Family and Parenting 3-Book Bundle. Michael Reist

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      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.

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