A Blog by

The Fuzzy Fluffy Super-Cute Health Threat In Your Backyard

A day-old chick.
A day-old chick.
Image via Shutterstock.net.

An epidemic is moving across the United States. It has invaded 35 states and sickened 324 people, including 88 children. It has put 66 people into hospitals, and one of the sick people has died. And the Centers for Disease Control and Prevention, responding as it always does to outbreaks that menace Americans, is struggling with how to stop its advance—because the things causing the epidemic are widely distributed across the country, come from many places, and are hard to trace back to their source.

And also, are super-cute. The cause is backyard chickens.

Since January, and continuing into June, there have been seven separate outbreaks of Salmonella—each caused by a different strain of the bacterium and each stretching over multiple states, from 16 down to seven—that have been proved to originate in live chicks and ducklings bought by mail or in feed stores and kept at home or at a school.

Baby chicks and ducklings and the birds they grow into may not sound like much of a threat. But in addition to the 324 cases they have caused this year (so far; the CDC plans to update the case count in the next two weeks), backyard poultry caused 252 cases of illness last year, 363 cases in 2014, 514 cases in 2013 (including 356 cases caused by one Salmonella strain); and 334 in 2012. That is 1,757 cases in 5 years.

If that doesn’t seem like much, consider that 2013-14 saw the largest recent outbreak of Salmonella caused by raw poultry, traced back to chicken produced by the California company Foster Farms. That outbreak generated an enormous public health response, months of media coverage, and lawsuits. It caused 634 known cases. Over the same time period, backyard poultry sickened 877. Yet those illnesses seem to still be flying (sorry) under the radar.

“If you ask someone, ‘Can you get Salmonella from eating undercooked poultry?’ they are absolutely going to say Yes,” Megin Nichols, a public health veterinarian in the CDC’s foodborne outbreak response and prevention branch, told me. “But if you ask them, ‘Can you get Salmonella from touching your backyard chicken?’ they don’t necessarily know that.”

How Salmonella outbreaks linked to backyard chicken have risen since the 1990s, based on CDC data.
How Salmonella outbreaks linked to backyard chicken have risen since the 1990s, based on CDC data.
Original from Behravesh et al., Clinical Infectious Diseases, May 2014

Some of that disconnect may be cognitive dissonance. People buy backyard chickens to opt out of an industrial food system they perceive as unhealthy—so it takes some mental gymnastics to confront that the birds providing homegrown eggs (and sometimes meat) might be hazardous too. But, Nichols said, it might also be lack of awareness—that Salmonella, which resides in chickens’ guts even when birds look  healthy, and exits their bodies in their droppings, can spread all over them as they perch and take dust baths and preen.

“On their feet, on their feathers, on their beaks,” Nichols said. “And in the areas where they live and roam. So people are exposed when they clean the coop or otherwise maintain the poultry environment. But we also see people, especially young children, cuddling and snuggling them and kissing them.”

Finally, add in that most people don’t know Salmonella, along with other foodborne illnesses, doesn’t only cause a few days or weeks of lying flat and sticking close to the bathroom. An increasingly solid body of research links it to lifelong illnesses from arthritis to digestive problems to circulatory damage that leads to high blood pressure, kidney failure and stroke.

Casey Barton Behravesh, a veterinarian with a public health doctorate who directs the CDC’s “One Health” office, said this is a new problem. Exposure to live poultry used to be rare, and pretty predictable: It occurred when children were given fuzzy newborn chicks in Easter baskets. “Then in the early 2000s, we noticed a growing trend of more and more outbreaks occurring, not linked to little chicks and ducklings, and not among kids getting sick,” she told me. “It was adults getting sick, people who reported having backyard flocks, which was something we had never seen before.”

Educational material on backyard-poultry disease outbreaks.
Educational material on backyard-poultry disease outbreaks.
Image courtesy the CDC; original here.

People are being made ill because they don’t recognize they are at risk—but the structure of the industry, and the systems set up to monitor it, aren’t helping. The federal program that surveys diseases in live chickens, the USDA’s National Poultry Improvement Plan (NPIP) was set up to protect chicken health, not human health. So it tracks Salmonella strains that make chickens sick, but not the ones that cause human outbreaks, and until recently, it focused on the vast commercial poultry trade where those strains would cause costly damage.

Denise Brinson, a veterinarian who is the NPIP’s director, told me that because of the backyard-associated outbreaks, the agency has worked with the CDC to create a program addressing small suppliers. In 2014, it began allowing hatcheries that supply the backyard trade—which sell birds to feed stores and hardware stores, as well as direct to consumers—to join a testing program scaled to the size of their businesses and to advertise that they have NPIP certification.

But to look for that, would-be poultry buyers have to know where the birds are coming from, and that turns out to be more difficult than it should be. Federal investigators including Behravesh documented in 2012 and 2014 that the process of getting chickens to market isn’t a supply chain, it’s a tangle. Birds come from 20 different hatcheries in the US, but many of those hatcheries have contract farmers doing the daily work, and then combine those clutches to make up the millions of birds they ship each year. Because some hatcheries specialize in only certain breeds, they also may “drop-ship”—buy and ship birds from other hatcheries—to make up orders as well.

And at the sales end, birds from different farms and hatcheries may be commingled in the same store pen—increasing the possibility that Salmonella can spread among them, and making traceback to the birds’ origin an extraordinarily difficult task.

