Why Does Asparagus Make Your Pee Smell Funny?

iStock
iStock

The asparagus has a long and storied history. It was mentioned in the myths and the scholarly writings of ancient Greece, and its cultivation was the subject of a detailed lesson in Cato the Elder's treatise, On Agriculture. But it wasn't until the turn of the 18th century that discussion of the link between asparagus and odorous urine emerged. In 1731, John Arbuthnot, physician to Queen Anne, noted in a book about food that asparagus "affects the urine with a foetid smell ... and therefore have been suspected by some physicians as not friendly to the kidneys." Benjamin Franklin also noticed that eating asparagus "shall give our urine a disagreeable odor."

Since then, there has been debate over what is responsible for the stinky pee phenomenon. Polish chemist and doctor Marceli Nencki identified a compound called methanethiol as the cause in 1891, after a study that involved four men eating about three and a half pounds of asparagus apiece. In 1975, Robert H. White, a chemist at the University of California at San Diego, used gas chromatography to pin down several compounds known as S-methyl thioesters as the culprits. Other researchers have blamed various "sulfur-containing compounds" and, simply, "metabolites."

More recently, a study demonstrated that asparagusic acid taken orally by subjects known to produce stinky asparagus pee produced odorous urine, which contained the same volatile compounds found in their asparagus-induced odorous urine. Other subjects, who normally didn't experience asparagus-induced odorous urine, likewise were spared stinky pee after taking asparagusic acid.

The researchers concluded that asparagusic acid and its derivatives are the precursors of urinary odor (compared, in different scientific papers, to the smell of "rotten cabbage," "boiling cabbage" and "vegetable soup"). The various compounds that contribute to the distinct smell—and were sometimes blamed as the sole cause in the past—are metabolized from asparagusic acid.

Exactly how these compounds are produced as we digest asparagus remains unclear, so let's turn to an equally compelling, but more answerable question:

WHY DOESN'T ASPARAGUS MAKE YOUR PEE SMELL FUNNY?

Remember when I said that some people don't produce stinky asparagus pee? Several studies have shown that only some of us experience stinky pee (ranging from 20 to 40 percent of the subjects taking part in the study, depending on which paper you read), while the majority have never had the pleasure.

For a while, the world was divided into those whose pee stank after eating asparagus and those whose didn't. Then in 1980, a study complicated matters: Subjects whose pee stank sniffed the urine of subjects whose pee didn't. Guess what? The pee stank. It turns out we're not only divided by the ability to produce odorous asparagus pee, but the ability to smell it.

An anosmia—an inability to perceive a smell—keeps certain people from smelling the compounds that make up even the most offensive asparagus pee, and like the stinky pee non-producers, they're in the majority.

Producing and perceiving asparagus pee don't go hand-in-hand, either. The 1980 study found that some people who don't produce stinky pee could detect the rotten cabbage smell in another person's urine. On the flip side, some stink producers aren't able to pick up the scent in their own urine or the urine of others.

Have you got a Big Question you'd like us to answer? If so, let us know by emailing us at bigquestions@mentalfloss.com.

What Do the Numbers and Letters on a Boarding Pass Mean?

iStock.com/Laurence Dutton
iStock.com/Laurence Dutton

Picture this: You're about to embark on a vacation or business trip, and you have to fly to reach your destination. You get to the airport, make it through the security checkpoint, and breathe a sigh of relief. What do you do next? After putting your shoes back on, you'll probably look at your boarding pass to double-check your gate number and boarding time. You might scan the information screen for your flight number to see if your plane will arrive on schedule, and at some point before boarding, you'll also probably check your zone and seat numbers.

Aside from these key nuggets of information, the other letters and numbers on your boarding pass might seem like gobbledygook. If you find this layout confusing, you're not the only one. Designer and creative director Tyler Thompson once commented that it was almost as if "someone put on a blindfold, drank a fifth of whiskey, spun around 100 times, got kicked in the face by a mule … and then just started puking numbers and letters onto the boarding pass at random."

Of course, these seemingly secret codes aren't exactly secret, and they aren't random either. So let's break it down, starting with the six-character code you'll see somewhere on your boarding pass. This is your Passenger Name Reference (or PNR for short). On some boarding passes—like the one shown below—it may be referred to as a record locator or reservation code.

A boarding pass
Piergiuliano Chesi, Wikimedia Commons // Public domain

These alphanumeric codes are randomly generated, but they're also unique to your personal travel itinerary. They give airlines access to key information about your contact information and reservation—even your meal preferences. This is why it's ill-advised to post a photo of your boarding pass to social media while waiting at your airport gate. A hacker could theoretically use that PNR to access your account, and from there they could claim your frequent flier miles, change your flight details, or cancel your trip altogether.

