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 circu
mstance 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.
The common source of these errors lies much deeper than any crude correlation to a political utility that most of us do not even recognize and would disavow if we did. The source lies, I believe, in a general view about causality that has either been beaten into us by a false philosophy about science and the natural world, or may even record an unfortunate foible in our brain’s evolved mode of operation. We favor simple kinds of explanations that flow in one direction from small, independent, constituent atoms of being, to complex and messy interactions among large bodies or organizations. In other words, and to use the technical term, we prefer to be “reductionists” in our causal schemes—to explain the physical behavior of large objects as consequences of atoms in motion, or to explain the social behavior of large animals by biological atoms called genes.
But the world rarely matches our simplistic hopes, and the admittedly powerful methods of reductionism don’t always apply. Wholes can be bigger than the sums of their parts, and interactions among objects cannot always be disaggregated into rules of action for each object considered separately. The rules and randomnesses of particular situations must often be inferred from direct and overt study of large objects and their interactions, not by reduction to constituent “atoms” and their fundamental properties. The three common errors of genetic explanation all share the same basic fallacy of reductionist assumptions.
1. We regard ourselves as sophisticated when we acknowledge that both genes and environment produce a given outcome, but we err in assuming that we can best express such a correct principle by assigning percentages and stating, for example, that “behavior A is 40 percent genetic and 60 percent environmental.” Such reductionist expressions pass beyond the status of simple error into the even more negative domain of entirely meaningless statements. Genetics and environment do interact to build a totality, but we need to understand why resulting wholes are unbreakable and irreducible to separate components. Water cannot be explained as two-thirds of the separate properties of hydrogen gas mixed with one-third of oxygen’s independent traits—just as wanderlust cannot be analyzed as 30 percent of a gene for feeble inhibition mixed with 70 percent of social circumstances that abet an urge to hit the road.
2. We think that we have reached some form of subtle accuracy in saying that many genes, not just a Davenportian unity, set the hereditary basis of complex behaviors. But we then take this correct statement and reintroduce the central error of reductionism by asserting that if 10 genes influence behavior A, and if the causes of A may be regarded as 50 percent genetic (the first error), then each gene must contribute roughly 5 percent to the totality of behavior A. But complex interactions cannot be calculated as the sum of independent parts considered separately. I cannot be understood as one-eighth of each of my great-grandparents (though my genetic composition may be roughly so determined); I am a unique product of my own interactive circumstances of social setting, heredity composition, and all the slings and arrows of individual and outrageous natural fortune.
3. We suppose that we have introduced sufficient caution in qualifying statements about “genes for” traits by admitting their only partial, and often quite small, contribution to an interactive totality. Thus, we imagine that we may legitimately talk of a “gay gene” so long as we add the proviso that only 15 percent of sexual preference records this cause. But we need to understand why such statements have no meaning and therefore become (as for the first argument above) worse than merely false. Many genes interact with several other factors to influence sexual preference, but no unitary and separable “gay gene” exists. When we talk about a “gene for” 10 percent of behavior A, we simply commit the old Davenportian fallacy on the “little bit pregnant” analogy.
As a concrete example of how a good and important study can be saddled with all these errors in public reporting (and also by less than optimally careful statements of some participating researchers), The New York Times greeted 1996 with a headline on the front page of its issue for January 2: “Variant Gene Tied to a Love of New Thrills.” The article discussed two studies published in the January 1996 issue of Nature Genetics. Two independent groups of researchers, one working with 124 Ashkenazi and Sephardic Jews from Israel, the other with a largely male sample of 315 ethnically diverse Americans, both found a clearly significant, if weak, association between propensity for “novelty-seeking” behavior (as ascertained from standard survey questionnaires) and possession of a variant of a gene called the D4 dopamine receptor, located on the eleventh chromosome, and acting as one of at least five receptors known to influence the brain’s response to dopamine.
