Researchers at Salk Institute in the US have uncovered how artificial light from smartphones and computers can disrupt sleep. The finding is more than just a curious study as it may lead to new treatments for migraines, insomnia, jet lag and circadian rhythm disorders.
How smartphones and computer disrupt sleep
Scientists found that 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, like migraines, insomnia and circadian rhythm disorders.
Researchers said that these disorders have been tied to:
- Cognitive dysfunction
- Insulin resistance
- Metabolic syndrome and more
The results, published in the journal Cell Reports, may lead to new treatments for such health issues including jet lag.
Artificial light is to blame
“This lifestyle causes disruptions to our circadian rhythms and has deleterious consequences on health,” Panda said.
The science behind it
The backs of our eyes contain a sensory membrane called the retina, whose innermost layer contains a tiny 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, signalling levels of ambient light directly to the brain to regulate consciousness, sleep and alertness.
“Compared to other light-sensing cells in the eye, melanopsin cells respond as long as the light lasts, or even a few seconds longer,” said staff scientist Ludovic Mure.
“That’s critical because our circadian clocks are designed to respond only to prolonged illumination,” Mure added.
Arrestins are necessary for melanopsin to continue responding to prolonged illumination
The researchers used molecular tools to turn on the production of melanopsin in retinal cells in mice.
They discovered that some of these cells have the ability to sustain light responses when exposed to repeated long pulses of light, while others become desensitised.
The researchers were surprised to find that arrestins are in fact necessary for melanopsin to continue responding to prolonged illumination.
In mice lacking either version of the arrestin protein (beta arrestin 1 and beta arrestin 2), the melanopsin-producing retinal cells failed to sustain their sensitivity to light under prolonged illumination.
“Our study suggests the two arrestins accomplish regeneration of melanopsin in a peculiar way,” Panda said.
“One arrestin does its conventional job of arresting the response, and the other helps the melanopsin protein reload its retinal light-sensing co-factor,” Panda said, adding, “When these two steps are done in quick succession, the cell appears to respond continuously to light.”