Zoobiquity Read online

  On the night of January 18, 1991, during the Gulf War, Scud missiles launched by Iraqi troops began exploding in Israeli communities. Citizens were alerted by howling air-raid sirens that blared from outdoor speakers and on the radio and TV. Since there was a terrifying possibility that the bombs were carrying chemical payloads in addition to their explosive power, the frightened populations had been instructed to don gas masks and seek shelter when they heard the wail of a siren.

  In the maternity ward of a Tel Aviv-area hospital that night, three women were in labor. As is standard practice, they had been fitted with fetal heart monitors that strapped around their bellies to keep track of their babies’ heartbeats. At three a.m., a sudden, terrifying shriek of a Scud alert siren penetrated the walls of the maternity ward—and, apparently, the wombs of the expectant mothers. As hospital staff scrambled to put gas masks on themselves and their patients, the nurses noticed something highly unusual on the fetal monitors. The heart rates of all three of the about-to-be-born infants suddenly and unexpectedly.… plummeted. From a healthy and brisk 100 to 120 beats per minute they slowed by half, to a frightening 40 to 60. The tiny hearts “lay low” like this for two minutes and then returned to normal.

  All three babies, who hadn’t yet even heard their parents’ voices outside the womb, responded physiologically, with bradycardia, to the sound of danger. Some of the slowing may have resulted from the sounds of the siren itself and some from maternal stress hormones entering the fetus’s body in response to the siren. Either way, these obstetrical observations strongly suggest that even prior to birth itself, we’re equipped with unconscious anti-predator defenses, including a potent alarm bradycardia response. All three babies were ultimately born healthy, as well as apparently armed with the full complement of survival instincts we all possess but rarely think about.

  Hiding in the face of danger—what scientists call crypsis—is one of nature’s most common and effective strategies for staying out of a predator’s stomach. Some animals depend on body shapes and camouflage to help them hide. And some conceal themselves by performing instinctive or learned behaviors like freezing, hiding, or crouching. Many animals do all of these. The stillness of a slowed heartbeat is just one of many tools prey animals employ to help them “disappear,” at least as far as a predator is concerned.

  Freezing, hiding, and crouching—with the help of slowed hearts—connect our nervous systems to the vast range of species with whom we share common ancestry. Examining fainting through the lens of veterinary medicine allowed me to reframe this common but puzzling cardiac event as a possible anti-predation strategy. And this hypothesis, in turn, helped me understand the powerful feedback loop between heart and brain that results, for some of us, in lost consciousness or passing out. Exploring why took me into the watery habitat of our ancient ancestors.

  Astronotus ocellatus, commonly known as an oscar, is a freshwater fish related to tilapia. Energetic and affectionate, oscars’ reputation as “puppies of the aquarium” comes from the enthusiastic greetings they give their owners, complete with tail wagging, acrobatic flips, and finger nibbling. But when oscars get stressed out—for example, when you’re cleaning their tank—they can seemingly go lifeless. Lying on their sides, completely still, they lose color and breathe more slowly. Their fins stop moving. They sometimes stay this way even when nudged.

  If I were able to place an aquatic version of my stethoscope over the heart of that very still—yet alive—fish at the bottom of the tank, I would hear another clue as to why fainting may have survived so many grueling rounds of natural selection. Or, rather, the clue would be in what I wouldn’t hear: a robustly beating heart. Instead, I’d notice the familiar, super-slow rhythm of a bradycardic heart, dominated by lengthy pauses between beats.§

  To understand the significance of this decelerated, less noticeable heart rhythm, consider the physiology of a master predator: the shark. Along with certain other underwater predators, like rays and catfish, sharks come equipped with heartbeat detectors. Called ampullary organs, these specialized sensory cells pick up the weak electrical pulses put out by the beating hearts of other fish. The hunters’ internal ears may also scan for fish heartbeats, picking out the lub-dubs like doctors do through stethoscopes. Predators can lock onto the telling signals and home in on them with lethal accuracy, even when their target is some distance away or hiding under sand. Which means: underwater, a beating heart can be a deadly giveaway.‖

  Every one of us has this “tell.” Whether you’re a human being, a salamander, or a canary, your telltale heart starts beating in the early days after conception and keeps going until the day you die.

