New light therapy help teens to sleep more


Teenagers got 43 more minutes of sleep a night after a four-week intervention that reset their body clocks and helped them go to bed earlier, a study from the Stanford University School of Medicine has shown.

The treatment had two components: brief, early morning flashes of bright, broad-spectrum white light to reset the teens’ circadian clocks, and cognitive behavioral therapy that motivated them to try earlier bedtimes.

The findings will be published online Sept. 25 in JAMA Network Open.

“Using a passive light therapy during sleep, we can help teens get an extra 43 minutes of sleep every single night,” said senior author Jamie Zeitzer, Ph.D., associate professor of psychiatry and behavioral sciences.

The light was delivered by a device in the teens’ bedrooms that was programmed to deliver 3-millisecond flashes of light every 20 seconds during the last few hours of sleep.

The brief flashes of light did not wake the teens. Zeitzer’s previous research on jet lag had shown that exposure to short flashes of light can trick the brain into adjusting to a new time zone, even during sleep.

Chronic sleep deprivation is common in teenagers, Zeitzer said.

The body’s circadian clock, which controls daily rhythms of when we sleep and when we’re awake, is naturally set later in teens than in children or in adults, meaning that teens often don’t feel sleepy until late at night.

Teens might also stay up late because of such social influences as homework and electronic device use. Early school start times often require them to wake up before they’re fully rested, further contributing to sleep deprivation.

Prior studies tested whether cognitive behavioral therapy alone could help teens go to sleep earlier. Successes were modest:

After the treatments, teens went to sleep 10 to 15 minutes sooner, on average. But these interventions might have put participants at odds with their own body clocks, asking them to try to fall asleep before they were tired, a behavior that is difficult to sustain, Zeitzer said.

“We have a biological drive to stay awake in the hours before we normally go to sleep,” he said. “So our team wondered if we could adjust the circadian timing, having the teens essentially move their brains to Denver while they’re living in California.”

In the first four-week portion of the new study, researchers tested light therapy alone in a group of 72 teenagers.

For four weeks, half the participants were exposed to the frequent brief light flashes during the final three hours of their normal sleep period.

The remaining participants received a sham light therapy treatment, consisting of three bright flashes of light per hour—too little to reset their body clocks.

Although the light therapy caused the teens who were exposed to it to feel more tired earlier at night, they still stayed up late. Using the light alone was not enough to increase the amount of time they slept.

“We had to convince teens to try to go to sleep earlier,” Zeitzer said.

So, in the second four-week phase of the study, researchers recruited 30 teens; half of them received light therapy during their final two hours of sleep, and half had sham light therapy.

But in this phase of the study, all of the teens also participated in four one-hour sessions of cognitive behavioral therapy to encourage them to go to sleep earlier.

Therapists worked with each teen to identify areas of their lives they cared about that would be better if they had more sleep—such as academics, physical appearance or athletic performance—and used these to help motivate the teens.

The cognitive behavioral therapy also included giving them information about the body clock, sleep hygiene and strategies for waking up earlier on weekends.

In addition to the extra sleep, participants who received both light therapy and cognitive behavioral therapy went to bed an average of 50 minutes earlier than participants who had only cognitive behavioral therapy.

In addition, the participants receiving both therapies were six times more successful than those receiving only cognitive behavioral therapy at maintaining consistent bedtimes.

Prior studies of light therapy for resetting the circadian clock have shown that the early morning flashes of light must continue daily to be effective, Zeitzer said.

“The cool part, for an intervention teens would potentially have to live with for years, is that it is completely passive. We set up the flashing light in the person’s bedroom and put it on a timer; they don’t have to wear a device, remember to turn it on, or do anything else.”

The flashing light used in the study was a programmable bridge beacon; it is not marketed as a sleep aid, Zeitzer said.

The next step, he said, is to figure out the best way to deliver brief cognitive behavioral therapy for improving sleep duration to large numbers of people.

The fate of ambient light: image-forming & nonimage-forming pathways

The primary sensory function of the eyes is to translate information contained in light into images [30]. This is accomplished primarily through two classes of retinal photoreceptors. Cones are color-sensitive photoreceptors while rods respond to changes in brightness and are particularly sensitive to dim light. Light information is converted by these photoreceptors, resulting in the stimulation of retinal ganglion cells (RGCs) that project to subcortical nuclei, including the lateral geniculate nucleus of the thalamus, ultimately terminating in the primary visual cortex and visual attention networks (Figure 1). These pathways provide the sensory information for vision and terminate in areas that process and interpret those sensory signals. For a complete review of the transformation from light information to visual interpretation, please see reference [30].

