The Mystery of the Wasting House-Cats

Forty years ago, feline hyperthyroidism was virtually nonexistent. Now it’s an epidemic — and some scientists think a class of everyday chemicals might be to blame.

BY EMILY ANTHES


Most days, the back room of the Animal Endocrine Clinic in Manhattan is home to half a dozen cats convalescing in feline luxury. They lounge in their own individual “condos,” each equipped with a plush bed, a raised perch and a cozy box for hiding. Classical music plinks softly from speakers overhead. A television plays cat-friendly videos — birds chirping, squirrels scampering. Patients can also tune in to the live version: A seed-stuffed bird feeder hangs directly outside each window.

One afternoon in April, a jet-black cat named Nubi assumed a predatory crouch in his condo as a brawny pigeon landed on a feeder. Dr. Mark Peterson, the soft-spoken veterinarian who runs the clinic, opened the door to Nubi’s condo and greeted the 12-year-old tom in a lilting, high-pitched voice. “How are you?” Peterson asked, reaching in to scratch his patient’s soft chin. Nubi, who typically is so temperamental that his owner jokes about needing a priest to perform an exorcism, gently acquiesced, then turned back to the bird. Peterson seemed eager to linger with each of Nubi’s four feline neighbors — Maggie, Biggie, Fiji and Napoleon — but, he warned, “these cats back here are radioactive.”

He meant that literally. The previous day, all five animals received carefully titrated doses of radioactive iodine, designed to destroy the overactive cells that had proliferated in their thyroid glands and flooded their bodies with hormones. These cats are among the millions suffering from hyperthyroidism, one of the most mysterious diseases in veterinary medicine. When Peterson entered veterinary school in 1972, feline hyperthyroidism seemingly didn’t exist; today, he treats nothing else. In the intervening decades, hyperthyroidism somehow became an epidemic in cats, and no one knows why. “I’ve devoted most of my time in the last 35 years to this,” said Peterson, who noted that he has treated more than 10,000 hyperthyroid cats, “and I still have more questions than I have answers.”

Although definitive answers remain elusive, scientists are narrowing in on one possible explanation: A steady drumbeat of research links the strange feline disease to a common class of flame retardants that have blanketed the insides of our homes for decades. But even as the findings may answer one epidemiological question, they raise another in its place. If household chemicals are wreaking havoc on the hormones of cats, what are they doing to us?

By the time Peterson met Sasha in the fall of 1978, the scrawny tuxedo cat was a regular at the Animal Medical Center in Manhattan. The 15-year-old had lost a profound amount of weight, despite a seemingly insatiable appetite. Her case stumped veterinarians, who had already ruled out many of the obvious culprits, including parasites, irritable-bowel disease and diabetes.

Peterson, who had become restless with his veterinary residency, was spending his time off attending endocrine rounds at New York Hospital. When he heard about Sasha’s symptoms, he thought of the thyroid, a gland that sits at the base of the neck and secretes hormones that regulate metabolism. In humans, weight loss and increased appetite are among the hallmark symptoms of hyperthyroidism, in which the gland churns out huge quantities of hormones, sending the body’s internal systems into overdrive.

Although cats weren’t known to develop the condition, Peterson thought the possibility was worth at least investigating. And so, one afternoon, he ferried Sasha to the hospital, where a sympathetic doctor had agreed to give the cat a thyroid scan. The image was unambiguous: There was a large mass on Sasha’s thyroid. The tumor was benign, but its inexhaustible cells were dumping thyroid hormones into her bloodstream. “We got all excited, and we didn’t know exactly what we were doing, but we removed the tumor,” Peterson says. “And the cat got better and gained like five pounds in six months.”

It was a happy ending for Sasha, but for Peterson and Gerald Johnson, the gastroenterologist at the Animal Medical Center, it was just the beginning. “Dr. Johnson said, ‘You know, I have these other cases that I haven’t been able to figure out,’ ” Peterson recalls. “So we thought: We’ll get them back. Let’s test them.” They quickly found four more cats with benign thyroid tumors and elevated levels of thyroid hormones. And the more they looked, the more hyperthyroid cats they found. “It didn’t take very long to get a dozen cases, and then 30 cases, and then 100 cases,” Peterson says. It was an astonishing discovery — dozens of pets wasting away from a disease that nobody knew existed.

In the summer of 1979, Peterson presented the first five cases of feline hyperthyroidism to a standing-room-only crowd at a veterinary conference in Seattle. There, he learned that hyperthyroid cats had recently begun turning up in Boston; the vets at Angell Memorial Animal Hospital would soon publish a paper on their first 10 patients. The reports set the veterinary world abuzz and raised some unsettling questions. “The first, among specialists, was, ‘How did we miss this?’ ” recalls Duncan Ferguson, a veterinarian and pharmacologist who was a co-author of a 1982 paper on the first cluster of cases to appear in Philadelphia. “We can’t believe it just sort of appeared. Is this a new disease?”