  But if a fish underwater could silence its beacon, it would become acoustically invisible. It might even be able to evade a predator. Anyone who’s seen a submarine movie will recognize this principle. The commander of a submarine being tracked by enemy sonar will invariably order his crew to “run silent”—which involves everything from shutting off radios to cutting the engine to suppress the heartbeat of the submarine. Once the threat has passed, they fire up the engines again and the sub speeds away to safety.

  Knowing this, we can see why natural selection might have favored fish that had the good fortune to faint their way out of becoming dinner. Having a heart that radically slows in response to real or perceived threats might have been a major advantage, offering protection before an attack even got under way. Fainting and “near fainting while conscious” may have evolved as a lifesaving “third option,” offering a protective alternative to the more storied “fight or flight.”

  As we know, the heart-slowing reflex triggered by states of high arousal, such as fear, pain, or distress, is a core feature of vasovagal fainting in human beings. Alarm bradycardia has protected animals across all classes of vertebrates, and persists in us today precisely because its protective power is so deeply embedded into the autonomic nervous system, which has been passed down from our ancient water-dwelling ancestors. This hypothesis connects the acutely slowing heart of a hunted fish in the water to a human fainter in the ER.

  In some ways, it’s hard to think of ourselves as prey. Human beings today are so dominant on our planet that we can (and do) wipe out whole species, sometimes without even knowing it. Most of us in developed countries will make it through our entire lives without ever facing a realistic threat from a nonhuman animal predator. An evolutionary vestige like fainting seems as ill-fitted to our modern times as a chariot repair shop. But a zoobiquitous approach lets us understand reflexes and behaviors in ourselves that mirror anti-predation strategies in other animals.

  Picture the myriad defenses nature has bestowed on many adult animals: quills, antlers, talons, noxious smells, and deadly poisons. While all can be useful during an attack, they also serve as “don’t mess with me” warnings that can prevent an attack in the first place. The same goes for a peculiar jumping maneuver among deer and gazelles called “stotting.” The stotting animal springs up, lands stiffly on all four legs, then springs up again and again, moving away from a predator as if on a pogo stick. Scientists argue about how this behavior helps an animal escape. It seems like a colossal waste of energy—energy that could be spent on running away. But the whole point seems to be to show off superb stamina. Stotting tells a predator that the animal has energy to spare and even thinking about giving chase is a waste of time.

  Wildlife biologists call these physical traits and behaviors “signals of unprofitability.” They send a clear message to a predator: Move along, find an easier target.

  We humans use signals of unprofitability for protection, too. Picture a bodyguard flexing his bulging biceps. Think about how you might instinctively pull yourself up to your full height and walk with an exaggerated swagger on an unnervingly quiet street at night. Imagine the sign on your lawn advertising that you have a burglar alarm inside, or the teams of lawyers employed by big companies to fight lawsuits. The message in each case is the same: Find another victim. This
one’s too much trouble.

  Indeed, maintaining and advertising a strong defense is a fundamental drive across species. In a conversation I had with the late Harvard evolutionary biologist Karel Liem, he explained that nearly every animal behavior has elements of self-protection, or anti-predation, at its core.

  And the physiology of fainting is no different. Simply being still can confer survival advantages. Of course, it doesn’t always work, but it does enough of the time to make it a respectable option of last resort.

  Yet respect is rarely the reaction that greets fainters. Alarm bradycardia, vagal nausea, freezing in place, feigning death, and full-on fainting are almost always taken as signs of weakness or cowardice, portrayed in literatura and film as shorthand for the lily-livered. Franklin Pierce’s episode of battlefield fainting, for example, landed him the moniker “the Fainting General,” which dogged him even after he became president of the United States in 1853. Few would characterize George H. W. Bush, Margaret Thatcher, David Petraeus, Fidel Castro, or Janet Reno as weak-willed, yet all suffered fainting spells while in office. To an observer, passing out might seem helpless, a physiologic act of surrender, even defeat. But, given fainting’s protective power, perhaps it’s time to revise this derogatory and uninformed view of syncope.