This gene exists in several forms, defined by differing lengths recording the number (anywhere from two to ten) of repeated copies of a particular DNA sub-unit within the gene. Individuals with a high number of repeated copies (that is, with a longer gene) tended to manifest a greater tendency for “novelty-seeking” behavior—perhaps because the longer form of the gene somehow acts to enhance the brain’s response to dopamine.
So far, so good—and very interesting. We can scarcely doubt that heredity influences broad and basic aspects of temperament—a bit of folk wisdom that surely falls into the category of “what every parent with more than one child knows.” No one should feel at all offended or threatened by the obvious fact that we are not all born entirely blank, or entirely the same, in our mixture of the broad behavioral propensities defining what we call “temperament.” Certain genes evidently influence particular aspects of brain chemistry; and brain chemistry surely affects our moods and behaviors. We know that basic and powerful neurotransmitters like dopamine strongly impact our moods and feelings (particularly, for dopamine, our sensations of pleasure). Differing forms of genes that affect the brain’s response to dopamine may influence our behaviors—and a form that enhances the response may well incline a person toward “novelty-seeking” activities.
But the long form of the D4 receptor does not therefore become the (or even a) “novelty-seeking” gene, and these studies do not show that novelty seeking can be quantified and explained as a specified percent “genetic” in origin—although statements in this form dominated popular reports of these discoveries. Even the primary sources—the two original reports in Nature Genetics and the accompanying editorial feature entitled “Mapping Genes for Human Personality”—and the excellent Times story (representing the best of our serious press) managed, amidst their generally careful and accurate accounts, to propagate all three errors detailed above.
The Times reporter committed the first error of assigning separable percentages by writing “that about half of novelty-seeking behavior is attributable to genes, the other half to as yet ill defined environmental circumstances.” Dr. R. P. Ebstein, principal author of one of the reports, then stated the second error of adding up effects without considering interactions when he argued that the long form of the D4 gene accounts for only about 10 percent of novelty-seeking behavior. If, by the first error, the totality of novelty seeking can be viewed as 50 percent genetic, and if D4 accounts for 10 percent of the totality, then we can infer that about four other genes must be involved (each contributing its 10 percent for the grand total of 50 percent genetic influence). Ebstein told the Times reporter: “If we assume that there are other genes out there that we haven’t looked at yet, and that each gene exerts more or less the same influence as the D4 receptor, then we would expect maybe four or five genes are involved in the trait.”
But the most significant errors, as always, fall into the third category of mis-proclaiming “genes for” specific behaviors—as in the title of the technical report from Nature Genetics, previously cited: “Mapping Genes for Human Personality
.” (If our professional journals so indulge and err, imagine what the popular press makes of “gay genes,” “thrill genes,” “stupidity genes,” and so on.) First of all, the D4 gene by itself exerts only a weak potential influence upon novelty-seeking behavior. How can a gene accounting for only 10 percent of the variance in a trait be proclaimed as a “gene for” the trait? If I decide that 10 percent of my weight gain originated from the calories in tofu (because I love the stuff and eat it by the ton), this item, generally regarded as nutritionally benign, does not become a “fatness food.”
More importantly, genes make enzymes, and enzymes control the rates of chemical processes. Genes do not make “novelty-seeking” or any other complex and overt behavior. Predisposition via a long chain of complex chemical reactions, mediated through a more complex series of life’s circumstances, does not equal identification or even causation. At most, the long form of D4 induces a chemical reaction that can, among other possible effects, generate a mood leading some people to greater openness toward behaviors defined by some questionnaires as “novelty seeking.”
In fact, a further study, published in 1997, illustrated this error in a dramatic way by linking the same long form of D4 to greater propensity for heroin addiction. The original Times article of 1996 had celebrated the “first known report of a link between a specific gene and a specific normal personality trait.” But now the same gene—perhaps via the same route of enhanced dopamine response—also correlates with a severe pathology in other personalities. So what shall we call D4—a “novelty-seeking” gene in normal folk, or an “addiction” gene in troubled people? We need instead to reform both our terminology and our concepts. The long form of D4 induces a chemical response. This response may correlate with many different overt behaviors in people with widely varying histories and genetic constitutions.