Nothing plugged your tooth in. What you felt is the same phenomenon that has split scientists since the 1780s, and dentists were already arguing about it in print in 1880. You supplied the parts yourself: two different metals and a mouthful of saliva.

Quick answer

Biting aluminum foil can hurt when the foil touches a metal filling or crown. The two dissimilar metals and your saliva form a tiny battery, and the small current it produces stimulates the nerve inside the tooth. Dentists call this galvanic shock.

A twitching frog and a grumpy physicist

The story starts before dentistry cared. In 1786, the Italian physician Luigi Galvani found that a frog’s leg would twitch under certain conditions, including when two different metals touched it. He concluded that the twitch came from an innate ‘animal electricity’ inside the tissue.

Alessandro Volta, a professor at the University of Pavia, disagreed. Volta argued that the frog was not the source of anything. The current came from the two different metals, and the leg was just a very sensitive detector. The frog was reacting to the metals, not generating the charge.

The argument was productive. Around 1800, Volta built the voltaic pile, a stack of metal discs separated by an electrolyte layer, as an early battery that needed no living tissue. In the modern account, Volta was right about the metals and Galvani was onto something about nerves. Both halves matter for your teeth.

Your mouth is a very good battery jar

A battery needs two different metals and a conductive liquid between them. Saliva is salty and full of ions, so it fits the role well. An amalgam filling or a gold crown supplies one metal. The foil supplies aluminum, a different one.

When the foil touches the filling, the pair forms a small galvanic cell. Dental sources describe the aluminum as the anode and the filling as the cathode. Current flows through the wet tooth toward the nerve, the nerve fires, and your brain reports pain. Volta’s metals and Galvani’s twitching tissue are both present, only the tissue is yours.

The sources we checked describe the effect as needing metal already in the mouth, such as a filling, crown or braces. A tooth with no metal work has nothing for the foil to pair with. Some dental pages cite exact current figures for the sensation, but they disagree with each other, so we’re leaving those out.

Dentists noticed this in the 1800s

Nineteenth-century dentists were fascinated by this, and often worried about it. Amalgam fillings were new and controversial. In October 1847, The Dental Register printed ‘Galvanic Action and Amalgam’ by E. Slack, M.D. The page images are archived at PubMed Central, but the text isn’t searchable, so we can’t tell you what Slack concluded.

Later, Henry S. Chase of St. Louis, an M.D. and D.D.S., published ‘Some Observations and Experiments Connected with Oral Electricity’ in The American Journal of Dental Science in May 1878. In February 1880 he published an article in The Independent Practitioner with a title that doesn’t hedge: ‘Every Tooth Containing a Metallic Filling Is a Galvanic Battery in Active Operation.’

Not everyone agreed. The same journal ran a rebuttal, ‘No “Battery” in a Tooth,’ and a further article, ‘Straining at a Gnat’ by Chas. E. Francis, M.D., appeared there in May 1885. We could confirm titles, authors and dates but could not read the text of these scans. So we know the argument happened, and we don’t know who won the round.

The part most people miss

The foil isn’t special. Any two dissimilar metals can do this job. Dental writers describe the same kind of shock when different metals in a single mouth touch each other, for example when the fillings on opposite jaws meet as you bite. The foil just happens to be a thin, aluminum-heavy scrap that ends up between your teeth at dinner.

The ‘battery’ also works by contact. Aluminum foil is only a problem when it touches metal, and it stops once the contact ends. The sources we read describe the pain as a quick zap rather than lasting damage, though none of them measured how long it lasts. One trade article did suggest that galvanic currents could damage bone, but it seemed to mean long-term exposure, not a single bite on a baked potato.

So the modern discomfort you feel is a small echo of the 1786 frog experiment. Two metals, a wet conductor and a reacting nerve are all it takes. Volta would say the metals did it, and Galvani would say the nerve reacted. Your tooth demonstrates both at once.

Sources

Today’s RDH, ‘Galvanized Shock: Some Dental Patients Can Still Experience a Shocker.’

Queen’s Park Dental, ‘Why Biting Down on Aluminum Foil Hurts.’

PubMed Central archive of historical dental journals: E. Slack, ‘Galvanic Action and Amalgam,’ The Dental Register (1847); Henry S. Chase, ‘Some Observations and Experiments Connected with Oral Electricity,’ American Journal of Dental Science (1878); Henry S. Chase, ‘Every Tooth Containing a Metallic Filling Is a Galvanic Battery in Active Operation,’ The Independent Practitioner (1880); Chas. E. Francis, ‘Straining at a Gnat,’ The Independent Practitioner (1885).

Wikipedia, ‘Alessandro Volta.’

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galvanic shock FAQs

Why does aluminum foil hurt my teeth?

When foil touches a metal filling or crown, the two different metals and your saliva form a small galvanic cell. The resulting current stimulates the tooth’s nerve, which your brain reads as a sharp zap.

Is the shock from biting aluminum foil dangerous?

The sources we checked describe it as a brief, uncomfortable zap rather than lasting damage, and none of them said a single incident is harmful. If a tooth stays sensitive afterward, mention it to your dentist.

Can it happen if I have no fillings?

The dental sources we consulted describe the effect as needing existing metal in the mouth, such as amalgam fillings, gold or metal crowns, or braces. Without a metal to pair with the aluminum, the effect described there doesn’t occur.

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Klar wasn’t chasing a hairstyling mystery. He studies yeast and cell division at the National Cancer Institute, and he had a hunch that the tiny spiral on top of your head might be wired to the same genetic switch that decides whether you write with your left hand or your right. What he found in that mall wasn’t proof, exactly. But it was strange enough, and stubborn enough, that scientists are still arguing about it decades later.

Quick answer

Most people’s hair whorls spin clockwise (roughly 85-90% in typical population samples, though the exact figure shifts by country), and researchers have found that counterclockwise whorls show up far more often in left-handed people. The leading explanation is that whorl direction and handedness may share an early genetic or developmental origin, though scientists disagree on exactly how strong or reliable that link really is.

A geneticist, a mall, and a lot of staring at strangers

Amar Klar’s method was refreshingly low-tech: stand somewhere heads are visible, tally the direction of each whorl, move on. Across his surveys of the general population, he recorded that about 92% of people had a clockwise whorl and roughly 8% counterclockwise — a number that lines up closely with figures reported in later summaries of his work. He hadn’t asked anyone their dominant hand, but he didn’t need to for the first step, since roughly 90% of people are right-handed, and the two ratios were suspiciously close.

