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Messy Metaphors

Mrs. Munroe has a good group of students this year. Grade eights can be a challenge — precariously balanced as they are between childhood and adolescence, their hormones overcharged and as volatile as nitroglycerin — but for the most part, she can’t complain. Only two of her students trouble her, and for very different reasons.

Joey is pure energy. Unfortunately, he rarely puts it to good use. He disrupts classes, swears at teachers, and bullies his classmates mercilessly. Over half a dozen students have complained to Mrs. Munroe about him. One claimed Joey stole his backpack and threw it onto the school roof. Another said Joey shoved her in the janitor’s closet and held the door shut until after the second period bell rang. Still another showed Mrs. Munroe her binder, which had been stabbed repeatedly with a pen and defaced with permanent marker. She claimed Joey did it.

Though Joey terrorizes his peers more or less without prejudice, a few students actually look up to him. He flouts rules with an abandon they find hopelessly alluring. He chain-smokes during his lunch hour, standing defiantly just a few feet off of school property, where the teachers are powerless to stop him. He regales anyone who will listen with stories of binge drinking and illicit sex. Mrs. Munroe is pretty sure the sex talk is pure bravado, but the drinking, at least, she believes to be true. Joey has shown up to school flush-faced and giddy on more than one occasion, the smell of stale beer on his breath. None of her punishments seem to have any effect on his behaviour. He careens through life like a transport truck with its brakes cut, flirting with disaster and constantly gaining speed.

Mrs. Munroe’s other problem child is Erika, though a less empathetic teacher would hardly consider her a problem at all. She never acts out, or breaks rules, or draws any attention to herself whatsoever. This is not to say she’s an ideal student — she doesn’t participate in class, and often fails to do her homework. Her test performance is spotty; sometimes she scores very well, but at other times she hands tests in with many questions left unanswered.

For the first few weeks, Mrs. Munroe suspected that Erika had some sort of learning disability, but she has become convinced this is not the case. The work Erika does complete is of exceptional quality. She writes eloquently, and can solve fairly complex math problems without struggle. The trouble is that, more often than not, she simply doesn’t bother to do the work. She doesn’t seem to have the energy. She smiles wanly when Mrs. Munroe talks to her about her assignments, shrugs off her teacher’s concerns, and completes just enough of her schoolwork to get by and stay under the radar.

The other students sometimes tease Erika, but she’s not a very satisfying target. Getting a rise out of her is pretty much impossible. A few children give half-hearted attempts now and then, but mostly they just leave her be. She has few friends, and during lunch she sits alone, pushing food around her plate. Her thin arms bear scars from frequent cuts and gashes. These wounds are not the hallmarks of domestic violence — Mrs. Munroe has never spotted bruises, black eyes, or taped-up fingers. They look self-inflicted.

On the surface, Joey and Erika seem like polar opposites. Joey’s personality is aggressive and forceful; Erika’s is shy and yielding. Joey does everything he can to draw attention to himself; Erika does everything she can to avoid it. Joey torments others; Erika torments herself. Yet these two seemingly disparate conditions share a common root. Psychologists have found that, beyond the superficial differences in behaviour, aggression and depression are often different symptoms for the same disease: poverty, neglect, emotional distance, and abuse by parents. Spending time with troubled children can often reveal the truth of this seemingly self-contradictory notion. Withdrawn, shy students and bullies alike often share deep-seated and painful insecurities rooted in their family environment. Given this connection, it may not be all that surprising that the same few genes can make a child susceptible to anxiety and aggression, apathy and hyperactivity. The body of research supporting this notion is new and fairly small, but like a well-nourished child, it is growing with astounding speed.

“Internalizing behaviours” are, in a way, the invisible cost of maltreatment. They do not call attention to themselves; if anything, they strive to hide from view. Erika, the self-mutilating student we described earlier, perfectly exemplifies internalizing behaviour. She’s shy, withdrawn, constantly fatigued, and prone to depression. Her intelligence and talent are hamstrung by her overwhelming sense of apathy, a black hole sucking away her every ounce of energy and optimism, leaving her feeling hopeless and alone. Nervousness and anxiety are also frequent symptoms of internalizing behaviour, though they can be difficult to see. If Erika experiences them, she hides them well behind a veil of lethargy and indifference.

