by Sam Kean
Given this disarray, it’s easy to understand the excitement, even hype, that attended the recent discovery of a purported master gene for language. In 1990 linguists inferred the gene’s existence after studying three generations of a London family known only (for privacy) as the KEs. In a simple pattern of single-gene dominance, half the KEs suffer from a strange suite of language malfunctions. They have trouble coordinating their lips, jaws, and tongues, and stumble over most words, becoming especially incomprehensible on the phone. They also struggle when asked to ape a sequence of simple facial expressions, like opening their mouths, sticking out their tongues, and uttering an uuuuaaaahh sound. But some scientists argue that the KEs’ problems extend beyond motor skills to grammar. Most of them know the plural of book is books, but seemingly because they’ve memorized that fact. Give them made-up words like zoop or wug, and they cannot figure out the plural; they see no connection between book/books and zoop/zoops, even after years of language therapy. They also fail fill-in-the-blank tests about the past tense, using words like “bringed.” The IQs of affected KEs sink pretty low—86 on average, versus 104 for nonaffected KEs. But the language hiccups probably aren’t a simple cognitive deficit: a few afflicted KEs have nonverbal IQ scores above average, and they can spot logical fallacies in arguments when tested. Plus, some scientists found that they understand reflexives just fine (e.g., “he washed him” versus “he washed himself”), as well as passive versus active voice and possessives.
It baffled scientists that one gene could cause such disparate symptoms, so in 1996 they set out to find and decode it. They narrowed its locus down to fifty genes on chromosome seven and were tediously working through each one when they caught a break. Another victim turned up, CS, from an unrelated family. The boy presented with the same mental and mandibular problems, and doctors spotted a translocation in his genes: a Philadelphia-like swap between the arms of two chromosomes, which interrupted the foxp2 gene on chromosome seven.
Like vitamin A, the protein produced by foxp2 clamps onto other genes and switches them on. Also like vitamin A, foxp2 has a long reach, interacting with hundreds of genes and steering fetal development in the jaw, gut, lungs, heart, and especially the brain. All mammals have foxp2, and despite billions of years of collective evolution, all versions look pretty much the same; humans have accumulated just three amino acid differences compared to mice. (This gene looks strikingly similar in songbirds as well, and is especially active when they’re learning new songs.) Intriguingly, humans picked up two of our amino-acid changes after splitting from chimps, and these changes allow foxp2 to interact with many new genes. Even more intriguingly, when scientists created mutant mice with the human foxp2, the mice had different neuron architecture in a brain region that (in us) processes language, and they conversed with fellow mice in lower-pitched, baritone squeaks.
Conversely, in the affected KEs’ brains, the regions that help produce language are stunted and have low densities of neurons. Scientists have traced these deficits back to a single A-for-G mutation. This substitution altered just one of foxp2’s 715 amino acids, but it’s enough to prevent the protein from binding to DNA. Unfortunately, this mutation occurs in a different part of the gene than the human-chimp mutations, so it can’t explain much about the evolution and original acquisition of language. And regardless, scientists still face a cause-and-effect tangle with the KEs: did the neurological deficits cause their facial clumsiness, or did their facial clumsiness lead to brain atrophy by discouraging them from practicing language? Foxp2 can’t be the only language gene anyway, since even the most afflicted in the KE clan aren’t devoid of language; they’re orders of magnitude more eloquent than any simian. (And sometimes they seemed more creative than the scientists testing them. When presented with the puzzler “Every day he walks eight miles. Yesterday he_____,” instead of answering, “walked eight miles,” one afflicted KE muttered, “had a rest.”) Overall, then, while foxp2 reveals something about the genetic basis of language and symbolic thought, the gene has proved frustratingly inarticulate so far.
Even the one thing scientists had all agreed on with foxp2—its unique form in humans—proved wrong. Homo sapiens split from other Homo species hundreds of thousands of years ago, but paleogeneticists recently discovered the human version of foxp2 in Neanderthals. This might mean nothing. But it might mean that Neanderthals also had the fine motor skills for language, or the cognitive wherewithal. Perhaps both: finer motor skills might have allowed them to use language more, and when they used it more, maybe they found they had more to say.
