Science is great. It’s what took us from constantly dying from plague in the dark ages to only very rarely contracting the plague in the modern world (and treating it with antibiotics if we do).

But science doesn’t know everything – and some of the things it can’t explain are almost embarrassingly mundane. So here are six things you’ve almost certainly done in your daily life that, as it stands, defy science in some way.

Use Acetaminophen (aka Paracetamol)

Acetaminophen – you may know it as Tylenol, or paracetamol if you’re outside the US – is so ubiquitous as a pain reliever that you’ve probably never stopped to wonder how it works. Which is lucky, because nobody really knows.

Take a look at the physicians' note that comes with the pills and you’ll see a less-than-comforting message: “Although the analgesic effect of acetaminophen is well established, the site and mode of action have not been clearly elucidated.”

In other words: we know it works, but we don’t know how or why. There are some hypotheses, though – the most common explanation you’ll likely get from a doctor is that it might block prostaglandins, the chemical messengers in the brain that let us know we’re in pain.

There also seems to be some evidence that paracetamol affects our serotonin levels. While serotonin is commonly thought of as a “happy hormone,” regulating mood disorders and helping us feel less anxious and depressed, it actually has a role in a whole bunch of things. These include sleep, regulating body heat, sex – and, yes, pain.

If serotonin is the key to acetaminophen’s success, though, it may raise more questions than it answers. Serotonin’s role in pain is complicated, and while doctors do sometimes prescribe antidepressants for chronic pain, it’s yet another medication that, while it seems to work on pain, we don’t really understand how – and that's because...

Pretty much any depression medication

Have you heard the good news? Ketamine, the party drug most favored by our parents, has turned out to be something of a miracle cure for depression, thus proving that not all horse medications are a bad idea.

How does it work? It inhibits glutamate release, scientists say. No wait – it’s something to do with serotonin. Does ketamine somehow restore the synapses and neurons that get lost through depression? Is it even the ketamine itself at all – perhaps it’s actually what the drug gets turned into by our bodies. Maybe it’s none of those explanations – or maybe it’s all of them.

As you may have gathered, the exact mechanism by which ketamine treats depression is still a subject of some debate. And maybe that’s to be expected – it’s hardly a first-line treatment, after all. But as it turns out, even most of our regular treatments for depression – in fact, even depression itself – aren’t completely understood, even by experts.

“A lot of what we think about antidepressants is still speculative,” explains WebMD. “We don't really know if low levels of serotonin or other neurotransmitters ‘cause’ depression, or if raising those levels will resolve it. We don't know enough about brain chemistry to say what's ‘balanced’ or ‘unbalanced.’

“It's possible that antidepressants have other unknown effects, and that their benefits don't have as much to do with neurotransmitter levels as they might with other effects, such as regulating genes that control nerve cell growth and function.”

Even the very oldest depression medication – lithium, which has been used as a mood stabilizer and soft drink additive for over 150 years, and possibly as long as 1,600 – follows this “it works, but darned if we know how” pattern.

“Although we don’t know exactly how lithium works to treat bipolar disorder, researchers believe it works in the brain to boost the levels of certain chemicals, including serotonin,” wrote Kevin Le, a pharmacist for GoodRx Health.

But “although it’s an old medication, lithium is one of the most effective for treating bipolar disorder,” he explained. “Because of this, it remains a first-choice medication, despite its risks, side effects, and drug interactions.”

Yawn

We yawn all the time: when we’re tired, when we’ve just woken up; when we’re bored, or when we’re about to start something new. You’re probably yawning right now – it’s so contagious that just thinking about a yawn can set one off.

“People who sky-dive say they tend to yawn before jumping. Police officers say they yawn before they enter a difficult situation,” Adrian Guggisberg, a professor of clinical neuroscience at the University of Geneva, told the New York Times.

But why do we do it? You may have heard it’s to increase the oxygen levels in our blood and keep us alert – that idea was debunked all the way back in 1987.

A more modern idea is that the movement and airflow serve to cool down our brain, staving off sleep. “When our body temperature is warmer, we feel more tired and sleepy,” explained psychologist and yawn-expert Andrew Gallup, also in NYT.

“It could be that evening yawns are triggered to try to antagonize sleep onset, so we yawn at night in an attempt to maintain some state of arousal or alertness,” he said.

However, it’s possible yawning doesn’t have a physical effect at all – another theory says that it’s more of a psychosocial phenomenon. There’s some research to support this: brain imaging has shown spikes in the empathy and social areas of people watching someone yawn, and we seem to “catch” yawning more from people we know than strangers. Dogs – surprisingly empathetic animals – can catch yawning from their favorite humans (as can elephants, strangely enough), while babies – notoriously evil – don’t do it at all, even with their own mothers.

So do we yawn for psychological reasons or physical ones? Maybe it’s both. Or maybe it’s neither! “The real answer so far is we don’t really know why we yawn,” Guggisberg explained.