You might also see a random standalone letter on your boarding pass. This references your booking class. "A" and "F," for instance, are typically used for first-class seats. The letter "Y" generally stands for economy class, while "Q" is an economy ticket purchased at a discounted rate. If you see a "B" you might be in luck—it means you could be eligible for a seat upgrade.

There might be other letters, too. "S/O," which is short for stopover, means you have a layover that lasts longer than four hours in the U.S. or more than 24 hours in another country. Likewise, "STPC" means "stopover paid by carrier," so you'll likely be put up in a hotel free of charge. Score!

One code you probably don’t want to see is "SSSS," which means your chances of getting stopped by TSA agents for a "Secondary Security Screening Selection" are high. For whatever reason, you've been identified as a higher security risk. This could be because you've booked last-minute or international one-way flights, or perhaps you've traveled to a "high-risk country." It could also be completely random.

Still confused? For a visual of what that all these codes look like on a boarding pass, check out this helpful infographic published by Lifehacker.

Have you got a Big Question you'd like us to answer? If so, send it to bigquestions@mentalfloss.com.

Does Having Allergies Mean That You Have A Decreased Immunity?

iStock.com/PeopleImages
iStock.com/PeopleImages

Tirumalai Kamala:

No, allergy isn't a sign of decreased immunity. It is a specific type of immune dysregulation. Autoimmunity, inflammatory disorders such as IBS and IBD, and even cancer are examples of other types of immune dysregulation.

Quality and target of immune responses and not their strength is the core issue in allergy. Let's see how.

—Allergens—substances known to induce allergy—are common. Some such as house dust mite and pollen are even ubiquitous.
—Everyone is exposed to allergens yet only a relative handful are clinically diagnosed with allergy.
—Thus allergens don't inherently trigger allergy. They can but only in those predisposed to allergy, not in everyone.
—Each allergic person makes pathological immune responses to not all but to only one or a few structurally related allergens while the non-allergic don't.
—Those diagnosed with allergy aren't necessarily more susceptible to other diseases.

If the immune response of each allergic person is selectively distorted when responding to specific allergens, what makes someone allergic? Obviously a mix of genetic and environmental factors.

[The] thing is allergy prevalence has spiked in recent decades, especially in developed countries, [which is] too short a time period for purely genetic mutation-based changes to be the sole cause, since that would take multiple generations to have such a population-wide effect. That tilts the balance towards environmental change, but what specifically?

Starting in the 1960s, epidemiologists began reporting a link between infections and allergy—[the] more infections in childhood, [the] less the allergy risk [this is called hygiene hypothesis]. Back then, microbiota weren't even a consideration but now we have learned better, so the hygiene hypothesis has expanded to include them.

Essentially, the idea is that the current Western style of living that rapidly developed over the 20th century fundamentally and dramatically reduced lifetime, and, crucially, early life exposure to environmental microorganisms, many of which would have normally become part of an individual's gut microbiota after they were born.

How could gut microbiota composition changes lead to selective allergies in specific individuals? Genetic predisposition should be taken as a given. However, natural history suggests that such predisposition transitioned to a full fledged clinical condition much more rarely in times past.

Let's briefly consider how that equation might have fundamentally changed in recent times. Consider indoor sanitation, piped chlorinated water, C-sections, milk formula, ultra-processed foods, lack of regular contact with farm animals (as a surrogate for nature) and profligate, ubiquitous, even excessive use of antimicrobial products such as antibiotics, to name just a few important factors.

Though some of these were beneficial in their own way, epidemiological data now suggests that such innovations in living conditions also disrupted the intimate association with the natural world that had been the norm for human societies since time immemorial. In the process such dramatic changes appear to have profoundly reduced human gut microbiota diversity among many, mostly in developed countries.

Unbeknownst to us, an epidemic of absence*, as Moises Velasquez-Manoff evocatively puts it, has thus been invisibly taking place across many human societies over the 20th century in lock-step with specific changes in living standards.

Such sudden and profound reduction in gut microbiota diversity thus emerges as the trigger that flips the normally hidden predisposition in some into clinically overt allergy. Actual mechanics of the process remain the subject of active research.

We (my colleague and I) propose a novel predictive mechanism for how disruption of regulatory T cell** function serves as the decisive and non-negotiable link between loss of specific microbiota and inflammatory disorders such as allergies. Time (and supporting data) will tell if we are right.

* An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases Reprint, Moises Velasquez-Manoff

** a small indispensable subset of CD4+ T cells.

This post originally appeared on Quora. Click here to view.

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