All of which means the onus is on individuals to protect themselves: owners of live poultry in backyard or schools, people who visit those owners, even people who handle baby chicks in the stores where they are sold. The CDC’s advice is to keep separate clothes and shoes to wear for feeding birds and cleaning their coops; make sure anyone who touches the birds or their area washes their hands right away; and remember that, no matter how adorable they are, backyard poultry are a food source, not a pet. Despite the temptation, they shouldn’t be smooched or snuggled—especially not by young children, whose immature immune systems put them at greater risk of infection.

“We do think that raising backyard poultry can be a fun and educational experience,” Nichols said. “But it is not the right experience for everyone.”

A Blog by

The Little Boy Who Should’ve Vanished, but Didn’t

He was 12 years old. He was a slave. He’d had no schooling. He was too young, too unlettered, too un-European; he couldn’t have done this on his own. That’s what people said.

Picture of a drawing of an older man and a young boy facing  a vanilla plant with their backs to the viewer
Drawing by Robert Krulwich
Drawing by Robert Krulwich

Edmond (he had no last name—slaves weren’t allowed them) had just solved a botanical mystery that had stumped the greatest botanists of his day. In the early 1800s he was a child on a remote island in the Indian Ocean, and yet, against overwhelming odds, Edmond would get credit for his discovery—and for the most surprising reasons. I want to tell you his story. So I’ll start here, with a plant.

Picture of a drawing of a vanilla plant
Drawing by Robert Krulwich
Drawing by Robert Krulwich

This is a vanilla plant (or my version of one). It’s a vine. It climbs, sometimes way high, and when it flowers and is visited by a pollinator, it produces a bunch of long, stringy beans. Properly treated, those beans give off the flavor we associate with vanilla.

Picture of a drawing of Anne of Austria holding a mug of hot chocolate
Drawing by Robert Krulwich
Drawing by Robert Krulwich

When Spanish explorers brought vanilla from Mexico, it was mixed with chocolate and became a classy sensation, fancied by kings, queens, and, pretty soon, everybody else. In his book Vanilla: Travels in Search of the Vanilla Orchid, journalist Tim Ecott reports that Anne of Austria, daughter of Philip III of Spain, drank it in hot chocolate. Madame de Pompadour, one of the great hostesses (and mistresses) of King Louis XV, flavored her soups with it.

Picture of Madame de Pompadour with a bowl of steaming soup in front of her
Drawing by Robert Krulwich
Drawing by Robert Krulwich

Francisco Hernandez, physician to King Philip II of Spain, called it a miracle drug that could soothe the stomach, cure the bite of a venomous snake, reduce flatulence, and cause “the urine to flow admirably.”

Picture of a drawing of a man peeing
Drawing by Robert Krulwich
Drawing by Robert Krulwich

And, best of all, it was a sexual picker upper. Bezaar Zimmerman, a German physician, claimed in his treatise “On Experiences” (1762) that, “No fewer than 342 impotent men, by drinking vanilla decoctions, have changed into astonishing lovers of at least as many women.”

Picture of a drawing of a woman laying her head on the shoulder of a man standing next to a vanilla bottle
Drawing by Robert Krulwich
Drawing by Robert Krulwich

Demand, naturally, shot sky high. By the late 18th century, a ton of Mexican vanilla was worth, writes Ecott, “its weight in silver.”

With profit margins growing, a few plants were hustled out of Mexico to botanical gardens in Paris and London, then on to the East Indies to see if the plant would grow in Europe or Asia.

It grew, but it wouldn’t fruit, wouldn’t produce beans. Flowers would appear, bloom for a day, fold up, and fall off. With no beans, there could be no vanilla extract, and therefore nothing to sell. The plant needed a pollinator. In Mexico a little bee did the deed. Nobody knew how the bee did it.

Picture of a drawing of a bee saying 'Shhhhh'
Drawing by Robert Krulwich
Drawing by Robert Krulwich

What to do? In the 1790s people knew about plant sex. Bees, they knew, were pollinators.

If people could only figure out where vanilla’s sexual parts were hiding, they could become bee substitutes.

Enter the 12-Year-Old

They kept trying. One plantation owner, Ferréol Bellier-Beaumont, on the island of Réunion halfway between India and Africa, had received a bunch of vanilla plants from the government in Paris. He’d planted them, and one, only one, held on for 22 years. It never fruited.

The story goes that one morning in 1841, Bellier-Beaumont was walking with his young African slave Edmond when they came up to a surviving vine. Edmond pointed to a part of the plant, and there, in plain view, were two packs of vanilla beans hanging from the vine. Two! That was startling. But then Edmond dropped a little bomb: This wasn’t an accident. He’d produced those fruits himself, he said, by hand-pollination.

No Way

Bellier-Beaumont didn’t believe him—not at first. It’s true that months earlier the older man had shown Edmond how to hand-pollinate a watermelon plant “by marrying the male and female parts together,” but he’d had no success with vanilla. No one had.

But after his watermelon lesson, Edmond said he’d sat with the solitary vanilla vine and looked and probed and found the part of the flower that produced pollen. He’d also found the stigma, the part that needed to be dusted. And, most important, he’d discovered that the two parts were separated by a little lid, and he’d lifted the flap and held it open with a little tool so he could rub the pollen in. You can see what Edmond did in this video:

Edmond had discovered the rostellum, the lid that many orchid plants (vanilla included) have, probably to keep the plant from fertilizing itself. Could you do it again, Bellier-Beaumont asked? And Edmond did.

This was news. Big news. Bellier-Beaumont wrote his fellow plantation owners to say Edmond had solved the mystery, then sent him from plantation to plantation to teach other slaves how to fertilize the vanilla vine.

And so the Indian Ocean vanilla industry was born.