The real test came next. Klar tracked down a separate group of people who specifically had counterclockwise whorls and asked about their handedness directly. If whorl direction and handedness were unrelated, you’d expect this group to be about 90% right-handed too, just like everyone else. Instead, it split close to 50/50 between right-handers and non-right-handers. Something about growing a counterclockwise whorl seemed to erase the usual right-handed advantage.

One gene trying to do two jobs

Klar published his data in the journal Genetics in 2003 and proposed a tidy explanation: a single gene, with a dominant version that pushes a person toward both a clockwise whorl and right-handedness. If you inherit even one copy of that dominant version, the theory goes, you’ll likely be a clockwise-whorled righty. But if you end up with two copies of the recessive version, the gene stops steering — your whorl direction and your handedness both become, in effect, a coin flip.

It’s an elegant idea, and it would explain why left-handed and ambidextrous people show something close to an even split of whorl directions while right-handed people overwhelmingly cluster clockwise. But ‘elegant’ and ‘confirmed’ are different things. A single gene controlling something as complex as hand preference, brain lateralization, and hair follicle geometry all at once is a bold claim, and follow-up studies haven’t all agreed. Some later research found no significant link between whorl direction and handedness or language dominance at all, and modern genetics generally treats handedness as influenced by dozens of genes, not one master switch.

The part most people miss

The other tempting explanation for cowlicks — that they spin whichever way the Coriolis effect nudges them, the same force people blame for draining toilets swirling differently in each hemisphere — is a joke that escaped the lab. French pediatric geneticist Marjolaine Willems and her colleagues actually tested it, comparing hair whorls in twins and unrelated children born in France versus Chile, on opposite sides of the equator. Their verdict, delivered with a straight face in the citation for their 2024 Ig Nobel Prize in Anatomy: ‘if toilets aren’t subject to Coriolis forces, hair certainly isn’t either.’ Their real finding was more interesting anyway — identical twins matched each other’s whorl direction far more often than chance would predict, but counterclockwise whorls were also noticeably more common among the Chilean children than the French ones, hinting that whorl direction isn’t pure genetics. Something in early development, possibly linked to the womb environment, appears to nudge it too.

Sources

Wikipedia’s entry on ‘Hair whorl,’ which summarizes Amar Klar’s 2003 findings and the genetic model built around them, along with the criticism that later research has raised.

The Conversation, ‘Why aren’t you a lefty? A geneticist finds clues in kangaroos and shopping malls’ (2018), which details Klar’s mall-based data collection and his proposed single-gene mechanism.

Scientific American, ‘Does the Coriolis Effect Cause Your Cowlick?’, covering Marjolaine Willems’s twin and cross-hemisphere study and its 2024 Ig Nobel Prize in Anatomy.

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cowlicks FAQs

Do most people’s cowlicks really spin clockwise?

Yes. Population surveys generally find clockwise whorls are the majority pattern, though the exact percentage varies by study and country, ranging from roughly half in some Japanese samples to over 80% in some U.S. and German samples.

Is it true that left-handed people are more likely to have a counterclockwise cowlick?

Research by geneticist Amar Klar found left-handed people were far more likely than right-handed people to have a counterclockwise whorl, but the link isn’t absolute, and other studies have failed to replicate a strong association.

Does the Coriolis effect cause hair whorl direction?

No. Researchers who studied this directly, including the team behind a 2024 Ig Nobel Prize-winning study, concluded the Coriolis effect is far too weak to influence something as small as a hair follicle.

Is cowlick direction purely genetic?

It appears to be influenced by genetics but not determined by it alone. Twin studies show identical twins often share whorl direction, but not always, and environmental factors during early development may also play a role.

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The condition is called HAFE, it has a genuine 1981 medical paper behind it, and decades of follow-up research have found the original explanation was only half right. Here’s what’s really going on inside your body at 35,000 feet and 14,000 feet, and why the full answer turned out to be stranger than ‘gas expands when pressure drops.’

Quick answer

Airplane cabins are pressurized to feel like roughly 8,000 feet of altitude, not sea level, and that lower pressure lets trapped intestinal gas expand — by as much as 30% according to aerospace medicine estimates — so it has to escape. The same pressure drop happens on mountains and even short drives to elevation, a phenomenon doctors formally named High-Altitude Flatus Expulsion, or HAFE, in 1981.

The doctors who named it

In February 1981, physicians Paul S. Auerbach and York E. Miller published a short paper in the Western Journal of Medicine titled, with admirable directness, ‘High Altitude Flatus Expulsion (HAFE).’ They described a gastrointestinal syndrome triggered by ascent: as atmospheric pressure falls, gas already sitting in the colon expands, and the frequency and volume of flatulence goes up until you descend again, at which point it resolves on its own.

They weren’t the first to notice. A Russian physician and naturalist named Joseph Hamel documented the effect on Mont Blanc as early as 1820, describing ‘pneumatic flatulence’ alongside shortness of breath and fatigue during the ascent — though the observation was largely forgotten for over 150 years. In 1972, a physician named E.Y. Davis documented the same thing among Everest-region trekkers in a paper called ‘Flatulence Accompanying Rigorous Trekking,’ published in the Kathmandu Medical Bulletin. There was even harder data behind it: a 1969 study by Greenwald, Allen, and Bancroft in the Journal of Applied Physiology had already measured abdominal gas volume changing at altitude versus at ground level. Auerbach and Miller just revived the syndrome and gave it its lasting name — and its acronym.

Then someone took it to the airport

The mountaineering finding eventually migrated indoors, onto airplanes, courtesy of a 2013 paper in the New Zealand Medical Journal called ‘Flatulence on Airplanes: Just Let It Go,’ by Hans Pommergaard, Jakob Burcharth, Anders Fischer, and Jacob Rosenberg of Copenhagen’s Herlev Hospital, along with William Thomas of Sheffield Teaching Hospitals in England.

Their argument was pure applied physics: a cabin held at around 565 mmHg of pressure — the equivalent of 8,000 feet — versus roughly 760 mmHg on the ground means gas in your gut genuinely expands in volume during flight. The average person already produces 0.7 to 1 liter of intestinal gas a day and passes it about 10 times, and the authors’ actual medical recommendation was to let it happen rather than hold it in, since suppression just causes discomfort and bloating. Their proposed fix, only partly tongue-in-cheek: charcoal-lined seat cushions, blankets, and even underwear to absorb the odor, since ordinary cushions already blunt roughly half of it.

