Zoobiquity (18 page)

This is a very important point. Our behavioral relationship with potentially addictive neurochemicals begins from the minute we enter the world (and quite possibly before). Suckling has been found to produce an internal opioid hit, a chemical reward for this basic, life-sustaining task. Indeed, Panksepp and others believe the suite of “attachment” neurochemicals are many and powerful, and that some of the codes for releasing them are set in earliest infancy. Various elements of a child’s young life—including physical health, “wiring,” but
also, significantly, parenting—influence how their personal lockbox will respond to increasingly challenging environments.

Like younger children, adolescents, too, have highly malleable brains. Pouring external sources of powerful reward chemicals into the brain at precisely the point it’s trying to calibrate the system can have lifelong effects. It can influence tolerance levels and response sensitivity. Across species, a zoobiquitous look at addiction suggests that delaying the age of first use could have powerful protective effects.
Extensive study of the effect of alcohol exposure on adolescent rodents and nonhuman primates has shown alcohol’s long-term effects on the adult brains of these young mammalian imbibers. Along with impaired cognitive function, early use in these animals may increase their risk of alcohol addiction later in life.

In the United States, we’ve tried prohibition and “just say no” campaigns. We’ve set the drinking age at twenty-one and the illegal drug use age at never. None of these interventions has completely stopped teenagers from going after what they want.

But the evidence suggests it’s wise for parents to try harder to delay their children’s first exposures and, perhaps, to teach them natural ways of achieving those chemical rewards: through exercise, physical and mental competition, or “safe” risk-taking, such as performing.

In some individuals, whether cedar waxwings or late-night partiers, intoxication can lead to tragedy. In humans it’s linked to higher rates of motor vehicle accidents, suicides, homicides, and accidental injury. In the wild, intoxicated animals, too, are at greater risk. They can more easily be picked off by predators, miss out on opportunities to mate, or fly into walls.

But nature provides its own abstinence program. Access to plants, berries, and other food sources in the wild vary with seasonality, weather, competition, and many other factors, including predation. And these variations automatically reduce access to substances that might otherwise lead to addiction. It’s like a wild version of having one’s coke dealer leave New York for Miami between November and March. This lack of ongoing access to substances, coupled with the increased risk of death to an intoxicated animal in the jungle, desert, or savannah, makes the possibility of humanlike addiction in the wild unlikely.

Recovery from addiction may involve restoring the integrity of the
lockbox we’re born with. Substance abusers can learn healthy behaviors that provide the same (albeit less potent) good feelings they used to seek from a bottle, a pill, or a needle. In fact, that may be what makes some rehab programs so effective for certain addicts. If you look at the behaviors these programs encourage—socializing, companionship, anticipation, planning, and purpose—they’re all part of an ancient, calibrated system that doles out internal neurochemical rewards.

Ironically, one way to fight addiction may be with addiction, replacing a dependence on heavily refined drugs with the hard work that makes life worth living. The endorphin release of physical work and exercise. The adrenaline rush of healthy competition and risk in games or business. The exquisite anticipation of planning, serving, and at last eating a great meal. The opioid rush of being part of an actual flesh-and-blood social network. Or the warming satisfaction of helping others. The term “natural high” may sound as dated as a John Denver song, but it’s not a metaphor. It’s the ancient reward that motivates and sustains all animals, including us.

The magnitude 6.7 earthquake struck at 4:31 a.m. on January 17, 1994. I was jolted out of bed, my heart pounding as I waited along with millions of others around Los Angeles for the ground to stop shaking. When it finally did, I drove to the hospital, adrenaline and caffeine blasting away my haze of fatigue. Not knowing whether we’d soon be receiving a few cuts and bruises or facing a large-scale catastrophe, I entered the UCLA emergency room. In that moment, I couldn’t have predicted how completely the morning’s geological shift would shake my perspective on medicine over a decade later.

At the time I was a “flea,” to use the macho, old-school surgeons’ derogatory term for overly analytic internal medicine nerds. I embraced the nickname, enthusiastically hopping up and down while spouting medical minutiae and arcane diagnoses whenever my superiors hove into earshot. On cue, I could explicate the cryptic presentation of Behçet’s disease. With dorky rectitude, I competed with other fleas to recall the fifth and sixth diagnostic criteria for relapsing polychondritis. Never in the history of medicine, we told ourselves, was anyone as passionate about Churg-Strauss vasculitis or Rasmussen’s encephalitis.

