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Databyte: Lights Out!

Paying attention to artificial light and natural sleep cycles

By June H. Kim

Published August 15, 2013

If the best part of waking up is a hot cup of coffee, are we forced to grin and bear the rest? From the daily thumping of my snooze button to my first hour at work, I often find that, ironically, I am never as tired as when I’m waking up.

According to a recent study published in the journal Current Biology, this paradox has actually persisted as far back as the advent of artificial lighting. Indeed, electricity may help explain why we so loathe waking up on Mondays.

The study, led by Dr. Kenneth P. Wright, Jr., Director of the Sleep and Chronobiology Laboratory at the University of Colorado Boulder, suggests that indoor lighting, while allowing us to work and play at all hours of the night, has altered the natural sleep cycle that our bodies go through each day. At night, our bodies release the hormone melatonin, which makes us sleepy and cues us to go to bed. In the morning, melatonin levels rapidly decline, prodding us to make the most out of the daylight. This circadian clock then winds itself again as the sun begins to set. That’s the plan at least.

At night, our eyes are constantly flooded with artificial light, whether from light bulbs or our omnipresent electronic devices. Combined with reduced exposure to actual sunlight, the authors contend that artificial light has rewired our natural circadian clocks. Instead of timing the release and offset of melatonin to the sunset and sunrise, respectively, our bodies are fooled into believing the day lasts much longer into the night. And this may lead to sleep disorders.

For two weeks, the researchers followed a small group of adults living in Boulder, Colorado. In the first week, the study participants went about their normal routines while wearing a motion-sensing device that measured when they were sleeping as well as their exposure to light, both natural and artificial. At the end of the week, melatonin levels were measured to record the timing of their circadian clocks.

Ideally, this scenario should be compared to a near identical week, involving the same individuals, going through the same routines, and at the same time, but without the availability of artificial lighting at night. This way, any differences in sleep patterns between the two “groups” could be attributed to the primary difference between the two scenarios: exposure to light at night.

The researchers instead used a type of modified crossover study, in which the exposure was altered for the same period of time in which the study participants were observed. Immediately after the first week, they whisked the study participants off into the woods for seven days of camping. Wearing the same devices they wore in the first week, the study participants were forbidden from using flashlights or cell phones, limiting their nighttime light exposure to that of a small campfire. As with the first week, melatonin levels were again measured overnight.

Compared to the first week, the participants were exposed to four times the amount of natural light while camping. However, as the sun is not available at the flick of a switch, light exposure at night was the opposite. After sunset in the week camping, the participants didn’t see the light of day until sunrise the next morning.

Remarkably, by the end of the second week of the study, in which participants were camping, the circadian clocks of everyone synched to match the timing of the sunrise and sunset. This is in stark contrast to the end of the first week, when the average timing of the ebb and flow of melatonin occurred nearly two hours later. As illustrated in the figure, melatonin levels began to recede over an hour after the participants woke up. After the second week, the average time of melatonin offset occurred nearly an hour prior to waking up.

For the myriad of people with fixed, early rising schedules, having a delayed sleep phase can lead to difficulties falling asleep at reasonable hours as well as poor cognitive functioning upon waking. Of course, sleeping beyond the delayed offset of melatonin is the best option, but one that is unfortunately not available for many school-aged adolescents and young adults. Alarmingly, the sleep phase of adolescents has been shown to delay markedly with age, despite increasingly earlier schedules.

With the first school bells ringing as early as 7:00 a.m., when does the fog of melatonin begin to dissipate? Hopefully before kids grow weary of school altogether.

Predictably, delayed sleep phase has been linked to significant deficits in academic performance as well as behavioral and psychological problems. In fact, symptoms of delayed sleep phase are often mistaken for those of ADHD, and treatments like morning light therapy that help advance sleep phase (e.g. turning a “night owl” into an “early bird”) have been shown to reduce the core symptoms of ADHD.

Reviews of recent studies have suggested that children with ADHD often have co-occurring sleep problems and more pronounced daytime sleepiness. Could we be diagnosing the wrong deficit?

Of course, treating sleepiness with stimulants seems perfectly logical. One more cup of coffee for the road. But why go through this daily cycle? Turn off the lights. Put down the tablet. Go camping.

Edited by Dana March

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The views and opinions expressed on this website are solely those of the authors and do not represent those of the Department of Epidemiology, the Mailman School of Public Health, or Columbia University.