The part most people miss

The tidy ‘gas just expands’ story turned out to be incomplete. A 2013 pilot study in Medical Hypotheses, led by Graham Slaney, drove eight volunteers up into the Australian Alps to an altitude of about 5,900 feet — roughly Denver’s elevation, far below where Hamel or later mountaineers had climbed — and still found flatus frequency more than doubled after ascent, with participants recording around 14 expulsions each over an 18-hour window. Stranger still, the surge wasn’t instant: it built over several hours, suggesting the gas wasn’t just old air stretching out under lower pressure. The researchers proposed that carbon dioxide was actively diffusing out of the bloodstream and into the gut in response to the pressure change, effectively manufacturing new gas rather than only expanding what was already there. So the real story isn’t a single simple gas law — it’s your blood chemistry and your plumbing responding to elevation together, which is also why the effect shows up at modest ski-town altitudes, not just on 14,000-foot peaks.

Sources

Paul S. Auerbach and York E. Miller, ‘High Altitude Flatus Expulsion (HAFE),’ Western Journal of Medicine, February 1981.

Hans C. Pommergaard, Jakob Burcharth, Anders Fischer, William E.G. Thomas, and Jacob Rosenberg, ‘Flatulence on Airplanes: Just Let It Go,’ The New Zealand Medical Journal, 2013.

Graham Slaney et al., ‘High Altitude Syndromes at Intermediate Altitudes: A Pilot Study in the Australian Alps,’ Medical Hypotheses, 2013, plus the historical record of Joseph Hamel’s 1820 Mont Blanc expedition, as summarized on PubMed and Wikipedia’s entry on High-altitude flatus expulsion.

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HAFE (High-Altitude Flatus Expulsion) FAQs

Why do I fart more on airplanes specifically?

Airplane cabins are pressurized to roughly the equivalent of 8,000 feet of altitude, well below sea-level pressure, which lets intestinal gas expand and increases how much and how often you need to pass it.

Is HAFE dangerous?

No — High-Altitude Flatus Expulsion is uncomfortable, not harmful, and resolves on its own once you return to lower altitude or land. Doctors who’ve studied it actually recommend letting it out rather than holding it in.

At what altitude does this start happening?

Research has found increased flatulence at altitudes as modest as about 5,900 feet, a 2013 Australian Alps study found, though the phenomenon was first documented during an 1820 Mont Blanc ascent well above 11,000 feet.

Is it just trapped gas expanding, or something else?

Both. Lower pressure does expand existing gas, but a 2013 study suggests the body may also generate additional gas by letting carbon dioxide diffuse from the bloodstream into the intestines during ascent.

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This isn’t a coincidence or a nervous reaction to icy water. It’s a real, well-documented physiological reflex called cold diuresis, or immersion diuresis, and the paper trail on it stretches from an 18th-century pamphlet about the healing powers of English spa water to a U.S. Air Force doctor who spent a week floating in a tank to help figure out what happens to astronauts in orbit.

Quick answer

Cold water constricts the blood vessels in your skin and limbs, shoving extra blood into your core. Your body reads that surge of central blood volume as “too much fluid on board” and tells your kidneys to start filtering it out as urine, fast — which is why the urge to pee can hit within minutes of getting cold.

A pamphlet about the healing waters of Bath

The first known write-up of this effect wasn’t a physiology paper — it was a sales pitch. In 1764, a physician named Sutherland published a book promoting the medicinal virtues of the mineral waters at Bath and Bristol, England. Buried in a section on treating dropsy (the old term for fluid retention), he noted that patients who bathed in cold water started urinating more afterward. He didn’t know why. He just wrote it down.

It took nearly 150 years for anyone to test the obvious follow-up question: was it the cold, or just being wet? In 1909, a researcher named Gibson showed that cold exposure alone — no water required — could trigger the same increase in urine output. The mystery had a mechanism worth chasing, even if nobody yet knew what it was.

The Air Force doctor who floated for a week

The story jumps forward to the early 1960s and, of all places, the space race. NASA and the military wanted to know what happens to the human body when it’s suddenly relieved of the everyday work of fighting gravity — because in orbit, blood that normally pools in the legs shifts up into the chest, exactly the way it does when cold water squeezes it there from the outside. Water immersion became a cheap, Earth-bound way to fake that fluid shift.

In 1962, researchers Margaret Jackson and Duane Graveline published a study in the Journal of Applied Physiology tracking volunteers through six-hour stretches of full water immersion, measuring exactly how their kidneys responded to that redirected blood. Graveline wasn’t just a lab researcher — three years later, in June 1965, he was selected as one of NASA’s scientist-astronauts. He resigned that August, before ever flying a mission, but the immersion research he helped pioneer became a foundation for understanding how fluid shifts, whether from cold water or zero gravity, force the kidneys into overdrive.

The part most people miss

Here’s the twist: scientists still don’t agree on the exact hormonal wiring behind cold diuresis. The long-standing explanation was that cold suppresses antidiuretic hormone (ADH), the signal that normally tells kidneys to hold onto water, so without it your kidneys just let fluid pass straight to the bladder. But in 1974, researcher Stefan Lennquist and colleagues argued the bigger driver might simply be pressure — cold-induced vasoconstriction raises blood pressure enough that kidneys flush more fluid on their own, no hormone drop required. Later work has muddied that further, finding that other hormones, including atrial natriuretic peptide, released when the heart’s upper chambers stretch from the extra incoming blood, and reduced aldosterone both play a role too. Divers Alert Network, which studies this constantly because it affects nearly every diver on every dive, describes it simply as the body dumping fluid to relieve pressure it thinks it doesn’t need. The honest answer is that it’s not one single switch — it’s several overlapping systems responding to the same signal, and researchers are still sorting out which one deserves top billing.

Sources

Institute of Medicine, “Nutritional Needs in Cold and High-Altitude Environments” (National Academies Press), chapter on cold stress and human fluid balance, which traces the research history from Sutherland’s 1764 observation through Gibson (1909) and Lennquist et al. (1974).

M. M. Jackson and D. E. Graveline, “Diuresis Associated with Prolonged Water Immersion,” Journal of Applied Physiology, 1962.

