Family and Parenting 3-Book Bundle. Michael Reist

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СКАЧАТЬ 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.

      Chapter 5

      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. СКАЧАТЬ