Every baseball season, 73-year-old Fred Crittenden plants himself in front of his television in his small one-bedroom apartment an hour north of Toronto.

"Oh, I love my sports — I love my Blue Jays," says Crittenden. "They need me to coach 'em — they'd be winning, I'll tell ya." He listens to the games in his apartment. He doesn't watch them, because he can't see.

"I went blind," Crittenden recalls, when "I was 35 years young."

Crittenden has retinitis pigmentosa, an inherited condition that led to the deterioration of his retinas. He lost all his rods (the cells that help us see in dim light) and all his cones (the cells that let us see color in brighter light). Within a single year, in 1985, Crittenden says he went from perfect vision to total blindness.

"The last thing I saw clearly," he says, thinking back, "it was my daughter, Sarah. She was 5 years old then. I used to go in at night and just look at her when she was in the crib. And I could just barely still make her out — her little eyes or her nose or her lips or her chin, that kind of stuff. Even to this day it's hard."

Crittenden says it took him about a year to come to terms with his blindness. Today, more than 35 years later, he doesn't see light. "It's total darkness," he reports. Still, he manages just fine. There's plenty he doesn't need help with — including syncing up with the 24-hour day/night cycle.

At night, Crittenden listens to sports or his talking book machine. He's asleep by 11, and out of bed every morning about 6:30, no alarm needed. That may not seem remarkable, except that our circadian clocks are deeply influenced by light.

Marla Feller, a neurobiologist at the University of California, Berkeley, says, "If you never saw any light, you would slowly shift your sleep cycle so that you'd start falling asleep later and later. But what happens is, every day you go out and look at the sun — and it entrains this circadian clock to be on the 24-hour cycle."

So Crittenden is something of a mystery. He's blind, but his internal clock marches to the 24-hour beat of a sunlit world, give or take a few minutes. This isn't the case for all individuals who are blind. So what's going on with him?

This brings us to Iggy Provencio, a biologist at the University of Virginia who, in grad school in the '90s, was studying the African clawed frog. "The frog is really a disgusting-looking animal," he chuckles. "It has very slimy skin."

That skin contains cells that darken with pigment when they detect light, which helps the frogs blend in with the streambed below. Provencio discovered the molecule responsible for the light detection, which he called melanopsin. And it wasn't just in the frog's skin. He and his team found it in the retina of the frogs, and of mice too.

"We were looking through the microscope," Provencio recalls, "and I told my colleague who was with me, 'We are the first people in the world to actually view a completely novel sensory system in mammals' " — including humans.

Melanopsin isn't in our rods or cones. Rather, it's inside big neurons called melanopsin cells, which are parked in a different layer of the retina. "Imagine an octopus with its tentacles reaching out," says Michael Do, a neurobiologist at Boston Children's Hospital and the Harvard Medical School. "The melanopsin cells — their arms reach out and overlap with the arms of other melanopsin cells to form a mesh over the retina."

The entire mesh is sensitive to light, especially bright, blue light. The sun makes a lot of that light, as, to a lesser extent, do our phones, tablets, screens and some other indoor lights, streetlights and headlights. The tentacles of those melanopsin cells radiate all over our brains.

"I think it's something like 30 brain regions are contacted directly by these cells," says Do. "One place is the structure at the base of the brain that is our master circadian clock." It's called the suprachiasmatic nucleus, and it uses the light information fed to it by melanopsin cells to instruct the rest of our body when it's time to sleep and when it's time to wake up. The melanopsin cells also help influence hunger, temperature control, migraine pain and maybe even our mood and how we learn.

Satchin Panda, a chronobiologist at the Salk Institute, says there have been lab experiments where mice had their melanopsin switched off. "These mice, they can sense light to some extent," he says, but things are off kilter.

For instance, give them a lab-mouse version of jetlag — where one day, you suddenly shift when the lights get turned on and shut off — and "these mice, instead of taking seven days to reset to the new time zone, they will take a month," Panda says. (There's variability in the system, which is why some people have a harder time adjusting to daylight saving time or a change in time zones than others.)

So that's the mystery we started with, solved: Fred Crittenden has no functioning rods or cones, but, he does have melanopsin cells.

Crittenden's experience offers insight into an important system in the brain and retina (beyond rods and cones) that is maintained in certain people who are blind. This system of special melanopsin cells is likely what allows Crittenden's brain to use light to help synchronize his internal clock.

It's these cells that tell his body to start a new day every morning — to make sure he's awake when Sarah, his daughter (who's 42 now) gives him a call.

"She usually calls me every other day, to see how I'm doing and that kind of stuff," Crittenden says fondly. "She's a good girl."

When we spoke, Crittenden had a photo of Sarah in his apartment. In it, she's smiling. The photo was hanging in his bedroom, opposite the window. And on a clear day, a shaft of sunlight would flash through that window and light up Sarah's face.

This story is part of our periodic science series "Finding Time — a journey through the fourth dimension to learn what makes us tick."

Another version premiered during a live show in 2016 at the Charles Hayden Planetarium at the Museum of Science, Boston.

Copyright 2022 NPR. To see more, visit https://www.npr.org.

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