De Vries was not alone in rediscovering Mendel’s notion of independent, indivisible hereditary instructions. That same year de Vries published his monumental study of plant variants, Carl Correns, a botanist in Tübingen, published a study on pea and maize hybrids that precisely recapitulated Mendel’s results. Correns had, ironically, been Nägeli’s student in Munich. But Nägeli—who considered Mendel an amateur crank—had neglected to tell Correns about the voluminous correspondence on pea hybrids that he had once received from “a certain Mendel.”
In his experimental gardens in Munich and Tübingen, about four hundred miles from the abbey, Correns thus laboriously bred tall plants with short plants and made hybrid-hybrid crosses—with no knowledge that he was just methodically repeating Mendel’s prior work. When Correns completed his experiments and was ready to assemble his paper for publication, he returned to the library to find references to his scientific predecessors. He thus stumbled on Mendel’s earlier paper buried in the Brno journal.
And in Vienna—the very place where Mendel had failed his botany exam in 1856—another young botanist, Erich von Tschermak-Seysenegg, also rediscovered Mendel’s laws. Von Tschermak had been a graduate student at Halle and in Ghent, where, working on pea hybrids, he had also observed hereditary traits moving independently and discretely, like particles, across generations of hybrids. The youngest of the three scientists, von Tschermak had received news of two other parallel studies that fully corroborated his results, then waded back into the scientific literature to discover Mendel. He too had felt that ascending chill of déjà vu as he read the opening salvos of Mendel’s paper. “I too still believed that I had found something new,” he would later write, with more than a tinge of envy and despondency.
Being rediscovered once is proof of a scientist’s prescience. Being rediscovered thrice is an insult. That three papers in the short span of three months in 1900 independently converged on Mendel’s work was a demonstration of the sustained myopia of biologists, who had ignored his work for nearly forty years. Even de Vries, who had so conspicuously forgotten to mention Mendel in his first study, was forced to acknowledge Mendel’s contribution. In the spring of 1900, soon after de Vries had published his paper, Carl Correns suggested that de Vries had appropriated Mendel’s work deliberately—committing something akin to scientific plagiarism (“by a strange coincidence,” Correns wrote mincingly, de Vries had even incorporated “Mendel’s vocabulary” in his paper). Eventually, de Vries caved in. In a subsequent version of his analysis of plant hybrids, he mentioned Mendel glowingly and acknowledged that he had merely “extended” Mendel’s earlier work.
But de Vries also took his experiments further than Mendel. He may have been preempted in the discovery of heritable units—but as de Vries delved more deeply into heredity and evolution, he was struck by a thought that must also have perplexed Mendel: How did variants arise in the first place? What force made tall versus short peas, or purple flowers and white ones?
The answer, again, was in the garden. Wandering through the countryside in one of his collecting expeditions, de Vries stumbled on an enormous, invasive patch of primroses growing in the wild—a species named (ironically, as he would soon discover) after Lamarck: Oenothera lamarckiana. De Vries harvested and planted fifty thousand seeds from the patch. Over the next years, as the vigorous Oenothera multiplied, de Vries found that eight hundred new variants had spontaneously arisen—plants with gigantic leaves, with hairy stems, or with odd-shaped flowers. Nature had spontaneously thrown up rare freaks—precisely the mechanism that Darwin had proposed as evolution’s first step. Darwin had called these variants “sports,” implying a streak of capricious whimsy in the natural world. De Vries chose a more serious-sounding word. He called them mutants—from the Latin word for “change.”I
De Vries quickly realized the importance of his observation: these mutants had to be the missing pieces in Darwin’s puzzle. Indeed, if you coupled the genesis of spontaneous mutants—the giant-leaved Oenothera, say—with natural selection, then Darwin’s relentless engine was automatically set in motion. Mutations created variants in nature: long-necked antelopes, short-beaked finches, and giant-leaved plants arose spontaneously in the vast tribes of normal specimens (contrary to Lamarck, these mutants were not generated purposefully, but by random chance). These variant qualities were hereditary—carried as discrete instructions in sperm and eggs. As animals struggled to survive, the best-adapted variants—the fittest mutations—were serially selected. Their children inherited these mutations and thus generated new species, thereby driving evolution. Natural selection was not operating on organisms but on their units of heredity. A chicken, de Vries realized, was merely an egg’s way of making a better egg.