In I841, Réunion exported no vanilla. By 1848, it was exporting 50 kilograms (.0055 tons) to France; by 1858, two tons; by 1867, 20 tons; and by 1898, 200 tons. “By then,” Tim Ecott writes, “Réunion had outstripped Mexico to become the world’s largest producer of vanilla beans.”

Picture of a drawing of a graph showing vanilla exports from Reunion
Drawing by Robert Krulwich
Drawing by Robert Krulwich

The planters were getting rich. What, I wondered, happened to Edmond?

Well, he was rewarded. His owner gave him his freedom. He got a last name, Albius. Plus, his former owner wrote the governor, saying he should get a cash stipend “for his role in making the vanilla industry.”

The governor didn’t answer.

Edmond left his master and moved to town, and that’s when things went sour.

He fell in with a rough crowd, somehow got involved in a jewelry heist, and was arrested, convicted, and sentenced to five years in jail. His former owner again wrote the governor.

“I appeal to your compassion in the case of a young black boy condemned to hard labor … If anyone has a right to clemency and to recognition for his achievements, then it is Edmond … It is entirely due to him that this country owes [sic] a new branch of industry—for it is he who first discovered how to manually fertilize the vanilla plant.”

Picture of a drawing that says Entirely Due to Him
Drawing by Robert Krulwich
Drawing by Robert Krulwich

The appeal worked. Edmond was released. But what catches my eye here is Bellier-Beaumont’s choice of “entirely.” Our new vanilla business, he says, is “entirely” due to Edmond. He’s giving the former slave full credit for his discovery and retaining none for himself. That’s rare.

Then, all of a sudden, Edmond had a rival. A famous botanist from Paris—a scholar, a high official knighted for his achievements—announced in the 1860s that he, and not the slave boy, had discovered how to fertilize vanilla.

Picture of a drawing of a man with a beard holding a vanilla plant and looking suspicious
Drawing by Robert Krulwich
Drawing by Robert Krulwich

Jean Michel Claude Richard claimed to have hand-pollinated vanilla in Paris and then gone to Réunion in 1838 to show a small group of horticulturists how to do it. Little Edmond, he presumed, had been in the room, peeked, and then stolen the technique.

So here’s a prestigious scholar from the imperial capital asserting a claim against a 12-year-old slave from a remote foreign island. What chance did Edmond have?

Picture of a drawing of a young boy who was a slave facing off with an old scholarly French man
Drawing by Robert Krulwich
Drawing by Robert Krulwich

He was uneducated, without power, without a voice—but luckily, he had a friend. Once again, Edmond’s former master, Bellier-Beaumont, jumped into action, writing a letter to Réunion’s official historian declaring Edmond the true inventor. The great man from Paris, he said, was just, well, mis-remembering.

He went on to say that no one recalled Richard showing them how to fertilize orchids, but everybody remembers, four years later, Edmond teaching his technique to slaves around the island. Why would farmers invite Edmond to teach “if the process were already known?”

“I have been [Richard’s] friend for many years, and regret anything which causes him pain,” Bellier-Beaumont wrote, “but I also have my obligations to Edmond. Through old age, faulty memory, or some other cause, M. Richard now imagines that he himself discovered the secret of how to pollinate vanilla, and imagines that he taught the technique to the person who discovered it! Let us leave him to his fantasies.”

The letter was published. It’s now in the island’s official history. It survives.

Picture of an etching of Edmond Albius with the vanilla plant in his hands
Etching of more adult Edmond Albius
Etching of more adult Edmond Albius

And Yet, a Miserable End

Edmond himself never prospered from his discovery. He married, moved back to the country near Bellier-Beaumont’s plantation, and died in 1880 at age 51. A little notice appeared in the Moniteur, the local paper, a few weeks after he died. Dated Thursday, 26 August, 1880, it read: “The very man who at great profit to his colony, discovered how to pollinate vanilla flowers has died in the hospital at Sainte-Suzanne. It was a destitute and miserable end.” His long-standing request for an allowance, the obituary said, “never brought a response.”

Picture of the Edmond Albius Statue in
The statue of Edmond in Réunion
Photograph courtesy of Yvon/Flickr

But a hundred years later, the mayor of a town on Réunion decided to make amends. In 1980 or so, a statue was built to honor Edmond. Writer Tim Ecott decided to take a look. He bought a bus ticket on the island’s “Vanilla Line,” rode to the stop marked “Albius,” got off, and there, standing by himself is Edmond (in bronze or concrete? I can’t tell). He’s dressed, Ecott says, like a waiter, with a narrow bow tie and jacket. He’s not wearing shoes: Slaves weren’t allowed shoes or hats. But he’s got a street named after him, a school named after him. He has an entry on Wikipedia. He’s survived.

Picutre of a drawing of a man with a beard holding a vanilla plant and looking sad
Drawing by Robert Krulwich
Drawing by Robert Krulwich

And the guy who tried to erase him from history, Richard? I looked him up. He also has a Wikipedia entry. It describes his life as “marred by controversy,” mentions his claim against Edmond, and concludes that “by the end of the 20th century,” historians considered the 12-year-old boy “the true discoverer.” So despite his age, poverty, race, and status, Edmond won.

This is such a rare tale. It shouldn’t be. But it is.

Editor’s Note: This post has been updated to correctly reflect the title of Tim Ecott’s book.

Two books recount Edmond’s story. Tim Ecott’s Vanilla: Travels in Search of the Vanilla Orchid is the most thorough and original, but How to Fly a Horse: The Secret History of Creation, Invention and Discovery by Kevin Ashton tells the same tale and marvels that a slave on the far side of the world, poor and non-white, could get credit for what he’d done. There is also Ken Cameron’s Vanilla Orchids: Natural History and Cultivation, a book that contains Thomas Jefferson’s handwritten recipe for vanilla ice cream.

