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Knowledge Is Power

Unlike depression, anxiety, and other internalizing behaviours, externalizing behaviours are highly visible. We see them in graffiti-covered storefronts and kicked-over newspaper vending boxes; in bars or on buses, where a furtive glance or an arm brushed accidentally against a shoulder turns in an instant into a shouting match; and on the news, in stories of robbery, domestic violence, and murder. Think of Joey from our last chapter. A classic example of externalizing behaviour, he drew attention to himself at every opportunity, openly flaunting rules, disrupting class, and bullying anyone who dared to meet his eye. Unlike Erika, who could be easily overlooked by a teacher less empathetic than Mrs. Munroe, Joey saw to it that he was noticed. To Erika, attention was a vile tincture, a medicine she hated taking and that didn’t seem to do her any good; to Joey, it was a drug.

The negative effects of externalizing behaviour ripple outward from the individual, affecting his family, his peers, his co-workers, and ultimately his community — and we use “his” here deliberately. Boys are far more likely than girls to exhibit externalizing behaviour in response to a stressful environment. Girls, by contrast, are more likely to suffer from depression or anxiety, though internalizing behaviours are significantly less gendered than externalizing behaviours.

Hundreds of studies have shown that stress caused by verbal and physical violence, mental illness, and substance abuse greatly increases children’s chances of suffering from excessive aggression, alcoholism, and ADHD. Though this correlation is well-documented, it is not incontrovertible. Plenty of children come from stressful homes yet grow up to be well-adjusted adults. What benevolent force saves them from the downward spiral of anger and violence that claims so many of their peers? Is it blind luck? Is it social support? Or do they possess some innate genetic filter that keeps environmental pollutants out of their systems?

A Canary in the Coal Mine

A 2005 study led by Sara Jaffee compared the effects of a stressful home environment on identical and fraternal twins. Fraternal twins are conceived when two eggs are fertilized by two different sperm, while identical twins occur when a fertilized egg — called a zygote — splits into two separate organisms during its first few replications. Identical twins have identical genomes, which explain their great physical similarities. Fraternal twins, on the other hand, are simply two siblings who shared a womb. Genetically speaking, they are no more alike than a typical brother and sister.

In technical terms, identical and fraternal twins are distinguished by their zygosity, or the number of fertilized eggs from which they were born. Identical twins, born from a single zygote, are called monozygotic, while fraternal twins are called dizygotic.[21]

Zygosity	Twin type	DNA in common
Dizygotic	Fraternal (non-identical) twins	50 percent
Monozygotic	Identical twins	100 percent

The goal of Jaffee’s study was to show that a person’s genes were correlated to his or her sensitivity to the long-term effects of maltreatment. She developed a framework that stratified children’s risk of exhibiting externalizing behaviour based on their zygosity and the presence or absence of externalizing symptoms in their twins. This premise may seem confusing, but it is actually fairly simple. If a trait has a genetic link, then one of your relatives possessing that trait increases your chances of possessing it as well. The closer that relative is to you genetically, the more alleles you share, and the greater the odds that you both display the same version of a given trait. Dizygotic twins have roughly 50 percent of their polymorphisms in common, so the odds of them sharing a genetic trait are approximately one in two. Monozygotic (identical) twins, on the other hand, have 100 percent of their polymorphisms in common, so the odds of them not sharing a genetic trait are slim to none (although it is possible for a gene to mutate shortly after the zygote separates, and certain genetic traits can be switched on or off by the environment, a phenomenon we will address in more detail later in this book). Therefore, if you observe a genetic trait in one dizygotic twin, there is a decent chance it will be visible in the other twin as well; observe the same trait in a monozygotic twin, and its presence in the other twin is basically guaranteed.

Bearing this in mind, Jaffee developed a 4-point scale of genetic risk, its underlying principle being that a symptom in one twin predicts the presence of that same symptom in the other twin. Your sibling becomes a sort of canary in the coalmine of your genes, their behaviours a genetic portent of what you may one day face.

The lowest-risk children were those whose monozygotic (identical) twins showed no signs of externalizing behaviour. Considering these twins share all of their DNA, the absence of a genetic trait in one twin can safely predict its absence in the other. Next were children whose dizygotic twins showed no signs of externalizing behaviour. Though the trait could arise from the 50 percent of alleles the children don’t share, we can at least guarantee that one half of their DNA is safe. Riskier still were children whose dizygotic twins showed signs of externalizing behaviour. At this level of the scale, we have confirmed that the trait exists within the subject’s immediate family. Perhaps they inherited it or perhaps they did not, but it is a confirmed possibility. Lastly, children whose monozygotic (identical) twins showed signs of externalizing behaviour were the highest risk of all. If one twin has the trait, and the trait comes from a polymorphic variation, then the other twin almost certainly has the offending variation, too.