It had taken two excruciatingly slow decades for Hugo de Vries to become a convert to Mendel’s ideas of heredity. For William Bateson, the English biologist, the conversion took about an hour—the time spent on a speeding train between Cambridge and London in May 1900.II That evening, Bateson was traveling to the city to deliver a lecture on heredity at the Royal Horticultural Society. As the train trundled through the darkening fens, Bateson read a copy of de Vries’s paper—and was instantly transmuted by Mendel’s idea of discrete units of heredity. This was to be Bateson’s fateful journey: by the time he reached the society’s office on Vincent Square, his mind was spinning. “We are in the presence of a new principle of the highest importance,” he told the lecture hall. “To what further conclusions it may lead us cannot yet be foretold.” In August that year, Bateson wrote to his friend Francis Galton: “I am writing to ask you to look up the paper of Mendl [sic] [which] seems to me one of the most remarkable investigations yet made on heredity and it is extraordinary that it should have got forgotten.”
Bateson made it his personal mission to ensure that Mendel, once forgotten, would never again be ignored. First, he independently confirmed Mendel’s work on plant hybrids in Cambridge. Bateson met de Vries in London and was impressed by his experimental rigor and his scientific vitality (although not by his continental habits. De Vries refused to bathe before dinner, Bateson complained: “His linen is foul. I daresay he puts on a new shirt once a week”). Doubly convinced by Mendel’s experimental data, and by his own evidence, Bateson set about proselytizing. Nicknamed “Mendel’s bulldog”—an animal that he resembled both in countenance and temperament—Bateson traveled to Germany, France, Italy, and the United States, giving talks on heredity that emphasized Mendel’s discovery. Bateson knew that he was witnessing, or, rather, midwifing, the birth of a profound revolution in biology. Deciphering the laws of heredity, he wrote, would transform “man’s outlook on the world, and his power over nature” more “than any other advance in natural knowledge that can be foreseen.”
In Cambridge, a group of young students gathered around Bateson to study the new science of heredity. Bateson knew that he needed a name for the discipline that was being born around him. Pangenetics seemed an obvious choice—extending de Vries’s use of the word pangene to denote the units of heredity. But pangenetics was overloaded with all the baggage of Darwin’s mistaken theory of hereditary instructions. “No single word in common use quite gives this meaning [yet] such a word is badly wanted,” Bateson wrote.
In 1905, still struggling for an alternative, Bateson coined a word of his own. Genetics, he called it: the study of heredity and variation—the word ultimately derived from the Greek genno, “to give birth.”
Bateson was acutely aware of the potential social and political impact of the newborn science. “What will happen when . . . enlightenment actually comes to pass and the facts of heredity are . . . commonly known?” he wrote, with striking prescience, in 1905. “One thing is certain: mankind will begin to interfere; perhaps not in England, but in some country more ready to break with the past and eager for ‘national efficiency.’ . . . Ignorance of the remoter consequences of interference has never long postponed such experiments.”
More than a
ny scientist before him, Bateson also grasped the idea that the discontinuous nature of genetic information carried vast implications for the future of human genetics. If genes were, indeed, independent particles of information, then it should be possible to select, purify, and manipulate these particles independently from one another. Genes for “desirable” attributes might be selected or augmented, while undesirable genes might be eliminated from the gene pool. In principle, a scientist should be able to change the “composition of individuals,” and of nations, and leave a permanent mark on human identity.
