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Authors: Stephen Jay Gould

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—that is, of
our
“greatest interest” to exclude by vetting and restricting immigration, lest American heredity be overwhelmed with a deluge of permanent bad genes from the wretched refuse of foreign lands.

To illustrate Davenport's characteristic style of argument, and to exemplify his easy slippage between supposed scientific documentation and overt political advocacy, we may turn to his influential 1915 monograph entitled
The Feebly Inherited
(publication number 236 of his benefactors, the Carnegie Institute of Washington), especially to part 1 on “Nomadism, or The Wandering Impulse, With Special Reference to Heredity.” The preface makes no bones about either sponsorship or intent. With three of America's wealthiest and most conservative families on board, one could hardly expect disinterested neutrality toward the full range of possible results. The Carnegies had endowed the general show,
while Davenport paid homage to specific patrons: “The cost of training the field-workers was met by Mrs. E. H. Harriman, founder and principal patron of the Eugenics Record Office, and Mr. John D. Rockefeller, who paid also the salaries of many of the field-workers.”

Davenport's preface also boldly admits his political position and purposes. He wishes to establish “feeble inhibition” as a category of temperament leading to inferior morality. Such a formulation will provide a one-two punch for identification of the eugenically unfit—bad intellect
and
bad morals. According to Davenport, the genetic basis of intelligence had already been documented in numerous studies of the feebleminded. But eugenics now needed to codify the second major reason for excluding immigrants and discouraging or denying reproductive rights to the native unfit—bad moral character (as in Davenport's fallback position, documented earlier in this essay, for restricting Jewish immigration when he could not invoke the usual charge of intellectual inferiority). Davenport writes:

A word may be said as to the term “feebly inhibited” used in these studies. It was selected as a fit term to stand as co-ordinate with “feeble-minded” and as the result of a conviction that the phenomena with which it deals should properly be considered apart from those of feeble-mindedness.

To allay any doubt about his motivations, Davenport then makes his political point up front. Feeble inhibition, leading to immorality, may be more dangerous than feeblemindedness, leading to stupidity:

I think it helps to consider separately the hereditary basis of the intellect and the emotions. It is in this conviction that these studies are submitted for thoughtful consideration. For, after all, the chief problem in administering society is that of disordered conduct, conduct is controlled by emotions, and the quality of the emotions is strongly tinged by the hereditary constitution.

Davenport then selects “nomadism” as his primary example of a putatively simple Mendelian trait—the product of a single gene—based on “feeble inhibition” and leading almost inevitably to immoral behavior. He encounters a problem of definition at the very outset of his work, as expressed in an opening sentence that must be ranked as one of the least profound in the entire history
of science! “A tendency to wander in some degree is a normal characteristic of man, as indeed of most animals, in sharp contrast to most plants.”

How then shall the “bad” form of wanderlust, defined as a compulsion to flee from responsibility, be distinguished from the meritorious sense of bravery and adventure—leading to “good” wanderlust—that motivated our early (and largely northern European) immigrants to colonize and subdue the frontier? Davenport had warmly praised the “good” form in his 1911 book as “the enterprising restlessness of the early settlers … the ambitious search for better conditions. The abandoned farms of New England point to the trait in our blood that entices us to move on to reap a possible advantage elsewhere.”

In a feeble attempt to put false labels on segments of complex continua, Davenport identified the “bad” form as “nomadism,” defined as an inability to inhibit the urge we all feel (from time to time) to flee from our duties, but that folks of normal and decent morality suppress. Nomads are society's tramps, bums, hoboes, and gypsies—“those who, while capable of steady and effective work, at more or less regular periods run away from the place where their duties He and travel considerable distances.”

Having defined his quarry (albeit in a fatally subjective way), Davenport then required two further arguments to make his favored link of a “bad” trait (rooted in feeble inhibition and leading to immoral behavior) to a single gene that eugenics might labor to breed down and out: he needed to prove the hereditary basis, and then to find the “gene,” for nomadism.