Children exhibiting internalizing behaviours often feel the same anger as those exhibiting “externalizing behaviour” (think of the rebellious and irascible Joey), but they tend to turn it on themselves, where it manifests in body mutilation, drug use, or eating disorders. They draw their pain inward, but that doesn’t mean it can’t be felt by those around them. Depression throbs like a wound in a family’s flank, one we can spot and bandage with antidepressants, but are all too often unable to actually heal. Though hard to notice at times, internalizing behaviours can be diagnosed, and researchers are growing increasingly confident in their prediction of what causes them. Unfortunately, the answer is complex, subject to variation, and incomplete.

This is not to say it isn’t useful. As the following studies will show, even a partial understanding of what causes internalizing behaviours can make treating them significantly easier.

Nothing to Fear but Fear Itself

Mice make ideal test subjects. Though less intelligent than their distant cousins, rats (themselves popular among researchers), mice are smart enough to train, have short birth cycles, and reproduce prodigiously, allowing researchers to observe the effects of an experiment over multiple generations without waiting years for the results to come in. Female mice reach sexual maturity when only 8 weeks old, and can birth 5 to 10 litters per year, each of which contains anywhere from 3 to 14 mice. That’s a lot of births, and a lot of mice. It’s also an ideal opportunity for selective breeding, and over the years scientists have produced dozens of different strains of mice, each with their own behavioural ticks, temperaments, and characters.

Interestingly, this quest for new and better experimental fodder has itself become grounds for an experiment. What makes these mice different from one another? The obvious answer would be their genes. A series of small mutations occurring over the span of multiple generations have manifested themselves in the mice’s tiny brains, changing how each breed looks and behaves. Mice, spanning as many as six generations in a single year, can evolve a lot quicker than humans, who hobble miles behind them with a 20-year generational lag. When assisted by the informed hands of professional breeders, a mouse’s evolutionary timeframe can be easily put on fast forward.

But Dr. Michael Meaney and his team questioned this assumption in their 2004 study. To them, a purely genetic explanation for interspecies variation seemed too simplistic. Differences between breeds could be pretty radical, and natural selection is a notoriously slow process, often taking thousands or tens of thousands of years to produce very slight adjustments to the genome. Even when factoring in human intervention, Meaney felt that things were going too fast for genes alone to manage. Something else must be working behind the scenes as well. To prove it, he first selected two very different breeds of mice. The first, called Type A, were skittish, docile, and easily frightened by new places or objects. The second, called Type B, were confident, curious, and almost wholly indifferent to threat.

Mouse Type	Mouse Behaviour
Type A	skittish, docile, and react strongly to stress
Type B	confident, curious, and more or less unfazed by new places or experiences

Meaney took both breeds and performed a cross-fostering study. Six hours after they were born, Type A and Type B mice were taken from their mothers and randomly fostered to mothers of the opposite type. Type A mothers raised Type B infants, and Type B mothers raised Type A infants, hence “cross-fostering.” As a control, some infants were taken and fostered to mothers of the same type — Type A infants with Type A mothers and Type B infants with Type B mothers. The mothers raised their adoptive offspring as their own, and Meaney let the infants reach maturity without any further intervention on his part.

When the mice were roughly 70 days old, they participated in a step-down test. Each mouse was placed on a small raised platform in the centre of an open plain. Meaney observed the mouse’s behaviour for the next five minutes, noting in particular its willingness to explore its new surroundings — though “explore” is perhaps overselling it. The study broke exploration down into three stages: extending the head over the edge of the platform, stepping two feet off of the platform, and stepping completely off of the platform. Hardly a venture worthy of Magellan or Columbus, but for a laboratory-raised rodent weighing little more than an ounce, step-down testing can be a truly harrowing experience. It evokes a deep-seated fear in a creature whose survival strategies have, for thousands of years, relied principally on its ability to scurry and hide. Aloft on a platform, surrounded by flat, open terrain devoid of grass or rocks or any sort of protective crevice or camouflage, they sense the atavistic dread of their wild ancestors, ears and eyes and nose trained to detect the first sign of an incoming hawk, fox, or bobcat. When confronted with the step-down test, docile mice tend to freeze, overcome by terror, while their more adventurous peers waste little time in exploring the boundaries of their new habitat.

It should come as no surprise, then, that Type A mice tend to take far longer than Type B mice to progress through the stages of exploration. Occasionally, Type A mice don’t leave the platform at all, but remain exactly where they’re placed, rigid with terror, until the experimenters remove them. Type B mice, on the other hand, barely hesitate before leaping nimbly from the platform and sniffing inquisitively around the perimeter of the cage.

