What do our minds owe to our nature, and what to our nurture? The question has long been vexed, in no small part because until recently we knew relatively little about the nature of nature—how genes work and what they bring to the biological structures that underlie the mind. But now, 50 years after the discovery of the molecular structure of DNA, we are for the first time in a position to understand directly DNA’s contribution to the mind. And the story is vastly different from—and vastly more interesting than—anything we had anticipated.

The emerging picture of nature’s role in the formation of the mind is at odds with a conventional view, recently summarized by Louis Menand. According to Menand, “every aspect of life has a biological foundation in exactly the same sense, which is that unless it was biologically possible it wouldn’t exist. After that, it’s up for grabs.” More particularly, some scholars have taken recent research on genes and on the brain as suggesting a profoundly limited role for nature in the formation of the mind.

Their position rests on two arguments, what Stanford anthropologist Paul Ehrlich dubbed a “gene shortage” and widespread, well-documented findings of “brain plasticity.” According to the gene shortage argument, genes can’t be very important to the birth of the mind because the genome contains only about 30,000 genes, simply too few to account even for the brain’s complexity—with its billions of cells and tens of billions of connections between neurons—much less the mind’s. “Given that ratio,” Ehrlich suggested, “it would be quite a trick for genes typically to control more than the most general aspects of human behavior.”

According to the brain plasticity argument, genes can’t be terribly important because the developing brain is so flexible. For instance, whereas adults who lose their left hemisphere are likely to lose permanently much of their ability to talk, a child who loses a left hemisphere may very well recover the ability to speak, even in the absence of a left hemisphere. Such flexibility is pervasive, down to the level of individual cells. Rather than being fixed in their fates the instant they are born, newly formed brain cells—neurons—can sometimes shift their function, depending on their context. A cell that would ordinarily help to give us a sense of touch can (in the right circumstances) be recruited into the visual system and accept signals from the eye. With that high level of brain plasticity, some imagine that genes are left on the sidelines, as scarcely relevant onlookers.

All of this is, I think, a mistake. It is certainly true that the number of genes is tiny in comparison to the number of neurons, and that the developing brain is highly plastic. Nevertheless, nature—in the form of genes—has an enormous impact on the developing brain and mind. The general outlines of how genes build the brain are finally becoming clear, and we are also starting to see how, in forming the brain, genes make room for the environment’s essential role. While vast amounts of work remain to be done, it is becoming equally clear that understanding the coordination of nature and nurture will require letting go of some long-held beliefs.

How to Build a Brain

In the nine-month dash from conception to birth—the flurry of dividing, specializing, and migrating cells that scientists call embryogenesis—organs such as the heart and kidney unfold in a series of ever more mature stages. In contrast to a 17th century theory known as preformationism, the organs of the body cannot be found preformed in miniature in a fertilized egg; at the moment of conception there is neither a tiny heart nor a tiny brain. Instead, the fertilized egg contains information: the three billion nucleotides of DNA that make up the human genome. That information, copied into the nucleus of every newly formed cell, guides the gradual but powerful process of successive approximation that shapes each of the body’s organs. The heart, for example, begins as a simple sheet of cell that gradually folds over to form a tube; the tube sprouts bulges, the bulges sprout further bulges, and every day the growing heart looks a bit more like an adult heart.

Even before the dawn of the modern genetic era, biologists understood that something similar was happening in the development of the brain—that the organ of thought and language was formed in much the same way as the rest of the body. The brain, too, develops in the first instance from a simple sheet of cells that gradually curls up into a tube that sprouts bulges, which over time differentiate into ever more complex shapes. Yet 2,000 years of thinking of the mind as independent from the body kept people from appreciating the significance of this seemingly obvious point.

The notion that the brain is drastically different from other physical systems has a long tradition; it can be seen as a modernized version of the ancient belief that the mind and body are wholly separate—but it is untenable. The brain is a physical system. Although the brain’s function is different from that of other organs, the brain’s capabilities, like those of other organs, emerge from its physical properties. We now know that strokes and gunshot wounds can interfere with language by destroying parts of the brain, and that Prozac and Ritalin can influence mood by altering the flow of neurotransmitters. The fundamental components of the brain—the neurons and the synapses that connect them—can be understood as physical systems, with chemical and electrical properties that follow from their composition.

