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Now it’s medicine’s turn. I was in the right place at the right time to put takotsubo together with capture myopathy. (You’ll find more on this finding in Chapter 6, “Scared to Death.”) Zoobiquity encourages similar interdisciplinary experiences for other physicians. And this field-merging approach could have other important benefits. If studies funded by the National Institutes of Health expanded the boundaries of their inquiry by adding the simple question “Do animals get ______?” the benefits of scientific investigation could be vastly amplified.
A comparative approach could extend far beyond the walls of a human or veterinary hospital. It could help aspiring businessmen or middle school girls navigate complex hierarchies—by exposing similar challenges within a school of salmon or a herd of bighorn sheep. It points out the overlaps in the ways animals protect and defend their territories—and how and why we humans create borders, castes, kingdoms, and prisons. It dangles the possibility that human parenting could be informed by a greater knowledge of how our animal cousins solve issues of child care, sibling rivalry, and infertility.
Of course, human beings are unique as a species. Contained in our mere 1.4 percent genetic difference from chimpanzees are the physical, cognitive, and emotional features responsible for Mozart, the Mars rover, and the study of molecular biology itself. But the magnificent glare of this crucial but tiny percentage blinds us to our 98.6 percent sameness. Zoobiquity encourages us to look away, for a moment, from the obvious yet narrow range of differences and embrace the many enormous similarities.
Sadly, Spitzbuben the tamarin later died—not, I hasten to add, because of my attempt to befriend her. After her necropsy (the term for an animal autopsy), I took a slide of some of her heart cells to one of the most respected cardiac pathologists in the country, a colleague of mine at UCLA, Michael Fishbein.
As we peered through Fishbein’s microscope, I noted how the damaged heart muscle cells seemed ensnared and strangled by the surrounding tissue. I felt a jolt of dreadful recognition as I spotted familiar-looking pink and purple shapes illuminated in the glaring white circle of the microscope’s frame. Although the abnormal cardiac cells belonged to a furry, tailed tree dweller, they were essentially identical to human heart cells with the disease.
But this was more than a cellular display of our common ancestry with animals. The patterns illustrated a simple fact well known to veterinarians but unknown or ignored by modern physicians. Animals and humans share a vulnerability to the same infections, illnesses, and injuries.
As he had done so many times before with human heart specimens, Fishbein studied the slide carefully before he spoke. “Cardiomyopathy,” I recall him observing. “Could be viral—looks just like a human’s.”
His phrase contained the essence of zoobiquity. Undistracted by fur and a tail, we saw, under that microscope, not “heart disease in a tamarin” but, rather, “heart disease in a primate”—gorilla, gibbon, chimpanzee, tamarin … or human.
As I heard Fishbein’s words, my single-species focus officially died. Emerging in its place was zoobiquity, a connecting, species-spanning approach to the diagnostic challenges and therapeutic puzzles of clinical medicine. I would never look at another heart, human or animal, the same way again.
*One of Virchow’s most illustrious students was the Canadian doctor William Osler, revered by American medical students as a father of modern medicine. What’s less well known to physicians is that veterinarians also consider Osler a father of their profession. He was a key advocate for the comparative method and influential in shaping what became McGill University’s School of Veterinary Medicine in Montreal.
†One of the first modern efforts at unification came in the 1960s from the eminent veterinary-epidemiologist Calvin Schwabe, who is regarded as a pioneer of this field.
‡The movement has gone by several different names over the years, including comparative medicine and One Medicine.
TWO
The Feint of Heart
Why We Pass Out
An urban hospital’s emergency room only occasionally resembles its television doppelgängers on shows like Grey’s Anatomy and House, M.D. Yes, we do see those whirlwinds of frantic activity around gunshot wounds, heart attacks, and drug overdoses. But in between come the calmer, less grim interludes. They arrive in the form of familiar characters: the hypochondriac, the overly vigilant parent, and, of course, the fainter.