All that’s certain is that the foxp2 discovery makes another debate about Neanderthals, over Neanderthal art, more urgent. In caves occupied by Neanderthals, archaeologists have discovered flutes made from bear femurs, as well as oyster shells stained red and yellow and perforated for stringing on necklaces. But good luck figuring out what these trinkets meant to Neanderthals. Again, perhaps Neanderthals just aped humans and attached no symbolic meaning to their toys. Or perhaps humans, who often colonized Neanderthal sites after Neanderthals died, simply tossed their worn-out flutes and shells in with Neanderthal rubbish, scrambling the chronology. The truth is, no one has any idea how articulate or artsy-fartsy Neanderthals were.
So until scientists catch another break—find another KE family with different DNA flaws, or root out more unexpected genes in Neanderthals—the genetic origins of language and symbolic art will remain murky. In the meantime we’ll have to content ourselves with tracing how DNA can augment, or make a mess of, the work of modern artists.
No different than with athletes, tiny bits of DNA can determine whether budding musicians fulfill their talents and ambitions. A few studies have found that one key musical trait, perfect pitch, gets inherited with the same dominant pattern as the KE language deficit, since people with perfect pitch passed it to half their children. Other studies found smaller and subtler genetic contributions for perfect pitch instead, and found that this DNA must act in concert with environmental cues (like music lessons) to bestow the gift. Beyond the ear, physical attributes can enhance or doom a musician as well. Sergei Rachmaninoff’s gigantic hands—probably the result of Marfan syndrome, a genetic disorder—could span twelve inches, an octave and a half on the piano, which allowed him to compose and play music that would tear the ligaments of lesser-endowed pianists. On the other mitt, Robert Schumann’s career as a concert pianist collapsed because of focal dystonia—a loss of muscle that caused his right middle finger to curl or jerk involuntarily. Many people with this condition have a genetic susceptibility, and Schumann compensated by writing at least one piece that avoided that finger entirely. But he never let up on his grinding practice schedule, and a jerry-built mechanical rack he designed to stretch the finger may have exacerbated his symptoms.
Still, in the long, gloried history of ailing and invalid musicians, no DNA proved a more ambivalent friend and ambiguous foe than the DNA of nineteenth-century musician Niccolò Paganini, the violin virtuoso’s violin virtuoso. The opera composer (and noted epicurean) Gioacchino Rossini didn’t like acknowledging that he ever wept, but one of the three times he owned up to crying* was when he heard Paganini perform. Rossini bawled then, and he wasn’t the only one bewitched by the ungainly Italian. Paganini wore his dark hair long and performed his concerts in black frock coats with black trousers, leaving his pale, sweaty face hovering spectrally onstage. He also cocked his hips at bizarre angles while performing, and sometimes crossed his elbows at impossible angles in a rush of furious bowing. Some connoisseurs found his concerts histrionic, and accused him of fraying his violin strings before shows so they’d snap dramatically midperformance. But no one ever denied his showmanship: Pope Leo XII named him a Knight of the Golden Spur, and royal mints struck coins with his likeness. Many critics hailed him as the greatest violinist ever, and he has proved almost a singular exception to the rule in classical music that only composers gain immortality.
Paganini rarely i
f ever played the old masters during his concerts, preferring his own compositions, which highlighted his finger-blurring dexterity. (Ever a crowd-pleaser, he also included lowbrow passages where he mimicked donkeys and roosters on his violin.) Since his teenage years, in the 1790s, Paganini had labored over his music; but he also understood human psychology and so encouraged various legends about the supernatural origins of his gifts. Word got around that an angel had appeared at Paganini’s birth and pronounced that no man would ever play the violin so sweetly. Six years later, divine favor seemingly resurrected him from a Lazarus-like doom. After he fell into a cataleptic coma, his parents gave him up for dead—they wrapped him in a burial shroud and everything—when, suddenly, something made him twitch beneath the cloth, saving him by a whisker from premature burial. Despite these miracles, people more often attributed Paganini’s talents to necromancy, insisting he’d signed a pact with Satan and exchanged his immortal soul for shameless musical talent. (Paganini fanned these rumors by holding concerts in cemeteries at twilight and giving his compositions names like “Devil’s Laughter” and “Witches’ Dance,” as if he had firsthand experience.) Others argued that he’d acquired his skills in dungeons, where he’d supposedly been incarcerated for eight years for stabbing a friend and had nothing better to do than practice violin. More sober types scoffed at these stories of witchcraft and iniquity. They patiently explained that Paganini had hired a crooked surgeon to snip the motion-limiting ligaments in his hands. Simple as that.
