Insomnia is a process that can be triggered by exposure to artificial light.
According to the American Sleep Association, approximately 50 to 70 million American adults experience some form of sleep disorder. The term insomnia is used to describe the inability to fall, and stay, asleep. About 30 percent of American adults report issues with insomnia, of which 10 percent report having been diagnosed with chronic insomnia. These numbers are gradually on the rise.
But what if the increase in numbers is not only attributed to diet, genetics and lifestyle but also something that may seem completely unrelated, like artificial light?
Researchers at the Salk Institute in San Diego have identified cells in the eye that are responsible not only for processing artificial light but also for communicating with the body’s internal circadian rhythm, which helps us sleep.
Before electric light, life was synchronized to the cycles of day and night. Humans were exposed to little or no light at night. With exposure to only the natural light from the environment, the body’s internal circadian rhythm became synchronized with the rise and fall of the sun.
However, with the invention of artificial light, the so-called “day” could be extended, and the body’s natural circadian rhythm is disrupted. This leads to the onset of various health consequences.
Light is one of the major external cues the body uses to differentiate between day and night, and exposure to light at night not only leads to a desynchronized circadian rhythm, but also introduces health and mood disorders. In a more relatable case, a desynchronized circadian rhythm may lead to a lack of sleep, and sleep deprivation is associated with an increase in negative emotions.
In a study published in Nature in 2017, exposure to artificial light at night is linked to an increased risk of breast cancer, metabolic disorders, and psychiatric and behavioral disorders.
In a recent study, Salk scientists Ludovic Mure and Satchidananda Panda discovered cells in the eye that process ambient light to synchronize the body’s internal clock.
In the back of the eye is a membrane known as the retina that contains photoreceptor cells — classes of cells that respond to light. One class of photoreceptors, called intrinsically photosensitive retinal ganglion cells (ipRGCs), react to light to activate a protein known as melanopsin to suppress melatonin — a hormone responsible for inducing sleep. Melanopsin has been shown to be most responsive to blue light, which is why blue light is known to boost attention and moods.
Mure explained how melanopsin interacts with circadian rhythm.
“Compared to other light-sensing cells in the eye, melanopsin cells respond as long as the light lasts, or even a few seconds longer,” Mure said in a press release. “That’s critical, because our circadian clocks are designed to respond only to prolonged illumination.”
With their most recent work, Mure and Panda were surprised to discover that melanopsin required arrestin proteins in order to continue responding to light. Arrestin proteins, in other cases, are responsible for stopping certain receptors from working, but, for some reason, arrestin activated melanopsin.
Panda described this unusual function of arrestin.
“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 retina light-sensing co-factor. When these two steps are done in quick succession, the cell appears to respond continuously to light.”
Through understanding melanopsin and its interaction with ambient light, Mure and Panda hope to determine the relationship between melanopsin and the internal circadian rhythm in order to help improve the quality of life for patients diagnosed with insomnia.