As trivial as it might seem, fainting—what doctors call syncope—is so prevalent that it accounts for 3 percent of ER visits and 6 percent of hospitalizations in the United States. In UCLA’s emergency department, we care for plenty of TV drama–worthy cases, including the victims of earthquakes, multicar crashes, and gang wars. But we also have fainters coming in almost every night—in fact, emergency rooms handle more fainting episodes than they do firearms injuries, suicide attempts, and third-degree burns combined.
About a third of all adults have fully fainted at least once in their lives. Nearly all of us have experienced that woozy, prefaint feeling, where all you can do is grope for a nearby chair and hang your head over your knees. And it’s nothing to laugh at: syncope can be a symptom of serious heart ailments and can also cause severe injury—for instance, if you crack your head on your trip to the floor.
A cardiologist routinely cares for fainting patients. Although it may seem like an ailment of the brain, syncope is actually a complex interplay between the brain and the heart. At UCLA’s medical school, where I lecture on fainting, I explain that a loss of consciousness often occurs when the brain is abruptly deprived of blood and oxygen. The specific causes vary, but more often than not, the heart is a prime suspect.
We all know that we can get dizzy when we stand up too fast. That kind of fainting comes from the basic physics challenge of moving liquid blood around the body against gravity. And fainting caused by a serious heart condition—where the heart is unable to pump a steady supply of blood to the brain—is relatively easy to diagnose.
But for the more storied form of syncope—the emotionally triggered faint that’s been employed as a plot point by writers from Shakespeare and Austen to J. K. Rowling and Stephen King—its basic cause remains a mystery.
Yet this kind of fainting, called vasovagal syncope (VVS), is so common that casualty assistance officers delivering the news of a soldier’s death to family members are trained to treat it. Nurses deal with fainting so often during blood draws that they keep ammonia inhalants (modern-day smelling salts) within arm’s reach. And every obstetrician knows that some of the biggest fainters around are the husbands of women in labor. At the point of highest emotion (the baby’s head crowning or popping out of the uterus during a C-section) the thunk of the father’s head hitting the floor occasionally precedes the cry of the newborn.
Yet all my intellectual knowledge and hands-on experience with fainting didn’t prepare me for what I would encounter when I took my twelve-year-old daughter to get her ears pierced. Instead of entrusting her pure, unsullied lobes to the high school kid at the mall jewelry store, I had, in my maternal wisdom, chosen the cleanest, safest venue I could think of: the starched and sterilized medical office of a family friend who’s a plastic surgeon. On the happy day, my excited daughter settled into a comfortable, overstuffed chair designed for recipients of Botox injections. She gave me a brave smile. The doctor marked her ears with a green pen. He held up a hand mirror so my daughter could approve the placement. Then he drew out the silver piercing gun … I watched my daughter’s smile fade … The gun moved closer and closer to her head … and had almost reached her left ear when—crash! Before I could even say, “You’re doing great, honey,” she had keeled over.
Believe me, my daughter wasn’t in that office under duress. For years she had been begging me for pierced ears; she wanted to be there. And we could not have chosen a less threatening environment. Yet some instinct in her body or mind had insisted that she’d be better off unconscious than “present” in that moment. And clea
rly her brain and heart had followed orders and triggered a fainting response.
Later, as I mulled it over, I found myself focusing on the convoluted logic of fainting. If that piercing gun had been a real weapon, wouldn’t she have been better off making an escape or putting up a fight, rather than falling helpless at the feet of the attacker? How has this odd response remained in the gene pool? Why didn’t evolution take out the fainters long ago, in favor of fighters and fliers?*
For clues to puzzles about human bodies and behaviors, we can look to creatures whose daily realities are less detached from their evolutionary roots than are the lives of modern Western urbanites. Vasovagal syncope is the perfect starting point for a zoobiquitous expedition. I realized that I had never, despite years of treating human fainters, thought to ask one basic question: Do animals faint?