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Figure 1.
Schematic representation of the destinations for ambient light entering the eye.hDMN: Hypothalamic dorsomedial nucleus; IGL: Intergeniculate leaflet; ipRGC: Intrinsically photosensitive retinal ganglion cell; LC: Locus coeruleus; LGN: Lateral geniculate nucleus; OPN: Olivary pretectal nucleus; PG: Pineal gland; SCN: Suprachiasmatic nucleus; SPVN: Supraparaventricular nucleus; VLPO: Ventrolateral preoptic nucleus.

An additional class of photoreceptor was discovered in the early 2000s and is the starting point for the nonimage-forming (NIF) pathway [31–34]. This third type of photoreceptor is expressed directly by a small proportion of RGCs (termed intrinsically photosensitive RGCs; ipRGCs). These ipRGCs are maximally sensitive to blue light (λ = 460–480 nm) and less so to longer wavelengths including green, amber and red [31]. ipRGCs, combined with information regarding illuminance and color from the rods and cones, then directly project to regions involved in the regulation of or influence the actions of (Figure 1):

  • Circadian rhythms. Projections from the ipRGCs to the suprachiasmatic nucleus (SCN), the primary biological clock for all circadian processes, can directly induce entrainment of either expected or aberrant circadian rhythms [31,35].
  • Melatonin suppression. Stimulation of ipRGCs results in melatonin suppression via the SCN’s projections to the pineal gland as well as the paraventricular nucleus of hypothalamus and superior cervical ganglion [34,36–38].
  • Sleep–wake cycle regulation. In conjunction with the above-mentioned melatonin suppression pathways, direct projections from the ipRGCs go to the ventrolateral preoptic nucleus, subparaventricular nucleus and lateral hypothalamus [34]. The SCN may additionally influence the action of the hypothalamus’s dorsomedial nucleus, and locus coeruleus, affecting the lateral hypothalamus secretion of orexin [33,34].
  • Cognition. The aforementioned pathways regulating circadian rhythms, melatonin suppression and sleep–wake cycles additionally exert both direct and indirect influences on cognition and alertness [26].
  • Emotional processing and mood. The amygdala, a primary site of emotional processing and integration, receives direct ipRGC projection [34,39].
  • Intracranial nociception. ipRGCs project to the trigeminovascular neurons of the thalamus that transmit nociceptive information from the dura to the cortex [40].
  • Pupillary constriction. ipRGCs directly project to the olivary pretectal nucleus [32–34], which in turn project to the Edinger–Westphal nucleus. The cumulative action of this pathway is pupillary constriction. For a complete review of the effects of mTBI on the pupillary light reflex, including NIF pathway contributions, please see [41].

As can be seen, light has the powerful potential to alter numerous biological and cognitive processes through this NIF pathway. Given the complex interactions between circadian timekeepers, hormone and neurotransmitter secretion pathways, cognition, and emotions, light has the potential to positively or negatively influence how individuals function at a very basic level. Consequently, using light as a therapeutic intervention has the potential to directly influence recovery and function following mTBI. In the following sections, we review potential areas of intervention and, where possible, expected outcomes from using light as a therapy.

mTBIs & their consequences

mTBIs are a change or disruption in the normal functioning of the brain subsequent to an external force applied to the head or body [42,43]. Typical guidelines for distinguishing mTBIs from more severe TBIs include a mechanism indicative of mTBI; loss of consciousness <30 min (if at all); post-traumatic amnesia <24 h; Glasgow Coma Scale scores 13–15; and lack of gross abnormalities on traditional neuroimaging [42,44,45]. The effects of a single mTBI are often viewed as transient and may include somatic symptoms, sleep–wake disturbances, and cognitive and behavioral disruptions. However, while these effects are common, the individual manifestations of these are highly individualized and may depend on premorbid functioning and the location and mechanism of injury [46]. Additionally, many individuals experience persistent symptoms associated with an mTBI, and recent findings indicate that the incidence of long-lasting mTBI-related functional decrements may be underestimated [42]. Here we provide an overview of mTBI-related consequences that may be positively affected by light therapy, with an emphasis on sleep and sleep-related consequences given the previously identified NIF-pathway effects.

