Why too much screen time disruptes sleep? & Nbsp | & nbspPhoto Credit: & nbspThinkstock
Washington DC: By now, we all know that spending too much time staring at screens – be it computers, phones, iPads – plays havoc with sleep. But do you know why? Researchers have identified how certain cells in the eye process ambient light and reset our internal clocks, the daily cycles of physiological processes known as the circadian rhythm.
When these cells are exposed to artificial light late into the night, our internal clocks can get confused, resulting in a host of health issues. The study, conducted by Salk Institute researchers, has been published in the journal Cell Reports.
The results may lead to new treatments for migraines, insomnia, jet lag and circadian rhythm disorders, which have been linked to cognitive dysfunction, cancer, obesity, resistance to insulin, metabolic syndrome and more.
"We are continually exposed to artificial light, whether from screen time, spending the day indoors or staying awake late at night," said Salk Professor Satchin Panda, senior author of the study. "This lifestyle causes disruptions to our circadian rhythms and has deleterious consequences on health."
The backs of our eyes contain a sensory membrane called the retina, whose inner layer contains a small subpopulation of light-sensitive cells that operate like pixels in a digital camera. When these cells are exposed to ongoing light, a protein called melanopsin continually regenerates within them, signaling levels of ambient light directly into the brain to regulate consciousness, sleep and alertness. Melanopsin plays a pivotal role in synchronizing our internal clock after 10 minutes of illumination and, under bright light, suppresses the hormone melatonin, responsible for regulating sleep.
"Compared with other light-sensing cells in the eye, melanopsin cells respond as long as the light dances, or even a few seconds longer," said Ludovic Mure, the first author of the paper. "That's critical, because our circadian clock is designed to respond only to prolonged illumination."
In the new work, the Salk researchers used molecular tools to turn on production of melanopsin into retinal cells in mice. They discovered that some of these cells have the ability to maintain light response when exposed to repeated light impulses while others become desensitized.
Conventional wisdom has held that proteins called arrestins, which stop the activity of certain receptors, should stop cells' photosensitive response within seconds of lights coming on. The researchers were surprised to find that arrestins were in fact needed for melanopsin to continue responding to prolonged illumination.
In mice lacking either the version of the arrestin protein (beta arrestin 1 and beta arrestin 2), the melanopsin-producing retinal cells failed to maintain their sensitivity to light under prolonged illumination. The reason, it turns out, is that arrestin helps melanopsin regenerate in the retinal cells.
"Our study suggests the two arrestins to accomplish the regeneration of melanopsin in a special way," Panda said. "One arrestin makes its conventional job of arresting the response, and the other helps the melanopsin protein reload its retinal light-sensing co-factor. When these two steps are done in quick succession, the cell appears to respond continuously to light."
By better understanding the interactions of melanopsin in the body and how the eyes react to light, Panda hopes to find new targets to counter skewed circadian rhythms due to, for example, artificial illumination. Previously, Panda's research team discovered that chemicals called opsinamides could block melanopsin's activity in mice without affecting their vision, offering a potential therapeutic avenue to address hypersensitivity to light experienced by migraine sufferers. .