Yet even as late as the 1990s, latter-day dualists might have thought that the brain developed by different principles. There were, of course, many hints that genes must be important for the brain: identical twins resemble each other more than nonidentical twins in personality as well as in physique; mental disorders such as schizophrenia and depression run in families and are shared even by twins reared apart; and animal breeders know that shaping the bodies of animals often leads to correlated changes in behavior. All of these observations provided clues of genetic effects on the brain.

But such clues are achingly indirect, and it was easy enough to pay them little heed. Even in the mid-1990s, despite all the discoveries that had been made in molecular biology, hardly anything specific was known about how the brain formed. By the end of that decade, however, revolutions in the methodology of molecular biology—techniques for studying and manipulating genes—were beginning to enter the study of the brain. Now, just a few years later, it has become clear that to an enormous extent the brain really is sculpted by the same processes as the rest of the body, not just at the macroscopic level (i.e., as a product of successive approximation) but also at the microscopic level, in terms of the mechanics of how genes are switched on and off, and even in terms of which genes are involved; a huge number of the genes that participate in the development of the brain play important (and often closely related) roles in the rest of the body.

In retrospect, this should scarcely be surprising. Though neurons—the principal cells of the brain—look very different from other cells, with their long, spindly axons that can span the length of the body and their bushy dendrites that collect messages from other neurons, at heart they are merely specializations on a universal cellular theme. Like most any other cell, a neuron contains a nucleus filled with DNA, mitochondrial power plants, membranes to keep invaders out, and so forth. Even a neuron’s distinctive specializations are really just variations on common biological themes; axons, for example, depend on essentially the same cytoskeleton proteins as many other cells. All of which means that the life cycle of a neuron is much the same as the life cycle of any other cell.

Which is not so terribly different from the life cycle of a human being. A neuron is born, it takes up a career (say as a motor neuron or a sensory neuron), moves perhaps to a new home, and eventually dies. The life choices of cells—whether neurons or liver cells—are what give the brain and body the texture that they have. All the successive approximation that formulates a brain or heart is driven by the actions of individual cells, which in turn are driven in no small part by the genes contained within their nuclei.

In the last couple of years, developmental neuroscientists have begun to understand this process in detail, to the point where they can directly alter it by flipping the right genetic switches. Researchers have been able to grow mice with abnormally large brains by inducing extra cell division, trick differentiating neurons that would ordinarily produce excitatory neurotransmitters into producing inhibitory ones, and coax neurons that would otherwise be bound for the cortex to instead head underground to a subcortical area known as the striatum. Genes guide every bit of this process, with as much precision in the brain as elsewhere in the body.

The supervisory power of genes holds even for the most unusual yet most characteristic parts of neurons: the long axons that carry signals away from the cell, the tree-like dendrites that allow neurons to receive signals from other nerve cells, and the trillions of synapses that serve as connections between them. What your brain does is largely a function of how those synaptic connections are set up—alter those connections, and you alter the mind—and how they are set up is no small part a function of the genome. In the laboratory, mutant flies and mice with aberrant brain wiring have trouble with everything from motor control (one mutant mouse is named “reeler” for its almost drunken gait) to vision. And in humans, faulty brain wiring contributes to disorders such as schizophrenia and autism.

Proper neural wiring depends on the behavior of individual axons and dendrites. And this behavior once again depends on the content of the genome. For example, much of what axons do is governed by special wiggly, almost hand-like protuberances at the end of each axon known as growth cones. Growth cones (and the axonal wiring they trail behind them) are like little animals that swerve back and forth, maneuvering around obstacles, extending and retracting feelers known as filopodia (the “fingers” of a growth cone) as the cone hunts around in search of its destination—say in the auditory cortex. Rather than simply being launched like projectiles that blindly and helplessly follow whatever route they first set out on, growth cones constantly compensate and adjust, taking in new information as they find their way to their targets.

Growth cones don’t just head in a particular direction and hope for the best. They “know” what they are looking for and can make new plans even if experimentally induced obstacles get in their way. In their efforts to find their destinations, growth cones use every trick they can, from “short-range” cues emanating from the surface of nearby cells to long-distance cues that broadcast their signals from millimeters away—miles and miles in the geography of an axon. For example, some proteins appear to serve as “radio beacons” that can diffuse across great distances and serve as guides to distant growth cones—provided that they are tuned to the right station. Which stations a growth cone picks up—and whether it finds a particular signal attractive or repellent—depends on the protein receptors it has on its surface, in turn a function of which genes are expressed within.