A survey of any veterinarian’s patients quickly confirms that yes, they sometimes do. In dog breeds from rottweilers to Chihuahuas, syncope can follow everyday activities like barking and jumping, frolicking, grooming, and bathing. Some canines faint when they’re roused to sudden activity after being at rest. Some vasovagal fainting in dogs and cats happens when they’re physically restrained against their will, an especially terrifying situation for many pets. Remarkably, as is the case with many humans, some pet patients have been reported to faint in response to needles: a Yorkie after a blood draw … a kitten after having urine drawn from its bladder with a syringe … a Cavalier King Charles after a vaccination.
What about wild animals? This is a harder question to get at, but zoo veterinarians have seen chimpanzees faint, especially when the animals are stressed or dehydrated. Wildlife veterinarians have seen screech owls and juncos fall into a torporlike state when they’re handled during blood draws. And Charles Darwin reported catching a robin that “fainted so completely that for a time I thought it dead.” He also saw a terrified canary “not only tremble and turn white about the base of the bill, but faint.”
Fainting episodes often begin in the same way and in the same situations as the well-known fight-or-flight response. When animals, including human animals, sense a possibly mortal threat, adrenaline and other hormones (called catecholamines) flood into our bloodstreams. Our hearts race. Our blood pressures soar. We breathe faster. Crucially, we get a burst of energy, allowing us to either escape from the threat or battle it off.
But as you’ll soon see, the old duality of “fight or flight” needs an update. Many animals have at their disposal an additional trick to boost their odds of living through a dangerous encounter. It’s not just fight or flight. It’s fight, flight, or faint.
Remarkably, fainting begins the same way as the other two fear responses—with a high-emotion stressor and a surge of adrenaline. But from there fainting follows a different route. Instead of the heart beating faster (tachycardia), it plummets (bradycardia). Instead of blood pressure surging, it plunges. Detecting low-pressure, slow-moving blood, sensors throughout the body signal to the brain that something is terribly wrong: a failing heart or a catastrophic loss of blood. In a protective response, the brain shuts the system down by fainting.
For anyone who’s had a racing pulse after being scared, this slowing of the heart seems counterintuitive. But you’ve felt it. Imagine that wave of intense nausea you had when you lost your passport in Beijing or discovered a partner was cheating on you. Reflect on that “I think I’m going to vomit” feeling that washed over you following a career-jeopardizing mistake or a near miss between your carful of kids and a sixteen-wheeler. It’s also the woozy feeling you may get before stepping in front of an audience, as you anticipate hundreds or thousands of eyes being trained on you. (For more on the heart’s sometimes deadly response to eye gaze, see Chapter 6, “Scared to Death.”)
That extreme, sick feeling is the vagal response. It’s caused by the part of the nervous system responsible for “digesting and resting”: the parasympathetic system. For a few crucial seconds the sympathetic system (which controls “fight or flight”) withdraws and the parasympathetic system takes over. A pulse check during those awful moments of vagal nausea would reveal a slowed heart rate. In some cases, but not all, it slows enough to cause a loss of consciousness, what most of us call a faint.
Although losing a passport won’t induce dread in a chipmunk, other stressful situations will. Alarm-triggered slowing of the heart has been documented across the animal kingdom. Woodchucks, rabbits, fawns, and monkeys have all shown marked slowing of the heart (and a decrease in blood pressure) in response to fear. Willow grouse, caimans, cats, squirrels, mice, alligators, many species of fish, and, yes, even chipmunks display this cardiac trick as well. And while it isn’t always followed by a faint (it isn’t always in people, either), this switch to a vagal state and the slowing of the heart in response to stress is as commonplace as it is curious. It’s exactly what happened to my daughter in the ear-piercing chair. For years, I’ve known this by the human medical term “fear-induced, vagally mediated bradycardia.” Once I started looking into it, I came across a different term, one used by veterinarians: “alarm bradycardia.” It sounded enticingly similar to our term—not to mention more succinct. And sure enough, the two terms describe exactly the same condition.
