The Violinist's Thumb: And Other Lost Tales of Love, War, and Genius, as Written by Our Genetic Code

by Sam Kean

  After suffering an aortic aneurysm on April 13, 1955, Einstein found himself the subject of an international death watch. He finally succumbed to internal hemorrhaging at 1:15 a.m. on April 18. His body arrived shortly thereafter at a local hospital in Princeton, New Jersey, for a routine autopsy. At this point the pathologist on duty, Thomas Harvey, faced a stark choice.

  Any one of us might have been tempted the same way—who wouldn’t want to know what made Einstein Einstein? Einstein himself expressed interest in having his brain studied after he died, and even sat for brain scans. He decided against preserving the best part of himself only because he loathed the thought of people venerating it, the twentieth-century equivalent of a medieval Catholic relic. But as Harvey arranged the scalpels in his autopsy room that night, he knew humankind had just one chance to salvage the gray matter of the greatest scientific thinker in centuries. And while it may be too strong to say stole, by 8 a.m. the next morning—without next-of-kin permission, and against Einstein’s notarized wish for cremation—Harvey had shall we say liberated the physicist’s brain and released the body to the family without it.

  The disappointment started immediately. Einstein’s brain weighed forty-three ounces, at the low end of normal. And before Harvey could measure anything more, word of the relic spread, just as Einstein had feared. During a discussion in school the next day about the loss of Einstein, Harvey’s son, normally a laconic lad, blurted out, “My dad’s got his brain!” A day later, newspapers across the country mentioned Harvey’s plans in their front-page obits. Harvey did eventually convince the remaining Einsteins, who were sure peeved, to grant permission for further study. So after measuring its dimensions with calipers and photographing it for posterity with his 35 mm black-and-white camera, Harvey sawed the brain into 240 taffy-sized hunks and lacquered each one in celloidin. Harvey was soon mailing the blobs in mayo jars to neurologists, confident that the forthcoming scientific insights would justify his peccadillo.

  Fragments of Einstein’s brain, shellacked in hard celloidin after the physicist’s death in 1955. (Getty Images)

  This certainly wasn’t the first autopsy of a famous person to take a lurid turn. Doctors set aside Beethoven’s ear bones in 1827 to study his deafness, but a medical orderly nicked them. The Soviet Union founded an entire institute in part to study Lenin’s brain and determine what makes a revolutionary a revolutionary. (The brains of Stalin and Tchaikovsky also merited preservation.) Similarly, and despite the body being mutilated by mobs, Americans helped themselves to half of Mussolini’s brain after World War II, to determine what made a dictator a dictator. That same year the U.S. military seized four thousand pieces of human flesh from Japanese coroners to study nuclear radiation damage. The spoils included hearts, slabs of liver and brain, even disembodied eyeballs, all of which doctors stored in jars in radiation-proof vaults in Washington, D.C., at a cost to taxpayers of $60,000 per year. (The U.S. repatriated the remains in 1973.)

  Even more grotesquely, William Buckland—in a story that’s possibly apocryphal, but that his contemporaries believed—topped his career as a gourmand when a friend opened a silver snuffbox to show off a desiccated morsel of Louis XIV’s heart. “I have eaten many strange things, but have never eaten the heart of a king,” Buckland mused. Before anyone thought to stop him, Buckland wolfed it down. One of the all-time raciest stolen body parts was the most private part of Cuvier’s patron, Napoleon. A spiteful doctor lopped off L’Empereur’s penis during the autopsy in 1821, and a crooked priest smuggled it to Europe. A century later, in 1927, the unit went on sale in New York, where one observer compared it to a “maltreated strip of buckskin shoelace.” It had shriveled to one and one-half inches, but a urologist in New Jersey bought it anyway for $2,900. And we can’t wrap up this creepy catalog without noting that yet another New Jersey doctor disgracefully whisked away Einstein’s eyeballs in 1955. The doctor later refused Michael Jackson’s offer to pay millions for them—partly because the doc had grown fond of gazing into them. As for the rest of Einstein’s body, take heart (sorry). It was cremated, and no one knows where in Princeton his family scattered the ashes.*

  Perhaps the most disheartening thing about the whole Einstein fiasco is the paltry knowledge scientists gained. Neurologists ended up publishing only three papers on Einstein’s brain in forty years, because most found nothing extraordinary there. Harvey kept soliciting scientists to take another look, but after the initial null results came back, the brain chunks mostly just sat around. Harvey kept each section wrapped in cheesecloth and piled them into two wide-mouthed glass cookie jars full of formaldehyde broth. The jars themselves sat in a cardboard box labeled “Costa Cider” in Harvey’s office, tucked behind a red beer cooler. When Harvey lost his job later and took off for greener pastures in Kansas (where he moved in next door to author and junkie William S. Burroughs), the brain rode shotgun in his car.