As the newly appointed chief resident in internal medicine, I was also treating real patients with more familiar-sounding maladies. But during this year, with the grunt work of internal medicine residency behind me and the rigors of subspecialty still ahead, I threw myself into the exciting and decidedly cerebral pursuit of medical oddities. At a teaching hospital like UCLA, this isn’t just tolerated; it’s encouraged.

But all that changed when the earthquake shot up from fifteen miles beneath Earth’s crust with the fastest ground acceleration ever recorded in urban North America. Apartment buildings slumped. Freeways snapped. The scoreboard at Anaheim stadium toppled onto several hundred (thankfully empty) seats. Thousands of people all over Southern California were injured.

Instantly I was propelled out of the arcane, into the here and now. Throughout the day we treated serious wounds and minor scrapes. Amid the blur and drama of the days right after what became known as the Northridge quake, a curious trend emerged. Although I didn’t notice it then, it held a special significance for me as a budding cardiologist.

On the day of the earthquake, and for twenty-four hours right afterward, the heart attack rate around Los Angeles spiked. L.A.’s coroner noted a fourfold increase in cardiac deaths. As later reported in the
New England Journal of Medicine
, nearly five times as many Angelenos suffered what we call a cardiac event that day, compared to the same day in January in the years before and after. The conclusion: at least some Southern Californians had been scared to death when the earthquake struck.

This research, although fascinating, had little day-to-day effect on my practice of medicine. Most of the time I was treating patients who were not extremely fearful. So it sat on my mental shelf of medical curiosities for several years, until the day a wildlife veterinarian showed me a telling video.

The scene opened on a quiet, curved stretch of beach. Waves glinted in the morning sunshine. Suddenly, an explosion cracked the stillness. A flock of shorebirds burst off the water. They flapped madly toward the center of the lake, chased by a giant unfurling rectangle of net detonating from the cannon. Most of the birds escaped and resettled on the mild waves. But two dozen or so didn’t make it. Before they could get airborne, the mesh had grabbed them and trapped them in place.

There the video ended, but my vet colleague filled me in on what happened next. A capture team sprinted to the ensnared birds. Working quickly, the biologists plucked the struggling animals one by one from the net, carefully detangling wings, beaks, and claws. Calmly but hurriedly, they placed the animals into plastic crates with perforated lids.

The caught birds would be tagged, recorded, and released, to provide vital information on the species’ health and migration routes. But some individuals would never fly again. Startled by the cannon shot, panicked by the confining net, terrified by the grasping human hands, they had died on the spot.

What I realized as I watched the video was that, although separated by place, time, and species, those shore birds connected to the humans who’d died from heart attacks during the Northridge earthquake. And more than that, the bird deaths connected physiologically with a type of cardiac arrest that kills tens of thousands of people every year, called sudden cardiac death. Exploring the overlap between fear-triggered “heart attacks” in animals and humans could expand the scientific understanding of sudden cardiac death. And it could help safeguard patients from an unseen threat within each of their bodies.

Like Angelenos after the Northridge quake, people all around the world take the shock and drama of earthquakes, tornadoes, and tsunamis literally to heart.
Admissions to hospitals for chest pain, arrhythmias, and even death are as predictable after natural disasters as power outages, Red Cross tents, and Anderson Cooper’s tight T-shirts.

Man-made calamities, too, jerk hearts out of their normal rhythms. In the early days of the Gulf War, in 1991, Iraqi forces began sending Scud missiles into suburban Tel Aviv and other areas of Israel. During that week of bombing, civilians faced the terrifying possibility of being blown up at any moment. Air-raid sirens suddenly and shrilly discharged around the clock.
Statisticians combing through the numbers later uncovered a potent piece of data: rates of cardiac events during that frightening week exceeded expected numbers. More Israelis may have died from the physiology of panic and dread than from actual Scud impacts. As a military strategy, the Scud explosions themselves were nearly useless. The much more effective wartime weapon may have been terror.

After the al Qaeda attacks of 9/11, frightened people across the United States hunkered down in their homes, wondering when the next hit might come. According to data collected from heart-disease patients with recording devices implanted in their hearts,
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the anxiety of those terrifying days carried grave cardiac risks.
The number of life-threatening heart rhythms detected and shocked surged to 200 percent of normal. And this trend was not only seen at the plane crash sites in New York City, Washington, D.C., and Pennsylvania, but in other parts of the country, too. The physical impact of fear touched Americans whose only connection to the disaster came through their eyes and ears—fixed on horrifying TV images and descriptions of planes crashing, buildings collapsing, and human beings leaping from smoke and flames.