His arguments for a genetic basis must be judged as astonishingly weak, even by the standards of his own generation (and despite the renown of his work, attributable, we must assume in retrospect, to its consonance with what most readers wanted to believe rather than to the quality of Davenport's logic or data). He simply argued, based on four dubious analogies, that features akin to nomadism emerge whenever situations veer toward “raw” nature (where genetics must rule), and away from environmental refinements of modern human society. Nomadism must be genetic because analogous features appear as “the wandering instinct in great apes,” “among primitive peoples,” in children (then regarded as akin to primitives under the false view that ontogeny recapitulates phylogeny), and in adolescents (where raw instinct temporarily overwhelms social inhibition in the
Sturm and Drang
of growing up). The argument about “primitive” people seems particularly weak, since a propensity for wandering might be regarded as well suited to a lifestyle based on hunting mobile game, rather than identified as a mark of inadequate genetic constitution (or any kind of genetic constitution at all). But Davenport, reversing the
probable route of cause and effect, pushed through any difficulty to his desired conclusion:

If we regard the Fuegians, Australians, Bushmen and Hottentots as the most primitive men, then we may say that primitive man is nomadic…. It is frequently assumed that they are nomadic because they hunt, but it is more probable that their nomadic instincts force them to hunting rather than agriculture for a livelihood.

Davenport then pursues his second claim—nomadism as the product of a single gene—by tracing pedigrees stored in his Eugenics Record Office. On the subjective criterion of impressions recorded by fieldworkers, or written descriptions of amateur informants (mostly people who had submitted their family trees in response to a general appeal for data), Davenport marked all nomads in his table with a scarlet
W
(for
Wanderlust
, the common German term for “urge to roam”). He then examined the distribution of
W'
s through families and generations to reach one of the most peculiar and improbable conclusions ever advanced in a famous study: nomadism, he argued, is caused by
a single gene
, a sex-linked recessive located on what would later be identified as the female chromosome.

Davenport reached this conclusion by arguing that nomadism occurred in families with the same distribution as hemophilia, colorblindness, and other truly sex-linked recessive traits. Such a status can be legitimately inferred from several definite patterns of heredity. For example, fathers with the trait do not pass it to their sons (since the relevant gene resides on the X-chromosome and males only pass a Y-chromosome to their sons). Mothers with the trait pass it to all their sons, but none of their daughters when the father lacks the trait. (Since the feature is recessive, an afflicted mother must carry the gene on both X-chromosomes. She passes a single X to her son, who must then express the trait, for he has no other X-chromosome. But a daughter will receive one afflicted X-chromosome from her mother and one normal X-chromosome from her father; she will therefore not express the trait because her father's normal copy of the gene is dominant.) Davenport knew these rules, so his study didn't fail on this score. Rather, his criteria for identifying “nomadism” as a discrete and scorable “thing” remained so subjective, and so biased by his genetic assumptions, that his pedigree data can only be judged as worthless.

Davenport's summary reached (and preached) a eugenic crescendo: “The wandering instinct,” he stated, “is a fundamental human instinct, which is, however,
typically inhibited in intelligent adults of civilized peoples.” Unfortunately, however, people who express the bad gene
W
(the scarlet letter of wanderlust) cannot achieve this healthy inhibition, and become feckless nomads who run from responsibility by literal flight. The trait is genetic, racial, and undesirable. Immigrants marked by
W
should be excluded (and many immigrants must be shiftless wanderers rather than brave adventurers), while nomadic natives should be strongly encouraged, if not compelled, to desist from breeding. Davenport concludes:

The new light brought by our studies is this: The nomadic impulse is, in all the cases, one and the same unit character. Nomads, of all kinds, have a special racial trait—are, in a proper sense, members of the nomadic race. This trait is the absence of the germinal determiner that makes for sedentariness, stability, domesticity.