Which is not to say that he or she has the trait.

Anyone who has met a set of identical twins could tell you that the term “identical” is not, in the most technical sense, accurate. Spend enough time with them and you will be able to distinguish one from the other just by looking at them. The telltale sign may be a mole or a freckle, or a slight difference in height or weight, or a result of their varying mannerisms and inflections. Though casual acquaintances may not be capable of discerning one from the other by appearance alone, a brief conversation should suffice. The “identical” aspects of monozygotic twins rarely extend to their personalities. In fact, identicals often exaggerate the differences between each other, perhaps in order to more firmly establish unique identities. A twin girl who is slightly more extroverted than her identical sibling will make a point of acting as outgoing as possible, while her more reserved twin will draw further inward. These behaviours change the way each twin is treated by her teachers, her peers, and even her own family, which in turn reinforces the differences between them.

Living things are more than the sum of their parts. Genes are not our overlords, especially when it comes to complex behavioural traits. One’s environment is equally important, and we would expect the home life of these children to play an important role in their development (or lack thereof) of externalizing behaviours. Jaffee is, of course, aware of this, which is why her study grouped children based on environmental factors as well as genetic ones. More specifically, she considered whether or not they had been physically maltreated.

Interviewers asked the twins’ mothers a series of “probe questions” designed to elicit conversation about their children’s past maltreatment without coming across as accusatory or hostile. Questions included “Do you remember any time when your child was disciplined severely enough that he may have been hurt?” and “Did you worry that you or someone else may have harmed or hurt your child?” The interviewers chose their words carefully, avoiding any implications that the mother may have been at fault. If the mother reported any maltreatment, the interviewer probed for details, keeping careful notes on what happened, when, how often, and if the police or child services were involved. They also kept an eye out for subtler clues, observing how the mother and child acted during their conversation. A nervous glance, downcast eyes, fidgeting, and increased tension in the presence of the father, or any hint at a darker truth was noted, analyzed, and used to determine whether the child was potentially being maltreated. The evidence didn’t need to be ironclad; for inclusion in the study’s test group, children could be classified either probable or definite cases of maltreatment.

Jaffee took the maltreated and non-maltreated cohorts (containing 307 and 809 children, respectively), subdivided each of them into groups based on her 4-point risk scale, and tallied the frequency of conduct problems in each group, as reported by the children’s mothers and teachers. Conduct problems included fighting, bullying, lying, stealing, cruelty to people or animals, vandalism, and breaking rules. As expected, each degree up the maltreatment risk scale correlated to an increase in conduct disorder in both cohorts. Lowest risk children, regardless of whether or not they were maltreated, were less likely to act out than children of the same cohort in the next bracket up. However, within each risk group, the maltreated children were more likely to exhibit conduct disorders than the non-maltreated children. Moreover, the gap between risk levels was wider in maltreated than non-maltreated children. As the risk level rose, the amount of maltreated children displaying conduct disorders increased considerably more than it did in the non-maltreated cohort. In the lowest genetic risk group, maltreatment caused conduct disorders to rise 2 percent compared to non-maltreated children of the same risk level; in the highest genetic risk group, the increase was 24 percent.

Jaffee, S.R., Caspi, A., Moffitt, T.E., Dodge, K.A., Rutter, M., Taylor, A., and Tully, L.A. (2005). “Nature × Nurture: Genetic Vulnerabilities Interact with Physical Maltreatment to Promote Conduct Problems.” Development and Psychopathology, 17(1), 67–84.

Jaffee’s study is a helpful example of how genes and environment interact. Maltreatment affected children negatively regardless of their genetic risk; maltreated children were more likely to misbehave than non-maltreated children in every risk group. Predicting how much more likely is where genes came into play. Though an excellent model, the weakness of Jaffee’s study lies in its generality. Much like Meaney’s experiments with Type A and Type B mice, Jaffee showed that genes influence our susceptibility to abuse without targeting any one gene. In order to understand the relationship between genes and environment, we need to narrow our focus to a precise genetic target.

