The Vegetable That Reveals How Privately You Smell the World

A person eats dinner. Asparagus, perhaps, alongside whatever else was on the plate. Thirty minutes later they return from the bathroom with a slightly bewildered look, because something has happened that no one warned them about. A sharp, sulfurous smell has risen from the toilet bowl, unmistakable and faintly alarming, the kind of odor that makes a person glance around as if to confirm they are alone. Within fifteen minutes of the first bite, sometimes less, the green vegetable on the dinner plate has left an unambiguous signature in the body’s plumbing.

And yet, seated at the same table, someone else has eaten the same spears and noticed nothing at all. Not a faint trace. Nothing. To this second person the entire phenomenon sounds like a strange joke, an old wives’ tale, the kind of thing people insist is real but never seems to occur to them. Both people are telling the truth. Both are correct. The contradiction is not a matter of imagination or sensitivity or hygiene. It is a small, elegant demonstration of one of the stranger facts about being human: that two bodies can process the same meal in chemically identical ways and still inhabit completely different sensory worlds.

The story of asparagus and urine is, on its surface, a piece of bathroom trivia. Underneath, it is a centuries-long detective story that turns out to be less about a vegetable than about the deeply private, genetically scripted nature of perception itself.

A puzzle older than chemistry

People noticed the smell long before anyone could explain it. The connection between asparagus and a peculiar odor in urine was common enough knowledge in the 18th century that learned men felt entitled to comment on it in print. In 1731, the Scottish physician John Arbuthnot, a friend of Jonathan Swift and a fixture of London’s intellectual circles, noted in a treatise on diet that asparagus “affects the urine with a foetid smell.”¹ He was simply recording something his readers would have recognized at once.

Benjamin Franklin, never one to let an indelicate subject go unexamined, weighed in as well. In a satirical letter written in the early 1780s and addressed (mockingly) to the Royal Academy of Brussels, Franklin proposed that the academy turn its attention to more practical chemistry, observing along the way that “a few stems of asparagus eaten shall give our urine a disagreeable odour.”² He found the matter genuinely worth thinking about, a stance that has aged better than the prudishness of his contemporaries.

For all this casual familiarity, no one had the faintest idea what was actually responsible. The smell was obviously sulfurous, the rotten-egg, struck-match family of odors, but chemistry in the 18th century lacked the tools to isolate the molecule doing the work. The vegetable was suspected, convicted, and sentenced in the court of common observation, yet the actual culprit remained unidentified for more than a hundred years after Arbuthnot’s note.

The first serious attempt came late in the 19th century. In 1891, the chemist Marcel Nencki, working in the rapidly professionalizing field of biochemistry, proposed that the offending substance was methanethiol, a simple sulfur compound also known as methyl mercaptan.³ It was a reasonable guess and, as it turned out, partly correct. But the puzzle was more crowded than a single molecule. What made asparagus so distinctive was not only the smell but the speed. Most foods that alter the body’s odors do so slowly, over hours, as digestion grinds through them. Asparagus acts almost immediately, releasing its chemical signature within minutes, a swiftness that pointed to something unusual in the plant itself.

The molecule found nowhere else

The answer lies in a compound the asparagus plant manufactures and almost nothing else in the vegetable kingdom does. It is called asparagusic acid, a sulfur-containing molecule that takes its name directly from the plant. Asparagusic acid serves the plant’s own purposes, helping to defend its roots against parasitic worms, and it has no obvious business smelling of anything. The trouble begins only when a human being eats it.

Digestion breaks asparagusic acid down quickly, and the breakdown products are a small family of volatile sulfur compounds. The word volatile is doing important work here. These molecules are light, chemically restless, and eager to escape from liquid into the air, which is precisely why they reach the nose so readily and so fast. The principal offender is the same methanethiol Nencki suspected over a century ago, the gas responsible for the smell of rotting cabbage and a contributor to bad breath. Alongside it ride relatives such as dimethyl sulfide, dimethyl disulfide, and dimethyl sulfone, each adding its own note to what researchers have, with admirable restraint, described as a pungent bouquet.⁴

The reason a small serving produces such a disproportionate effect comes down to the extraordinary sensitivity of the human nose to this particular chemistry. Methanethiol is detectable at concentrations measured in parts per billion. The olfactory system evolved to treat sulfur compounds as urgent information, because in nature they often signal decay, spoilage, or danger. A nose tuned to detect a few molecules of rot in a forest will have no difficulty flagging the contents of a toilet bowl after dinner. The asparagus did not produce much of the compound. It did not need to.