Of course, no one would now defend Davenport's extreme view that single genes determine nearly every complex human behavior. Most colleagues eventually rejected Davenport's theory during his own career, especially since he lived into the 1940s, long past the early flush of Mendelian enthusiasm, and well past our modern recognition that complex traits usually record the operation of many genes, each with a small and cumulative effect (not to mention a strong, and often predominant influence from nongenetic environmental contexts of growth and expression). A single gene for anger, conviviality, contemplation, or wanderlust now seems as absurd as a claim that one assassin's bullet, and nothing else, caused World War I, or that Darwin discovered evolution all by himself, and we would still be creationists if he had never been born.

Nonetheless, in our modern age of renewed propensity for genetic explanations (a valid and genuine enthusiasm when properly pursued), Davenport's general style of error resurfaces on an almost daily basis, albeit in much more subtle form, but with all the vigor of his putative old gene—yes, he did propose one—for stubbornly persistent behavior.

No sensible critic of biological determinism denies that genes influence behavior; of course they do. Moreover, no honorable skeptic would argue that genetic explanations should be resisted because they entail negative political, social, or ethical connotations—a charge that must be rejected for two primary reasons. First, nature's facts stand neutral before our ethical usages. We have, to be sure, often made dubious, even tragic decisions based on false genetic claims. But in other contexts, valid arguments about the innate and hereditary basis of
human attributes can be profoundly liberating. Consider only the burden lifted from loving parents who raise beautiful and promising children for twenty years, and then “lose” them to the growing ravages of schizophrenia—almost surely a genetically based disease of the mind, just as many congenital diseases of other bodily organs also appear in the third decade of life or even later. Generations of psychologists had subtly blamed parents for unintentionally inducing such a condition, then viewed as entirely “environmental” in origin. What could be more cruel than a false weight of blame added to such an ultimate tragedy? Second, we will never get very far, either in our moral deliberations or in our scientific inquiries, if we disregard genuine facts because we dislike their implications. In the most obvious case, I cannot think of a more unpleasant fact than the inevitable physical death of each human body, but no sane person would bet on extended stability for a society built on the premise that King Prospero will reign in his personal flesh forever.

However, if we often follow erroneous but deeply rooted habits of thinking to generate false conclusions about the role of heredity in human behavior, then these habits should be exposed and corrected—all the more vigorously if such arguments usually lead to recommendations for action that most people would also regard as ethically wrong (involuntary sterilization of the mentally retarded, for example). I believe that we face such a situation today, and that the genetic fallacies underlying our misusages bear a striking similarity in style and logic to Davenport's errors, however much we have gained in subtlety of argument and factual accuracy.

Throughout the history of genetics, political misuse has most frequently originated from claims for “biological determinism”—the argument that a given behavior or social situation can't be altered because people have been “built that way” by their genes. Once we attribute something we don't like to “genes,” we tend either to make excuses, or to make less effort for change. In the most obvious, egregious, and persisting example, many people still argue that we should deny educational benefits and social services to groups (usually races or social classes) falsely judged as genetically inferior on average, because their poverty and misfortune He in their own heredity and cannot be significantly ameliorated by social intervention. Thus, history shows a consistent linkage between genetic claims cast in this mold and conservative political arguments for maintenance of an unjust status quo of great benefit to people currently in power.

Of course, no serious student of either genetics or politics would now advance this argument in Davenport's style of “one gene, one complex behavior.” That
is, no one talks today about
the
gene for stupidity, promiscuity, or lack of ambition. But a series of three subtle—and extremely common—errors lead all too often to the same eugenical style of conclusion. Somehow we remain fascinated with the idea that complex social behaviors might be explained, at least in large part, by inherited “atoms” of behavioral propensity lying deeply within individuals. We seem so much more satisfied, so much more intrigued, by the claim that a definite gene, rather than a complex and inextricable mix of heredity and social circumstances, causes a particular phenomenon. We feel that we have come much nearer to a real or essential cause when we implicate a particle within an individual, rather than a social circumstance built of multiple components, as the reason behind a puzzling behavior. We will avidly read a front-page headline entitled “gay gene found,” but newspapers will not even bother to report an equally well documented story on other components of homosexual preference with a primary social root and no correlated genetic difference.

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