Researchers are now in a position where they can begin to understand and even manipulate those genes. In 2000, a team of researchers at the Salk Institute in San Diego took a group of thoracic (chest) motor neurons that normally extend their axons into several different places, such as axial muscles (midline muscles that play a role in posture), intercostal muscles (the muscles between the ribs), and sympathetic neurons (which, among other things, participate in the fast energy mobilization for fight-or-flight responses), and by changing their genetic labels persuaded virtually the entire group of thoracic neurons to abandon their usual targets in favor of the axial muscles. (The few exceptions were a tiny number that apparently couldn’t fit into the newly crowded axial destinations and had to find other targets.)

What this all boils down to, from the perspective of psychology, is an astonishingly powerful system for wiring the mind. Instead of vaguely telling axons and dendrites to send and accept signals from their neighbors, thereby leaving all of the burden of mind development to experience, nature in effect lays down the cable: it supplies the brain’s wires—axons and dendrites—with elaborate tools for finding their way on their own. Rather than waiting for experience, brains can use the complex menagerie of genes and proteins to create a rich, intricate starting point for the brain and mind.

The sheer overlap between the cellular and molecular processes by which the brain is built and the processes by which the rest of the body is built has meant that new techniques designed for the study of the one can often be readily imported into the study of the other. New techniques in staining, for instance, by which biologists trace the movements and fates of individual cells, can often be brought to bear on the study of the brain as soon as they are developed; even more important, new techniques for altering the genomes of experimental animals can often be almost immediately applied to studies of brain development. Our collective understanding of biology is growing by leaps and bounds because sauce for the goose is so often sauce for the gander.

Nature and Nurture Redux

This seemingly simple idea—that what’s good enough for the body is good enough for the brain—has important implications for how we understand the roles of nature and nurture in the development of the mind and brain.

Beyond the Blueprint

Since the early 1960s biologists have realized that genes are neither blueprints nor dictators; instead, as I will explain in a moment, genes are better seen as providers of opportunity. Yet because the brain has for so long been treated as separate from the body, the notion of genes as sources of options rather than purveyors of commands has yet to really enter into our understanding of the origins of human psychology.

Biologists have long understood that all genes have two functions. First, they serve as templates for building particular proteins. The insulin gene provides a template for insulin, the hemoglobin genes give templates for building hemoglobin, and so forth. Second, each gene contains what is called a regulatory sequence, a set of conditions that guide whether or not that gene’s template gets converted into protein. Although every cell contains a complete copy of the genome, most of the genes in any given cell are silent. Your lung cells, for example, contain the recipe for insulin but they don’t produce any, because in those cells the insulin gene is switched off (or “repressed”); each protein is produced only in the cells in which the relevant gene is switched on. So individual genes are like lines in a computer program. Each gene has an IF and a THEN, a precondition (IF) and an action (THEN). And here is one of the most important places where the environment can enter: the IFs of genes are responsive to the environment of the cells in which they are contained. Rather than being static entities that decide the fate of each cell in advance, genes—because of the regulatory sequence—are dynamic and can guide a cell in different ways at different times, depending on the balance of molecules in their environment.

This basic logic—which was worked out in the early 1960s by two French biologists, François Jacob and Jacques Monod, in a series of painstaking studies of the diet of a simple bacterium—applies as much to humans as to bacteria, and as much for the brain as for any other part of the body. Monod and Jacob aimed to understand howE. coli bacteria could switch almost instantaneously from a diet of glucose (its favorite) to a diet of lactose (an emergency backup food). What they found was that this abrupt change in diet was accomplished by a process that switched genes on and off. To metabolize lactose, the bacterium needed to build a certain set of protein-based enzymes that for simplicity I’ll refer to collectively as lactase, the product of a cluster of lactase genes. Every E. coli had those lactase genes lying in wait, but they were only expressed—switched on—when a bit of lactose could bind (attach to) a certain spot of DNA that lay near them, and this in turn could happen only if there was no glucose around to get in the way. In essence, the simple bacterium had an IF-THEN—if lactose and not glucose, then build lactase—that is very much of a piece with the billions of IF-THENs that run the world’s computer software.

The essential point is that genes are IFs rather than MUSTs. So even a single environmental cue can radically reshape the course of development. In the African butterfly Bicyclus anynana, for example, high temperature during development (associated with the rainy season in its native tropical climate) leads the butterfly to become brightly colored; low temperature (associated with a dry fall) leads the butterfly to become a dull brown. The growing butterfly doesn’t learn (in the course of its development) how to blend in better—it will do the same thing in a lab where the temperature varies and the foliage is constant; instead it is genetically programmed to develop in two different ways in two different environments.

