Back in the day, the 1980s to be specific, there was a brief fad around amber-on-black computer screens (as opposed to green-on-black or white-on-black) for supposed ergonomic reasons. My computer had one, along with its 5 ¼” floppy drives (remember those?).
More recently, with kids texting at night and people logging late hours on computers and devices, there’s been a recognition that artificial light at night is bad for sleep and disruptive to physiology overall, with blue light increasingly recognized as the culprit.
That’s given birth to some new fads. You can now download programs to eliminate blue light from your computer screen at night or buy amber-tinted glasses for computing and gaming to “filter the harsh spectra” of light. Airlines are using “mood” lighting to mimic sunrises and sunsets, which supposedly reduces jetlag.
In a paper in Neuron last week, Alan Emanuel and Michael Do, PhD, of the F.M. Kirby Neurobiology Center at Boston Children’s Hospital and Harvard Medical School provide some science to support and inform these fads, as well as the use of light therapy for conditions like seasonal affective disorder.
Emanuel and Do looked under the hood of our non-image visual system—how it handles different kinds of light to help stabilize and tune our circadian and sleep/wake responses. Specifically, they looked at the principal regulators of our circadian clock—light-sensing cells known as intrinsically photosensitive retinal ganglion cells (ipRGCs).
Taking the long view
IpRGCs can respond to light independently of the rods and cones that handle image vision and, unlike those cells, message the brain directly. Each ipRGC has some 10,000 melanopsin molecules that capture light. (Interestingly, melanopsin more closely resembles photosensitive molecules found in flies and squid than those in humans and other mammals.)
IpRGCs can signal the brain for sustained periods—hours long—in contrast to the rapid-shutter responses typical of other cells in the retina. The researchers’ first question was: why? They stimulated ipRGCs from the mouse retina in a dish with pulses of light and measured their electrical output. They found a system exquisitely tuned to the “big picture” of light.
First, once they’re activated, melanopsin molecules tend to stay active. If you glance out the window on a sunny day, melanopsin molecules activated during that glance continue to signal for minutes afterward, even in darkness. Another glance activates additional molecules. The more melanopsin molecules that get activated, the stronger the signals that ipRGCs send to your brain. “Since melanopsin adds up the amount of light you see, brief exposures can give very long-lasting effects,” says Do.
IpRGCs tally photons over many minutes in order to generate signals that reflect the overall light level. “The brain uses these signals to synchronize its internal clock with local time,” says Do. “If ipRGCs responded to momentary changes in light level—from a flash of lightning or a passing cloud—their signals would fluctuate and push the clock to be constantly set and reset, potentially making its reading unclear.”
A flash of amber
And here’s where color comes in. Each melanopsin molecule is a three-way switch that is flipped by light. The switch has two “off” positions that keep the cell silent and one “on,” activated position. Each “off” position is pushed to the “on” position by a different hue of light (specifically, cyan and violet). But since these hues are found in practically all common light sources, melanopsin and ipRGCs can respond to a broad range of illumination conditions, provided the light is bright enough.
Indeed, when Emanuel tried spectra from multiple common light sources—fluorescent lights, LED lights, mercury lamps, xenon (in car headlights), sunlight, sunset—he saw that they produced very similar melanopsin activity. The cyan and violet within all of these spectra dominated the ipRGCs’ responses.
With most spectra of light, the cell will keep signaling the brain long after the light source is gone. But there’s one hue with a different effect: amber. Amber light activates the cells while it’s on, but when it’s off, the cell’s activity goes off too. What’s more, an ipRGC that is activated by sunlight—and would ordinarily remain activated for many minutes of subsequent darkness—can be silenced by giving a pulse of amber light.
Ever since melanopsin’s discovery, people had speculated it was a simple off/on switch. But this couldn’t account for all its capabilities. “Melanopsin functions with much greater flexibility than we had anticipated,” says Do. “This degree of flexibility from a single molecule is impressive.”
So maybe I was on to something, typing my graduate school papers on an amber screen. Using amber lights at night could control ipRGCs’ tendency to keep signaling the brain afterward, throwing off people’s circadian clock and causing insomnia. “In a way, amber is an innocuous source of lighting,” says Do.
The beauty of blue
On the flip side, he says, we now have solid evidence for using blue lighting for therapeutic applications—where you want the light response to be sustained. It’s been known that blue light boxes work better than white ones, but it hasn’t been fully known why.
The research findings could help provide proper specs for light therapy for shift workers and people with seasonal affective disorder, as well as efforts to mitigate dysfunctional sleep/wake cycles, which have been linked to cancer, obesity, mental illness and other disorders.
“We can use this new information to design environments more deliberately,” says Do.