Here was the crux of Meaney’s experiment. If Type A mice’s skittishness and Type B mice’s fearlessness comes hardwired into their genes, then they should exhibit it regardless of who raised them. However, if their dispositions were instead the product of their environment, then adopted mice should behave much like their step brothers and stepsisters, even though they are born from different breeds.

So which was it? Here’s the strange thing: it was sort of both.

When raised by Type A mothers, Type A mice acted as skittish as ever. They performed poorly on the step-down test, leaving their platforms with great reluctance or freezing with catatonic fright. But when raised by Type B mothers, Type A mice passed the test with flying colours, exploring their cage with the same gusto as their natural-born Type B brothers and sisters. Though mother mice don’t teach their offspring how to react to step-down testing in the conventional sense — few if any of the mothers will have ever even experienced such a thing — something in Type B mice’s maternal behaviour imparts in their foster children a bravado they would have otherwise lacked.

It seems that nurture has won the day. Except that Type B mice would beg to differ. Unlike their Type A peers, Type B mice displayed the same inquisitive, devil-may-care attitudes regardless of who raised them. When raised by Type A mothers, they nevertheless acted like their other biological siblings, sniffing eagerly around the testing site.

	Raised by Type A mothers	Raised by Type B mothers
Type A mice	Skittish, fearful, performed poorly on test	Fearless, curious, performed well on test
Type B mice	Fearless, curious, performed well on test	Fearless, curious, performed well on test

You can see why questions like “nature or nurture?” don’t have easy answers. They seem to lead us only to more questions. Why do environmental influences only work one way? How can Type B mothers subvert the ingrained timidity of Type A mice while Type A mothers are powerless to uproot the brash gusto of their adopted Type B offspring? What separates these two breeds? Meaney’s study can’t answer these questions, but it does at least pose them. And in science, new questions can be just as important as answers.

Of Mice and Men

Dr. Meaney’s study left us wondering what made Type A mice bend like putty beneath the sculpting hands of their environment, while Type B mice were, behaviourally speaking, rigid as stones. Enquiring scientific minds, spellbound as ever by those vast molecular blueprints, turned once again to genes. Of course, as an answer to Meaney’s questions, “genes” is distressingly vague. For the theory to hold any weight, its aim would have to be narrowed considerably. It would have to focus on one gene in particular.

Dr. Joan Kaufman suspected the culprit might be the serotonin transporter gene, known by the tongue-twisting moniker 5-HTTLPR.[18] As we discussed last chapter, the 5-HTT gene comes in two different varieties, long (l) and short (s), so named because one of them is built from a larger nucleotide sequence, making it physically longer than the other. In genetic parlance, these varieties are called alleles. Everybody has the same genes, but not everyone has the same alleles, which is why we are not all genetically identical. For instance, imagine two individuals named Tim and Patricia. Tim has brown eyes and Patricia has blue eyes. The gene determining their eye colour is largely similar — it sits on the same chromosome, is more or less the same length, contains an almost identical series of nucleotides, and does the same job in either of them. It is, essentially, the same gene, except that very slight changes have caused it to produce a different outcome in Tim than it does in Patricia. Tim has the brown eye allele of the eye colour gene, while Patricia has the blue eye allele.

Almost every gene in the human body comes in different alleles, which accounts for the tremendous variety of traits between individuals. In the 5-HTT gene’s case, the short allele is less efficient than the long allele, meaning it can generate fewer serotonin transporters in a given time. As serotonin is responsible for regulating mood, digestion, and a number of other important biological functions, a less efficient 5-HTT can, under the wrong circumstances, cause a lot of trouble.

5-HTT sits on the 17th chromosome of every human being and non-human primate, and is present in a similar form in most mammals. Since humans have two copies of chromosome 17, they also have two copies of 5-HTT, and they make good use of both of them. This means that a person can have two long alleles (l/l), two short alleles (s/s), or one copy of each (l/s).

Dr. Kaufman knew about 5-HTT ’s relationship with mood disorders. Many studies have suggested a correlation between 5-HTT and depression. A similar number have implicated it in cases of anxiety and alcoholism. What more likely culprit could there be? Her intuition bolstered by past research, Kaufman hypothesized that the s/s allele of the 5-HTT gene would increase a child’s chances of suffering from depression. This is not to say the allele actually made children depressed, only that it provided a foothold for the true causes of depression — in this case, negative environmental influences caused by abusive or neglectful parents — to latch onto.

