When scientists started investigating BEN, they thought that it might be a gradual, cumulative form of lead poisoning. Researchers working in a Serbian endemic village found high levels of lead in patients’ blood and hair, as well as in the local flour: the miller had been using a lead-based grout to repair his millstone. The government duly dismantled 36 water mills in Serbia. Further investigation, however, revealed that BEN patients in other villages didn’t have high levels of lead in their blood, and many had never used water mills.
My father compares BEN research to the story of the blind men and the elephant: everyone noticed something different and built a theory around it, and nobody saw the whole picture. Data from one village, or the expertise of one specialist, or the aftereffects of one environmental trauma, would indicate a solution, only to crumble in light of other data. Virologists, studying a village where all the BEN patients had hidden in an oak forest during the Second World War, attributed the disease to a virus native to oak forests. A Serbian geochemist, citing the low selenium content of soil in Serbia, suggested that BEN was triggered by selenium deficiency. In five villages in Kosovo, Muslims, who made up half the population, were found to be 25 times less likely than Christians to get BEN. Virologists argued that the disease was a virus transmitted by pigs, and that Muslims were spared by their avoidance of pig husbandry. Geneticists, believing BEN to be hereditary, saw the same data and ascribed the lower incidence among Muslims to their ethnic makeup. Confusingly, the Muslims in Bulgaria, known as “white gypsies,” often did get BEN, though actual Gypsies did not, and was that because of their genes or because they didn’t work on farms? A Bulgarian researcher claimed that he had identified a chromosomal marker, but nobody else could find it.
In the 1950s, the Bulgarian village of Karash was hit particularly hard by the disease. The communist government, having decided that the problem lay in the village itself, shut Karash down and relocated the population to Sofia. Twenty years later, some of the Karash exiles began to develop BEN, but those who had moved as children never got the disease—only those who had lived in Karash for 15 years or more. BEN, it seemed, was a super-slow time bomb. Fifteen years of exposure would set the clock ticking.
A shift in BEN studies came in the 1970s. A charismatic Danish veterinarian named Palle Krogh had been studying a strange outbreak of kidney disease affecting pigs in Danish slaughterhouses. There were no obvious differences between the lives of the sick pigs and those of the healthy ones. The only clue was that the disease seemed to worsen after rainy summers. Krogh eventually determined that the pigs’ grain had been contaminated by a fungal toxin called ochratoxin A, which produced effects not unlike BEN: the kidney damage was similar, and both were aggravated by wet weather. Sure enough, when tests were run in Yugoslavia, ochratoxin A was found in the blood and the urine of BEN patients, as well as in their grain supply.
Continued research, however, revealed that ochratoxin A was far more common than initially suspected: it appears in grains, coffee beans, wine, and other stored substances all over the world. Some of the highest levels of contamination have been recorded in countries with no known BEN-like disease. The story of ochratoxin illustrates the fundamental challenge in epidemiology: proof of exposure isn’t the same thing as proof of causation. Every day, we’re exposed to countless potential pathogens and toxins, most of which don’t make us sick. Identifying the “right” toxin is particularly difficult when the disease affects the kidney, an organ whose main function is to clear the blood of toxins.
Oddly, or perhaps not so oddly, Palle Krogh himself died of kidney cancer, in 1990. Krogh’s tumor was later dissected and analyzed by a group of his colleagues, including Tatu. Tatu suspected that the cancer had been caused by ochratoxin. My father pointed out that Krogh had been a chain smoker—smoking is a leading cause of renal carcinoma—and Tatu conceded that he could remember Krogh waving a cigarette in excitement at his latest findings. Nonetheless, it was difficult not to be struck by the death from kidney cancer of a scientist who had devoted many years to the study of nephrotoxic and possibly carcinogenic mold.
Two days later, in a high-ceilinged coffeehouse in Zagreb, my father and I met with Bojan Jelaković, a mild-mannered Croatian nephrologist who has worked closely with Grollman on the aristolochic-acid theory. He took us on a tour of an endemic region two hours southeast of Zagreb. We passed the towering grain silos of an industrial-looking mill. According to Jelaković and Grollman, such mills are eradicating BEN, because they combine wheat from so many different farms that the aristolochic acid is diluted. Patients we spoke to at a local dialysis clinic confirmed that they had once ground their own flour from their own wheat, but had switched to bigger communal mills after the war.
