscience & Biobehavioral Reviews​, ​33​(6), 793-806.


Twomey, R. (2016, January 6). Xbox addict, 20, killed by blood clot after 12-hour gaming

sessions. ​Daily Mail.​ Retrieved from


Whitford, T. J., Rennie, C. J., Grieve, S. M., Clark, C. R., Gordon, E., & Williams, L. M. (2006).

Brain maturation in adolescence: Concurrent changes in neuroanatomy and

neurophysiology. ​Human Brain Mapping,​ ​28(​ 3), 228-237. doi:10.1002/hbm.20273

Wahlstrom, K. L., Dretzke, B. J., Gordon, M. F., Peterson, K., Edwards, K., & Gdula, J.
(2014).​Examining the Impact of Later High School Start Times on the Health and

Academic Performance of High School Students: A Multi-Site Study​. Retrieved from

Center for Applied Research and Educational Improvement website:


Wolfson, A. R., & Carskadon, M. A. (2005). A survey of factors influencing high school start

times. NASSP Bulletin, 89(642), 47-66. doi: 10.1177/019263650508964205

Yoo, S., Gujar, N., Hu, P., Jolesz, F. A., & Walker, M. P. (2007). The human emotional brain

without sleep — a prefrontal amygdala disconnect. ​Current Biology​, ​17​(20), R877-R878.


Yoo, S., Hu, P. T., Gujar, N., Jolesz, F. A., & Walker, M. P. (2007). A deficit in the ability to

form new human memories without sleep. ​Nature Neuroscience​, ​10​(3), 385-392.