To prove her hypothesis, Kaufman gathered 101 children ages 5 to 15 for her study, 57 of whom had been removed from their parents’ custody by the State of Connecticut Department of Children and Families due to allegations of abuse or neglect. The other 44 participants formed a “community control,” meaning they came from similar socioeconomic backgrounds to the test group (their families earned $25,000 a year or less and came from the same geographic region) but had never experienced maltreatment.

Next, Kaufman assessed each child’s behaviour to determine if he or she was depressed. Though depression is often considered a somewhat intangible state of being — we’ve all felt down or depressed at some point in our lives, and for all sorts of reasons — it is also a distinct psychological disorder (known officially by the name Major Depressive Disorder, or MDD) that can be empirically diagnosed. This was the kind of depression Kaufman was looking for, and to find it, she used a diagnostic model called the Short Mood and Feelings Questionnaire, which was originally developed by psychiatrist Adrian Angold. The Short Mood and Feelings Questionnaire is a survey used by psychologists, sociologists, and other researchers to a) determine whether or not a child is depressed, and b) quantify their level of depression on a numeric scale. It is easy to use and highly accurate, making it an ideal tool for experiments dealing with a large number of children, particularly those in which degrees of depression matter — where “is he depressed?” is less important than “how depressed is he?”

With all her data in place, Kaufman ran a series of statistical analyses and measured the findings against her hypothesis. She believed children with the l/l allele of the 5-HTT gene would be least susceptible to the long-term effects of abuse, and children with the s/s allele would be most susceptible, with l/s children falling somewhere in the middle.

The data proved her right, though “somewhere in the middle” veered a lot closer to the l/l side of things. Among abused and maltreated children, l/l and l/s children were equally likely to suffer from depression. Children with the s/s allele, on the other hand, were nearly twice as likely as l/l and l/s children to be depressed. This discrepancy did not exist in the non-maltreated children, who were less likely to be depressed than their maltreated peers regardless of their genotype.

Without exposure to abuse, 5-HTT doesn’t much matter. Or rather, it likely matters in some way we haven’t yet discovered, but for the purposes of fending off depression in supportive homes, s/s and l/l both work well enough. When children have stable upbringings, the environment allows their serotonin transporters some leeway, asking only that they function at a certain basic level. Under such lenient conditions, both l/l and s/s alleles have no trouble meeting demand.

Among abused children, however, that benchmark level of functionality doesn’t cut it. When burdened by an emotionally fraught environment, children’s serotonin transporters need to run at full capacity. If the serotonin transporters aren’t up to the task, then things break down and children suffer. We can’t yet say for sure what this breakdown entails, but we can make an educated guess. Serotonin helps regulate mood — along with dopamine, it is one of the two chemicals responsible for allowing us to feel pleasure. Transporters are a protein product vital to the processing of serotonin in the human brain, and 5-HTT is responsible for building them. The better it does its job, the more serotonin transporters there are doing theirs and the smoother the whole system runs. Switch the l/l allele for the less efficient s/s model and production dips. That’s fine if serotonin is in low demand, but if the body needs more to cope with the stress it is continually bombarded with at home, and if demand can’t match supply…. You see the problem.

Kaufman, J., Yang, B.Z., Douglas-Palumberi, H., Houshyar, S., Lipschitz, D., Krystal, J.H., and Gelernter, J. (2004). “Social Supports and Serotonin Transporter Gene Moderate Depression in Maltreated Children.” Proceedings of the National Academy of Sciences of the United States of America, 101(49), 17316–17321.

Though different in a lot of ways, Meaney’s cross-fostering experiment and Kaufman’s maltreatment studies suggest a similar relationship between genes and environment. In Meaney’s experiment, Type A mice had the equivalent of the s/s allele, while Type B mice had the l/l. When reared in adverse conditions (remaining with “scaredy-mouse” Type A mothers), the Type A mice succumbed to environmental pressure, adopting the timid disposition that is the hallmark of their breed. However, when brought to a more stable, supportive environment (being cross-fostered to “tougher” Type B mothers) their timidity failed to develop. Conversely, Type B mice — the resilient l/l children of the rodent world — were unaffected by the troubled Type A environment, maintaining their extroverted personalities regardless of who raised them.