Divers Alert Network (DAN), “Immersion Diuresis,” health resource on the mechanism behind fluid loss during water immersion.

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cold diuresis FAQs

What is it called when cold water makes you need to pee?

It’s known as cold diuresis or immersion diuresis — a reflex where cold-triggered blood vessel constriction pushes extra blood to your core, prompting your kidneys to filter out fluid faster.

Does this happen in cold air too, not just cold water?

Yes. Researchers confirmed as early as 1909 that cold exposure alone, without water, triggers the same increased urine production — it’s part of why you tend to pee more in winter.

Is needing to pee in cold water a sign something’s wrong?

No, it’s a normal protective reflex. It only becomes a concern during prolonged cold-water exposure, where the fluid loss can contribute to dehydration and speed up hypothermia risk.

Can you prevent or reduce cold diuresis?

Research from the 1950s found that moderate exercise during cold exposure can reduce the effect, likely because muscle activity helps counteract the blood-shifting vasoconstriction.

Why does the urge feel almost instant?

Vasoconstriction in the skin and limbs begins within minutes of cold exposure, and the resulting pressure signal reaches the kidneys quickly — so if your bladder already had some fluid in it, the extra output can tip it into urgent territory fast.

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For decades scientists assumed this was just about looking out the window. It isn’t. The real answer involves a 1970s theory about your inner ear lying to your eyes, a study that spun people in circles for science, and an evolutionary hypothesis that treats vomiting as a leftover poison alarm. And it turns out the driver’s immunity has a very specific expiration date — one the self-driving car industry is racing to solve right now.

Quick answer

Carsickness comes from a mismatch between what your inner ear feels and what your eyes see — your vestibular system registers turns and stops your eyes can’t confirm, especially if you’re reading or on a phone. Drivers mostly escape it because they control the wheel and can see and anticipate every motion before it happens, not just react to it.

The argument happening inside your skull

In 1975, British psychologists John Reason and Joyce Brand published a book that became the standard reference on the subject, simply titled ‘Motion Sickness.’ Their sensory conflict theory (sometimes called sensory rearrangement theory) argued that nausea isn’t triggered by motion itself — it’s triggered by disagreement between your senses about what’s happening. Your vestibular system, the fluid-filled canals in your inner ear, feels every turn, stop, and sway. But if your eyes are locked on a stationary book page or phone screen, they’re reporting that you’re sitting still. Your brain, faced with two contradictory motion reports it can’t reconcile, treats the confusion as a red-alert glitch worth getting sick over.

It’s a strange system when you think about it — your body isn’t reacting to something dangerous, it’s reacting to a disagreement between two of its own instruments. That framing turned out to explain a huge range of motion sickness triggers, from ships and flight simulators to, later, virtual reality headsets.

The steering wheel effect

But sensory conflict alone doesn’t explain why the person holding the wheel so rarely feels it, even though their inner ear is registering the exact same turns and stops as everyone else in the car. In 1991, researchers Boris Rolnick and Robert Lubow published a study in the journal Ergonomics titled ‘Why is the driver rarely motion sick? The role of controllability in motion sickness.’ They paired up subjects and spun them in a rotating chair designed to provoke nausea — one person in each pair actually controlled the rotation and their own head movements, while their partner was spun through the identical motion passively, with no control at all. The people with control reported significantly less sickness, even though the physical motion each pair experienced was engineered to match.

The takeaway: it isn’t just what you see or how your head moves that matters — it’s whether your brain knows what’s coming next. A driver is constantly generating a mental forecast of the next turn, the next brake, the next lane change, a fraction of a second before it happens. Passengers only get the after-the-fact version. That gap between prediction and surprise, more than the motion itself, seems to be what makes stomachs turn.

The part most people miss

Here’s the twist: the driver’s immunity isn’t really about being a driver. It’s about being the one in control and looking ahead — which means as soon as you take the wheel away, the immunity disappears, even for someone who’s driven that same road a thousand times. Researchers at Mcity, the University of Michigan’s driverless-vehicle testing facility, have flagged motion sickness as a real obstacle to self-driving car adoption, precisely because the technology turns every former driver into a passive passenger with nothing to predict. Up to a third of Americans are considered highly susceptible to motion sickness under ordinary conditions, and autonomous vehicles risk putting all of them in the one seat that never used to bother them. Uber took the problem seriously enough to file a patent application for a ‘sensory stimulation system’ (U.S. Patent 9,789,880) back in March 2016, and it was granted in October 2017 — a setup that uses lights, seat movement, and even puffs of air to warn a passenger’s body about a turn just before it happens, essentially trying to hand back the forecasting ability that steering wheels used to provide for free.

Sources

John Reason and Joyce Brand’s 1975 book ‘Motion Sickness’ (Academic Press), which established the sensory conflict theory still cited in motion sickness research today.

Boris Rolnick and Robert Lubow, ‘Why is the driver rarely motion sick? The role of controllability in motion sickness,’ Ergonomics, 1991.

Mcity, University of Michigan’s driverless-vehicle research center, on its work measuring and mitigating motion sickness in autonomous vehicles.

U.S. Patent 9,789,880 B2, ‘Sensory stimulation system for an autonomous vehicle,’ assigned to Uber Technologies, filed March 3, 2016 and granted October 17, 2017.

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carsickness FAQs

Why do I get carsick reading in the car but not when I’m driving?

Reading fixes your eyes on something that appears stationary, while your inner ear still feels every turn and stop — that visual-vestibular mismatch is the classic trigger. Drivers rarely read while driving, and they’re also anticipating the car’s movements instead of just feeling them arrive.

Does looking at the horizon actually help with carsickness?

Yes — looking ahead at a fixed, distant point gives your eyes a steady reference that roughly matches what your inner ear is sensing, reducing the sensory conflict that triggers nausea.

Will self-driving cars make motion sickness worse?

Researchers, including teams at the University of Michigan’s Mcity facility, expect it could, since former drivers lose the anticipatory control that used to protect them and become passive passengers instead.

Is carsickness the same thing as seasickness?

They share the same underlying mechanism — sensory conflict between the inner ear and the eyes — which is why the general theory developed by Reason and Brand covers cars, boats, planes, and even virtual reality.

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Bean never set out to settle the fingernail-versus-toenail question directly, but his decades of obsessive note-taking became the backbone of what we now know about nail growth in general. And the short version is: your fingernails are winning a race your toenails don’t even know they’re running.