A Blog by

Easter Chicks: Cute, Fluffy, and Probably Bad For You

In the United States—and for that matter in much of the world—the foodborne disease Salmonella is a major public health problem. Here, it causes an estimated 1 million cases every year. We tend to think of those cases, and most foodborne illness, as minor episodes of needing to stay close to the bathroom—but every year, 19,000 of them end up in the hospital and almost 400 people die. And even if they survive, people aren’t necessarily out of danger; after decades of dismissing foodborne illness as unimportant and self-limited, researchers are beginning to understand that it can have lifelong consequences.

So it’s important, as much as possible, to identify the sources of Salmonella infection, and to alert people to the ways in which they can protect themselves.

And that’s why the Centers for Disease Control and Prevention, the CDC, is worried about those fluffball Easter chicks that might be appearing in households this weekend, as well as the juvenile poultry that backyard farmers and urban locavores may begin buying as the weather warms.

As I mentioned in my intro post yesterday, I also am writing for National Geographic‘s food site, The Plate, and I have a new post up there about the under-appreciated danger posed by live baby poultry. Whether you are buying them for immediate adorableness on top of an Easter basket, or eventual eggs or meat in a small-scale coop, most of us find baby chicks irresistible, in the hard-wired way that makes us melt before kittens and babies too. So we cradle them, and cuddle them, and smooch them on top of the head. But we forget that, just like babies of every other species, they are poop machines. And Salmonella travels in poop.

There are millions of baby chicks and other poultry sold every year: several millions pounds’ worth, according to the US Post Office, which ships most of them. In the past several years, they have caused significant outbreaks: 363 people in 43 states in 2014; 158 people ill, in 30 states in 2013; 195 people sick in 27 states in 2012; and 316 people sick in 43 states in the years before that.

This isn’t an argument against buying baby poultry, especially not if you’re doing it for small-scale egg or meat production. (Animal welfare organizations urge not buying baby animals just for Easter, because of the likelihood they will be dumped.)

But it is a plea on behalf of something I’m probably going to be saying a lot as we go forward: Don’t forget to wash your hands.

A Blog by

Introducing Germination: Diseases, Drugs, Farms, and Food

When I was a kid, my favorite part of school wasn’t class — even though I loved studying, and liked showing off what I knew. It wasn’t the uniforms, though my boarding school’s dresses and blazers, and shoes for indoor and outdoor games, were a puzzle that came together differently every time. And it certainly wasn’t the food: School dinner in England was a mystery of boiled sprouts and stewed rhubarb, even if the Texas high school lunches that came after taught me how to make Frito pie.

What I loved most about school, with a fierceness that bordered on devotion, were school supplies. The incense of a just-sharpened pencil. The order in a fresh box of pen cartridges. And more than anything, the promise in a new notebook, and the anticipation of filling its empty, perfect pages with everything I would discover and learn.

I’m feeling a similar thrill now, viewing this new space at Phenomena. Welcome to Germination, a blog that will explore public health, global health, and food production and policy—and ancient diseases, emerging infections, antibiotic resistance, agricultural planning, foodborne illness, and how we’ll feed and care for an increasingly crowded world.

If you followed me here from my previous blog Superbug at Wired, thanks, and get comfortable. If I’m a new discovery for you, here’s a capsule bio. I’m a freelance journalist working mostly for magazines (Wired,  Scientific American, Nature, Slate, the Atlantic, the Guardian and Modern Farmer, along with an array of women’s magazines). I’ve written two books so far—Superbug, about the global rise of antibiotic resistance, and Beating Back the Devil, about the Epidemic Intelligence Service, the disease-detective corps of the US Centers for Disease Control and Prevention—and am working on a third, about how we came to use antibiotics in agriculture, and what a mistake that turned out to be.

Before I was a magazine writer, I was a newspaper reporter, doing mostly investigative work: on the causes of cancer clusters, the social effects of drug trafficking, and a mysterious illness in reservists that turned out to be the first cases of Gulf War Syndrome. In my last newspaper job, I covered the CDC, under orders from the editor who hired me to “get in there and tell us these people’s stories.” I spent a lot of time talking my way into investigations and onto planes in the middle of the night. It was enormous fun.

Me, at TED, on March 18, 2015. Original here/a>.
Me, at TED, on March 18, 2015. Original here.
Maryn McKenna speaks at TED2015 - Truth and Dare, Session 6, March 16-20, 2015, Vancouver Convention Center, Vancouver, Canada. Photo: Bret Hartman/TED

I’m also a Senior Fellow of the Schuster Institute for Investigative Journalism at Brandeis University, and just finished a fellowship at MIT. I do some video. And I just gave a TED talk, on imagining what the world will be like after we’ve used up antibiotics. (The video has not gone up yet, but I’ll let you know when it does.)

As a journalist, my interest is complexity, inadvertence, and unintended consequences. (My Phenomena colleague Ed Yong jokes that he covers the “Wow” beat; I think of what I do as the “Oops” beat.) We got to widespread resistance because we wanted to cure infections quickly; we got to factory farming because we wanted to ensure affordable food. There isn’t (much) malfeasance in either of those endeavors,  but there is a ton of good intentions—and good intentions gone bad are a rich, rewarding subject. We might be here a while.