However ludicrous, that last explanation hits closest to the mark. Because beyond Paganini’s passion, charisma, and capacity for hard work, he did have unusually supple hands. He could unfurl and stretch his fingers impossibly far, his skin seemingly about to rip apart. His finger joints themselves were also freakishly flexible: he could wrench his thumb across the back of his hand to touch his pinky (try this), and he could wriggle his midfinger joints laterally, like tiny metronomes. As a result, Paganini could dash off intricate riffs and arpeggios that other violinists didn’t dare, hitting many more high and low notes in swift succession—up to a thousand notes per minute, some claim. He could double- or triple-stop (play multiple notes at once) with ease, and he perfected unusual techniques, like left-handed pizzicato, a plucking technique, that took advantage of his plasticity. Normally the right hand (the bow hand) does pizzicato, forcing the violinist to chose between bowing or plucking during each passage. With left-handed pizzicato, Paganini didn’t have to choose. His nimble fingers could bow one note and pluck the next, as if two violins were playing at once.
Beyond being flexible, his fingers were deceptively strong, especially the thumbs. Paganini’s great rival Karol Lipiski watched him in concert one evening in Padua, then retired to Paganini’s room for a late dinner and some chitchat with Paganini and friends. At the table, Lipiski found a disappointingly scanty spread for someone of Paganini’s stature, mostly eggs and bread. (Paganini could not even be bothered to eat that and contented himself with fruit.) But after some wine and some jam sessions on the guitar and trumpet, Lipiski found himself staring at Paganini’s hands. He even embraced the master’s “small bony fingers,” turning them over. “How is it possible,” Lipiski marveled, “for these thin small fingers to achieve things acquiring extraordinary strength?” Paganini answered, “Oh, my fingers are stronger than you think.” At this he picked up a saucer of thick crystal and suspended it over the table, fingers below, thumb on top. Friends gathered around to laugh—they’d seen the trick before. While Lipiski stared, bemused, Paganini flexed his thumb almost imperceptibly and—crack!—snapped the saucer into two shards. Not to be outdone, Lipiski grabbed a plate and tried to shatter it with his own thumb, but couldn’t come close. Nor could Paganini’s friends. “The saucers remained just as they were before,” Lipiski recalled, “while Paganini laughed maliciously” at their futility. It seemed almost unfair, this combination of power and agility, and those who knew Paganini best, like his personal physician, Francesco Bennati, explicitly credited his success to his wonderfully tarantular hands.
Of course, as with Einstein’s violin training, sorting out cause and effect gets tricky here. Paganini had been a frail child, sickly and prone to coughs and respiratory infections, but he nevertheless began intensive violin lessons at age seven. So perhaps he’d simply loosened up his fingers through practice. However, other symptoms indicate that Paganini had a genetic condition called Ehlers-Danlos syndrome. People with EDS cannot make much collagen, a fiber that gives ligaments and tendons some rigidity and toughens up bone. The benefit of having less collagen is circus flexibility. Like many people with EDS, Paganini could bend all his joints alarmingly far backward (hence his contortions onstage). But collagen does more than prevent most of us from touching our toes: a chronic lack can lead to muscle fatigue, weak lungs, irritable bowels, poor eyesight, and translucent, easily damaged skin. Modern studies have shown that musicians have high rates of EDS and other hypermobility syndromes (as do dancers), and while this gives them a big advantage at first, they tend to develop debilitating knee and back pain later, especially if, like Paganini, they stand while performing.