The lesson of the last five years of research in developmental neuroscience is that IF-THENs are as crucial and omnipresent in brain development as they are elsewhere. To take one recently worked out example: rats, mice, and other rodents devote a particular region of the cerebral cortex known as barrel fields to the problem of analyzing the stimulation of their whiskers. The exact placement of those barrel fields appears to be driven by a gene or set of genes whose IF region is responsive to the quantity of a particular molecule, Fibroblast Growth Factor 8 (FGF8). By altering the distribution of that molecule, researchers were able to alter barrel development: increasing the concentration of FGF8 led to mice with barrel fields that were unusually far forward, while decreasing the concentration led to mice with barrel fields that were unusually far back. In essence, the quantity of FGF8 serves as a beacon, guiding growing cells to their fate by driving the regulatory IFs of the many genes that are presumably involved in barrel-field formation.

Other IF-THENs contribute to the function of the brain throughout life, e.g., supervising the control of neurotransmitters and participating (as I will explain below) in the process of laying down memory traces. Because each gene has an IF, every aspect of the brain’s development is in principle linked to some aspect of the environment; chemicals such as alcohol that are ingested during pregnancy have such enormous effects because they fool the IFs that regulate genes that guide cells into dividing too much or too little, into moving too far or not far enough, and so forth. The brain is the product of the actions of its component cells, and those actions are the products of the genes they contain within, each cell guided by 30,000 IFs paired with 30,000 THENs—as many possibilities as there are genes. (More, really, because many genes have multiple IFs, and genes can and often do work in combination.)

From Genes to Behavior

Whether we speak of the brain or other parts of the body, changes in even a single gene—leading to either a new IF or a new THEN—can have great consequences. Just as a single alteration to the hemoglobin gene can lead to a predisposition for sickle-cell anemia, a single change to the genes involved in the brain can lead to a language impairment or mental retardation.

And at least in animals, small differences within genomes can lead to significant differences in behavior. A Toronto team, for example, recently used genetic techniques to investigate—and ultimately modify—the foraging habits of C. elegans worms. Some elegansprefer to forage in groups, others are loners, and the Toronto group was able to tie these behavioral differences to differences in a single amino acid in the protein template (THEN) region of a particular gene known as npr-1; worms with the amino acid valine in the critical spot are “social” whereas worms with phenylalanine are loners. Armed with that knowledge and modern genetic engineering techniques, the team was able to switch a strain of loner C. elegansworms into social worms by altering that one gene.

Another team of researchers, at Emory University, has shown that changing the regulatory IF region of a single gene can also have a significant effect on social behavior. Building on an observation that differences in sociability in different species of voles correlated with how many vasopressin receptors they had, they transferred the regulatory IF region of sociable prairie voles’ vasopressin receptor genes into the genome of a less sociable species, the mouse—and in so doing created mutant mice, more social than normal, with more vasopressin receptors. With other small genetic modifications, researchers have created strains of anxious, fearful mice, mice that progressively increase alcohol consumption under stress, mice that lack the nurturing instinct, and even mice that groom themselves constantly, pulling and tugging on their own hair to the point of baldness. Each of those studies demonstrates how behavior can be significantly changed when even a single gene is altered.

Still, complex biological structures—whether we speak of hearts or kidneys or brains—are the product of the concerted actions and interactions of many genes, not just one. A mutation in a single gene known as FOXP2 can interfere with the ability of a child to learn language; an alteration in the vasopressin gene can alter a rodent’s sociability—but this doesn’t mean that FOXP2 is solely responsible for language or that vasopressin is the only gene a rat needs in order to be sociable. Although individual genes can have powerful effects, no trait is the consequence of any single gene. There can no more be a single gene for language, or for the propensity for talking about the weather, than there can be for the left ventricle of a human heart. Even a single brain cell—or a single heart cell—is the product of many genes working together.