Building the Human Brain

In 2006, Kaufman performed a follow-up study in order to confirm and expand upon her initial findings. Her new experiment was identical in structure to her old one, except that it included an extra variable: a gene on the eleventh chromosome called BDNF. BDNF codes for brain-derived neurotrophic factor, a protein responsible for developing and maintaining brain cells. Studies have linked the gene to child-onset depression, and Kaufman hypothesized that it might worsen symptoms of depression in children already made vulnerable by the l/s or s/s 5-HTT allele. To confirm this, she genotyped (or genetically tested) children in search of a specific polymorphism (or variety) of the BDNF gene.

Like 5-HTT, BDNF has two alleles of interest to researchers: “val” and “met.”[19] They work on exactly the same principle as 5-HTT ’s long (l) and short (s) alleles. Val is the more common and stable allele, the equivalent of l, and met is the rarer, more troublesome allele, the equivalent of s. As with 5-HTT, BDNF is active on both chromosomes. Individuals can be val/val, val/met, or met/met (the equivalent of l/l, l/s, and s/s, respectively).

The val/met and met/met alleles are associated with a number of neurological conditions, including Alzheimer’s disease, Parkinson’s disease, eating disorders, depression, and bipolar disorder. People with val/met or met/met alleles also perform relatively poorly on tests measuring their ability to remember places or events. This may come as a result of the val/met and met/met alleles’ effect on the hippocampus, a region of the brain responsible for transitioning memories from short-term to long-term storage. On average, people with the val/met or met/met allele have a smaller hippocampus by volume than those with the more common val/val allele.

Considering BDNF ’s role as a developer of neural tissue, it’s not hard to imagine how even a small mutation in the gene could greatly impair functionality in an organ as intricate as the brain. If one’s hippocampus somehow shrank, its ability to consolidate short-term memories into long-term ones would be reduced, which would explain why individuals with the val/met or met/met allele perform poorly on memory recollection tests while doing as well as their val/val peers on tasks that scarcely involve the hippocampus, such as learning new words and planning ahead — their hippocampi have been built with a suboptimal protein material. The hippocampus still works, of course, or anyone with a met allele would be functionally brain-dead. But it works, broadly speaking, a little less well than it could. Memories come a bit slower, slip away quicker, and make easier prey for Alzheimer’s, which regularly chooses the hippocampus as its first target.

Of course, this is only half the story. The environment always has its say as well, which is why Kaufman included BDNF in her gene-by-environment study. She wondered if rather than directly causing these ailments, the val/met and met/met alleles might, like the s/s 5-HTT allele, simply make the individual more susceptible to them.

Kaufman’s new experiment mirrored its predecessor. As in her previous study, participants were 5 to 15 years old and recruited in the same manner — maltreated and non-maltreated children were drawn from the same community and lived in similar socioeconomic environments. The only difference between them was that maltreated children, unlike the control children, had at some point been taken from their parents for a minimum of 96 hours due to allegations of abuse.

Kaufman divided the children into two groups based on their BDNF genotype, creating a val/val group and a val/met group.[20] She treated each group as a separate study and recompiled her data. In both groups, maltreated children with s/s 5-HTT alleles were the most likely to exhibit symptoms of depression. But among this statistically disadvantaged group, those who also had the val/met BDNF allele were more susceptible still.

Among the val/val group, maltreated children with the s/s 5-HTT genotype scored an average of 5 points higher on the depression scale (meaning they were more depressed) than maltreated children with the protective l/l alleles; in the val/met group, this discrepancy more than doubles. The val/met genotype acts as a kind of susceptibility multiplier, expanding the gap between s/s and l/l children, but only when those children were maltreated. Among children who were not maltreated, neither the BDNF nor the 5-HTT allele they possessed had a more than marginal impact on their odds of suffering from depression.

Kaufman’s findings paint a bleak picture for val/met, s/s children living in abusive conditions. Is there any hope for these kids at all? Are the odds so thoroughly stacked against them that they are, in effect, born into lives of poverty, addiction, and crime? The statistics may seem damning, but we prefer to reject such fatalism. And lucky for us, Kaufman’s study offers a tangible cause for optimism.

During her study, Kaufman asked participating children to list people in their lives whom they confide in, count on financially, tell good or bad news to, have fun with, and approach when they have a problem. Children described their relationships with each person they mentioned, and told researchers how often they were able to see him or her. Kaufman used this information to measure each child’s level of social support. The more people children named as supportive presences, and the more often they were able to see these people, the higher their rating on Kaufman’s social support index.

