Tech Shortcuts for Life

Brain Science Explains Why Blue Light Blockers Help You Sleep

Hack your brain for more energy and better sleep

Tech Shortcuts for Life is a weekly column from Thomas Smith on Debugger exploring the apps, automations, gadgets, and other tech tricks that can make your life more efficient.

While driving through San Francisco in late 2020, I saw a billboard for a curious product: Blokz glasses from tech-centric eyewear company Zenni. The glasses, which range in price from around $30 to $200+, promise to “protect your eyes from blue light,” which the company claims is responsible for all kinds of evils, from “blurred vision” to “disrupted sleep.”

Zenni’s glasses are just the latest salvo in an ongoing war on blue light. Android phones now come standard with a Night Mode which filters out blue light from the phone’s screen. Apple has an equivalent mode called Night Shift. One of the signature features on the highest-end Amazon Kindle e-reader is a mode that shifts the device’s LEDs from blue light to a nice, warm yellow at night. A 2018 article in The Observer even called blue light “the tobacco of the digital age.”

While the dangers of blue light have almost certainly been blown out of proportion by savvy marketers, parts of their claims are true. Blue light, it turns out, really does impact our brains. Understanding why requires peering deep into the retina, meeting (real) blind mice, and exploring one of the most fascinating neuroscience discoveries of the last 30 years. It also reveals a variety of easy brain hacks which can potentially improve your mood, lower your blood pressure, make you more productive at work, and help you sleep better at night.

While the dangers of blue light have almost certainly been blown out of proportion by savvy marketers, parts of their claims are true.

As you may remember from high school biology, the human eye has two different kinds of photoreceptors, or light-sensitive cells: rods and cones. Rods allow you to see in low-light conditions — like when you’re stumbling down a dark hallway to the bathroom in the middle of the night. Rods aren’t very precise, though, and they only allow you to see in black and white. When a bit more light is available, your eyes switch to using cones. These allow for the high-resolution, full-color vision we experience during most of our waking hours.

Until the early 20th century, rods and cones were assumed to be the only light-sensitive cells in the human eye. In 1923, though, a scientist named Clyde Keeler made a strange discovery. Keeler had mistakenly bred mice with no rods or cones in their retinas. As he described in a 1923 paper titled Blind Mice (he didn’t say how many, but I hope it was three of them), his mutant mice couldn’t see, but their pupils still responded to light. That didn’t make sense. Without traditional photoreceptors, the mice shouldn’t have responded to light at all. But somehow, they did.

Keeler believed his results might indicate a breakthrough — the existence of a totally new kind of photoreceptor. But his contemporaries disagreed. They thought it was more likely that Keeler’s blind mice weren’t totally blind. Some of their rods and cones must still be present — not enough to see, but enough that their pupils still responded to light. It wasn’t until 70 years later — in the 1990s — that scientists finally had the technology to pursue Keeler’s theory more fully. In 1991, neuroscientist Russell Foster and his colleagues engineered mice who completely lacked the genes for rods and cones. Their pupils still responded to light.

Our circadian clocks are pretty good. Left on their own, they naturally measure out a nearly 24-hour day, regulating the release of hormones, helping to make us hungry at the right times, and ensuring we get sleepy at night.

So Foster and his team removed their eyes. With no eyes, the mices’ brains stopped showing any response to light, as the team expected. But then, something even stranger started to happen. The blinded mice lost their ability to regulate their circadian rhythms. Over time, their rhythms started to drift, until they had no idea when they were supposed to sleep and started running on their wheels in the middle of the night. Somehow, removing the mice’s eyes had made their internal clocks go haywire.

In 2002, scientists David M. Berson, Felice A. Dunn, and Motoharu Takao finally figured out why. Keeler, it turns out, had been right all along. Mice, humans, and other animals really do have a third kind of photoreceptor — the intrinsically photosensitive retinal ganglion cell, or ipRGC. These specialized cells are located just downstream of our other photoreceptors. They use a molecule called melanopsin to detect light. And they’re responsible for all kinds of important functions — from the pupillary light response that Keeler originally observed in 1923, to controlling our sleep/wake cycles, to regulating our moods. It was a stunning result and the culmination of nearly 100 years of study.

Our classical photoreceptors, the rods and cones, work by signaling the precise location at which photons of light hit our eyes. This precision is what allows us to see — knowing exactly where photons are coming from allows our brains to start to piece together the edges, gradients, and other features that make up a scene, and ultimately lead to the process we call “seeing.” Rods and cones are also fast, signing the presence of light within around 100 milliseconds of its arrival in our eyes.

ipRGCs, though, work differently. Rather than signaling the precise location of incoming light, ipRGCs provide our brains with information about light’s overall intensity. They’re also much slower than rods and cones, taking seconds or more to start signaling that light has hit them, and even longer to stop once the light goes away. In short, they’re ambient light detectors —while they do relatively little to help us see images, ipRGCs tell our brains detailed information about the overall levels of light in our environment.

ipRGCs are wired differently, too. Classical photoreceptors send their signals to the thalamus, and then on to the occipital lobe toward the back of the brain, and ultimately to the cortical regions used for image formation. ipRGCs, on the other hand, send signals to different places, including the suprachiasmatic nucleus (SCN). The SCN contains the body’s circadian clock — it’s the brain region that keeps our bodies synchronized with the rise and set of the sun.