Sleepiness & fatigue

High-quality sleep is an essential component of all aspects of human performance. Current recommendations for adequate sleep recommend 7–9 h of sleep per night for adults. Despite these recommendations, chronic sleep loss (<5.5 h/night of sleep) in the USA is reaching epidemic levels [47]. For individuals with chronic sleep loss, the consequences are numerous including increased somatization [48,49], poor emotional processing and responsiveness (e.g., increased incidence of depression and anxiety) [50–52], impaired cognition (vigilant attention, executive function, working and long-term memory) [53–56] and poor motor performance [57–59], as well as increased risk for general health issues including diabetes [60–62], cardiovascular disease [60,63], neurodegeneration [64,65] and overall poorer quality of life [66]. While the exact nature of this trend toward chronically undersleeping is not fully understood, work–life stress (e.g., increased expectations for high job-related hours, social stress) as well as the highly prevalent use of fluorescent lighting and blue-shifted light-emitting diode screens at night [67–69] are all implicated.

Compounding the endemic social issue of chronic sleep loss, detrimentally altered sleep is among the most common short- and long-term consequences of mTBI [70–74]. Indeed subjectively perceived traumatic brain injury (TBI)-related sleep–wake disruption is reported by plausibly as many as 70% of all individuals who sustain a TBI (regardless of severity) [70,74,75]. Individuals with mTBI commonly self report insomnia [74–79] and hypersomnolence (excessive sleepiness) [71,75,80–86], though hypersomnia [80,85,87,88] and circadian rhythm sleep disorders [82,89] are also reported. Objectively, these reports are often corroborated by poor sleep efficiency, higher than usual wake after sleep onset and sleep latency, as well as more fragmented sleep and changes in sleep architecture [87,90–95]. Clinically, it is important to recognize that post-mTBI insomnia may be misdiagnosed as a circadian phase issue, specifically delayed sleep phase syndrome [89]. Consequently, individuals sustaining an mTBI may be at an increased risk for all of the aforementioned sleep-related health and performance outcomes without treatment for mTBI-related alterations.

The mechanisms by which mTBI induces altered sleep are not fully understood. However, there are implications from both human studies and animal models that suggest any combination of possible mechanisms including altered circadian hormone regulation (e.g., melatonin release) [96–98] and reductions in neurotransmitter function (e.g., loss of or damage to wake-promoting, orexin-secreting neurons in the hypothalamus) [99–101] among others may be responsible.

In addition to these possible mechanisms of post-mTBI sleep changes, sleep loss or low-quality sleep may impede and impair healing following mTBI. There is considerable evidence indicating that decreases in sleep quantity and quality, both in humans and animals as well as apart from and in relation to mTBI, may impair hippocampal neurogenesis, disrupt ATP production thereby extending the mTBI-initiated neurometabolic cascade [102,103], prolong neuroinflammation [104], impede metabolic waste removal in the brain [105], alter cerebrovascular responsiveness and compromise glymphatic removal of phosphorylated tau [105–107]. Collectively, these effects of sleep disruption may contribute to the short- and long-term clinical presentation of mTBI as well as precipitate the neurodegenerative conditions, particularly tau-related pathologies (e.g., chronic traumatic encephalopathy), commonly thought to be associated with repetitive head trauma.


As noted, an mTBI may induce a sequela whereby disrupted circadian rhythms lead to sleep dysfunction, culminating in daytime sleepiness or fatigue. Broadly, daytime fatigue is associated with decreased alertness and vigilant attention capabilities. Indeed, a recent study demonstrates that evidence of increased fatigue and decreased alertness in an mTBI sample are closely related concepts that are difficult to disentangle [86]. Furthermore, mTBI is associated with degraded alertness and vigilance in both the short and long term [86,108,109]. With regards to daytime alertness, phototherapy may provide a nonpharmacological route for improving daytime functioning in post-mTBI individuals.


mTBIs additionally exert a substantial, negative impact on various cognitive functions, including working memory, attention, executive function and visuospatial processing [20,110–117]. While deficits in these cognitive domains are generally resolved soon after injury (e.g., most within a month, many within 3 months postinjury), there is evidence to suggest subtle, persistent deficits that linger well beyond this clinically accepted time course. Additionally, there are individuals in whom the full impact of these deficits does not resolve quickly.

Apart from mTBI, increasing sleep need as well as sleep deprivation conditions induce marked deterioration in the cognitive capabilities of individuals [53,118–120]. Given the impact of mTBI on sleep, daytime sleepiness and fatigue, it is reasonable to posit that many of the observed cognitive deficits, particularly those that linger beyond the general clinical time course, may be mediated by sleep-related changes.


Depression and increased reporting of depressive symptoms are common following mTBI. The incidence of post-mTBI depression may be as high as 42% in adults and 22% in children and adolescents [121–124]. Premorbid depression is a risk factor for prolonged recovery from mTBI and may be associated with postconcussion symptoms, as well as sleep disruption, impaired cognition and other post-mTBI psychiatric symptoms (e.g., anxiety) [17,20,125–129]. Therefore, ameliorating post-mTBI depression may improve overall symptom presentation and be associated with improvements in sleep and cognitive function.