  In the past fifteen years, though, Harvey’s persistence has been justified, a little. A few cautious papers have highlighted some atypical aspects of Einstein’s brain, on both microscopic and macroscopic levels. Coupled with loads of research into the genetics of brain growth, these findings may yet provide some insight into what separates a human brain from an animal brain, and what pushes an Einstein a few standard deviations beyond that.

  First, the obsession with overall brain size has given way to obsessing over the size of certain brain parts. Primates have particularly beefy neuron shafts (called axons) compared to other animals and can therefore send information through each neuron more quickly. Even more important is the thickness of the cortex, the outermost brain layer, which promotes thinking and dreaming and other flowery pursuits. Scientists know that certain genes are crucial for growing a thick cortex, partly because it’s so sadly obvious when these genes fail: people end up with primitively tiny brains. One such gene is aspm. Primates have extra stretches of DNA in aspm compared to other mammals, and this DNA codes for extra strings of amino acids that bulk up the cortex. (These strings usually start with the amino acids isoleucine and glutamine. In the alphabetic abbreviations that biochemists use for amino acids, glutamine is usually shortened to Q [G was taken] and isoleucine to plain I—which means we probably got an intelligence boost from a string of DNA referred to, coincidentally, as the “IQ domain.”)

  In tandem with increasing cortex size, aspm helps direct a process that increases the density of neurons in the cortex, another trait that correlates strongly with intelligence. This increase in density happens during our earliest days, when we have loads of stem cells, undeclared cells that can choose any path and become any type of cell. When stem cells begin dividing in the incipient brain, they can either produce more stem cells, or they can settle down, get a job, and become mature neurons. Neurons are good, obviously, but each time a neuron forms, the production of new stem cells (which can make additional neurons in the future) stops. So getting a big brain requires building up the base population of stem cells first. And the key to doing that is making sure that stem cells divide evenly: if the cellular guts get divided equally between both daughter cells, each one becomes another stem cell. If the split is unequal, neurons form prematurely.

  To facilitate an even split, aspm guides the “spindles” that attach to chromosomes and pull them apart in a nice, clean, symmetrical way. If aspm fails, the split is uneven, neurons form too soon, and the child is cheated of a normal brain. To be sure, aspm isn’t the gene responsible for big brains: cell division requires intricate coordination among many genes, with master regulator genes conducting everything from above, too. But aspm can certainly pack the cortex with neurons* when it’s firing right—or sabotage neuron production if it misfires.

  Einstein’s cortex had a few unusual features. One study found that, compared to normal elderly men, his had the same number of neurons and the same average neuron size. However, part of Einstein’s cortex, the prefrontal cortex, was thinner, which gave him a greater density of neurons. Closely p
acked neurons may help the brain process information more quickly—a tantalizing find considering that the prefrontal cortex orchestrates thoughts throughout the brain and helps solve multistep problems.

  Further studies examined certain folds and grooves in Einstein’s cortex. As with brain size, it’s a myth that simply having more folds automatically makes a brain more potent. But folding does generally indicate higher functioning. Smaller and dumber monkeys, for instance, have fewer corrugations in their cortexes. As, interestingly, do newborn humans. Which means that as we mature from infants to young adults, and as genes that wrinkle our brains start kicking on, every one of us relives millions of years of human evolution. Scientists also know that a lack of brain folds is devastating. The genetic disorder “smooth brain” leaves babies severely retarded, if they even survive to term. Instead of being succulently furrowed, a smooth brain looks eerily polished, and cross sections of it, instead of showing scrunched-up brain fabric, look like slabs of liver.