Quick answer

Fingernails grow roughly two to three times faster than toenails — about 3.5 millimeters a month for fingernails versus about 1.6 millimeters a month for toenails, according to a 2010 measurement study of healthy young adults. Nobody has proven exactly why, but the leading theories point to blood flow and everyday wear and tear on the hands.

The doctor who turned his thumbnail into a lab notebook

William B. Bean spent most of his career as a professor of internal medicine at the University of Iowa, with a stint running the Institute for Medical Humanities at the University of Texas Medical Branch in Galveston. But his most famous contribution to science had nothing to do with a hospital ward. Starting at age 32, he began tracking the growth of his own left thumbnail, filing his findings the way other scientists track sunspots or tide charts.

The pattern he found was striking: growth slowed steadily with age. His thumbnail grew about 0.123 millimeters a day when he was 32, and by the time he was 67 that had dropped to 0.095 millimeters a day. He also noticed that his fingernails, overall, grew noticeably faster than his toenails — an observation that later, more formal studies would confirm with actual control groups instead of one very patient man.

Blood, trauma, and why the gap is real

In 2010, researchers led by Sopa Yaemsiri measured nail growth in 22 healthy young American adults using a standardized filing-and-marking protocol, the same basic idea Bean had pioneered decades earlier. Their numbers: fingernails grew an average of 3.47 millimeters a month, toenails just 1.62 millimeters a month. Within each hand and foot there were quirks too — the little fingernail was the slowest grower on the hand, while the big toenail was the fastest on the foot.

Nobody has nailed down (sorry) the single cause of the fingernail-toenail gap, but two explanations keep coming up. One is circulation: hands sit closer to the heart than feet do, and nail growth tracks pretty closely with blood flow to the digit — which is also why nails grow slower in cold weather, when blood vessels constrict. The other is wear and tear, sometimes called the terminal trauma theory: fingers get bumped, typed on, and used constantly, and the body may respond to that repeated low-grade stress by sending more blood and nutrients to the nail matrix, the living tissue under the skin where new nail is actually made.

The part most people miss

Bean’s fingernail obsession outlived him by decades, and in a strange twist it eventually paid off in the most Bean-appropriate way possible. In September 2025, the Ig Nobel Prize in Literature — the annual award for research that first makes people laugh, then makes them think — was given posthumously to William B. Bean for his 35-year single-nail study, with his son Bennett Bean accepting on his behalf at the ceremony at Boston University. The judges singled out Bean’s actual write-ups, which apparently wandered into references to Moby-Dick and medieval astrology while reporting keratin growth rates. It’s a reminder that Bean wasn’t just running an experiment; he was having fun with it, one thumbnail scratch at a time.

Sources

William B. Bean, “A Note on Fingernail Growth,” Journal of Investigative Dermatology, 1953, volume 20, pages 27-31, documenting his first 10 years of self-observation.

William B. Bean, “Nail Growth: 30 Years of Observation,” Archives of Internal Medicine, 1974, volume 134, pages 497-502, and “Nail Growth. Thirty-Five Years of Observation,” Archives of Internal Medicine, 1980, volume 140, pages 73-76.

Sopa Yaemsiri et al., “Growth rate of human fingernails and toenails in healthy American young adults,” Journal of the European Academy of Dermatology and Venereology, 2010.

Coverage of the 2025 Ig Nobel Prize in Literature awarded to William B. Bean, reported by Improbable Research (organizer of the Ig Nobel Prizes) and Science Friday.

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nail growth rate FAQs

How much faster do fingernails grow than toenails?

About two to three times faster. Fingernails grow roughly 3.5 millimeters a month on average, compared to about 1.6 millimeters a month for toenails.

Why do fingernails grow faster than toenails?

There’s no single proven answer, but the leading theories are better blood circulation in the hands (which are closer to the heart) and constant minor bumps and use of the fingers, which may stimulate the nail matrix to grow faster.

Who discovered that fingernails grow faster than toenails?

Formal measurement studies confirmed it, but physician William B. Bean’s 35-year self-study of his own thumbnail, published between 1953 and 1980, was an early and influential source of data on human nail growth rates, including the fingernail-toenail difference.

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That failed experiment did something more useful than confirming a theory ever could — it killed one. Nearly four decades later, researchers still haven’t agreed on a single explanation for the most ordinary thing a human body does. What they’ve found instead is stranger, and more interesting, than “you’re just tired.”

Quick answer

The best-supported theory is that yawning helps cool an overheated brain: the deep breath and jaw stretch boost blood flow and pull in cooler air. It’s not proven beyond doubt, and it doesn’t explain everything — contagious yawning, the kind you catch from someone else, seems to run on a separate social circuit that scientists still can’t fully map.

The professor who tried to gas a yawn out of people

Robert Provine spent decades treating yawns like a naturalist tracking an elusive animal — cataloguing when people did it, how long it lasted (about six seconds, remarkably consistent from person to person), and what triggered it. His 1987 study, published in Behavioral and Neural Biology, was designed to finally test the oxygen-deficit idea that had been the default explanation for centuries. Volunteers breathed air spiked with carbon dioxide, then pure oxygen, then were run hard enough on exercise to double their breathing rate. None of it moved yawn frequency at all.

The conclusion was almost anticlimactic: yawning has nothing to do with gas exchange. It runs on its own clock in the brain, tied to something else entirely — and that opened the door for a very different theory to take over.

A cold pack solves half the puzzle

Psychologists Andrew Gallup and Gordon Gallup picked up where Provine left off, proposing that yawning isn’t about oxygen but temperature — specifically, cooling an overheated brain. In a 2007 study, they had people watch videos of others yawning while either holding a cold pack to their forehead or breathing only through their nose. Both groups caught far fewer yawns than people breathing normally through the mouth. Gallup later tracked yawning across seasons in Tucson, Arizona, and found people yawned less in summer, when outdoor air was as hot as body temperature or hotter — cooling air wouldn’t help, so the body apparently didn’t bother.