Pleasure, Anger, and Dopamine

Dopamine is, arguably, the most powerful motivator in the human brain’s arsenal. Without it our entire species would collapse into despondency, indifference, and extinction. But dopamine is no good on its own. In order to reap its benefits, our brains need a way to process it. For this, we have a protein product called a dopamine receptor, a tiny neurological trigger fired by contact with a dopamine molecule. The human brain has many different types of these receptors, but perhaps none has come under more scientific scrutiny than the DRD4 family, a class of dopamine receptors implicated in a host of adverse conditions, including schizophrenia, Parkinson’s disease, bipolar disorder, anorexia nervosa, bulimia nervosa, and drug addiction. A protein product, DRD4 is coded for by the DRD4 gene, and much of its reputation as a hotbed of neurological strife comes from a single allelic variation called the 7-repeat allele. As its name suggests, 7-repeat is a variation of the DRD4 gene where a brief sequence of 48 nucleotides (the microscopic molecules from which genes are constructed) repeats seven times.

Repetition is not what makes the 7-repeat unusual; different varieties of DRD4 have the same sequence repeated anywhere from two to eleven times. What makes the 7-repeat allele unique is its weaker-than-average reaction to dopamine, compared with other versions of DRD4. To put it crudely, the 7-repeat allele is not all that good at its job. While its compatriots handle influxes of dopamine with ease, 7-repeat struggles to stay on target. This idiosyncrasy has made 7-repeat a subject of great interest to scientists across multiple disciplines, as a person’s neurological response to dopamine influences, on a very fundamental level, how that person behaves. It seems inevitable that such an infamous allele — particularly one so intimately involved in regulating human behaviour — would catch the eye of perceptive scholars studying child development.

Among those paying attention were Dutch researchers Marian Bakermans-Kranenburg and Marinus Van IJzendoorn. Together, the two professors from Leiden University in the Netherlands have spearheaded multiple studies investigating the effects of 7-repeat on children’s behaviour. They are, arguably, among the world’s foremost experts on the subject. And they have found a link between the troublesome gene, early rearing environments, and children’s behaviour that you, having read the results of Joan Kaufman’s studies earlier this chapter, may find awfully familiar.

First, Bakermans-Kranenburg and Van IJzendoorn recruited 47 mothers when their children were 10 months old and followed them until the children were three. They visited each mother at home and filmed her performing normal, unstructured activities — cleaning, cooking, feeding, or changing or playing with her child, etc. Mothers weren’t told what the two researchers were looking for, or even whether they or their children were the focus of the study. They were instructed to act as normally as possible and, after a brief period of self-consciousness, settled quickly into their typical routine.

Bakermans-Kranenburg and Van IJzendoorn studied the tapes, documenting the behaviour of each mother-child pair. In the children’s case, they were interested in signs of externalizing behaviour — talking back, hitting, throwing food and toys, fits of anger, hyperactivity, any outward display of excessive aggression or unchecked energy. For mothers, the focus was a bit different. Less attention was paid to actions, and more to interactions. Bakermans-Kranenburg and Van IJzendoorn wanted to gauge something called maternal sensitivity, a variable that measures how adept mothers are at anticipating, interpreting, and responding to their children’s needs.

Mothers’ actions were rated on the Maternal Sensitivity Scale, a sociological measure comprised of four categories: a mother’s awareness of her child’s signals of needs or wants, her accurate interpretation of those signals, the appropriateness of her response, and how promptly she responded. Mothers who scored on the upper half of the scale — meaning they responded quickly and appropriately to their children’s needs — were placed in the high-sensitivity group, and mothers on the lower half — those who responded slowly or infrequently to their children, or who misinterpreted their needs — were classified low sensitivity.

To acquire the study’s final variable, researchers took DNA samples from each child participating in the study and determined which polymorphism (or variation) of the DRD4 gene they possessed. More specifically, they wanted to know whether or not the children had the infamous 7-repeat allele. Bakermans-Kranenburg, Van IJzendoorn, and their observation team were kept clear of the results of these tests until after they had reviewed the tapes and submitted their appraisals of mother and child behaviour. Sequestering data is critical in these types of studies, where objectivity is a goal that is exceedingly difficult to reach, and the slightest potential for bias in the researcher can poison the entire experiment. If the researchers charged with scoring mother-infant behaviour knew which children had the volatile 7-repeat allele, they could — either consciously or unconsciously — rank them higher on the externalizing behaviour scale in order to prove their hypothesis correct. This problem — called confirmation bias — is a constant hazard to experiments in the social sciences, and researchers must guard against it vigilantly.