  Einstein had unusual wrinkles and ridges in the cortex of his parietal lobe, a region that aids in mathematical reasoning and image processing. This comports with Einstein’s famous declaration that he thought about physics mostly through pictures: he formulated relativity theory, for instance, in part by imagining what would happen if he rode around bareback on light rays. The parietal lobe also integrates sound, sight, and other sensory input into the rest of the brain’s thinking. Einstein once declared that abstract concepts achieved meaning in his mind “only through their connection with sense-experiences,” and his family remembers him practicing his violin whenever he got stuck with a physics problem. An hour later, he’d often declare, “I’ve got it!” and return to work. Auditory input seemed to jog his thinking. Perhaps most telling, the parietal wrinkles and ridges in Einstein’s lobes were steroid thick, 15 percent bigger than normal. And whereas most of us mental weaklings have skinny right parietal lobes and even skinnier left parietal lobes, Einstein’s were equally buff.

  Finally, Einstein appeared to be missing part of his middle brain, the parietal operculum; at the least, it didn’t develop fully. This part of the brain helps produce language, and its lack might explain why Einstein didn’t speak until age two and why until age seven he had to rehearse every sentence he spoke aloud under his breath. But there might have been compensations. This region normally contains a fissure, or small gap, and our thoughts get routed the long way around. The lack of a gap might have meant that Einstein could process certain information more speedily, by bringing two separate parts of his brain into unusually direct contact.

  All of which is exciting. But is it exciting bunkum? Einstein feared his brain becoming a relic, but have we done something equally silly and reverted to phrenology? Einstein’s brain has deteriorated into chopped liver by now (it’s even the same color), which forces scientists to work mostly from old photographs, a less precise method. And not to put too fine a point on it, but Thomas Harvey coauthored half of the various studies on the “extraordinary” features of Einstein’s brain, and he certainly had an interest in science learning something from the organ he purloined. Plus, as with Cuvier’s swollen brain, maybe Einstein’s features are idiosyncratic and had nothing to do with genius; it’s hard to tell with a sample size of one. Even trickier, we can’t sort out if unusual neurofeatures (like thickened folds) caused Einstein’s genius, or if his genius allowed him to “exercise” and build up those parts of his brain. Some skeptical neuroscientists note that playing the violin from an early age (and Einstein started lessons at six) can cause the same brain alterations observed in Einstein.

  And if you had hopes of dipping into Harvey’s brain slices and extracting DNA, forget it. In 1998, Harvey, his jars, and a writer took a road trip in a rented Buick to visit Einstein’s granddaughter in California. Although weirded out by Grandpa’s brain, Evelyn Einstein accepted the visitors for one reason. She was poor, reputedly dim, and had trouble holding down a job—not exactly an Einstein. In fact Evelyn was always told she’d been adopted by Einstein’s son, Hans. But Evelyn could do a little math, and when she started hearing rumors that Einstein had canoodled with various lady friends after his wife died, Evelyn realized she might be Einstein’s bastard child. The “adoption” might have been a ruse. Evelyn wanted to do a genetic paternity test to settle things, but it turned out that the embalming process had denatured the brain’s DNA. Other sources of his DNA might still be floating around—strands in mustache brushes, spittle on pipes, sweated-on violins—but for now we know more about the genes of Neanderthals who died fifty thousand years ago than the genes of a man who died in 1955.

  But if Einstein’s genius remains enigmatic, scientists have sussed out a lot about the everyday genius of humans compared to that of other primates. Some of the DNA that enhances human intelligence does so in roundabout ways. A two-letter frameshift mutation in humans a few million years ago deactivated a gene that bulked up our jaw muscles. This probably allowed us to get by with thinner, more gracile skulls, which in turn freed up precious cc’s of skull for the brain to expand into. Another surprise was that apoE, the meat-eating gene, helped a lot, by helping the brain manage cholesterol. To function properly, the brain needs to sheathe its axons in myelin, which acts like rubber insulation on wires and prevents signals from short-circuiting or misfiring. Cholesterol is a major component of myelin, and certain forms of apoE do a better job distributing brain cholesterol where it’s needed. ApoE also seems to promote brain plasticity.