One noticeable difference between animal and human fainting is that, while animals frequently get alarm bradycardia, they seem to fully faint less often than humans. Then again, for every actual faint we see in the ER, we know there are many more cases where people feel the swoon, the nausea, the light-headedness of bradycardia while never completely blacking out. It isn’t unreasonable to call this syndrome, both in humans and animals, “near-fainting while conscious.” And since so many species do it, it brings us back to a fundamental question: Do animals whose hearts go into super slo-mo at times of high stress have a survival advantage?
There are a few possible answers, the first of which you’ve probably already guessed. Alarm bradycardia can help an animal feign death and thus possibly fool a predator into passing it by.
One study demonstrated that inexperienced foxes could be fooled by ducks whose slowed nervous responses made them seem dead. Older foxes, though, having been tricked out of a meal or two in the past, had wised up. These savvy hunters knew to kill the duck on the spot or possibly bite its legs off, to ensure that it didn’t miraculously “rise from the dead.”
This trick of the heart and mind has saved people from imminent, actual harm. In 1941, twenty-one-year-old Nina Morecki was fleeing a concentration camp and her Nazi pursuers in the Polish woods when she fainted. After regaining consciousness, she found herself surrounded by the dead bodies of her less fortunate comrades. Other grim analogues might include those survivors of mass killings who play dead until they can escape. This strategy has been described in survivors’ accounts from the Babi Yar massacre during World War II, the Rwandan genocide in 1994, and shooting rampages like the one at Virginia Tech in 2007.
Another common side effect of near fainting while conscious is both disgusting and tactically brilliant. A vagal state can make an animal lose control of its bodily functions. Some animals urinate or defecate under extreme emotion or fear. Many predators find urine or feces repugnant and will leave. Dogs are known to retreat at the smell of skunk; frightened shrews produce such foul odors from their anal pockets that even ravenous badgers keep their distance. Vomiting by the would-be prey can have the same conveniently repellant effect on the predator.
This potentially embarrassing loss of bodily control in response to fear is one vestige we humans probably wish we’d evolved out of. But in fact it may occasionally serve a protective function for us as well. Rape-prevention educators sometimes instruct women to urinate or vomit if rape is imminent. In some cases, the attacker will be repulsed and withdraw. A more common phenomenon is seen in women who successfully avoid sexual assault by fainting or by entering a “near fainting while conscious” state. Psychologists have studied cases of this and compared them to immobility reactions i
n animals. They suggest that when fighting back isn’t an option, not struggling may defuse the situation and reduce the likelihood of rape.† While far from foolproof, fainting succeeds enough of the time to warrant a serious consideration of its evolutionary roots.
It’s a grim irony that the one group of people who may best understand the vital role fainting plays in giving the body a needed respite is a group dedicated to inflicting pain: torturers. Many narratives taken from torture victims contain a nauseatingly familiar refrain. Under the terror and physical violation, many victims pass out. But, horrifically, when they come to, the torturer is cued to resume his assault. You could say that by overriding the body’s protective response—the faint—the torturer adds yet another level of affliction, the way sleep deprivation keeps a body from having a restorative break.‡
A slowed heart offers another key survival advantage. It helps a vulnerable animal keep still. Canadian scientists studying white-tailed deer tracked what happened when they played recorded wolf howls to fawns. The baby deer responded with “very predictable” alarm bradycardia, slowing their hearts and quieting their bodies. Think of the survival edge this physiological trick gives to fawns, who often get left alone for long periods while their mothers go off to forage. A slowed heart rate keeps them from rustling around when danger is nearby. In other words, it helps them hide. Is this physiology present in young humans?
This is the kind of experiment we would never do on infants; terrifying them on purpose to test their heart rates would certainly get the researcher excoriated, if not arrested. And yet, remarkably, an accident of geopolitical fate has given us a small window into how the very youngest members of our own species respond to primal terrors.