That explains the yawn itself. It doesn’t explain why yawns spread through a room like gossip. A 2008 study by Ramiro Joly-Mascheroni and colleagues found that dogs catch yawns too: 21 of 29 dogs tested yawned after watching a stranger yawn at them — the first evidence that contagious yawning crosses the species line, though the study didn’t test whether an owner’s yawn worked any better than a stranger’s. A 2013 follow-up by Teresa Romero, Akitsugu Konno, and Toshikazu Hasegawa answered that question, finding dogs yawned significantly more often for their own owners than for an unfamiliar person — hinting that contagion runs on social bonding, not just heat. For years, that fed a popular idea: catching yawns is a sign of empathy. Then in 2014, Duke University geneticist Elizabeth Cirulli tested 328 volunteers and found the opposite — empathy barely mattered. The only real predictor was age; older adults simply caught fewer yawns, and even that explained just 8% of the variation. Most of why yawning spreads from person to person is, officially, still unexplained.

The part most people miss

If yawning were really about being tired or bored, it would be strange that fetuses do it. Durham University researcher Nadja Reissland used 4D ultrasound to scan fifteen healthy fetuses repeatedly between 24 and 36 weeks of gestation and found them yawning as often as six times an hour early on, tapering off as birth approached — long before anything resembling boredom or sleep deprivation could apply. More recent work has pushed the mystery further: a February 2026 study led by Damiano Menin at the University of Ferrara, published in PLOS ONE, tracked 32 fetuses and found that the ones who yawned more often tended to be born at slightly lower weight, a possible marker of mild prenatal stress rather than sleepiness. If that holds up, the very first yawns of our lives may have nothing to do with being tired at all — they might be an early stress or brain-development signal, decades before anyone thinks to stifle one in a meeting.

Sources

Robert Provine’s 1987 gas-exchange experiment, published in Behavioral and Neural Biology.

Andrew C. Gallup and Gordon G. Gallup’s thermoregulatory yawning research, Evolutionary Psychology (2007), and Gallup’s seasonal yawning study conducted in Tucson, Arizona.

Ramiro Joly-Mascheroni and colleagues’ 2008 study on contagious yawning in dogs, published in Biology Letters, and Teresa Romero, Akitsugu Konno, and Toshikazu Hasegawa’s 2013 follow-up on familiarity bias in contagious yawning by dogs, published in PLOS ONE.

Elizabeth Cirulli’s 2014 contagious-yawning and empathy study, Duke University School of Medicine, published in PLOS ONE.

Nadja Reissland’s fetal yawning research, Durham University, published in PLOS ONE (2012), and Damiano Menin’s fetal yawning and birth weight study, University of Ferrara, published in PLOS ONE (February 2026).

Explore more: More true stories about the human body.

yawning FAQs

Why do we yawn when we’re tired?

Nobody has proven the exact link, but the leading idea is that yawning helps regulate brain temperature and alertness during shifts in arousal state — not that it pulls in extra oxygen, which researchers ruled out in the 1980s.

Is yawning contagious to animals, not just humans?

Yes. A 2008 study found 21 of 29 dogs yawned after watching a stranger yawn at them, and a 2013 follow-up found dogs yawn even more often for their own owners than for strangers. Contagious yawning has also been documented in chimpanzees and other primates.

Does catching someone else’s yawn mean you’re empathetic?

That was the popular theory for years, but a 2014 Duke University study of 328 people found empathy barely predicted contagious yawning — age was the only meaningful factor, and even that explained just a small slice of the variation.

Do babies yawn before they’re born?

Yes. Ultrasound studies show fetuses yawning starting around 20-24 weeks of gestation, tapering off as birth nears, which suggests yawning is tied to brain development rather than tiredness or boredom.

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Charles Darwin agreed. In 1871 he listed the appendix among the human body’s “rudimentary” leftovers, a shrunken remnant of a plant-digesting pouch our leaf-eating ancestors supposedly no longer needed. That verdict stuck for generations, right up until a Duke University surgeon started looking at the appendix under a microscope instead of just cutting it out.

Quick answer

No — research increasingly suggests the appendix isn’t a functionless evolutionary leftover. It appears to act as a protected reservoir for beneficial gut bacteria, and it has evolved independently in mammals dozens of separate times, which is not something natural selection tends to do with junk.

The organ everyone loved to hate

For most of modern medical history, the appendix’s whole identity was the emergency it caused. Once Fitz named appendicitis and surgeons like Charles McBurney worked out how to diagnose and remove an inflamed appendix quickly, appendectomy became one of the most common operations in the world. If a body part’s main claim to fame is the surgery invented to yank it out, “useless” starts to sound like the obvious conclusion.

And Darwin’s vestigial-organ theory gave that hunch scientific cover. If the appendix was just a shrunken version of the cecum that plant-eating ancestors used to ferment tough vegetation, then in an omnivorous, cooked-food-eating species like us, it made sense that it had withered into a dangling, purposeless tube — one whose only job left was occasionally getting infected.

A safe house for the good bacteria

That story cracked open in 2007, when Duke University immunologist William Parker and surgeon R. Randal Bollinger, along with colleagues Andrew Barbas, Errol Bush, and Shu Lin, published a hypothesis in the Journal of Theoretical Biology. Parker’s lab had been studying biofilms — thin, protective layers of mucus, immune molecules, and bacteria — lining the gut, and the appendix turned out to be an unusually good place for one to hide.

The appendix sits tucked below the normal one-way traffic flow of the large intestine and is packed with lymphatic tissue that nurtures helpful microbes rather than attacking them. The researchers proposed that during a severe gut infection — cholera or dysentery, historically — the diarrhea that purges harmful bacteria could also wipe out the beneficial bacterial community living in the rest of the intestine. The appendix, off to the side and shielded from that flushing, could act as a reserve tank, reseeding the gut with good bacteria once the crisis passed. As Parker put it in Duke’s announcement of the findings, “the abundance of circumstantial evidence makes a strong case for the role of the appendix as a place where the good bacteria can live safe and undisturbed until they are needed.”

Evolution’s stubborn habit of rebuilding it

The clincher came from an unexpected direction: family trees. In 2013, evolutionary biologist Heather Smith at Midwestern University and colleagues examined the guts of 361 mammal species, tracking which ones had an appendix-like structure and mapping them onto the mammalian evolutionary tree. Published in Comptes Rendus Palevol, their analysis found that roughly 50 species have some version of an appendix — and those species are scattered so widely across unrelated branches of the tree that the structure must have evolved independently at least 32 separate times, possibly closer to 38.

That’s the opposite of what a true vestige should look like. A leftover organ typically traces back to a single ancestor and then slowly shrinks away in every descendant line. An organ that keeps getting reinvented from scratch, again and again, in species that aren’t closely related, is usually one that’s earning its keep.

