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
