Family and Parenting 3-Book Bundle. Michael Reist
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Название: Family and Parenting 3-Book Bundle

Автор: Michael Reist

Издательство: Ingram

Жанр: Секс и семейная психология

Серия:

isbn: 9781459730861

isbn:

СКАЧАТЬ 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 from the same community and lived in similar socioeconomic 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 СКАЧАТЬ