Widely considered the greatest violinist ever, Niccolò Paganini owed much of his gift to a genetic disorder that made his hands freakishly flexible. Notice the grotesquely splayed thumb. (Courtesy of the Library of Congress)
Constant touring wore Paganini down after 1810, and although he’d just entered his thirties, his body began giving out on him. Despite his growing fortune, a landlord in Naples evicted him in 1818, convinced that anyone as skinny and sickly as Paganini must have tuberculosis. He began canceling engagements, unable to perform his art, and by the 1820s he had to sit out whole years of tours to recuperate. Paganini couldn’t have known that EDS underlay his general misery; no doctor described the syndrome formally until 1901. But ignorance only heightened his desperation, and he sought out quack apothecaries and doctors. After diagnosing syphilis and tuberculosis and who knows what else, the docs prescribed him harsh, mercury-based purgative pills, which ravaged his already fragile insides. His persistent cough worsened, and eventually his voice died completely, silencing him. He had to wear blue-tinted shades to shield his sore retinas, and at one point his left testicle swelled, he sobbed, to the size of “a little pumpkin.” Because of chronic mercury damage to his gums, he had to bind his wobbly teeth with twine to eat.
Sorting out why Paganini finally died, in 1840, is like asking what knocked off the Roman Empire—take your pick. Abusing mercury drugs probably did the most intense damage, but Dr. Bennati, who knew Paganini before his pill-popping days and was the only doctor Paganini never dismissed in a rage for fleecing him, traced the real problem further back. After examining Paganini, Bennati dismissed the diagnoses of tuberculosis and syphilis as spurious. He noted instead, “Nearly all [Paganini’s] later ailments can be traced to the extreme sensitivity of his skin.” Bennati felt that Paganini’s papery EDS skin left him vulnerable to chills, sweats, and fevers and aggravated his frail constitution. Bennati also described the membranes of Paganini’s throat, lungs, and colon—all areas affected by EDS—as highly susceptible to irritation. We have to be cautious about reading too much into a diagnosis from the 1830s, but Bennati clearly traced Paganini’s vulnerability to something inborn. And in the light of modern knowledge, it seems likely Paganini’s physical talents and physical tortures had the same genetic source.
Paganini’s afterlife was no less doomed. On his deathbed in Nice, he refused communion and confession, believing they would hasten his demise. He died anyway, and because he’d skipped the sacraments, during Eastertide no less, the Catholic Church refused him proper burial. (As a result his family had to schlep his body around ignominiously for months. It first lay for sixty days in a friend’s bed, before health officials stepped in. His corpse was next transferred to an abandoned leper’s hospital, where a crooked caretaker charged tourists money to gawk at it, then to a cement tub in an olive oil proc
essing plant. Family finally smuggled his bones back into Genoa in secret and interred him in a private garden, where he lay for thirty-six years, until the church finally forgave him and permitted burial.*)
Paganini’s ex post facto excommunication fueled speculation that church elders had it in for Paganini. He did cut the church out of his ample will, and the Faustian stories of selling his soul couldn’t have helped. But the church had plenty of nonfictional reasons to spurn the violinist. Paganini gambled flagrantly, even betting his violin once before a show. (He lost.) Worse, he caroused with maidens, charwomen, and blue-blooded dames all across Europe, betraying a truly capacious appetite for fornication. In his most ballsy conquests, he allegedly seduced two of Napoleon’s sisters, then discarded them. “I am ugly as sin, yet all I have to do,” he once bragged, “is play my violin and women fall at my feet.” The church was not impressed.
Nevertheless Paganini’s hypersexual activity brings up a salient point about genetics and fine arts. Given their ubiquity, DNA probably encodes some sort of artistic impulses—but why? Why should we respond so strongly to the arts? One theory is that our brains crave social interaction and affirmation, and shared stories, songs, and images help people bond. Art, in this view, fosters societal cohesion. Then again, our cravings for art could be an accident. Our brain circuits evolved to favor certain sights, sounds, and emotions in our ancient environment, and the fine arts might simply exploit those circuits and deliver sights, sounds, and emotions in concentrated doses. In this view, art and music manipulate our brains in roughly the same way that chocolate manipulates our tongues.
Many scientists, though, explain our lust for art through a process called sexual selection, a cousin of natural selection. In sexual selection, the creatures that mate the most often and pass on their DNA don’t necessarily do so because they have survival advantages; they’re simply prettier, sexier. Sexy in most creatures means brawny, well-proportioned, or lavishly decorated—think bucks’ antlers and peacocks’ tails. But singing or dancing can also draw attention to someone’s robust physical health. And painting and witty poetry highlight someone’s mental prowess and agility—talents crucial for navigating the alliances and hierarchies of primate society. Art, in other words, betrays a sexy mental fitness.