It seemed to be. When Peterson later combed through old pathology reports for 7,000 feline necropsies, he found that the thyroid abnormalities he was seeing were rare until the late 1970s. But once the outbreak started, it spread fast. From 1979 to 1983, the vets at the Animal Medical Center saw three cases a month on average; by 1993, they were seeing more than 20. The disease hopscotched across the United States and then the world, striking cats in Canada, Europe, Japan, Australia and New Zealand.

Today, senior cats are routinely screened for hyperthyroidism, and about 10 percent will be found to have the disease. Owners can choose from a variety of treatments, including drugs, surgery or radioactive iodine, which destroys the hyperactive thyroid cells while sparing the healthy tissue. At his two clinics — the one in Manhattan and another in Bedford Hills, N.Y. — Peterson administers radioiodine to more than 300 cats each year. But for all the progress veterinarians have made in diagnosing and treating the disorder, it has been far trickier to determine its origin.

When hyperthyroidism first surfaced in cats, Peterson was confident that scientists would soon make sense of the curious condition. A number of researchers, including Peterson, became epidemiological detectives, searching for dietary, environmental and lifestyle factors that distinguished the hyperthyroid cats from healthy ones, and they turned up many leads. Among the many behaviors that appeared to put cats at risk: spending time indoors, using cat litter, eating canned food, eating fish-flavored canned food, eating liver-and-giblet-flavored canned food, drinking puddle water, sleeping on the floor, sleeping on bedding treated with flea-control products and living in a home with a gas fireplace.

Dr. Mark Peterson with a patient at his Manhattan clinic.CreditMark Peckmezian for The New York Times

It was a long and eclectic list, and from the 1980s to the early 2000s, scientists proposed a wide range of potential culprits, including chemicals used in canning and a toxic mystery substance in cat litter. Eventually, researchers homed in on another possibility: a class of flame retardants known as polybrominated diphenyl ethers (PBDEs). Beginning in the 1970s, large quantities of the chemicals were routinely added to many household goods, including couch cushions, carpet padding and electronics. PBDEs can be itinerant compounds; they leach from our sofas and TVs and latch onto particles of house dust, coating our floors and furniture. They drift into soil, water and air and slip into the bodies of animals, collecting in everything from the eggs of peregrine falcons to the blubber of beluga whales.

PBDEs also happen to have a chemical structure that resembles thyroid hormones and may mimic or compete with these hormones in the body, binding to their receptors and interfering with their transport and metabolism. By the mid-2000s, it was clear that they could alter thyroid function in rodents, birds and fish, and the United States and the European Union have now largely phased the chemicals out. (They remain ubiquitous, however; PBDEs take years to degrade, and many people still own products manufactured before they were taken off the market.)

As the health risks of PBDEs became clear, two scientists at the Environmental Protection Agency — Linda Birnbaum, a toxicologist, and Janice Dye, a veterinarian — began to wonder whether the chemicals might also be responsible for the rise of hyperthyroidism in cats. “How do cats behave?” says Birnbaum, who now directs the National Institute of Environmental Health Sciences and its National Toxicology Program. “They crawl on the floor. They sit on the couch. They lick their paws all the time. So anything in the dust, they’re going to end up ingesting.” If PBDEs were to blame, it would explain why the disease didn’t appear until the late 1970s, why it first emerged in the United States — where use of the chemicals was especially heavy — and why indoor cats seemed to be at particular risk.

Birnbaum and Dye started a small pilot study to scour the blood of 23 cats, including 11 with hyperthyroidism, for traces of PBDEs. The volumes of blood they collected were so small that the graduate student conducting the lab work worried that she might not detect anything. Her fears were unfounded: The cats had PBDE levels 20 to 100 times as high as those typically observed in American adults. Birnbaum and Dye, who reported their results in a 2007 paper, also found relatively large quantities of PBDEs in several types of cat food, particularly seafood-flavored canned foods.

Several years later, a group in Illinois discovered that pet cats had higher PBDE levels than feral ones and that hyperthyroid cats tended to live in homes that were particularly saturated with the flame retardants. In 2015, a Swedish team found that hyperthyroid cats had significantly higher levels of three types of PBDEs in their blood than healthy cats did. Last year, researchers in California reported a similar result: Total PBDE levels were higher in cats with hyperthyroidism than those without.

The findings are tantalizing but not definitive. Cats’ lengthening life spans may explain some of the increased incidence of the disease, and it’s possible that high PBDE levels are a result of hyperthyroidism, rather than a cause; the compounds, which are stored in fat, may be released into the bloodstream when cats lose weight. Even if flame retardants do contribute to the disease, they may not be the sole cause. Researchers at the California Department of Toxic Substances Control recently identified more than 70 different compounds that seem to be present in especially high concentrations in hyperthyroid cats. “It’s terribly complicated to nail,” says Ake Bergman, who led the Swedish study and is the director of the Swedish Toxicology Sciences Research Center. “Because you are, and I am, and we are all, including the cats, exposed to such a mixture of chemicals.”

