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Family and Parenting 3-Book Bundle - Michael Reist


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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.

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      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.

      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,


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