The mapping between genes and behavior is made even more complex by the fact that few if any neural circuits operate entirely autonomously. Except perhaps in the case of reflexes, most behaviors are the product of multiple interacting systems. In a complex animal like a mammal or a bird, virtually every action depends on a coming together of systems for perception, attention, motivation, and so forth. Whether or not a pigeon pecks a lever to get a pellet depends on whether it is hungry, whether it is tired, whether there is anything else more interesting around, and so forth. Furthermore, even within a single system, genes rarely participate directly “on-line,” in part because they are just too slow. Genes do seem to play an active, major role in “off-line” processing, such as consolidation of long-term memory—which can even happen during sleep—but when it comes to rapid on-line decision-making, genes, which work on a time scale of seconds or minutes, turn over the reins to neurons, which act on a scale of hundredths of a second. The chief contribution of genes comes in advance, in laying down and adjusting neural circuitry, not in the moment-by-moment running of the nervous system. Genes build neural structures—not behavior.

In the assembly of the brain, as in the assembly of other organs, one of the most important ideas is that of a cascade, one gene influencing another, which influences another, which influences another, and so on. Rather than acting in absolute isolation, most genes act as parts of elaborate networks in which the expression of one gene is a precondition for the expression of the next. The THEN of one gene can satisfy the IF of another and thus induce it to turn on. Regulatory proteins are proteins (themselves the product of genes) that control the expression of other genes and thus tie the whole genetic system together. A single regulatory gene at the top of a complex network can indirectly launch a cascade of hundreds or thousands of other genes leading to, for example, the development of an eye or a limb.

In the words of Swiss biologist Walter Gehring, such genes can serve as “master control genes” and exert enormous power on a growing system. PAX6, for example, is a regulatory protein that plays a role in eye development, and Gehring has shown that artificially activating it in the right spot on a fruit fly’s antenna can lead to an extra eye, right there on the antenna—thus, a simple regulatory gene leads directly and indirectly to the expression of approximately 2,500 other genes. What is true for the fly’s eye is also true for its brain—and also for the human brain: by compounding and coordinating their effects, genes can exert enormous influence on biological structure.

From a Tiny Number of Genes to a Complex Brain

The cascades in turn help us to make sense of the alleged gene shortage, the idea that the discrepancy between the number of genes and the number of neurons might somehow minimize the importance of genes when it comes to constructing brain or behavior.

Reflection on the relation between brain and body immediately vitiates the gene shortage argument: if 30,000 genes weren’t enough to have significant influence on the 20 billion cells in the brain, they surely wouldn’t have much impact on the trillions that are found in the body as a whole. The confusion, once again, can be traced to the mistaken idea of genome as blueprint, to the misguided expectation of a one-to-one mapping from individual genes to individual neurons; in reality, genomes describe processes for building things rather than pictures of finished products: better to think of the genome as a compression scheme than a blueprint.

Computer scientists use compression schemes when they want to store and transmit information efficiently. All compression schemes rely in one way or another on ferreting out redundancy. For instance, programs that use the GIF format look for patterns of repeated pixels (the colored dots of which digital images are made). If a whole series of pixels are of exactly the same color, the software that creates GIF files will assign a code that represents the color of those pixels, followed by a number to indicate how many pixels in a row are of the same color. Instead of having to list every blue pixel individually, the GIF format saves space by storing only two numbers: the code for blue and the number of repeated blue pixels. When you “open” a GIF file, the computer converts those codes back into the appropriate strings of identical bits; in the meantime, the computer has saved a considerable amount of memory. Computer scientists have devised dozens of different compression schemes, from JPEGs for photographs to MP3s for music, each designed to exploit a different kind of redundancy. The general procedure is always the same: some end product is converted into a compact description of how to reconstruct that end product; a “decompressor” reconstructs the desired end product from that compact description.

Biology doesn’t know in advance what the end product will be; there’s no StuffIt Compressor to convert a human being into a genome. But the genome is very much akin to a compression scheme, a terrifically efficient description of how to build something of great complexity—perhaps more efficient than anything yet developed in the labs of computer scientists (never mind the complexities of the brain—there are trillions of cells in the rest of the body, and they are all supervised by the same 30,000-gene genome). And although nature has no counterpart to a program that stuffs a picture into a compressed encoding, it does offer a counterpart to the program that performs decompression: the cell. Genome in, organism out. Through the logic of gene expression, cells are self-regulating factories that translate genomes into biological structure.