In the village of Kaniža, Jelaković showed us two churches standing face-to-face: one Croatian Catholic, with a white pointed steeple, and the other Ukrainian Orthodox, with an onion dome. These churches have come to stand for another famous “natural experiment” from the annals of BEN. Around 1905, a community of Ukrainian immigrants settled in Kaniža, having been offered free farmland by the Austro-Hungarian emperor. Although the Ukrainians kept their religion and did not intermarry with the Croats, they ended up getting sick just as frequently as the native villagers. The case proved that the disease isn’t inherited in the classical Mendelian sense.
In a nearby village, Jelaković showed us a so-called black house—left empty and gone to ruin after its occupants were stricken with BEN. He told us that a household of around a dozen people had died here in the 1970s. Next door, a boy and a girl watched us through the front windows, then pulled the curtains closed.
Like most BEN regions, this one is prone to flooding, and we had parked our cars by a monument to a 19th-century deluge alongside the Sava River. Across the river was Bosnia. There had been a bridge here before the war. “A wooden bridge,” Jelaković said. “A very beautiful one.”
We parted with Jelaković and drove across the river into Bosnia. At a hospital in the city of Odžak, we were given the use of an ambulette and a driver, so that we could visit BEN patients in nearby villages. We sat in a sunny garden with an elderly husband and wife, both of whom had BEN. They had heard of aristolochia by one of its local names (wolf’s paw), but they didn’t know what it looked like. We showed them photographs, and they said they might have seen it around but they didn’t pay much attention to weeds. When asked what they thought caused the disease, they immediately said water: more people got sick in the parts of the village that were prone to flooding, and fewer people were getting sick now, because of improvements to the water system. They noted that the disease didn’t affect anyone who lived in the hills, with the exception of women who had grown up in the lowlands and had moved to the hills only after getting married. We heard something similar in another village, where a man with BEN, who had lost his father, his aunt, and three siblings to the disease, told us about a neighbor who had no BEN in his family. “You see, he comes from the other side of the street,” the man said. It emerged that every house on one side of the street had one or several cases of BEN, but the other side, which was on slightly higher ground, was almost completely free of the disease. Annie Pfohl-Leszkowicz, a proponent of the ochratoxin theory, has cited similar patterns as evidence that BEN is caused by a fungal toxin: the healthy side of the street, she proposes, gets direct sunlight, which discourages the growth of mold.
In Odžak, my father and I met with Enisa Mesić, a nephrologist from nearby Tuzla. A magnetic presence, with a large head, copious dark hair, a deep voice, and piercing gray eyes, Mesić told us about the bureaucratic obstacles faced by BEN researchers. After the war, political power was decentralized in order to preserve equilibrium among different ethnic groups. As a result, Bosnia-Herzegovina now has no fewer than 13 ministries of health: one at the federal level, one for each of its 10 cantons, and one each for the self-governing Brčko District and the Republika Srpska. The two major centers for BEN research, in Tuzla and S
arajevo, are in cantons outside the endemic region, which means that before researchers can actually study any patients, they must submit requests to two different ministries.
Because of the war, nearly every patient’s file is missing at least four years. There is no central BEN database, and establishing one would require the cooperation of all 13 ministers of health. The municipalities used to have local databases, but these were discontinued after the war. When asked what had happened to the databases, Mesić ticked off their fates: “In Bijeljina, the archive probably still exists, but it’s difficult to access. In Šamac, it probably doesn’t exist anymore. In Odžak, it was destroyed in 1992, together with the hospital.”