Here’s what you can expect at Germination: reports on new scientific findings; inquiries into policy initiatives; profiles and interviews with researchers doing cool things; history; and, occasionally, whimsy. I have been writing for a year for National Geographic‘s food platform The Plate, and some posts that deal more purely with food will be loaned or cross-posted there. (About which: You make Frito pie by opening a serving-size bag of Fritos along the back seam and plopping in a ladle of chili and some shredded yellow cheese. It tastes best when served by a lunch lady in a hairnet and a Texas Longhorns jersey.) If you’d like to hear more about my plans, head over to The Loom, where my new colleague Carl Zimmer has kindly conducted a Q&A with me.

When I think back to being a kid at the start of a school year, the initial thrill might have been those pristine new notebooks—but the bigger thrill was filling them. Phenomena is the most exclusive science-writing club on the internet, and I’m excited to join it. Please come along.

(Much gratitude to Jonathan Eisen, PhD, for suggesting Germination as a blog name.)

A Blog by

Gefilte Fish: Why, Oy Why?

Jewish stories are brimming with miracles. When Pharaoh refuses to free the Jews, frogs fill up his bed, the Nile turns to blood, and the skies rain hail and fire. Later, a small unarmored boy uses a slingshot to slay a giant. Sometime after that, in the Holy Temple, a day’s worth of oil lights a menorah for eight. But for this shiksa, the biggest Jewish miracle of all is the acquired taste for gefilte fish.

I first encountered this flaccid culinary specimen in September 2007, when celebrating Rosh Hashanah at my new boyfriend’s parents’ house. It was my first time meeting them, and my first Rosh Hashanah, and I was trying my damnedest to blend in at the long table full of friendly Jews. I dipped apple slices into honey and (slowly) sipped Manischewitz. When somebody suggested the Gentile visitor put on a yarmulke, I complied and posed for a toothy photo.

So far, so good. Then my boyfriend’s mother, Marlene, came around behind me with a platter of brown-gray gelatinous lumps.

“Gefilte fish?” she asked.

“Um, what is it?” I said in the most polite voice I could muster.

“It’s fish mixed with bread,” said Howie, my boyfriend’s brother, eagerly forking one from the platter.

“OK, sure,” I said. I looked down at this supposed fish on my plate and took a tiny, tepid bite. I did not like it, which I guess was obvious from my face. Everybody laughed. “Well, you tried it!” Marlene said.

For the uninitiated: Gefilte fish is ground fish mixed with other ingredients, typically matzo meal, onions, vegetables, eggs, and seasonings. Small patties of this batter are poached in fish stock, chilled, and served cold and slimy.

Some gefilte recipes are sweet, others savory. The split appeared a couple of hundred years ago from something known as the “gefilte fish line” in Poland. Jews living west of the line ate sweet gefilte, whereas those east of the line ate a peppery version. (According to one Jewish historian, the fish line overlaps with a linguistic border between two types of Yiddish.)

Some Jewish families relish their homemade gefilte. “These recipes are sacred, held close and carefully passed from generation to generation,” says Aimee Levitt, a writer at The Chicago Reader. “My own family’s comes from my maternal great-grandmother, who only relinquished it mere months before she died. Every Passover, someone marvels at what a close call we had.”

Levitt’s Passover tradition is in jeopardy this year, she writes, because of a whitefish shortage in the Chicago area. Some Jews are resorting to tilapia or, gasp, to the many varieties of jarred gefilte found on grocery store shelves (the source of my first and only bite):



But seriously. Why?

Fish in general has been a Sabbath tradition for a long time. The first Jews thought fish encouraged fertility. “They believed the intoxicating odor on the Sabbath table would encourage couples to ‘be fruitful and multiply’ — which in Jewish tradition is encouraged on Friday night,” writes Tamara Mann of My Jewish Learning.

There’s also symbolism in the word itself. The Sabbath happens on the seventh day, and so many foods traditionally eaten on the Sabbath correspond to the number 7, explains Rabbi Aaron L. Raskin:

The Hebrew word for wine is yayin, spelled יין, yudyudnun. If one adds up the gematria of יין, it equals 70.

After Kiddush, everyone then washes and returns to the table to say the blessing on and eat challah bread. The gematria of חלה, challah, is 43, and 4 and 3=7.

After they eat the challah, of course they have gefilte fish. The word “fish,” דג (dag), is spelled dalet=4 and gimmel=3, equaling 7.

Alright, this is all starting to add up. I’m down with eating fish on the Sabbath. But why gefilte? Why butcher it so?

“The gastronomic considerations of this delicacy may seem the most obvious,” writes Rabbi Zushe Blech, of Monsey, New York. I beg to differ. Luckily the rabbi also provides a more credible reason*:

Shabbos is a day of rest where many types of labor are prohibited. One of the activities in which one may not be engaged on Shabbos relates to the separation of chaff from grain, which is known in Hebrew as Borer. This restriction extends to many types of separation, and the rules governing which types are permitted and which are not can be quite complicated. Eating fish is a common situation where Borer becomes a problem, since fish is often served whole and bones are not removed before serving. In order to avoid this concern, a custom developed, whereby the fish was filleted, ground, and stuffed back into the skin and then cooked.

That’s where the name comes from, by the way: Gefilte is derived from געפֿילטע פֿיש, the Yiddish word for “stuffed fish.” But wait, gefilte fish isn’t stuffed! What happened? I can’t find an explanation online, other than laziness: It was just easier to poach the stuffing rather than jam it back into the skin. I can’t help but think how much more appetizing the fish would be had the skin stayed in the picture.

I’m headed back to Marlene’s house tomorrow evening for Passover. She’s my mother-in-law now, so I don’t have to worry about fitting in. When she comes around with the gefilte platter, I’ll just say, “No, thank you,” and take two helpings of charoset.