  Fight, flight, or faint. Fainting is the body’s way of flipping a circuit breaker. It halts the action and perhaps even a pursuer. It can defuse conflict. It can enable escape. Fainting and its related spectrum of “slowing down” behaviors remain with us because over hundreds of millions of years they have helped animals evade death. Embedded in fainting’s ancient physiology is an important lesson for how we respond to the things that scare us. Fighting or fleeing your enemy may work some of the time. But when fighting is futile and fleeing not an option, just being still may offer an even more powerful form of protection.

  Teens at the ear-piercing salon, fawns hidden in leaves, blood donors, and fish escaping predators have all inherited fainting’s death-evading neurocircuitry. Their conversing hearts and minds have bestowed upon them a respite—a momentary, deceitful reprieve that for eons has sometimes meant a way out.

  *There are some theories. One, the “clot-production” hypothesis, posits that a slow heartbeat or full-on faint helps animals avoid bleeding to death after an attack, since slow-moving blood under low pressure clots better. The less plausible “human violent conflict” hypothesis suggests a Paleolithic-era origin, speculating that fainting evolved in women and children as a way of taking them (but not men) out of harm’s way during tribal warfare.

  †Female robberflies sometimes employ a similar tactic to thwart unwanted sexual advances. Writes entomologist Göran Arnqvist, “If grasped by a male, they exhibit thanatosis (playing dead). Once the female ceases to move the male apparently no longer recognizes the lifeless female as a potential partner, loses interest and so releases the female.” Whether or how this insect rape-prevention strategy has implication for human beings is unclear, but Arnqvist posits that since feigning death is so widespread in the insect world, females may have adapted this strategy to protect themselves from unwanted copulations.

  ‡Some experts believe that crucifixion is death by recurrent vasovagal syncope. During this horrible form of torture (from which the word excruciating is derived), you’re restrained from collapsing into a restorative horizontal position. You faint and recover without respite, and eventually succumb to low blood pressure and oxygen deprivation.

  §The fish heart has two cardiac chambers separated by a rudimentary valve; the mammalian heart has four chambers and four cardiac valves. When the heart’s valves close, they create clicks we call heart sounds. In humans, the shutting of the heart’s valves generates the iconic lub-dub sound.

  ‖The Volvo car company once offered a heartbeat detector as an option on some of its models. Volvo claimed the machine could alert you to the presence of an intruder in the backseat of your car before you got behind the wheel.

  THREE

  Jews, Jaguars, and Jurassic Cancer

  New Hope for an Ancient Diagnosis

  As veterans streamed home from Asia and Europe after World War II, doctors in the United States were battling a deadly threat on the home front. Five times the number of Americans who died at Iwo Jima and Omaha Beach were dying every year of heart disease. In response, the National Heart Institute launched what became the gold standard in long-term medical investigations: the Framingham Heart Study. Every two years, starting in 1948 and continuing today, thousands of men and women from that Massachusetts city go to special doctors. They give blood and other lab samples, have comprehensive physicals, and answer question after question about their eating, exercise, work, and leisure habits.

  As the data piled up over decades, researchers began to discern patterns. High blood pressure and smoking led to heart disease. Age and gender influenced risk. It’s hard to believe that this information we now accept as routine was ever unknown. Even today, Framingham’s half century (and counting) of statistics is paying dividends as researchers mine the data for long-term trends in stroke and dementia, osteoporosis and arthritis. The iconic study is now in its third generation, having enrolled many of the children and grandchildren of the original participants.

  Longitudinal medical studies—those with large populations and elongated time frames—are hard to pull off. What makes them so valuable is exactly what can make them so frustrating. Even when lots of people sign up, many drop out. Participants lose interest. They forget to go to their physicals. They move away and don’t leave a forwarding address. They blow off the third or thirteenth or thirty-third questionnaire.

  But the challenge hasn’t daunted Dr. Michael Guy. In 2012 he began enrolling three thousand participants in what is perhaps the most ambitious new longitudinal study in more than a decade. Its focus is cancer in a population that has a staggering 60 percent risk of dying from the disease.