In the early 1950s, the cats of Minamata, Japan, seemed to go mad all at once. They began to stagger, stumble and convulse, limbs flailing in every direction. They salivated uncontrollably. They hurled themselves at stone walls and drowned themselves in the sea. This “dancing-cat disease,” as it came to be known, was a warning — one that went unheeded.

The cat condos at the Animal Endocrine Clinic in Manhattan.CreditMark Peckmezian for The New York Times

In the spring of 1956, a 5-year-old Minamata girl suddenly lost control of her body. She dropped her food, wobbled when she walked and shuddered with convulsions, biting her tongue until it bled. Other city residents, including the girl’s 2-year-old sister, soon began to exhibit similar symptoms. Thousands of people eventually fell ill; many slipped into comas and died. In 1959, a physician identified the cause of the catastrophe: A local chemical plant had been dumping methylmercury into the bay, poisoning the fish and, ultimately, the humans and cats who ate them. “In retrospect, if we’d paid more attention to the dancing cats, we might have prevented some of the problems of mercury poisoning in the people,” says Peter Rabinowitz, who directs the University of Washington’s Center for One Health Research, which explores connections among human, animal and environmental health.

Environmental toxicants are equal-opportunity hazards; mercury, asbestos, pesticides and other compounds can cause health problems in humans and animals alike. For at least a century — since coal miners began using caged canaries to alert them to the presence of toxic gases — we have known that we can put these shared vulnerabilities to practical use. Sick animals can be sentinels, warning of looming threats to human health. For household chemicals, cats and dogs, which tend to spend nearly all their time in the home and happily hoover up whatever detritus falls on the floor, may be particularly useful sentinels. “Our household pets are exposed to many of the same kinds of chemicals that we are,” Birnbaum says. “I think if we see a health problem in our animals, especially one that has arisen very recently — genetics doesn’t change that quickly — I think it’s kind of raising the canary-in-the-coal-mine issue.”

Could hyperthyroid cats be modern-day canaries? We know that flame retardants accumulate in our own bodies; scientists find PBDEs in nearly every person they test, including newborns. “It’s almost 100 percent detection,” says Heather Stapleton, an environmental chemist and exposure scientist at Duke University. The compounds turn up in human blood, breast milk and tissue and can persist for years in fat.

Over the course of decades, human PBDE levels skyrocketed, increasing 100-fold from the 1970s to the early 2000s. (These levels now appear to be declining, most likely as a result of the phasing out of the chemicals.) The rate of human thyroid cancer more than doubled over the same time period. These parallel trends may be more than coincidence: Multiple studies have shown that men and women with high concentrations of PBDEs in their bodies tend to have altered levels of thyroid hormones circulating in their bloodstreams. Last year, researchers reported that thyroid problems were more common among American women with elevated levels of PBDEs in their blood. And at a conference this spring, Stapleton and her colleagues presented findings suggesting that long-term exposure to PBDEs may be a risk factor for papillary thyroid cancer; according to the unpublished data, living in a home with high levels of one type of PBDE in the dust more than doubled the odds of having the disease.

Thyroid hormones also play a crucial role in brain development; a deficiency of these hormones, known as hypothyroidism, may cause neurological abnormalities. If PBDEs cause unusual fluctuations in hormone levels in early life, they may do lasting damage. Scientists have found that those who are exposed to high concentrations of PBDEs in utero or during early childhood score lower on tests of motor skills and cognition. These findings are particularly worrisome given that young children — who are not uncatlike in their behavior, ingesting up to 200 milligrams of dust a day — tend to have higher body burdens of PBDEs than adults. The data are not conclusive, and the underlying mechanisms remain unclear. But further studies of cats could help scientists clarify what’s happening. “I remain convinced that paying more attention to what the animals are trying to tell us is a really good idea,” Rabinowitz says. “There are still many disease outbreaks in animals that remain sort of unexplored or unexplained.”

Rabinowitz, who created the online Canary Database to index papers on animal outbreaks that may be relevant to human health, thinks scientists and clinicians could be more strategic about connecting the dots between species. When he and his colleagues recently investigated the potential health risks of hydraulic fracturing, they discovered that skin problems were common in both the people and the dogs living near gas-extraction sites. “We’re finding that there was really some utility in asking about both people and animals when looking at a new hazard,” Rabinowitz says. He suggests that we consider linking the health records of pets and their owners.

For his part, Peterson remains steadfastly focused on cats, which keep showing up with thyroid hot spots that need to be injected with radiation. He will keep them as comfortable as possible during their stay at the “Hypurrcat Spa,” which is why he has converted the floor-to-ceiling pipe into a scratching post and keeps towel-lined baskets on the cold exam table. At his Bedford Hills clinic, which lacks windows for bird-watching, he has even installed a cage of gerbils in the cats’ line of sight. (“People always say, ‘Are the gerbils upset?’ ” he told me. “I think the gerbils like it, because they get to see new cats.”) Sitting in his Manhattan clinic’s waiting room, where the cats are encouraged to relax on the furniture, he said: “I love the animals. I love the animals more than people, I think.”