For a while this seemed to settle the matter. Asparagus contains a unique precursor, the body cleaves it into volatile sulfur compounds, the compounds are excreted in urine, the nose detects them. A clean chain of cause and effect. Except that it failed to explain the most interesting thing about the whole phenomenon, which is that a substantial number of perfectly healthy people insisted, sincerely and repeatedly, that it never happened to them at all.

The great asparagus debate

By the middle of the 20th century, this discrepancy had become a genuine scientific irritant. Surveys kept turning up people who reported smelling nothing in their own urine after eating asparagus, and the proportion was not trivial. This raised an obvious and surprisingly difficult question. Were these people somehow different in their bodies, failing to produce the smelly compounds in the first place? Or were they different in their noses, producing the compounds like everyone else but unable to perceive them?

The distinction matters enormously, and for decades it split researchers into two camps. The first theory proposed that the population divided into producers and non-producers. On this view, some people carried the metabolic machinery to break asparagusic acid down into volatile sulfur, and some simply did not, passing the precursor through the body chemically untouched and odorless. The second theory proposed exactly the opposite. Everyone produced the compounds, and the variation lay entirely in perception. Some people could smell the result; some were effectively blind to it.

The debate could only be resolved by doing something most scientists would rather avoid, which is to systematically smell other people’s urine. In the 1950s and again in studies through the following decades, researchers persuaded volunteers to eat asparagus and then to sniff the urine samples not only of themselves but of others, including the supposed non-producers.⁵ The results were quietly devastating to the production theory. People who could detect the smell could detect it in nearly everyone’s sample, including the urine of those who swore they produced no odor. The smell was there. The non-producers had simply been unable to notice their own.

A 1980 study sharpened this further, demonstrating that the apparent division between producers and non-producers tracked far better with the sniffer than with the producer. The same sample could be odorous to one person and odorless to another. The variation, in other words, lived in the nose. The inability to detect asparagus urine acquired a clinical name: asparagus anosmia, anosmia being the general term for the loss or absence of a sense of smell. What had looked like a difference in bodies turned out to be a difference in perception.

This did not entirely close the question. Careful researchers noted that there is probably some genuine variation in production too, that not every body breaks down asparagusic acid at exactly the same rate, and that the truth is likely a matter of degree rather than a clean binary.⁶ But the center of gravity had shifted decisively. The dominant story was no longer about what the kidneys excreted. It was about what the nose could read.

What the genome revealed

If the difference lived in perception, then it should be possible to find it written in the genes that build the smelling apparatus. In 2016, a team of researchers including the epidemiologist Lorelei Mucci at the Harvard T.H. Chan School of Public Health did exactly that, on a scale large enough to be persuasive. Drawing on data from two long-running health studies, they examined nearly 7,000 people of European-American ancestry who had answered a deceptively simple question: after eating asparagus, could they smell a distinctive odor in their urine?⁷

The answer divided the population almost cleanly. About 60 percent of the participants reported that they could not detect the smell at all. These were the anosmics, the people for whom the entire phenomenon was a rumor about a sensation they had never experienced. Far from being rare, the inability to smell asparagus urine turned out to be the majority condition, at least in this group.

Then the researchers did what the chemists of previous centuries could only dream of. They scanned the genome, comparing the DNA of detectors and non-detectors, looking for the genetic differences that separated the two. The strongest signal landed in a region of chromosome 1 dense with olfactory receptor genes, the stretch of DNA that codes for the molecular sensors lining the inside of the nose. They identified hundreds of genetic variants in this region associated with the inability to smell asparagus metabolites.⁷ The differences were tiny, single-letter changes in the genetic code, yet they were enough to determine whether a person’s smell receptors registered the sulfur or let it pass undetected.