Our circadian clocks are pretty good. Left on their own, they naturally measure out a nearly 24-hour day, regulating the release of hormones, helping to make us hungry at the right times, and ensuring we get sleepy at night. But they’re not perfect. Everyone’s circadian clock is just a bit off from a perfect 24-hour cycle. Without any external input, our circadian clocks would slowly “drift” away from the sun’s cycle over time, like an old analog clock with a bad battery that slowly loses a few minutes per day until it’s totally inaccurate.

What keeps our own clocks from drifting? Light. It turns out that our brains use the ambient light detected by our ipRGCs to synchronize our internal circadian clocks with the rise and set of the sun. When our ipRGCs detect light in the morning, they slowly start pinging the SCN with the message “There’s light here!” The SCN then adjusts our internal circadian clocks to match the actual cycle of day and night in our environment, in a process called entrainment. It’s as if you took that old analog clock and used your iPhone’s perfect digital clock to reset it each morning, ensuring that it stays accurate.

Because the ipRGCs keep our circadian clock synchronized with the sun, they have a huge impact on our cycles of sleep and wakefulness. ipRGC’s role in resetting our circadian clocks also explains why Foster’s mice ran on their wheels in the middle of the night. With no eyes (and thus no ipRGCs), they had no way to update their circadian clocks to the right time. Their clocks drifted over time until the mice had no idea whether it was day or night. Their internal rhythms were out of sync with the environment.

What does all this have to do with blue light? It turns out that iPRGCs are exquisitely sensitive to blue light. This makes sense, as the ipRGCs likely evolved to detect sunlight, which has a high color temperature, and thus, a blue tinge. When you expose your eyes to blue light, your ipRGCs fire continuously, telling your brain over and over that “It’s morning!” until the blue light goes away. They evolved to synchronize your circadian clock with the sun, and they’re quite good at this job.

In ancient times, that worked fine, because humans only encountered blue light during the day. Once the sun set, our ipRGCs stopped firing, and our bodies knew it was night. Now, that’s changed. Through our phones and other screens, we expose our ipRGCs to blue light at all hours of the day and night. When you look at your blueish iPhone screen right before bed, your ipRGCs detect the screen’s blue light, and start telling your brain that it’s morning.

Expect, of course, it’s not morning. And that causes all kinds of problems. In particular, exposing your eyes to blue light at night reduces your body’s production of the sleep hormone melatonin, which causes problems sleeping. It can also impact other bodily functions which are partially controlled by the ipRGCs and ambient light levels, including blood pressure, body temperature, and glucose release.

That’s where blue light-blocking glasses — as well as features like Night Shift — come in. By reducing your ipRGCs’ exposure to blue light at night, these products and features can potentially preserve your circadian rhythm, stopping your brain from thinking that it’s morning when it actually isn’t. Reducing blue light exposure at night has been shown to increase the production of melatonin, helping you sleep, and potentially improving other bodily functions, like blood pressure. It’s a simple brain hack you can implement tonight, just by enabling the blue light blocker on your phone, turning down artificial lights after the sun sets — or even wearing those blue light-blocking glasses.

If blue light causes so many issues, should you shut it out all the time? Absolutely not. It turns out that getting enough blue light exposure during the day is likely just as important as reducing blue light exposure at night. Exposing your ipRGCs to blue light in the morning is essential to maintaining your circadian clock. Without blue light, your brain has no idea when morning has arrived. In extreme cases, depriving your brain of blue light would make you like Foster’s mice — totally out of sync with the environment, waking in the middle of the night, and feeling sleepy during the day.

Studies have shown that exposure to bright, blueish light during the day can improve work performance and mood, help you feel more alert in the morning, and even fight depression. Harvard Medical School says that you should “expose yourself to lots of bright light during the day, which will boost your ability to sleep at night, as well as your mood and alertness during daylight.”

The impact of blue light, then, is all about timing. If you wear blue light-blocking glasses during the day or leave Night Shift on all the time, you’re probably doing more harm than good. By depriving your ipRGCS of blue light during the daytime, you’re preventing them from doing their job of properly updating your circadian clock. That may lead you to feel more tired during the day, or could even lower your mood and decrease your cognitive performance.

So after the sun goes down, don those Zenni glasses (or a cheaper pair from a company like TIJN) and switch your phone over to Night Mode or Night Shift to block out blue light. Switch off or dim artificial lights in your home, too, and avoid watching TV right before bed. But when the sun comes up in the morning, make sure to take the blue light glasses off, put your phone down, and go outside. Spend at least 30 minutes in natural light each morning — that’s how long it takes to fully entrain your circadian rhythms. Your ipRGCs — and your brain — will thank you.

Co-Founder & CEO of Gado Images. I write, speak and consult about tech, privacy, AI and photography. tom@gadoimages.com

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