Early in the 20th century, after the fall of the Ottoman Empire and the ensuing chaos in the Balkans, a new verb entered the English language: “Balkanize,” defined by the OED as “to divide (a region) into a number of smaller and often mutually hostile units, as was done in the Balkan Peninsula in the late nineteenth and early twentieth centuries.” Most European languages have an equivalent: the French balkaniser, the Italian balkanizzare, the German balkanisieren, and the Russian balkanizirovat'—attesting to the special relationship between the Balkan Peninsula and the human tendency toward division and faction. It’s an apt word to describe the study of Balkan nephropathy, and its fragmentation along geopolitical, ethnic, religious, linguistic, and even disciplinary lines. Researching the disease requires expertise in a wide range of fields—nephrology, epidemiology, genetics, oncology, microbiology, hydrogeology, botany, toxicology, biochemistry—each of which can be as hermetic and insular as a tiny country, with its own language, customs, and sovereignty.
The basic philosophical question surrounding BEN is whether it’s a big problem or a little one. For Arthur Grollman, BEN is part of a worldwide crisis of aristolochic-acid nephropathy: a story in which the true culprits are government agencies that fail to regulate herbal medications. When I met him later, at his apartment in Manhattan, he assured me that BEN was a closed case, and that a greater source of concern was the public health risk caused by the use of a variety of aristolochia in Chinese herbal medicine. He described his recent collaborations with researchers in Taiwan, where aristolochia is a commonly prescribed remedy, and where the reported incidence of upper-urinary-tract cancers is the highest in the world. Whereas a hundred women got sick in Belgium, Grollman says, millions of people may be at risk in Taiwan and China.
Researchers like Tatu, on the other hand, think that BEN is unique: although its causes may occur individually all over the world, their combined effect is specific to the endemic regions. For my father, too, the disease is defined by a set of particular locations. He thinks it’s significant that patients speak of doomed houses—that they feel it’s the places and not the people that are sick. He often quotes a remark by an old colleague, now deceased: “I could live in this town for twenty years, and I’d know which house to live in, to not get sick.”
On our last afternoon in Bosnia, the driver drove my father and me around the countryside to look for aristolochia. We stopped at a swamp overgrown with creeping tendrils, trembling fronds, and strange, earlike formations. We did not find aristolochia. We stopped by a cornfield, and walked along the perimeter and down one of the rows. A sudden commotion broke out among the cornstalks, a violent rustling and shaking, as if from the thrashing of some hidden beast. A moment later, the source of the disturbance revealed itself: a glossy, compact pheasant, running through the corn.
We got back into the van. The sun hung low over the late-summer fields. The cornstalks seemed to be standing around chaotically, like skinny, crazy people, their arms flung in all directions. As we drove past, there was one magical moment when they arranged themselves into rows and it was possible to see clearly all the way to the end, before they dissolved back into disorder.
JULIA COOKE
Amigos
FROM Virginia Quarterly Review
IF THERE WAS ONE THING Sandra knew well, it was hair. She knew hair from root to split end. In beauty school, she had learned the shape of the human head and how the best thing to do when trimming its hair was to section the skull into eighths. Her long nails shone red as she held her soft hands in front of her to demonstrate on an imaginary client. Her gold rings glinted. When she tired of haircutting techniques, she waved her hands quickly and her fingers sparked through the thick night like fireworks.
Sandra, like other girls who hung out where we sat on Havana’s waist-high seawall (malecón) where it hit Paseo, wore fashionable clothes of the barely there variety: diminutive shorts with interlocking C’s on back pockets, glittery heels, bras that peeked from tops, halters leaving midriffs bare. She dyed her own long, straight hair blue-black and lined her lips with the same dark pencil that she used around her eyes because shops hadn’t carried red in months. Her plastic nails were thick and whispery along the tips; she grabbed my forearm as we crossed the street on our way to the bathroom at a nearby gas station, dodging the cars that sped around the curve at Paseo. We went the long way to avoid the police who hung in the shadows on the intersection’s traffic island, keeping an eye on the strip. “The cars here, they’ll hit you. And if it’s him”—Sandra flicked her chin and pulled her hand down to mime a beard, the universal gesture for Fidel Castro—“they won’t stop. They’ll run you over and keep on going.”