  And his research team knows for sure that their test subjects aren’t likely to cheat or fib or flee. They won’t fudge answers on their surveys or tell a researcher only what she wants to hear. They’ll be loyal and enthusiastic and obedient. The researchers know this because they chose their participants deliberately and wisely. They are all golden retrievers.

  Before you start picturing a floppy-eared puppy in a sterile wire lab cage, let me explain. The dogs enrolled in the Canine Lifetime Health Project—a long-term cancer study Guy sometimes calls “Framingham for Dogs”—are beloved pets. Recruited from normal homes all over the United States, they live in yards and bedrooms, romp with children and other dogs, eat the food their owners carefully select and prepare for them. They walk neighborhood sidewalks and play fetch in local parks.

  Like the human participants in the Framingham study, each dog in the Canine Lifetime Health Project will be followed for the rest of its life. As the data roll in, epidemiologists, oncologists, and statisticians will scrutinize the dogs’ diets to see if nutrients or portion sizes contribute to developing cancer. They will pore over environmental exposures—from secondhand smoke to household cleansers. They will measure how far the dogs live from power lines and freeways to determine whether any cancers cluster in significant ways. The researchers will analyze the genetic code of each dog, comparing it to the others and to the complete canine genome (completed in 2005 on the DNA of a female boxer named Tasha).

  This unprecedented study, undertaken by the nonprofit Morris Animal Foundation, could radically shift our approach to cancer in dogs. And the effort may yield knowledge that will benefit not only future generations of pets but also the animals at the other end of the leash. Dog cancer has many stories to tell about human cancer: where it comes from, why it migrates, and, possibly, how to stop it in its tracks. A multispecies take on cancer research means our special relationship with man’s best friend is about to get even closer.

  Except for some grizzling on her muzzle, Tessa’s fur was glossy black—a striking contrast with her streetlight-
yellow vest. The bright garment, as snug as a Partridge Family costume, was covered with embroidered patches. A few advertised dog food companies. One identified Tessa as a “Dock Dog,” an elite animal athlete whose jumping and fetching prowess makes the average pet look like a Little Leaguer going up against Derek Jeter. But the most noticeable feature of Tessa’s vest were the two words stitched in black thread across her midriff: “Cancer Survivor.”

  Tessa is a black Labrador retriever I met in the spring of 2010 at a gathering of pet patients who had battled illnesses and won. Although a brown lesion on the gum behind her lower left fang was still visible, her mouth cancer had been in remission for two years. As I patted Tessa’s furry, wedge-shaped head, her owner, Linda Hettich, explained how she had discovered her dog had the disease. They were playing fetch and Tessa brought back a bloody tennis ball. A trip to the vet confirmed a cancer diagnosis, and Tessa went into treatment. Although Hettich’s distinct alto voice (she’s the noon anchor for a Los Angeles news radio station) conveyed gratitude that Tessa’s cancer had not returned, her face betrayed a certain grim anxiety. Tessa was not her first dog to have cancer. A few years earlier, her beloved mutt, Kadin, had died of it. Hettich admitted in a whisper that she sometimes wonders why two of her dogs have fought the disease.

  “With Kadin, there was a tremendous amount of guilt,” she told me. Now that Tessa has had cancer, she said, there are moments when she wonders, “I’m two for two—what did I do?”

  That didn’t surprise me a bit. I’d heard “What did I do?” before; that question frequently plagues many human cancer patients, too.

  One of my roles at UCLA involves caring for people who’ve developed heart problems as a side effect of their cancer treatments. Sometimes they share with me their personal theories for why they drew the cancer card. Often, it’s something they did: My cell phone. My deodorant. My char-grilled salmon. My microwave. My lipstick. My plastic Evian bottle. My years as a flight attendant. Or something they didn’t do: Missing church. Not exercising. Skipping mammograms. Something that was done to them: My father’s nicotine addiction. The fluoride in my water. The new carpet at my office. Or general stress: A lingering lawsuit. A mountainous credit card balance. Caring for an aging parent.