When all the data was in place, Bakermans-Kranenburg and Van IJzendoorn put it through rigorous analyses. The results were significant. For children with the 7-repeat allele, mothers’ behaviour greatly influenced their odds of acting out. The 7-repeat children with low-sensitivity mothers (mothers who misinterpreted their children’s needs, or who responded indifferently to them) exhibited a great deal of externalizing behaviour, while 7-repeat children with high-sensitivity mothers (mothers who understood their needs and met them promptly) barely showed any externalizing behaviour at all. They were less than half as likely as 7-repeat children with low-sensitivity mothers to talk back, act out, or show signs of ADHD. Children without the 7-repeat allele fell somewhere in the middle, though they were closer to the well-behaved 7-repeat high-sensitivity children than the defiant 7-repeat low-sensitivity children. Their mothers’ level of sensitivity didn’t make much difference to their odds of displaying externalizing behaviour.

Bakermans-Kranenburg, M.J., and Van IJzendoorn, M.H. (2006). “Gene–Environment Interaction of the Dopamine D4 Receptor (DRD4) and Observed Maternal Insensitivity Predicting Externalizing Behavior in Preschoolers.” Developmental Psychobiology, 48(5), 406–409.

Keep in mind that the women in the low-sensitivity group were not necessarily bad mothers. The study did not recruit parents accused of child abuse or neglect, nor did it focus on families from groups generally considered to be high-risk (impoverished, uneducated, suffering from alcoholism or drug addiction, prone to violence, etc.). Low-sensitivity mothers didn’t leave their children home alone for hours on end to go party, or drink themselves sick, or bully their children with taunts or smacks or insults. Some of them were absent-minded. Many of them were overworked and exhausted and didn’t have the energy or patience required to meet their children’s every immediate need, but loved their children all the same and wanted nothing but the best for them. The vast majority were probably doing their best, and would be horrified at the thought that their actions might be hurting their children. And yet, their children were over twice as likely to display aggressive or violent behaviour as those of high-sensitivity mothers — assuming, of course, the children in question had the 7-repeat allele of the DRD4 gene. That is not a small discrepancy, and it shows that in parenting, the little things matter just as much as the big ones.

Fixing the Problem

Having established a link between genes, maternal sensitivity, and children’s behaviour, Bakermans-Kranenburg and Van IJzendoorn strove to use this knowledge to help those children who were most at risk. Their study showed that children with the 7-repeat allele and low-sensitivity mothers were by far the most likely to display signs of externalizing behaviour. Having just one of the two traits — 7-repeat but a high-sensitivity mother, or a low-sensitivity mother but no 7-repeat — was pretty much as good as having neither. Therefore, it stood to reason that changing one of those two variables in vulnerable children would lower their risk considerably. Genes can’t change. Maternal behaviour can.

The two researchers recruited 157 families with children who exhibited signs of externalizing behaviour, such as aggression, hyperactivity, and hostilely defiant behaviour toward authority figures. The families were randomly assigned to either a test or control group. Families in the test group underwent an intervention program Bakermans-Kranenburg and Van IJzendoorn had developed.

Each family in the program received six home visits from female consultants called interveners. During these visits, the interveners observed how the family interacted, appraised their parenting strategies, and offered tips and suggestions for improved communication between parents and children. Each visit was themed, focusing on different skill sets, such as responding promptly to children’s signals, sharing emotions, and using positive reinforcement. The last two sessions were review, where interveners helped bolster previously learned skills. At the end of the program, parents received brochures filled with tips and exercises on the key issues of the intervention.

Meanwhile, the control group participated in a largely insubstantial program called a dummy intervention. Researchers contacted parents by phone and discussed parenting issues with them. Parents were encouraged to talk about their children’s development, but the “interveners” did no intervening whatsoever; they did not observe the participants’ parenting strategies, nor did they offer any tips on how to more effectively parent children with externalizing behaviour disorders. The entire point of the control was to make parents think they were participating in an intervention program without actually providing one. Bakermans-Kranenburg and Van IJzendoorn met with both groups a year after the program’s completion and noted the change, if any, in children’s externalizing behaviours.

The results were, at first glance, lukewarm. As expected, 7-repeat children benefited from the real intervention, but the effect was marginal; 7-repeats who underwent the intervention program scored an average of 2.5 points lower on the externalizing behaviour scale than 7-repeats in the control group, who received the deliberately ineffective “dummy” intervention. Non-7-repeat children varied even less. Although 2.5 points is enough to be statistically significant, given the respectable sample size of the study, it is hardly earth-shattering. The intervention program seemed like a dud.