This was the resolution of a debate that had run, in one form or another, since Benjamin Franklin’s day. The smell was not in the asparagus, exactly, nor in the kidneys, nor in any meaningful difference between one person’s metabolism and another’s. It was in the receptors, in a handful of mutations that decided whether a given nose was equipped to perceive a particular family of molecules. Some people had the hardware. Some people, through no fault of their own, did not.

The same dinner, two different worlds

Strip away three centuries of confusion and what remains is a small, almost philosophical fact. Two people eat the same spears at the same table. Inside both bodies, the same chemistry unfolds. Asparagusic acid is broken into the same volatile sulfur compounds, which are excreted in the same way, present in the same urine. The vegetable, chemically speaking, does precisely the same thing to both of them. And yet one person leaves the bathroom faintly horrified while the other notices nothing whatsoever, because the molecules that are demonstrably present simply do not exist for one of them. They are there, and they are unsmelled, which from the inside is indistinguishable from not being there at all.

It is tempting to treat the senses as windows, transparent openings through which the world arrives unaltered. The asparagus story is a reminder that they are nothing of the kind. They are translations, and every translation is selective. Your nose does not hand you the world; it hands you the portion of the world its receptors are built to detect, and the blueprint for those receptors was written before you were born. Two people standing in the same room, breathing the same air, are receiving different reports of reality, and neither has any way of knowing what the other is missing.

Asparagus is not the only place this shows up, merely the most comic. The herb coriander, called cilantro in much of the world, tastes bright and citrusy to most people and unpleasantly soapy to a minority, a difference linked to variation in olfactory receptor genes much like the ones that govern asparagus anosmia.⁸ Bitterness, sweetness, the intensity of certain odors, the very texture of a flavor, all vary from person to person in ways that are partly genetic and entirely invisible from the outside. We assume, because we have no choice, that others taste and smell roughly what we do. The evidence suggests they often do not.

There is something quietly humbling in this. We tend to argue about the world as if disagreements were failures of honesty or attention, as if a person who claims not to smell something must be mistaken or careless. The asparagus reveals a different possibility. Sometimes two people who flatly contradict each other are both reporting their experience accurately, because their experiences genuinely differ at the level of the molecule and the gene. The next time a green vegetable produces its notorious effect, or fails to, it is worth a moment’s attention. A humble spring vegetable, eaten and forgotten by millions, turns out to be carrying a small revelation about how separately, how privately, each of us experiences the only world we will ever know.

Sources

1. Arbuthnot, J., An Essay Concerning the Nature of Aliments, J. Tonson, 1731. — https://archive.org/details/essayconcerningn00arbu
2. Franklin, B., “To the Royal Academy of Brussels” (Fart Proudly), c. 1781. — https://en.wikipedia.org/wiki/Fart_Proudly
3. Nencki, M., “Ueber das Vorkommen von Methylmercaptan im menschlichen Harn nach Spargelgenuss,” Archiv für experimentelle Pathologie und Pharmakologie, 1891. — https://link.springer.com/article/10.1007/BF01977437
4. Pelchat, M. L. et al., “Excretion and Perception of a Characteristic Odor in Urine after Asparagus Ingestion,” Chemical Senses, 2011. — https://doi.org/10.1093/chemse/bjq081
5. Lison, M., Blondheim, S. H., Melmed, R. N., “A polymorphism of the ability to smell urinary metabolites of asparagus,” British Medical Journal, 1980. — https://doi.org/10.1136/bmj.281.6256.1676
6. Mitchell, S. C., “Food idiosyncrasies: beetroot and asparagus,” Drug Metabolism and Disposition, 2001. — https://doi.org/10.1124/dmd.29.4.539
7. Markt, S. C., Nuttall, E., Mucci, L. A. et al., “Sniffing out significant ‘Pee values’: genome wide association study of asparagus anosmia,” BMJ, 2016. — https://doi.org/10.1136/bmj.i6071
8. Eriksson, N. et al., “A genetic variant near olfactory receptor genes influences cilantro preference,” Flavour, 2012. — https://doi.org/10.1186/2044-7248-1-22

Related reading

• The Surgeon Who Measured Stool and Rewrote Nutrition
• The Drug That Learned to Be Dessert

More from the Plate edition →