The part most people miss

Here’s the twist FYI Tales readers should know: this case isn’t closed. Follow-up research on real patients has been messier than the safe-house story suggests. Some studies looking at whether people without an appendix suffer worse or more frequent Clostridioides difficile (C. diff) infections have found no protective effect at all, while others have reported a higher risk of C. diff after appendectomy. Nobody has run the controlled experiment nature would need to settle it. It’s also worth noting that appendicitis itself is far more common in industrialized, sanitized countries than in places with heavier microbial exposure — which fits an odd possibility: the appendix’s ancient bacterial-backup job may simply have less to do in a world of clean water and antibiotics, leaving it inflamed and idle more often than useful. So the honest version of this tale isn’t “scientists proved the appendix is essential.” It’s that the organ doctors spent a century treating as biological packing material turned out to be far more interesting, and far more argued-over, than anyone expected.

Sources

Duke Health, “Appendix Isn’t Useless at All: It’s a Safe House for Bacteria,” covering the 2007 Journal of Theoretical Biology hypothesis by William Parker, R. Randal Bollinger, and colleagues.

Science (AAAS), “Appendix Evolved More Than 30 Times,” covering the 2013 Comptes Rendus Palevol study led by Heather F. Smith of Midwestern University.

Hektoen International, “The Early Days in the History of Appendectomy,” on Reginald Heber Fitz’s 1886 naming of appendicitis and the rise of appendix surgery.

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appendix FAQs

Is the appendix completely useless?

Probably not. Research points to it acting as a protected reservoir for beneficial gut bacteria and as a hub of immune tissue, though scientists haven’t proven this beyond doubt.

Can you live a normal life without an appendix?

Yes. Appendectomy is common and safe, and most people notice no lasting effects — whatever the appendix does, the rest of the body seems to manage fine without it.

Why did Darwin think the appendix was vestigial?

In The Descent of Man (1871), Darwin listed the appendix as a shrunken remnant of a larger structure ancestral plant-eaters used for digestion, based on the limited anatomical evidence available at the time.

How many times has the appendix evolved in mammals?

A 2013 study by Heather Smith and colleagues found it evolved independently at least 32 times, and possibly as many as 38, across different mammal lineages.

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That staggered build isn’t folklore, it’s basic embryology, understood by dentists for well over a century. But the deeper question — why bother with two rounds of teeth instead of just building it right the first time — took a lot longer to answer properly. The clearest answer yet came in 2022, from a small Australian marsupial doing something scientists were pretty sure mammals had stopped doing 200 million years ago.

Quick answer

Humans are “diphyodont” — biology’s term for growing exactly two sets of teeth — because jaws grow but individual teeth don’t. Twenty small primary teeth get a child through infancy, when the jaw is too small for full-size teeth; once the jaw has grown enough, thirty-two larger, sturdier permanent teeth take over for the rest of a person’s chewing life. It’s a compromise inherited from ancestors who could regrow teeth indefinitely, traded away for a tighter, more precise adult bite.

A shark’s smile and Aristotle’s blunder

Most vertebrates don’t play by the two-set rule. Sharks, many reptiles, and most fish are “polyphyodont”: a permanent strip of tissue called the dental lamina keeps churning out replacement teeth for life, so a lost tooth is never a real loss. Mammals are the odd ones — most of us shut that assembly line down after just two runs.

Humans have been curious about tooth counts for a very long time, and not always accurately. In his 4th-century BCE work History of Animals, Aristotle claimed men have more teeth than women. The philosopher Bertrand Russell later needled him for it, pointing out that Aristotle was married twice and apparently never thought to count his own wives’ teeth. He’d have found the same number: both sexes get 20 baby teeth and up to 32 adult ones. It’s a good reminder that figuring out *why* we have two sets of teeth took a lot more than counting — it took real embryology.

Losing the assembly line

The dental lamina in sharks is a permanent, self-renewing structure — new teeth are always queued up behind the ones in use. Early mammal ancestors had a version of this too, but somewhere around 205 million years ago, most mammal lineages evolved a version of the dental lamina that breaks down and stops working after producing just two generations of teeth.

Why give up an endless supply of free replacement teeth? Because mammals need something reptiles and sharks generally don’t: precise occlusion — top and bottom teeth that interlock tightly for grinding food, not just piercing and swallowing it whole. A mouth that’s constantly swapping in loose new teeth doesn’t grind well. Two sets is the compromise: small teeth to get an infant through nursing and early chewing while the jaw is still tiny, then one clean, permanent upgrade once the jaw reaches adult size and needs a precision-fit set built to last. Even the permanent set arrives in waves — the second molars don’t start forming until roughly a child’s first birthday, and the third molars, the wisdom teeth, don’t begin until around age four or five.

The wallaby that broke the textbook

For decades, the textbook story was tidy: baby teeth come from the primary dental lamina, and adult replacement teeth sprout later from a separate structure called the successional lamina. Then in 2022, researcher Qamariya Nasrullah at Monash University, working with Marilyn Renfree at the University of Melbourne and Alistair Evans, published a study in the Journal of Mammalian Evolution that complicated that picture.

The team used a scanning technique called diceCT — staining soft tissue so it shows up on a CT scan — to watch tooth development in tammar wallabies from embryo to adult. Wallabies replace only their premolars, and those “replacement” teeth were assumed to come from the successional lamina, just like ours. Instead, the scans showed they were delayed baby teeth, still growing out of the original primary dental lamina — a hidden holdover from the ancestral, endlessly-replacing system mammals were supposed to have left behind.

The part most people miss

Here’s the part that rarely makes it into the two-sets-of-teeth explainer: the ancient assembly line isn’t gone from humans either — it’s just switched off. Researchers have identified rudimentary tissue for a theoretical third human dentition, suppressed during development by a protein called USAG-1. Kyoto University’s Katsu Takahashi spent nearly three decades studying that protein, and the startup he helped found, Toregem BioPharma, began first-in-human trials in 2024 of an antibody designed to block USAG-1 and wake those dormant buds up. In earlier animal studies, the same approach regrew real, functional teeth in mice, ferrets, and dogs. It’s still early-stage medicine, not a cure at the dentist’s office yet — but it means the “two sets and that’s it” rule your dentist taught you may not be the final chapter.