*This is the most popular explanation for why Jews eats gefilte, but some scholars are skeptical of it. Haym Soloveitchik, a Jewish historian at Yeshiva University, wrote in 1994:

“Popular lore has it that gefilte fish was introduced into the Sabbath menu to avoid the very problem of borer. [But] gefilte fish is an East European dish, and Jews had been eating fish on Sabbath for some fifteen centuries before this culinary creation. Even in Eastern Europe, I know of no instance of someone being labeled a mehallel Shabbas and run out of town for eating non-gefilte fish.”

Which, I must say, makes me feel a bit better about my aversion to the stuff.

A Blog by

So Science…Might Have Gotten It Wrong. Now What?

Last week, I wrote about a scientific paper that was published in the elite journal Nature in 1995. Within a couple of years, the findings of said paper were called into question by several other papers in different journals. As of today, nearly two decades since the original came out, nobody has replicated it. And yet, it’s still sitting there in the literature, still influencing others. It’s been cited nearly 1,000 times.

Some readers were angry with my post, arguing, for example, that “science’s self-correcting paradigm works over decades”. Indeed, that was my point. Science’s self-correction is generally very slow — perhaps, as many argue, too slow.

This week I learned about an unfolding scientific debate that’s got me thinking again about the challenge — the impossibility? — of swift and sure scientific correction. What does it mean when one group of researchers, or even two or three groups, can’t replicate a particular scientific finding? Does that necessarily mean it’s wrong? At what point should a scientist give up on a new idea for lack of supporting evidence?

That unfolding debate started in late 2011, when Chen-Yu Zhang’s team from Nanjing University in China found something pretty wild: bits of rice RNA floating in the bloodstreams of Chinese men and women. That might not seem so strange; rice was a primary ingredient of their diets, after all. But RNA molecules are pretty fragile. So the discovery shocked and intrigued many biologists.

“It’s just a very neat new physiologic mechanism,” says Ken Witwer, a molecular biologist at Johns Hopkins University in Baltimore. “How is it that a small RNA, or any RNA, could survive this trip from the mouth, with all these enzymes in saliva, down into the stomach, with the acidic environment there, and make it all the way into the gut, to the point that it could cross over into the blood? What form would this RNA have to be in to make that journey?”

Even more provocative: Zhang’s study also showed that in mice, those same tiny pieces of plant RNA — dubbed microRNA or miRNA, and made up of just two-dozen nucleotides, or letters of code — can shut down a gene involved in cholesterol uptake.

The study had big implications for medicine and our food supply. For instance, it suggested that researchers might be able to design oral RNA drugs for a host of diseases, “one of the holy grails” of the field, Witwer says. The data also provided evidence, at least according to a press release issued by Zhang, that miRNAs are “essential functional molecules” in Chinese herbal remedies. Finally, some people — like the author of a controversial* column published in The Atlantic — used the study to argue that genetically modified organisms (GMOs) are harmful to eat (despite loads of evidence to the contrary). (Update 7/9:  See below a response from the author of that column.)

Andres Rodriguez, via Flickr
Andres Rodriguez, via Flickr

So the paper made its media splash. And in the 21 months since its publication, the work has been cited in 42 other papers, according to Web of Knowledge.

A few of those could be considered replication studies. In one, David Galas of the Pacific Northwest Diabetes Research Institute, in Seattle, performed genetic sequencing of human blood samples and found low levels of miRNA from many species, including bacteria, fungi, insects, and plants. Galas’s team detected the same specific rice miRNA that Zhang had — dubbed miR-168 — albeit at far lower levels than Zhang had.

Two other follow-up studies were bankrolled by agricultural giant Monsanto (which, it must be said, sells GMOs and thus has a big stake in claims that they’re dangerous). The Monsanto researchers combed through large datasets of genetic sequences obtained from mammals, chickens, and insects, looking for any trace of plant miRNAs. They found them in some of the datasets, but again, at very low levels. And sometimes the data didn’t make sense — they found miR-168, for example, in animals that had never eaten food containing miR-168, suggesting that it could have been the result of a contamination, Witwer says. “We know that pollen has miRNAs in it, and depending on the time of the year, maybe we have more pollen contamination, even in our best labs, than at other times.”

The July issue of RNA Biology adds two more skeptical papers to the mix. In one of them, Witwer’s team fed monkeys a Silk fruit and protein shake, which happens to contain high levels of miR-168 and other plant miRNAs. The researchers tested the animals’ blood for miRNAs before the feeding and 1, 4, and 12 hours after the feeding.

The scientists used the same method that Zhang’s group had: polymerase chain reaction, or PCR, which allows researchers to identify specific segments of DNA or RNA by copying them over and over again, and then fluorescing the copies. When Witwer’s team used PCR to find miRNAs in the smoothies, the results were sensitive and consistent. But when looking at the monkeys’ blood, the PCR data were much more variable. “We weren’t completely confident in the accuracy of the method,” Witwer says.

So his team repeated the experiment using a newer and more precise type of PCR, called droplet digital PCR. This time, they again saw a lot of variability in the blood data, and no consistent differences between the samples taken before and after the animals ate the shakes. Witwer’s conclusion: Plant miRNAs probably don’t transfer into our blood after digesting it, at least not in quantities anywhere near what Zhang’s group had reported.

In the other new paper, Stephen Chan of the Brigham and Women’s Hospital in Boston found that healthy athletes did not carry detectable levels of plant miRNAs in their blood after eating fruit chock-full of those molecules. The scientists also couldn’t find this kind of transfer in experiments with mice and bees. “We conclude,” the paper states, “that horizontal delivery of microRNAs via typical dietary ingestion is neither a robust nor a frequent mechanism.”

