Family and Parenting 3-Book Bundle. Michael Reist
Читать онлайн книгу.
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.
Kaufman, J., Yang, B.Z., Douglas-Palumberi, H., Houshyar, S., Lipschitz, D., Krystal, J.H., and Gelernter, J. (2004). “Social Supports and Serotonin Transporter Gene Moderate Depression in Maltreated Children.” Proceedings of the National Academy of Sciences of the United States of America, 101(49), 17316–17321.
Though different in a lot of ways, Meaney’s cross-fostering experiment and Kaufman’s maltreatment studies suggest a similar relationship between genes and environment. In Meaney’s experiment, Type A mice had the equivalent of the s/s allele, while Type B mice had the l/l. When reared in adverse conditions (remaining with “scaredy-mouse” Type A mothers), the Type A mice succumbed to environmental pressure, adopting the timid disposition that is the hallmark of their breed. However, when brought to a more stable, supportive environment (being cross-fostered to “tougher” Type B mothers) their timidity failed to develop. Conversely, Type B mice — the resilient l/l children of the rodent world — were unaffected by the troubled Type A environment, maintaining their extroverted personalities regardless of who raised them.
Building the Human Brain
In 2006, Kaufman performed a follow-up study in order to confirm and expand upon her initial findings. Her new experiment was identical in structure to her old one, except that it included an extra variable: a gene on the eleventh chromosome called BDNF. BDNF codes for brain-derived neurotrophic factor, a protein responsible for developing and maintaining brain cells. Studies have linked the gene to child-onset depression, and Kaufman hypothesized that it might worsen symptoms of depression in children already made vulnerable by the l/s or s/s 5-HTT allele. To confirm this, she genotyped (or genetically tested) children in search of a specific polymorphism (or variety) of the BDNF gene.
Like 5-HTT, BDNF has two alleles of interest to researchers: “val” and “met.”[19] They work on exactly the same principle as 5-HTT ’s long (l) and short (s) alleles. Val is the more common and stable allele, the equivalent of l, and met is the rarer, more troublesome allele, the equivalent of s. As with 5-HTT, BDNF is active on both chromosomes. Individuals can be val/val, val/met, or met/met (the equivalent of l/l, l/s, and s/s, respectively).
The val/met and met/met alleles are associated with a number of neurological conditions, including Alzheimer’s disease, Parkinson’s disease, eating disorders, depression, and bipolar disorder. People with val/met or met/met alleles also perform relatively poorly on tests measuring their ability to remember places or events. This may come as a result of the val/met and met/met alleles’ effect on the hippocampus, a region of the brain responsible for transitioning memories from short-term to long-term storage. On average, people with the val/met or met/met allele have a smaller hippocampus by volume than those with the more common val/val allele.
Considering BDNF ’s role as a developer of neural tissue, it’s not hard to imagine how even a small mutation in the gene could greatly impair functionality in an organ as intricate as the brain. If one’s hippocampus somehow shrank, its ability to consolidate short-term memories into long-term ones would be reduced, which would explain why individuals with the val/met or met/met allele perform poorly on memory recollection tests while doing as well as their val/val peers on tasks that scarcely involve the hippocampus, such as learning new words and planning ahead — their hippocampi have been built with a suboptimal protein material. The hippocampus still works, of course, or anyone with a met allele would be functionally brain-dead. But it works, broadly speaking, a little less well than it could. Memories come a bit slower, slip away quicker, and make easier prey for Alzheimer’s, which regularly chooses the hippocampus as its first target.
Of course, this is only half the story. The environment always has its say as well, which is why Kaufman included BDNF in her gene-by-environment study. She wondered if rather than directly causing these ailments, the val/met and met/met alleles might, like the s/s 5-HTT allele, simply make the individual more susceptible to them.
Kaufman’s new experiment mirrored its predecessor. As in her previous study, participants were 5 to 15 years old and recruited in the same manner — maltreated and non-maltreated children were drawn