Why Do You Sneeze When You Look at the Sun?

Look directly at a bright light.

For about one in four people, that sentence ends with a sneeze.

Not because the light irritated anything. Not because of dust or pollen. Just — light. Bright light. Sneeze.

If that’s never happened to you, you probably think this sounds made up. If it has, you’ve been carrying around a small unexplained fact about yourself your whole life.

Here’s what’s actually happening.

Aristotle Noticed This

In around 350 BCE, Aristotle wrote in Book of Problems: “Why does the heat of the sun provoke sneezing?”

He thought it was warmth dilating the nostrils. He was wrong about the mechanism but right about the phenomenon. For the next 2,000 years, the question sat there largely unanswered — not because no one cared, but because the nervous system is hard to study and sneezing seemed like a low-priority mystery.

Francis Galton (the statistician, Darwin’s cousin, and obsessive cataloguer of human variation) surveyed it in 1883. He noticed it ran in families. Father sneezes at the sun, child sneezes at the sun. That suggested something genetic was going on.

It took another century to give it a name: ACHOO syndrome.

That’s not a joke. It stands for Autosomal Compelling Helio-Ophthalmic Outburst. Someone in the 1980s really committed to the acronym. The clinical term is photic sneeze reflex, but ACHOO is more honest about how the field felt about it.

The Numbers

Studies give different numbers — anywhere from 10% to 35% of people have it, depending on the population and how you ask. A 2010 genome-wide association study using data from 23andMe found roughly 23% of participants reported sneezing in bright light.

One in four. Maybe more. A reflex this common, this consistent, this heritable — and it took until the 21st century to get a decent molecular handle on it.

The genetics are straightforward: autosomal dominant, which means you only need one copy of the relevant variant. You got it from a parent. One of them sneezes when they walk outside. If you haven’t asked them, now you have something to talk about.

The region implicated in GWAS studies sits near chromosome 2q22.3. The specific gene or genes haven’t been nailed down with certainty — this is a reflex, not a disease, so research funding has not exactly flooded in.

The Wiring Problem

Your sneeze reflex is controlled by the trigeminal nerve — cranial nerve V, one of the large branching nerves of the face and skull. It handles sensation in your face, your sinuses, your teeth, your forehead. When something irritates your nasal passages, trigeminal signals reach the sneeze center in the brainstem, and a sneeze fires.

Your vision is carried by the optic nerve — cranial nerve II. It runs from your retinas back into the brain.

These two systems are not the same system. But they run close together, and they share some of the same brainstem real estate.

Here’s what’s thought to happen when you look at a bright light:

The light floods your retina. Your visual system fires. Your pupils need to constrict fast — that’s the pupillary reflex, driven by the parasympathetic nervous system. The signal travels through the Edinger-Westphal nucleus, which sends instructions down the ciliary ganglion to tighten your pupils.

In some people, that parasympathetic signal doesn’t stay neatly contained. It bleeds. It crosses into the trigeminal nucleus nearby. And the trigeminal nucleus doesn’t know that the signal originated in the eye — it just knows it got a signal. So it does what it does with signals: it starts a sneeze.

Your nose didn’t sense anything. Your face is fine. But the wiring is shared, and when one system fires hard, it leaks into the other.

Neural cross-talk. Your brain is not a clean collection of isolated modules. It’s layered, compressed, built on evolutionary scaffolding where new systems got added on top of old ones, sharing cables where they could. Efficiency and precision are in constant tension.

In most people, the insulation is good enough to keep pupillary signals from triggering sneezes. In one in four, there’s a bit of a short.

Why It Matters

This is not purely a curiosity.

The Royal Air Force has studied the photic sneeze reflex because jet pilots experience it when the cockpit canopy opens into bright sky. A sneeze during a critical moment — landing approach, evasive maneuver — is a real operational concern. A sneeze lasts about 150 milliseconds. At 500 mph, that’s not nothing.

The fix, for people who know they have it, is simple: don’t look directly at the light source. Wear sunglasses. Tilt your head. Most photic sneezers develop workarounds automatically, without ever knowing why they needed them.

What This Says About Reflexes

A reflex is supposed to be a clean input-output machine. Stimulus, response. The sneeze reflex exists to clear the airway when irritants enter the nose. Bright light is not an irritant. It is not in your nose. And yet, for millions of people, it reliably triggers the reflex.

This means the brain’s wiring is not error-free. It’s good enough — good enough to survive, good enough to reproduce, good enough to run as infrastructure for a hundred thousand generations without this particular cross-signal causing enough problems to get selected out.

The photic sneeze reflex has been in the human gene pool since at least Aristotle noticed it. It’s still here.

It’s not a bug. It’s not exactly a feature. It’s what happens when you build a nervous system out of borrowed parts, running shared pathways, optimized for mostly right.

Aristotle asked the question. Galton found the family pattern. Genetics located the chromosome. Neuroscience traced the trigeminal pathway.

And still, for about one in four people, stepping outside on a bright afternoon ends in a sneeze that no one fully asked for.

The wiring is just a little close.