Forest Wander, via Flickr
Forest Wander, via Flickr

So what do all of these studies say about this particular finding, and more generally, about science’s self-correcting process?

Less than two years after the original paper came out, at least five studies have followed it up. And in my (utterly non-expert) judgment, it seems like none of them meaningfully replicate Zhang’s paper. (Zhang has not responded to my request for comment; I will update the post if/when he does. Update, 7/8: Zhang has responded to my request for comment; see his full response at the bottom of this post.)

The studies are consistent in finding very low levels of plant miRNAs in people and a variety of other species. Witwer says that’s enough evidence of a non-result to move on from the whole idea. “I’m willing to help out if someone’s organizing an attempt to replicate something, but I’m probably not going to devote my lab to answering more questions on this issue,” he says. “We’ve convinced ourslves that we’re not seeing anything here.”

Others, though, aren’t ready to drop it. Galas, whose paper found miR-168 in low levels in human blood, says the only thing we know for sure is how difficult the question is to study. “The major result is that miRs are difficult to measure accurately,” he says. What’s more, he says, Witwer’s feeding experiments aren’t necessarily damning because their specifics differ from the original Zhang paper.

For Galas, the current data only makes the question more worthy of study by the RNA community, not less. “This is a an important topic to get pinned down — the potential for new biological phenomena is significant.”

This story helps explain why science’s self-correction process can’t be super-quick. It takes time for evidence to accumulate and show clear trends. That said, scientists could be better at making that correction process more efficient. One step, Witwer says, is transferring published data into public repositories that can be easily shared with the scientific community.

As Witwer reported in February, less than 40 percent of studies reporting microRNA sequencing data submitted that data to public databases. More interesting: The scientists who did share were more likely to have high-quality papers. The only paper in the analysis to be retracted, by the way, was one that did not share its raw data.

“I think that science can be self-correcting,” Witwer says, “but it requires people to do that correcting.”

*That column was rightfully struck down by science bloggers Emily Willingham and Christie Wilcox, and because of their posts, the author eventually amended it. The self-correction of the blogosphere is just a tad faster than the self-correction of science, eh? (UPDATE 7/9: The author of the column says his re-write had nothing to do with the bloggers; see his full comment here.)

UPDATE #1 (7/4): Also, just noticed that the incomparable Willingham beat me to this story a couple of weeks ago! Go check out her post at Forbes.

UPDATE #2 (7/8): Dr. Zhang sent me a lengthy letter in response to my request for comment about Dr. Witwer’s new study. You can read that (in .pdf form) by clicking here.

A Blog by

A New Culprit in China’s Tainted Milk Saga: Gut Bacteria

Wei Jia became a professor at The University of North Carolina at Greensboro in August of 2008, after 10 years working at the Shanghai Jiao Tong University. He is a specialist in metabolomics, meaning that he looks at the chemical byproducts, or metabolites, of cells, tissues and living things. He’s done chemical analyses of the blood of colorectal cancer patients, for example, and of the amniotic fluid of malnourished pregnant rats.

Just a month after Jia moved to the U.S., he and the rest of the world heard about a tragedy in his native country. Thousands of babies in China were sick with kidney stones and several had died after drinking formula laced with a ubiquitous and cheap industrial chemical called melamine.

Cory Doctorow

This was no accident, nor the result of naive incompetence. Dairy companies — nearly two dozen of them — had intentionally added melamine to the milk powder. The manufacturers knew melamine would artificially boost the protein content of the formula, even though the chemical can’t be digested. They thought it was harmless. And they were horribly wrong. Over the next few months, 300,000 children got sick and six died.

As soon as Jia found out, he called his old team of collaborators in Shanghai to start investigating this scientific head-scratcher: Why was melamine so toxic? “Because it’s not, really. It’s not supposed to be absorbable by the human body,” Jia says. Its LD-50 (“lethal dose-50”), or the dose at which 50 percent of those exposed would die, is 3161 mg/kg in rats, an incredibly low toxicity. So why had so many children gotten sick?

Jia’s team turned to studies done on melamine poisoning in pets, research triggered by another Chinese food scandal. Manufacturers in China had long been adding grain containing ground-up melamine to pet food and other animal feed as a cheap filler, and these products were sold in the United States and elsewhere. This came to light in Asia in 2004 and in the U.S. in 2007, when melamine killed 16 dogs and cats in the U.S. and made thousands of others sick. Some 60 million packages of pet food were recalled.

Scientists from the University of Georgia analyzed blood and tissue samples from cats and dogs that had died from the contaminated food. Kidney tissue from all of the animals contained not only melamine, but a chemical called cyanuric acid, which is a common by-product in the manufacturing of melamine, the study found. Jia’s team reported similar results in 2009. They gave rats melamine, cyanuric acid, or a mix of both, and found that tiny doses of melamine could lead to kidney failure, but only when paired with cyanuric acid. It turns out that together, melamine and cyanuric acid form crystals in the kidney that turn into dangerous kidney stones.

According to Jia, many researchers had assumed that the cyanuric acid had come from the pet food, just like melamine. But he suspected otherwise. He knew that in the environment, soil microbes in the Klebsiella family could interact with melamine to produce cyanuric acid. What if the same thing was happening in the gut of the sick pets and babies?

His rat study had shown that when the animals were given high doses of melamine alone, their urine contained a chemical signature — low phenylacetylglycine paired with high trimethylamine-N-oxide and 3-phenylpropionate, for the metabolomic geeks out there — that pointed to the metabolism of gut microbes. But that didn’t prove that microbes had anything to do with the poisoning.

