In a recent article published in Scientific Reports, researchers examined whether flash therapy, given during sleep, changed the sleep architecture to shift the human circadian clock.
Study: Moving time zones in a flash with light therapy during sleep. Image Credit: Bun Mihail/Shutterstock.com
The suprachiasmatic nucleus (SCN) in the hypothalamus governs the human circadian system and is highly sensitive to light exposure, especially during sleep time.
It receives all light information from rods, cones, and intrinsically photosensitive retinal ganglion cells (ipRGC) cells in the retina, which helps this human circadian pacemaker synchronize with the external light–dark cycle.
Traveling across multiple time zones temporarily offsets this synchronization, resulting in jet lag, i.e., disrupted sleep and wake, irritability, fatigue, and increased daytime sleepiness, which often persists for several days.
A potent light stimulus administered during sleep—flash therapy could help solve the jet lag problem quicker. It could be at least twice as effective as equiluminant continuous light, and preliminary evidence suggests it does not disturb sleep.
About the study
In the present study, researchers invited healthy participants (n=10) who completed two weeks of at-home sleep monitoring to stay in a time isolation suite for a 37-h in-laboratory portion.
In their first stay, they received no goggles, just a placebo, i.e., no flashlight therapy, whereas, in their second stay, they received two milliseconds (ms) of light flashes at 15-second intervals for 60 minutes starting 30 minutes after habitual sleep onset (HSOn).
All participants were instructed to sleep again if they awoke during flash therapy.
The researchers used changes in salivary dim light melatonin onset (DLMO) to assess circadian phase shift (Δϕ), defined as the difference in circadian timing between the test and placebo conditions, where H0 and H1 signified no phase change and significantly delayed circadian clock, respectively.
They measured sleep using polysomnography, and it depicted changes in sleep architecture and spectral power.
Further, the researchers used linear mixed models to determine duration spent in the wake (W), three stages of non-rapid eye movement (NREM) sleep, N1-N3, and rapid eye movement sleep (REM) sleep during 1-hour flash therapy versus during the control condition.
Notably, during N3, delta waves in the electroencephalograph (EEG) are the most predominant, implying the body is unlikely to wake due to flashes (external stimuli).
Moreover, the body is most sensitive to the circadian phase, which delays light triggers during N3.
Linear mixed models also indicated sleep architecture post-intervention, i.e., up to 6.5 hours. Finally, they used a Bayesian framework to examine differences in sleep stages due to the flash therapy to further validate linear model results.
DLMO showed that one hour of light therapy delayed the circadian clock by 1.13 ± 1.27 hours on average compared to 12 ± 20 min for placebo, with two participants exhibiting shifts of 6.4 and 3.1 h.
The researchers optimized flash light stimulus for time, duration, frequency, and intensity based on results from previous studies evaluating the efficacy of flash therapy in phase delaying the circadian clock. Yet, the observed responses in this study were highly variable.
In this study, researchers administered flash therapy during a limited range of sleep stages, predominantly during N2 and N3 and very little during wake, N1, or REM sleep.
During the intervention, there were no marked variations in the number of transitions from any sleep stage to wake, including N2/N3 to N1 sleep.
Likewise, there was no evidence of differences in duration spent in sleep stages during the 6.5 hours following the intervention.
In addition, there was no evidence of any direct interaction between the sleep stage and the magnitude of the circadian phase shift, necessitating more work to understand the effect of shorter-duration stimuli administered during specific stages of sleep.
Furthermore, Bayesian analyses supported the linear model results, with most Bayes Factors (B) providing minimal or anecdotal support for H1 or H0.
However, Bayesian assessment evidences a difference in the number of shifts from deeper to lighter stages of sleep and from sleep to waking during and following flash therapy compared to the placebo. Notably, delta enhancement is secondary to an evoked response and not an induction of delta activity.
To conclude, one hour of flash therapy during sleep evoked an enormous circadian shift, up to six hours, but with minimal or no impact on sleep architecture during or following the flash therapy.
Thus, this intervention might help delay the circadian clock in frequent travelers and shift workers.