“No physiological effect of yawning has been observed so far,” he told NYT. “That’s why we speculate.”

Wear glasses (or drink from a glass)

We defy you to explain glass without just pointing at a nearby window or tumbler and saying “that. That’s glass.” But don’t worry that you can’t come up with a good definition: glass – what it is, how it’s structured, why it even exists at all – is something that baffles scientists to this day.

There’s a common idea that glass is actually an incredibly slow-moving liquid, rather than a solid – which would certainly raise questions around how glass from around three and a half millennia ago can look so un-melty.

In fact, glass is a solid, but a particularly weird one: it’s what scientists call an amorphous solid. This means that its molecules are all disorganized like you’d expect to see in a liquid, rather than the regular crystalline structure that solids normally have.

But despite knowing what it looks like on a microscopic level, the fundamental structure of glass remains, ironically, opaque.

“The deepest and most interesting unsolved problem in solid state theory is probably the theory of the nature of glass and the glass transition,” Nobel prizewinning theoretical physicist Philip Warren Anderson wrote back in 1995. The question, basically, is what happens when a fluid becomes glass – how the molecules can seem to be arranged like a liquid, but behave like a solid, and what stops them from settling into a standard solid form.

Anderson optimistically thought this question could be solved “in the coming decade.” Unfortunately, he was wrong: as you may be aware, it’s now 2022 – and we still don’t really know what the heck glass actually is.

“Liquid and glass have the same structure, but behave differently,” Camille Scalliet, a glass theorist at the University of Cambridge, told Quanta Magazine. “Understanding that is the main question.”

Ride a bike

It’s very fitting that we describe something instinctive as “like riding a bike,” because it turns out most of us have pretty much no idea how to actually explain the activity.

Don’t get us wrong: science has worked out a lot of things that go into keeping a bicycle upright since the vehicle was invented more than 100 years ago. But even those scientists who study bike science for a living admit that the precise way those factors interact with each other are still a bit mysterious.

“If you take a bicycle, and you hold it with your hands and let go, it’s going to fall over, right?” said Jason Moore, assistant professor of biomechanical engineering at the University of Technology Delft, in the Netherlands.

“But […] there in fact is a speed at which it will not fall over,” he explained for the BBC’s CrowdScience series. “Maybe you’re at a hill, and you take your bike and let it roll down […] it'll bounce around and not really fall down – and it’s sort of odd, it doesn't stay up by itself, but it can stay up by itself too.”

Depending on who you ask, a bike may stay up for any number of reasons. A physicist may point to the gyroscopic effect of the wheels; an engineer might put it down to the materials or geometry of the bike; while a biomechanics expert might talk about the precise posture and position of the rider.

Here’s the problem, though: you can remove pretty much all of those qualities, and the bike will remain stable.

“There’s actually a long list over the last hundred years or so of people making those kinds of statements, and those are mostly wrong,” Moore said. “You can make some really funny looking bikes that still have the properties of a bike, but remove the causes that most people think are the reason the bike [is stable].”

“All these things are playing together … I can change one, or take one away; wiggle around the other things, and I get a bike that still counter steers or a bike that’s still self-stable,” he explained.

Have a butt

That’s right: butts! We all have ‘em, loyally perched underneath us as we sit on the toilet scrolling our phones. But have you ever stopped to consider why we have such monumental asses?

“Only humans have butts,” said Heather Radke, a journalist and author of the book Butts: A Backstory. And why that is is a question that’s only partly answered, she explained in the Vox podcast Unexplainable.

“The muscle and bone part [of the problem] is pretty well-studied,” Radke said. “Those muscles are big – they’re the biggest muscles in your body […]  [the] theory [is] that humans developed a set of adaptations that made them excellent long-distance runners, and one of the anatomical adaptations […] was the muscles and bones of the butt.”

But if Sir Mix-A-Lot taught us anything, it’s that our badonkadonks are far more than just muscle and bone. “The other half [of the question] is the fat,” Radke said, “and it's much more complicated – or at least it's much less known.”

The problem of explaining why humans are quite so bootylicious is two-fold, Radke explained. One is our own fault: historically, we’ve always got too caught up in racism and sexism to actually study butts in an objective way.

But the other side of it is purely practical: fat doesn’t leave a record.

“Bone leaves a fossil,” Radke said. “A muscle connects to a bone; we can learn what those muscles looked like based on the marks they leave on the bone. But there's no fossil record of fat, just like there's no fossil record of hair, or skin or whatever.”

While we know the reason for the amount of fat in a human butt – it’s due to the size of our brains, weirdly – the shape and location is yet to be fully accounted for. And perhaps we never will: Radke suggested that we may just be too close to butts, metaphorically speaking, to ever look at them scientifically.

“One of the lessons of the butt is how much we project on to it,” she said.

Of course, once we figure out the butt, we get to the anus – and that might be even harder to explain. So you know what? Maybe we should forget trying to understand things we use every day, and just stick simpler problems.

You know … like nuclear fusion.