Post-traumatic headache & pain

Post-traumatic headaches (PTH) and chronic pain are among the most common symptoms experienced by individuals recovering from mTBI. The incidence of PTH likely may be as high 90% [130–135], and the incidence of chronic pain may be as high as 75% [136]. Additionally, both PTH and chronic pain may mediate, or be mediated by, post-mTBI poor sleep, daytime sleepiness, cognitive deficits and depression [122,137–142]. Consequently, the aforementioned benefits of bright or blue light therapy for sleep, cognitive performance and depression may have positive effects on PTH and pain.Go to:

The effects of different types of light & applications to mTBI

Given the range of deficits and changes observed following mTBIs, as well as the known NIF pathways for light, light therapy has the potential to positively influence a wide range of cognitive, emotional and physiological functions. Below, we discuss the known effects of various aspects (colors, intensities) of light across the range of human performance. These findings are additionally summarized in Table 1.

Polychromatic white light

Polychromatic white light is essentially a broad-spectrum light. Because white light includes nearly all wavelengths, it also encompasses the blue light portion of the spectrum (∼460–448 nm) that selectively activates ipRGCs and therefore has important circadian and hormone-secreting properties [31]. Consequently, it could be expected that white or bright light therapy would induce changes in post-mTBI circadian rhythms, sleep and alertness.

A recent meta-analysis indicates that light therapy in general is effective in the treatment of sleep disorders that include circadian rhythm sleep disorders, insomnia, and sleep problems associated with Alzheimer’s disease and dementia [27]. This meta-analysis included randomized controlled trials and within-subject design studies utilizing polychromatic white light, and blue-enriched white light, as well as several studies utilizing monochromic blue light. Overall, positive effects for light therapy were observed for circadian shifts, bed and wake times, sleep onset latency, total sleep time, wake after sleep onset, sleep efficiency, sleepiness and alertness, sleep quality, insomnia symptoms and fatigue [27]. The authors additionally report that light intensity (ranging from 2000 to 10,000 lux in the majority of included studies) had positive effects on individuals with insomnia, with greater intensity increasing the beneficial effects of light therapy [27]. In estimating effect sizes, the authors did not distinguish the effects of bright light from those of blue light; however, only 9% of the included studies specifically examined blue light.

An additional systematic review by Souman et al. examined the effects of light therapy on alertness. Across the reviewed literature, there is the indication that increasing the intensity of polychromatic white light significantly increases subjective alertness [28]. However, this does not appear to translate into improved vigilance or reaction. Additionally, there is limited evidence for significant improvements in subjective or performance-based measures of alertness with blue-shifted polychromatic white light [28]. Cumulatively, these findings suggest that the intensity of polychromatic white light may have positive effects on subjective alertness.

Furthermore, polychromatic white light therapy has been shown to be effective in reducing depressive symptoms in individuals with diagnosed depression, including major depressive disorder. Recent meta-analyses indicate that light therapy, especially polychromatic white light, reduces depressive symptoms at post treatment compared with control participants and this effect is more pronounced for standalone light therapy than for studies using light as an adjunctive therapy [29,143]. The effect is additionally stronger when light therapy is used in the morning than any other time [29]. These effects were observed over studies including polychromatic white, green and pale blue light [29,143].

Monochromatic blue & blue-shifted white light

As previously noted with polychromatic white light, blue light therapy – including monochromatic blue and blue-enriched white light – alters circadian rhythms, particularly the timing of melatonin release, in individuals with a variety of sleep-disrupted conditions [27,144]. These studies demonstrate that short amounts (30 min or more) of focused and intentional daily light therapy in the morning effectively advances individuals’ circadian rhythms, evidenced by the timing of melatonin secretion. In general, the effects of phototherapy are condition dependent, but may include changes in circadian rhythm and improvements in sleep duration, self-reported sleep quality, insomnia symptoms and fatigue [27].

In addition to the direct effects of monochromatic blue light therapy on sleep quantity and quality, the appropriate timing of melatonin secretion is essential for maintaining normal daytime arousal and minimizing fatigue. There is robust evidence that blue-wavelength light is effective in acutely decreasing sleepiness and fatigue [145–152] as well as increasing concentrations of arousal-promoting hormones (e.g., cortisol) [153]. Furthermore, blue light therapy has positive effects on increasing alertness [145,147,149,152,154–169]. This phenomenon is present both during the day (e.g., morning blue light exposure) and night.