There were clubs and bars at the hotels that hulked over the crossroads—the mod Riviera, the shimmery Meliá Cohiba, the Jazz Café—but since few locals could afford drinks there, the tourists who wanted to meet real Cubanos hung out by the sea. Everyone, Cuban and foreign, loved the malecón, to sit facing the ocean and Miami and feel the spray on bare shins, or to turn toward the city and watch old cars roar slowly by, or, after a long night at the bars, to see the brightening sky pull itself away from the sea. On nights when there was no moon, you could nod approvingly at the fish that men in mesh tank tops caught on sheer line stretched from coils on the sidewalk. On hot days, you watched kids who leapt from the wall into high tide, their arms pinwheeling past the rocks that cragged up from the ocean.
So young men toted bongo drums and guitars, imitating the Buena Vista Social Club for a few dollars’ tip. Gentlemen in frayed straw fedoras asked tourists to pick up an extra beer at the gas station kiosk. Tired-looking women in Lycra shorts sang out the names of cones of roasted peanuts, cucuruchos de maní, and popcorn, rositas de maíz. Nonchalant girls cocked hips at the foreign men who walked past. Sandra had been taught the art of artifice to serve the Cuban Revolution through its beauty parlors, but she’d given up on hair. By the time she was 21, she’d been working as a prostitute for around five years. The dates changed every time I asked her. Either way, she made about three times in one night what she’d have been paid monthly at any of the government-owned salons.
In November 2011, when Cuban first daughter Mariela Castro Espín was in Amsterdam in her capacity as sexologist and director of Cuba’s Center for Sexual Education, she was interviewed on Radio Netherlands Worldwide. Castro, prim and deliberate in a turtleneck and tweed blazer, sat in a room with draping red curtains and feather boas and effused about Amsterdam’s red-light district. “I’ve enjoyed seeing how they do it,” she said. “What I admire is that they’ve been able to dignify and value the work that they do—because yes, it is a job.” She enunciated her Spanish so translators didn’t miss a word for the televised interview. Castro went on to explain how, as she put it, the principles are the same in Cuba as in Amsterdam, but the circumstances are different. She talked about how the malecón is a place of pride for Havanans, and she smiled broadly until she mentioned the people who sell sex there. “Some people go there to practice prostitution in a way that is bothersome for, above all, the tourist or foreigner,” and her agency is in close contact with the police to decrease the malecón prostitution, she said, without drawing too much attention from said tourist or foreigner.
This is what the Cuban government usually highlights w
hen it talks about women and prostitution: Before Fidel Castro’s revolution in 1959, women had represented only 13 percent of the workforce, and many were domestic servants. A large number were prostitutes, too—as a port city with a sexually liberal climate and a U.S.-backed puppet government, Havana was where yanquis had gone in search of louche, uninhibited nightlife from Prohibition on. In 1931, after the Volstead Act had tripled the numbers of tourists who visited the country in under 15 years, 7,400 women officially stated their professions as prostitutes. The city formerly known as “the Pearl of the Caribbean” was soon referred to as its brothel. Eradicating prostitution and increasing women’s rights was one of Castro’s stated goals. Forty years after the 1959 revolution, long after literacy drives had enabled the island’s rural residents to read and prostitutes had been trained as seamstresses and given jobs and day care for their children, 51 percent of Cuba’s scientists were women. Fifty percent of attorneys and 52 percent of medical doctors, too. Everyone was paid nearly equally—a doctor, male or female, made marginally more than a seamstress, around $20 a month in Cuban pesos.
Then, 20 years ago, the USSR fell and Soviet subsidies disappeared, and with them more than a third of Cuba’s GDP. The value of the peso plummeted, and rations of food, clothing, and other necessities that removed pressure from monthly stipends dwindled. Increasingly, women, and some men, began to trade sexual favors for, say, the fish that a neighbor caught or the bread that only a well-placed state employee got very much of. When the government pushed to increase tourism and Cuba drew closer to the global capitalist marketplace, those activities again had cash value. By 1995, around the same time that studies on gender parity in the workforce came out, the Italian travel magazine Viaggiare had given the island the dubious honor of being the number one global “paradise of sexual tourism.” The government, broke and desperate, did little to contradict this image. And though the economy lifted as Cuba rounded into the 21st century, and though the new decade saw police tossing the more obvious prostitutes into jail, sex was something that could be easily bought and sold in Havana.