Bakermans-Kranenburg and Van IJzendoorn were not to be dissuaded. Pushing the control group aside, they considered their data from a new angle. Perhaps, they thought, merely participating in the program wasn’t enough. A far more influential factor would be whether or not the parents who received this information actually did anything with it, or whether they promptly fell back into old habits after the intervention program concluded.

The two researchers set out to ascertain exactly that. They took parents who had participated in the real intervention, re-observed them interacting with their children, and broke them into two groups based on whether or not they had continued to follow the techniques prescribed by the program.

Suddenly, the intervention seemed far more promising. Among children with the DRD4 7-repeat allele, those whose parents took the program’s lessons to heart scored 6 points lower on the externalizing behaviour scale (meaning they were calmer, happier, and less prone to anger) than children whose parents chose not to follow the plan, a difference more than twice that between the intervention and control groups. Even among families in the dummy intervention group, those who had adopted a more engaged and interactive parenting style — be it through advice gleaned from a parenting book or the suggestion of a grandparent or simply by learning from their own experiences as parents — saw a precipitous drop in their children’s externalizing behaviour, with children scoring 4 points lower on the externalizing behaviour scale than those of less adaptive parents. The drops were less substantial in children without the DRD4 7-repeat allele, though even they showed a marked improvement.

Bakermans-Kranenburg and Van IJzendoorn’s intervention was a rousing success, but not because it was a brilliant or life-altering program. Its power didn’t come from comprehensive lesson plans or advanced technology or extensive funding — in fact, it possessed none of these traits, just half a dozen chats with an informed third party and several pages of accessible parenting literature. Nurses or social workers or perhaps even trained parents could provide programs like this in our communities.

The true success of the program rested on the parents’ desire to better understand and relate to their children. Without that spark, the program meant nothing.[22]

Bakermans-Kranenburg, M.J., IJzendoorn, M.H.V., Pijlman, F.T., Mesman, J., and Juffer, F. (2008). “Experimental Evidence for Differential Susceptibility: Dopamine D4 Receptor Polymorphism (DRD4 VNTR) Moderates Intervention Effects on Toddlers’ Externalizing Behavior in a Randomized Controlled Trial.” Developmental Psychology, 44(1), 293.

In the insular, almost solipsistic world of infant development, small actions have big consequences. Young brains grow at a feverish rate, and their constant, relentless expansion makes them ravenous for stimuli. Everything they see, hear, taste, touch, and smell is gobbled up, pored over, processed, and neatly filed away for future consideration. Much of it will ultimately be discarded, but a surprising amount of it will be absorbed and incorporated into the child’s beliefs, attitudes, and behaviour. Minds, as mysterious and intangible as they may seem, are rooted in the physical world. They are built experience by experience and neuron by neuron, materials as real — and as crucial — as the bricks and mortar of a house’s foundation. Mislay the bricks or skimp on the mortar and the house stands crooked or crumbles to the ground.

Sounds scary, doesn’t it? And you know what, it is scary. Parenting is a hard job. It requires creativity, discipline, intuition, compassion, tenacity, and wisdom. It comes with long hours, tremendous responsibility, and no pay. It forces you to become the parent your child needs you to be, to adapt your responses, emotions, and behaviours to the benefit of your child. It demands the best of you at all times. It is tough. But it is far from impossible. Your parents did it, after all, as did your grandparents before them, and your great-grandparents before them. Trailing behind you to the distant horizon of human history is a chain of parents thousands of generations long. Some of them did a better job than others. Yet every single one of them, in their own way, succeeded at humanity’s most important endeavour. They kept the ball rolling for another generation. If they could do it, surely you can too. Think of all the advantages you have over your ancestors 10 generations back. You have clean water and family doctors and hand sanitizer. You have penicillin and daycare and the polio vaccine. You have freedom from famine and pestilence and war. You have knowledge, more than any generation that came before you.

We also have civilizations and governments that can afford to attend more to the needs of families, encouraging and helping parents to be the sensitive, attentive people their children need them to be. Parenting needs to be recognized as the cornerstone of greater public health and supported in as many constructive ways as possible. But we are getting ahead of ourselves. There is much more evidence still to come that will reveal the true scope of parenting’s influence on individuals, families, and the societies in which they dwell.

Scientific studies, with their complex behavioural scales and near-inscrutable graphs, can seem abstract and sterile. But beneath the tables and jargon and rhetoric lies a rich and ever-deepening pool of knowledge. We are the beneficiaries of a grand and storied tradition of scientific inquiry, but also of practical experience. It is at the crossroads of these two variables that our understanding of early child development is at its most lucid. And perhaps no field of study gets it better than attachment theory.