In a new study, published today in Science Translational Medicine, Jia presents much stronger evidence for the idea that gut bacteria spur melamine to make cyanuric acid, leading to trouble.

The researchers first gave rats high doses of melamine paired with an antibiotic. The figure below shows the animals’ kidney cells. Rats exposed to melamine alone (right panel) developed some of the dreaded melamine-cyanuric acid crystals (see red arrow). But rats given the antibiotic (left panel) showed no crystals.

Kidney cells exposed to melamine and antibiotics (left) versus melanine alone (right). White arrows show mild hemorrhaging; red arrows show crystals, which turn into dangerous kidney stones. From Zheng et al., Science Translational Medicine 2013

In other experiments, the researchers mixed melamine with fecal samples taken from the rats. Cyanuric acid appeared after 24 hours, but didn’t show up at all in control mixtures without the fecal matter. Then, to narrow down what kind of bacteria might be responsible, the scientists performed a DNA analysis of the rat poop. They found seven species of Klebsiella, including one, called K. terrigena, which had been previously shown to convert melamine to cyanuric acid.

Finally, putting everything together, the researchers colonized the guts of rats with K. terrigena (by feeding a lot of it to them over four days). Kidney cells in these colonized rats were chock full of crystals, hemorrhaging and inflammation:

Zheng et al., Science Translational Medicine 2013
Zheng et al., Science Translational Medicine 2013

So, are gut microbes definitely the reason that the tainted milk made some kids sick? Not necessarily, Jia says, but it’s a strong possibility.

This type of bacteria is not a normal resident of the human gut. That might explain why the overwhelming majority of babies who were exposed to the tainted milk actually didn’t get sick.

So how would some of the kids (and pets) have picked up Klebsiella? Jia says that science can’t say for sure. But he notes that the babies who got sick tended to be from the countryside, rather than cities. “You could imagine that these kids, from relatively poor families, were exposed to a lot of dirt and soil, and may be more susceptible to having this type of bacteria,” he says.

Whether or not these gut microbes turn out to be the biological culprit in melamine poisoning, the data provide yet another example of the many ways that the bacteria that live on us, the so-called microbiome, can affect what we eat and how we live. The microbiome “can explain more and more problems that we were not able to explain in the past,” Jia says. “In the future, for toxicity and pharmacological studies, we need to redesign experiments to take this into consideration.”

In thinking about these possible microbial culprits, let’s not forget about the far more culpable human ones. In January of 2009, Chinese officials tried and sentenced 19 people who worked for the dairy manufacturers and knew about the melamine contamination: 15 went to jail for 2 to 15 years, 3 were imprisoned for life, and 1 received a suspended death sentence. In November of that year, two others were executed.

Just last month, meanwhile, grocery stores in Australia reported that baby formula is flying off their shelves, apparently because of a surge of demand from Chinese parents afraid to buy it in their own country.


Top photo by Jon Feinstein, Kowloon flyer by Cory Doctorow, both via Flickr

A Blog by

The Stuff of Hot

El chile gordo

Late Saturday evening, I was cutting jalapeños for the salsa for the next day’s barbeque party. I had a few other things on my mind — like my bean salad, and cleaning the bathroom, and figuring out what to write for this post — and so I forgot the lesson learned the last time I cut hot peppers: just wear gloves, you idiot. Five minutes later, my hands were on fire.

The stuff that makes jalapeños hot is a colorless, odorless compound called capsaicin, found mostly in the white pith that connects the seeds to the shell. Capsaicin works by binding to ‘TRPV1’ receptors in your nerve cells, which in turn sets off pain messages. Inside your mouth, small amounts of capsaicin makes for a pleasantly tingling spice, which I happen to love when mixed with the salt of a tortilla chip. But when rubbed in large quantities over both sides of both hands, capsaicin feels like a bad, bad sunburn.

A Blog by

My Coffee Problem

On Friday I woke up too early with a splitting headache and chest pain. This was alarming. In the shower, I tried to come up with a list of plausible explanations, but my mind found only one: the four cups of coffee I drank the day before. I wondered, is this how a heart attack begins? For the first time in eight years, I sat down at my desk to work without a mug of jolt.

The rational part of my brain knew why I had jumped to the worst-case scenario. I recently bought a genetic testing kit from 23andMe. After the initial shock about my melanoma risk variants, I calmed down and started digging into the rest of the data. Turns out I carry a variant for a condition that is, in some ways, more unnerving than skin cancer: slow caffeine metabolism.

A Blog by

A New Year’s Diet: Mind Control

First week of January. Like everybody else in America, I’m on a diet.

I’ve tried lots of diets over the years, and no matter how simple the particular rules — Fat is bad: stick to salads, whole grains and fruit! No no no, fat is good: lay off carbs, and eat lots of meat. Count calories. Count carbs. Are you getting enough fiber? Eat cookies all day! — following them is never easy.

Eating is what neuroscientists call a complex behavior. It’s not reflexive, like a knee jerk or sneeze, but rather depends on lots of brain systems. Real, painful hunger, of course, triggers eating. But so can the smell of bacon, even if you’ve already had breakfast. If you’re starving on a lettuce diet, good old willpower can (I’ve heard) override your urges to eat. And this complexity isn’t just a human thing. For lots of animals, feeding motivations can change with body temperature, sleep cycles and mating opportunities. Dozens of brain regions and hundreds of different kinds of brain cells have been tied to eating.

Which is why this study I’m about to gush about is so (mind the pun) startling. Scott Sternson‘s team from Janelia Farm compelled mice to voraciously eat by switching on just one type of neuron in their brains. Perhaps more provocative, the researchers got mice to completely stop eating by activating a different type of neuron.