Sources

Qamariya Nasrullah, Marilyn Renfree, and Alistair Evans, “From Embryo to Adult: The Complete Development and Unusual Replacement of the Dentition of the Tammar Wallaby (Macropus eugenii),” Journal of Mammalian Evolution (2022), published via Springer Nature Link.

The Conversation / Monash Lens, “Why do humans grow two sets of teeth? These marsupials are rewriting the story of dental evolution” (2022), reporting on the Monash University research team.

TeachMeAnatomy, “Development of Teeth,” for the timeline of permanent tooth germ formation before and after birth, including the delayed appearance of the second and third permanent molars.

Wikipedia, “Diphyodont,” for background on two-generation tooth replacement across mammals.

Toregem BioPharma (Kyoto University spinoff), official company information on Dr. Katsu Takahashi’s USAG-1 antibody research and its 2024 human clinical trials.

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two sets of teeth FAQs

Why do baby teeth fall out in the first place?

Baby teeth are sized for an infant’s small jaw and aren’t built to last a lifetime. As the jaw grows, the roots of primary teeth dissolve, making room for the larger, sturdier permanent teeth waiting underneath to push through.

How many teeth does a person grow in a lifetime?

Fifty-two, total — 20 primary (“baby”) teeth followed by 32 permanent teeth, including the four wisdom teeth that come in last, if they come in at all.

Are all of a baby’s permanent teeth already forming at birth?

Most, but not all. By birth, the tooth buds for the permanent incisors, canines, premolars, and first molars have already started developing beneath the baby teeth. The second molars don’t begin forming until around a child’s first birthday, and the third molars — wisdom teeth — don’t start until roughly age four or five.

Could humans actually grow a third set of teeth someday?

Possibly. Human trials beginning in 2024 are testing a drug that blocks a protein called USAG-1, which normally keeps dormant extra tooth buds from developing. It’s aimed first at people missing teeth from birth, and it’s still in early clinical testing.

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The color really does come from your immune system doing something specific and real. What it doesn’t do, according to the researchers who’ve actually tested the claim, is reliably tell you whether bacteria are involved at all.

Quick answer

Snot color mostly tracks how hard your immune system is working, not whether a virus or bacteria caused the problem. Green and yellow come from an iron-containing enzyme released by white blood cells as they fight off any invader — so a bad viral cold can turn snot just as green as a bacterial sinus infection.

The enzyme behind the green

In 2010, science writer Valerie Ross went looking for an answer to a question kids ask constantly, and got it from Dr. Harry Malech, a neutrophil specialist at the National Institute of Allergy and Infectious Diseases. Neutrophils are the immune cells that rush toward infection or irritation and start engulfing whatever’s causing trouble. To do that, they’re packed with an enzyme called myeloperoxidase — and myeloperoxidase happens to be loaded with iron.

‘Myeloperoxidase has a lot of iron in it, and in the environment provided by the surrounding snot, the iron turns a green color,’ Malech told Ross. It’s the same basic chemistry that makes blood red: iron-containing proteins tint fluid when they’re released in bulk. When neutrophils have been working for a while, they break down and spill their myeloperoxidase into the mucus, and the green gets more vivid the longer the immune response runs.

Then someone actually tested the belief

The trouble is that neutrophils show up for viral infections too — colds, flu, even allergic inflammation can summon them. So researchers started asking a more useful question: if you actually measure it, does mucus color predict bacteria? A pooled analysis of six multicentre studies (over 4,000 sputum samples), published in the European Respiratory Journal, found that green or yellow sputum was about 95% sensitive for bacterial presence — meaning if bacteria really were there, discolored mucus almost always showed it. But specificity was only around 15%. That’s the number that trips people up: it doesn’t mean colored mucus fails to rule bacteria out. It means colored mucus is bad at ruling bacteria in. A huge share of green or yellow samples showed up in people with no bacterial culture at all, so seeing the color tells you almost nothing about whether antibiotics would actually help.

In 2016, University of Adelaide microbiologist John Turnidge tackled the myth head-on in The Conversation, writing plainly that green or yellow mucus meaning bacterial infection ‘isn’t true.’ The color, he explained, is just a normal stage of inflammation — your immune system doing its job on a virus, most of the time — and antibiotics ‘provide no benefit’ for the colds, acute bronchitis, and sinus infections where the myth usually gets invoked.

The part most people miss

The part almost nobody clocks: you’re most contagious during the boring, clear, runny stage of a cold — not once the green, gunky, alarming-looking stuff shows up. By the time neutrophils have flooded in and turned things green, Turnidge noted, viral shedding has usually already dropped off. So the exact moment people start worrying they’re spreading germs is often the moment they’re least likely to be doing so. Where the myth itself came from is murkier — Turnidge suggests it’s a leftover mix-up with pus, which genuinely does signal bacterial infection in things like boils and abscesses, bleeding over into an assumption about mucus that never held up to testing.

Sources

The Conversation, ‘Health Check: does green mucus mean you’re infectious and need antibiotics?’ by John Turnidge, Affiliate Professor, University of Adelaide (August 15, 2016).

Scienceline, ‘What Makes Snot Turn Green?’ by Valerie Ross, quoting Dr. Harry Malech of the National Institute of Allergy and Infectious Diseases (February 1, 2010).

European Respiratory Journal, pooled analysis ‘Sputum colour and bacteria in chronic bronchitis exacerbations,’ reporting 94.7% sensitivity and roughly 15% specificity for sputum color as a marker of bacterial presence.

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snot color FAQs

Does green or yellow mucus mean I need antibiotics?

Not on its own. A large pooled study found colored mucus shows up in about 95% of cases where bacteria are present, but it also shows up constantly when bacteria aren’t — its specificity is only around 15%. So seeing color doesn’t confirm a bacterial infection, and most colds, bronchitis, and sinus infections clear up without antibiotics regardless of color.

Why does mucus turn green in the first place?

White blood cells called neutrophils release an iron-rich enzyme, myeloperoxidase, as they fight off infection or irritation. The iron tints the mucus green, the same way iron in blood makes it red.

When is a cold actually most contagious?

Usually during the early, clear, runny-nose phase — before mucus turns colored, not after. By the time green mucus shows up, viral shedding has often already declined.

When should mucus color actually worry me?

See a doctor if symptoms last more than about 10 days, keep worsening after initially improving, or come with high fever or facial pain — those patterns matter more than color alone.

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