Prior work has additionally demonstrated that blue light therapy increases activation in cognition-related, task-specific brain regions [157,159,170–176]. However, while light affects brain activation, the actual behavioral effects of blue light exposure are not quite as clear. Individual studies have demonstrated improvements in cognitive performance on working memory, digit recall, sustained attention and arithmetic tasks while others have shown no improvements or even reduced performance in response to light exposure [145,158,169,176–184]. It is thus unclear the extent to which blue light therapy may directly affect cognitive performance beyond those conferred by improvements or alterations in sleep, fatigue or overall alertness.

With respect to mood and affect, blue or blue-shifted light can variously cause [143,185] or improve [29,186] depressive symptoms depending on the timing of therapy (e.g., when timing coincides with or in opposition to naturally expected patterns). Mood disorders, including depression, are associated with the homeostatic maintenance of circulating stress hormones. Among these, glucocorticoids like cortisol exhibit circadian rhythmicity, with a night-time accumulation period and clearance during the day [187,188]. Thus, blue light that influences circadian rhythms, as previously described for sleep and melatonin, may impart a beneficial effect on glucocorticoid expression when utilized in circadian-optimal timings or may induce or worsen mood disorders when mistimed (e.g., night-time use of light-emitting diode screens).

However, one potential pitfall in the application of blue light therapy as described to this point is the exacerbation of PTH. The blue light-sensitive ipRGCs directly project to the trigeminovascular neurons in the thalamus [40]. Prior research related to migraine indicates that these neurons transmit nociceptive signals originating in the dura to cortex, thereby contributing to the perception of intracranial pain during a migraine [40]. Furthermore ipRGC inputs onto the trigeminovascular neurons may modulate the response to light by migraineurs. This neural mechanism may explain why individuals feel worse when exposed to light and preferentially seek dark rooms for relief (photophobia) when experiencing a migraine. While the overarching neural mechanisms of mTBI-related PTH resemble, but may not be exactly the same as those for migraine [140], light-based exacerbation of PTH and/or photophobic responses by individuals post-mTBI may likely have the same neural underpinning. Thus it is plausible that, despite the numerous potential benefits of blue light on circadian rhythms, fatigue, alertness and cognition following mTBI, blue-light or blue-shifted white light treatments may be poorly tolerated and may indeed worsen PTH in some individuals. At present, this specific possibility has not been directly explored in treatment studies using blue light for treating symptoms of mTBI, but research on this topic would be a welcome addition to the literature.

Monochromatic red light

For individuals seeking to enhance alertness without modifying their circadian rhythm (e.g., increasing daytime alertness in the presence of a normal circadian rhythm), utilizing blue light therapy may have unintended and unwanted effects, primarily on melatonin secretion. Interestingly, prior work has shown that longer wavelength light (e.g., red light) may have equally powerful alerting effects [157,160–164]. Red light is detected by L-cones in the retina, and the ipRGCs that are sensitive to blue light are not sensitive to the longer wavelengths (∼630 nm) of red light [31,33]. In some preliminary work, the alerting effects of red light were present both in the late afternoon and at night, and were comparable to the effects of blue light. While the mechanisms by which red light has an alerting effect are not fully understood, a plausible explanation is that it may influence the actions of subcortical regions apart from SCN resulting in alerting effects unrelated to melatonin secretion or suppression [159,170].

Monochromatic green light

While the use of blue light may exert its most profound effects on circadian phase advancement or resetting circadian rhythms that mediate sleep, blue light specifically suppresses melatonin secretion thereby inhibiting or delaying the actual onset of sleep. Though possibly beneficial for altering post-mTBI sleep timing or reducing daytime sleepiness and fatigue, this effect on melatonin does nothing for actually promoting night-time sleep. On the other hand, preliminary evidence from animal models suggests that green light (∼530 nm) indeed has a sleep-promoting function [189]. This has not yet been confirmed in human studies and the specific mechanisms are not described as yet, though multisynaptic M-cone projections to the ventrolateral preoptic area (involved in sleep promotion) and lateral hypothalamus (where wake-promoting orexin is secreted) may plausibly create this relationship [189,190].

As previously noted, blue light may also have the unintended consequence of aggravating PTHs. However, further research with migraineurs demonstrates that the use of green light has a positive effect on migraine symptoms, including at a minimum no exacerbation of the headache and at best a decrease in the intensity of symptoms [191]. This effect is observed relative to the use of white, blue, amber and red light. Additionally, animal models have demonstrated that green light confers antinociceptive benefits, both at the sensory threshold and with neuropathic pain [192]. Therefore, individuals with mTBI-related PTH or pain may benefit either from environments bathed in green light or from glasses, which preferentially filter the spectra of incoming light to preferentially include green light.

Journal information: JAMA Network Open
Provided by Stanford University Medical Center


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