Cascades are at the heart of this process of decompression, because the regulatory proteins that are at the top of genetic cascades serve as shorthand that can be used over and over again, like the subroutine of a software engineer. For example, the genome of a centipede probably doesn’t specify separate sets of hundreds or thousands of genes for each of the centipede’s legs; instead, it appears that the leg-building “subroutine”—a cascade of perhaps hundreds or thousands of genes—gets invoked many times, once for each new pair of legs. Something similar lies behind the construction of a vertebrate’s ribs. And within the last few years it has become clear that the embryonic brain relies on the same sort of genetic recycling, using the same repeated motifs—such as sets of parallel connections known as topographic maps—over and over again, to supervise the development of thousands or even millions of neurons with each use of a given genetic subroutine. There’s no gene shortage, because every cascade represents the shorthand for a different reuseable subroutine, a different way of creating more from less.

From Prewiring to Rewiring

In the final analysis, I think the most important question about the biological roots of the mind may not be the question that has preoccupied my colleagues and myself for a number of years—the extent to which genes prewire the brain—but a different question that until recently had never been seriously raised: the extent to which (and ways in which) genes make it possible for experience torewire the brain. Efforts to address the nature-nurture question typically falter because of the false assumption that the two—prewiring and rewiring—are competing ideas. “Anti-nativists”—critics of the view that we might be born with significant mental structure prior to experience—often attempt to downplay the significance of genes by making what I earlier called “the argument from plasticity”: they point to the brain’s resilience to damage and its ability to modify itself in response to experience. Nativists sometimes seem to think that their position rests on downplaying (or demonstrating limits on) plasticity.

In reality, plasticity and innateness are almost logically separate. Innateness is about the extent to which the brain is prewired, plasticity about the extent to which it can be rewired. Some organisms may be good at one but not the other: chimpanzees, for example, may have intricate innate wiring yet, in comparison to humans, relatively few mechanisms for rewiring their brains. Other organisms may be lousy at both: C. elegans worms have limited initial structure, and relatively little in the way of techniques for rewiring their nervous system on the basis of experience. And some organisms, such as humans, are well-endowed in both respects, with enormously intricate initial architecture and fantastically powerful and flexible means for rewiring in the face of experience.

The crucial point is that every technique for rewiring the brain has its origins, in one way or another, in the genome. Memory, for example, is a way of rewiring connections between neurons (or altering something inside individual neurons) that plainly depends on gene function: interfere with the process of synthesizing proteins from genes, and you interfere with memory. Closely related organisms (such as Aplysia, the sea slug that has been the central experimental animal for Nobel laureate Eric Kandel, and its rather dimwitted cousin, Dolabrifera dolabrifera) can differ significantly in their talents for learning, apparently as a function of a small difference in genomes. In simple, scientifically tractable organisms, scientists have begun to map out a range of different learning abilities and the sets of genes that underlie them. C. elegans worms, for example, have at least a dozen and a half learning-related genes, each with a particular role in a particular kind of learning. What an organism learns depends in no small part on what genes for learning it is born with.

We will advance beyond the nature-nurture controversy not by blurring (or denying) the distinction between genes and the environment but by understanding it better, and that means, among other things, investigating the precise function of our genes and how they make rewiring and learning possible. Matt Ridley recently wrote a book called Nature via Nurture—true because the IFs that regulate gene expression are responsive to the environment—but one could as easily conclude that it is really nurture that is via nature, for it is our genes that allow us to learn something from the environment.

One of the most intriguing possibilities is that we may eventually be able to improve our social interventions—education, welfare programs, and the like—by better understanding specific interactions between nature and nurture. To take an example, one recent study suggests that children with a certain version of a gene that produces an enzyme known as MAO-A (which metabolizes neurotransmitters such as serotonin and dopamine) are significantly more likely to become violent—but only if they were mistreated as children. In this way, an aspect of human behavior might be a bit like the body of the Bicyclus butterfly, driven to one form or another by genes that switch in response to environmental cues, one genotype yielding two different phenotypes for two different environments. Although these results are just a first study and establish only a correlation with the environment and not yet a causal relation, there is good biological reason to find such results plausible. Many organisms (including humans) have a vast array of genes for dealing with stress, and the regulatory IFs that control the production of enzymes like MAO-A might well be directly or indirectly sensitive to such stress.

Further studies of gene-environment interactions could eventually lead to a new way of identifying which children are at higher risk, and thus provide a new way of identifying children who might best profit from special day-care programs or home visits from social workers. Just as the new field of pharmacogenetics aims to match drugs to unique genetic physiology, a new field of therapeuto-genetics could use individual genetics to prescribe customized social interventions. As we come to see genes not as rigid dictators of destiny but as rich providers of opportunity, we may be able to use our growing knowledge of nature as a means to make the most out of nurture.