Kaufman, J., Yang, B.Z., Douglas-Palumberi, H., Grasso, D., Lipschitz, D., Houshyar, S., … and Gelernter, J. (2006). “Brain-derived Neurotrophic Factor–5-HTTLPR Gene Interactions and Environmental Modifiers of Depression in Children.” Biological Psychiatry, 59(8), 673–680.

Focusing solely on the maltreated cohort, Kaufman once again measured the effects of genes and environment on children’s depression scores. Except this time, instead of separating children into maltreated and non-maltreated groups, Kaufman divided the children into high support and low support groups, based on their answers to her social support questions. High support children knew a number of adults outside of their parents whom they regularly went to for advice, comfort, and support. These adults included grandparents, family friends, other relatives, favourite teachers, friends’ parents, and community members to whom the children had a strong connection. They were a frequent presence in the child’s life, providing the emotional and intellectual nourishment he or she might not necessarily have gotten at home. Low support children did not have this same advantage. They had few close relationships with adults outside of their parents (or perhaps none at all), and those whom they did trust were not always available to them.

Having constructed a new framework, Kaufman reassessed the data. Keep in mind, every child participating in this leg of the study experienced maltreatment at home. Living in houses fraught with anxiety, anger, and pain, it’s difficult to imagine that a kind word from a grandparent or uncle or extra attention from a particularly dedicated teacher could make much difference to how they behaved. Yet it did.

The results of Kaufman’s high support/low support study and her maltreated/non-maltreated study possess an eerie symmetry. In each experiment, the effects of 5-HTT and BDNF genotype are identical, with high support children filling in for the non-maltreated group. High support children were as impervious to genetic influence as non-maltreated children in spite of the fact that they had been abused. Their depression scores were on the whole higher, but they displayed none of the genetic volatility characteristic of abused children. Those with the s/s 5-HTT and val/met BDNF alleles — the devastating one-two punch of genetic oversensitivity — were no more depressed than children with the protective l/l and val/val alleles. The presence of stable, supportive adults in their lives mitigated the effects of an abusive home life, particularly among those who, because of an accident of genetics, would have been most affected.

Kaufman’s research can teach us two things. The first is that human intervention can trump genetics. When the odds are stacked against you, when your home life taxes your emotional and intellectual development, when not one but two genes undermine your brain’s ability to cope with the strain, even then you can find solace in a friendly face or a guiding hand or a shoulder to cry on. As fragile and beholden to the whims of their parents as children seem at times, they nevertheless have a stunning tenacity about them, an ability to derive comfort and support from wherever they may find it. This ability speaks volumes about the plasticity of child development. It also leads us to Kaufman’s second point: development is complex. Research has pushed aside the notion of predominance in either nature or nurture, ushering in a more nuanced paradigm of gene-by-environment interactions. In this new theory, the quality of a child’s environment influences how he or she behaves, but the extent of that influence is determined by the presence of certain genes. The environment sets the station but genes control the volume. And there isn’t just one volume knob, either. The 5-HTT gene can dial up depression a good 10 decibels, say, but then the BDNF gene can keep it capped there, or crank it up another 10. Suddenly our simple transistor radio has become a home stereo system. But then consider the moderating influences enjoyed by high support children. When the family environment is stable and supportive, does that dial down the depression? Does it dial up anything else? Where does that fit in our analogy? A separate bass or treble knob on the speakers themselves? The metaphor has grown ungainly. It falls apart.

Child development doesn’t take well to pithy metaphors. The human body is an immensely, perhaps even infinitely complex organism, a sprawling network of molecules responding to commands issued from both inside (our genes) and out (our environment). Genetic and environmental influences clash, converge, and collude with one another, holding court over a seething mass of cells that somehow function in perfect (or perhaps only near-perfect) harmony. Sometimes it seems the more we learn, the less we know. Fortunately, this isn’t the case. We don’t know everything, but we know quite a bit. A lot more now than we did 10 years ago, surely, and in another 10 years we’ll know a lot more still.

And, most important of all, we have learned how to harness this knowledge. Scientists and policy makers have already begun advocating for change in the way our communities support their most vulnerable children. But their research does not apply solely to cases of dire poverty or criminal abuse. It affects all children, even those from loving, supportive homes.