Читать книгу Introduction to Abnormal Child and Adolescent Psychology - Robert Weis - Страница 87

Genes guide our maturation, but they do not determine our development. Our genotype refers to the genetic code that we inherit from our parents. In contrast, our phenotype is the observable expression of our genetic endowment. Our phenotype is determined by the complex interaction between our genes and our environment (Grigorenko et al., 2016).

The diathesis–stress model can be used to explain the way genes and environments interact and affect development. According to this model, a child exhibits a disorder when an underlying genetic risk for the disorder is triggered by a stressful experience or life event. Both genetic risk and an environmental stressor are necessary for the disorder to emerge; the genetic risk or environmental experience alone is insufficient to bring about the disorder (Plomin et al., 2017).

We can see the usefulness of the diathesis–stress model in a famous study conducted by Avshalom Caspi and colleagues (2003). The researchers followed a large group of children from early childhood through early adulthood in order to examine the relationship between child maltreatment and depression later in life. As we might expect, children exposed to maltreatment were at risk for depression later in life. However, whether a maltreated child developed depression depended on his or her genotype (Figure 2.3).

Children who did not experience maltreatment were at low risk for depression later in life, regardless of their genes. However, children exposed to severe maltreatment displayed different outcomes, depending on their genotypes. Specifically, children who inherited one or two short alleles of the serotonin transporter gene were likely to develop depression in adulthood. Interestingly, this gene regulates the neurotransmitter serotonin, a chemical that plays an important role in mood regulation. The short version of this gene seems to place children at risk for depression if they also experience maltreatment. In contrast, children who inherited two long alleles of the serotonin transporter gene were not more likely to develop depression in adulthood, even if they were exposed to maltreatment. The long version of this gene seems to protect children from the effects of stressful life events.

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Figure 2.3 ■ The Diathesis–Stress Model

Note: Children’s likelihood of depression depends on their genetic risk and an environmental stressor (i.e., maltreatment). SS = two short alleles, SL = one short, one long allele, LL = two long alleles. Based on Caspi and colleagues (2003).

The diathesis–stress model is especially helpful in explaining multifinality, the tendency of children exposed to the same environmental stressor to show different developmental outcomes. In Caspi and colleagues’ (2003) study, maltreated children showed divergent outcomes depending on their genetic risk.