  Some genes lead to direct structural changes in the brain. The lrrtm1 gene helps determine which exact patches of neurons control speech, emotion, and other mental qualities, which in turn helps the human brain establish its unusual asymmetry and left-right specialization. Some versions of lrrtm1 even reverse parts of the left and right brain—and increase your chances of being left-handed to boot, the only known genetic association for that trait. Other DNA alters the brain’s architecture in almost comical ways: certain inheritable mutations can cross-wire the sneeze reflex with other ancient reflexes, leaving people achooing uncontrollably—up to forty-three times in a row in one case—after looking into the sun, eating too much, or having an orgasm. Scientists have also recently detected 3,181 base pairs of brain “junk DNA” in chimpanzees that got deleted in humans. This region helps stop out-of-control neuron growth, which can lead to big brains, obviously, but also brain tumors. Humans gambled in deleting this DNA, but the risk apparently paid off, and our brains ballooned. The discovery shows that it’s not always what we gained with DNA, but sometimes what we lost, that makes us human. (Or at least makes us nonmonkey: Neanderthals didn’t have this DNA either.)

  How and how quickly DNA spreads through a population can reveal which genes contribute to intelligence. In 2005 scientists reported that two mutated brain genes seem to have swept torrentially through our ancestors, microcephalin doing so 37,000 years ago, aspm just 6,000 years ago. Scientists clocked this spread by using techniques first developed in the Columbia fruit fly room. Thomas Hunt Morgan discovered that certain versions of genes get inherited in clusters, simply because they reside near each other on chromosomes. As an example, the A, B, and D versions of three genes might normally appear together; or (lowercase) a, b, and d might appear together. Over time, though, chromosomal crossing-over and recrossing will mix the groups, giving combos like a, B, and D; or A, b, and D. After enough generations, every combination will appear.

  But say that B mutates to B0 at some point, and that B0 gives people a hell of a brain tune-up. At that point it could sweep through a population, since B0 people can outthink everyone else. (That spread will be especially easy if the population drops very low, since the novel gene has less competition. Bottlenecks aren’t always bad!) And notice that as B0 sweeps through a population, the versions of A/a and D/d that happen to be sitting next to B0 in the first person with the mutation will also sweep through the population, simply because crossing over won’t have time to break the trio apart.
In other words, these genes will ride along with the advantageous gene, a process called genetic hitchhiking. Scientists see especially strong signs of hitchhiking with aspm and microcephalin, which means they spread especially quickly and probably provided an especially strong advantage.

  Beyond any specific brain-boosting genes, DNA regulation might explain a lot about our gray matter. One flagrant difference between human and monkey DNA is that our brain cells splice DNA far more often, chopping and editing the same string of letters for many different effects. Neurons mix it up so much, in fact, that some scientists think they’ve upended one central dogma of biology—that all cells in your body have the same DNA. For whatever reason, our neurons allow much more free play among mobile DNA bits, the “jumping genes” that wedge themselves randomly into chromosomes. This changes the DNA patterns in neurons, which can change how they work. As one neuroscientist observes, “Given that changing the firing patterns of single neurons can have marked effects on behavior… it is likely that some [mobile DNA], in some cells, in some humans, will have significant, if not profound, effects on the final structure and function of the human brain.” Once again viruslike particles may prove important to our humanity.

  If you’re skeptical that we can explain something as ineffable as genius by studying something as reductive as DNA, a lot of scientists are right there with you. And every so often a case like that of savant Kim Peek pops up—a case that so mocks our understanding of how DNA and brain architecture influence intelligence that even the most enthusiastic neuroscientist seeks the consolation of a stiff bourbon and starts to think seriously about going into administration.

  Peek, a Salt Lake City native, was actually a megasavant, a souped-up version of what’s impolitely but accurately known as an idiot savant. Instead of being limited to poignantly empty skills like drawing perfect circles or listing all the Holy Roman Emperors in order, Peek had encyclopedic knowledge of geography, opera, American history, Shakespeare, classical music, the Bible—basically all of Western Civ. Even more intimidating, Peek had Google-like recall of any sentence in the nine thousand books he’d memorized, starting at eighteen months old. (When finished with a book, he returned it to his shelf with the spine upside down to indicate he’d knocked it off.) If it makes you less insecure, Peek did know loads of useless crap, too, like the complete U.S. zip code system. He also memorized Rain Man, a movie he inspired, and knew Mormon theology in lobotomizing detail.*