“When power is discovered, man always turns to it,” Bateson wrote darkly. “The science of heredity will soon provide power on a stupendous scale; and in some country, at some time not, perhaps, far distant, that power will be applied to control the composition of a nation. Whether the institution of such control will ultimately be good or bad for that nation, or for humanity at large, is a separate question.” He had preempted the century of the gene.
* * *
I. De Vries’s “mutants” might actually have been the result of backcrosses, rather than spontaneously arising variants.
II. The story of Bateson’s “conversion” to Mendel’s theory during a train ride has been disputed by some historians. The story appears frequently in his biography, but may have been embellished by some of Bateson’s students for dramatic flair.
Eugenics
Improved environment and education may better the generation already born. Improved blood will better every generation to come.
—Herbert Walter, Genetics
Most Eugenists are Euphemists. I mean merely that short words startle them, while long words soothe them. And they are utterly incapable of translating the one into the other. . . . Say to them “The . . . citizen should . . . make sure that the burden of longevity in the previous generations does not become disproportionate and intolerable, especially to the females”; say this to them and they sway slightly to and fro. . . . Say to them “Murder your mother,” and they sit up quite suddenly.
—G. K. Chesterton, Eugenics and Other Evils
In 1883, one year after Charles Darwin’s death, Darwin’s cousin Francis Galton published a provocative book—Inquiries into Human Faculty and Its Development—in which he laid out a strategic plan for the improvement of the human race. Galton’s idea was simple: he would mimic the mechanism of natural selection. If nature could achieve such remarkable effects on animal populations through survival and selection, Galton imagined accelerating the process of refining humans via human intervention. The selective breeding of the strongest, smartest, “fittest” humans—unnatural selection—Galton imagined, could achieve over just a few decades what nature had been attempting for eons.
Galton needed a word for this strategy. “We greatly want a brief word to express the science of improving stock,” he wrote, “to give the more suitable races or strains of blood a better chance of prevailing speedily over the less suitable.” For Galton, the word eugenics was an opportune fit—“at least a neater word . . . than viriculture, which I once ventured to use.” It combined the Greek prefix eu—“good”—with genesis: “good in stock, hereditarily endowed with noble qualities.” Galton—who never blanched from the recognition of his own genius—was deeply satisfied with his coinage: “Believing, as I do, that human eugenics will become recognised before long as a study of the highest practical importance, it seems to me that no time ought to be lost in . . . compiling personal and family histories.”
Galton was born in the winter of 1822—the same year as Gregor Mendel—and thirteen years after his cousin Charles Darwin. Slung between the two giants of modern biology, he was inevitably haunted by an acute sense of scientific inadequacy. For Galton, the inadequacy may have felt particularly galling because he too had been meant to become a giant. His father was a wealthy banker in Birmingham; his mother was the daughter of Erasmus Darwin, the polymath poet and doctor, who was also Charles Darwin’s grandfather. A child prodigy, Galton learned to read at two, was fluent in Greek and Latin by five, and solved quadratic equations by eight. Like Darwin, he collected beetles, but he lacked his cousin’s plodding, taxonomic mind and soon gave up his collection for more ambitious pursuits. He tried studying medicine, but then switched to mathematics at Cambridge. In 1843, he attempted an honors exam in mathematics, but suffered a nervous breakdown and returned home to recuperate.
In the summer of 1844, while Charles Darwin was writing his first essay on evolution, Galton left England to travel to Egypt and Sudan—the first of many trips he would take to Africa. But while Darwin’s encounters with the “natives” of South America in the 1830s had strengthened his belief in the common ancestry of humans, Galton only saw difference: “I saw enough of savage races to give me material to think about all the rest of my life.”
In 1859, Galton read Darwin’s Origin of Species. Rather, he “devoured” the book: it struck him like a jolt of electricity, both paralyzing and galvanizing him. He simmered with envy, pride, and admiration. He had been “initiated into an entirely new province of knowledge,” he wrote glowingly to Darwin.
The “province of knowledge” that Galton felt particularly inclined to explore was heredity. Like Fleeming Jenkin, Galton quickly realized that his cousin had got the principle right, but not the mechanism: the nature of inheritance was crucial to the understanding of Darwin’s theory. Heredity was the yin to evolution’s yang. The two theories had to be congenitally linked—each bolstering and completing the other. If “cousin Darwin” had solved half the puzzle, then “cousin Galton” was destined to crack the other.
In the mid-1860s, Galton began to study heredity. Darwin’s “gemmule” theory—that hereditary instructions were thrown adrift by all cells and then floated in the blood, like a million messages in bottles—suggested that blood transfusions might transmit gemmules and thereby alter heredity. Galton tried transfusing rabbits with the blood of other rabbits to transmit the gemmules. He even tried working with plants—peas, of all things—to understand the basis of hereditary instructions. But he was an abysmal experimentalist; he lacked Mendel’s instinctive touch. The rabbits died of shock, and the vines withered in his garden. Frustrated, Galton switched to the study of humans. Model organisms had failed to reveal the mechanism of heredity. The measurement of variance and heredity in humans, Galton reasoned, should unlock the secret. The decision bore the hallmarks of his overarching ambition: a top-down approach, beginning with the most complex and variant traits conceivable—intelligence, temperament, physical prowess, height. It was a decision that would launch him into a full-fledged battle with the science of genetics.
Galton was not the first to attempt to model human heredity by measuring variation in humans. In the 1830s and 1840s, the Belgian scientist Adolphe Quetelet—an astronomer-turned-biologist—had begun to systematically measure human features and analyze them using statistical methods. Quetelet’s approach was rigorous and comprehensive. “Man is born, grows up and dies according to certain laws that have never been studied,” Quetelet wrote. He tabulated the chest breadth and height of 5,738 soldiers to demonstrate that chest size and height were distributed along smooth, continuous, bell-shaped curves. Indeed, wherever Quetelet looked, he found a recurrent pattern: human features—even behaviors—were distributed in bell-shaped curves.
Galton was inspired by Quetelet’s measurements and ventured deeper into the measurement of human variance. Were complex features such as intelligence, intellectual accomplishment, or beauty, say, variant in the same manner? Galton knew that no ordinary measuring devices existed for any of these characteristics. But where he lacked devices, he invented them (“Whenever you can, [you should] count,” he wrote). As a surrogate for intelligence, he obtained the examination marks for the mathematical honors exam at Cambridge—ironically, the very test that he had failed—and demonstrated that, to the best approximation, even examination abilities followed this bell-curve distribution. He walked through England and S
cotland tabulating “beauty”—secretly ranking the women he met as “attractive,” “indifferent,” or “repellent” using pinpricks on a card hidden in his pocket. It seemed no human attribute could escape Galton’s sifting, evaluating, counting, tabulating eye: “Keenness of Sight and Hearing; Colour Sense; Judgment of Eye; Breathing Power; Reaction Time; Strength and Pull of Squeeze; Force of Blow; Span of Arms; Height . . . Weight.”
Galton now turned from measurement to mechanism. Were these variations in humans inherited? And in what manner? Again, he veered away from simple organisms, hoping to jump straight into humans. Wasn’t his own exalted pedigree—Erasmus as grandfather, Darwin as cousin—proof that genius ran in families? To marshal further evidence, Galton began to reconstruct pedigrees of eminent men. He found, for instance, that among 605 notable men who lived between 1453 and 1853, there were 102 familial relationships: one in six of all accomplished men were apparently related. If an accomplished man had a son, Galton estimated, chances were one in twelve that the son would be eminent. In contrast, only one in three thousand “randomly” selected men could achieve distinction. Eminence, Galton argued, was inherited. Lords produced lords—not because peerage was hereditary, but because intelligence was.