Molecular geneticists conduct linkage and association studies to identify specific genes that may underlie certain disorders.
How Do Genetic and Environmental Factors Interact?
The Diathesis–Stress Model
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.
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.
Gene–Environment Correlation
The diathesis–stress model shows that both genes and environment influence development. A second influential model, developed by Sandra Scarr and Kathleen McCartney (1983), shows that genes and environments are not independent. According to the gene–environment correlation model, we sometimes select environments that complement our genotypes. Specifically, there are three types of gene–environment correlations: passive, evocative, and active.
Although our biological parents determine our genotype, they also determine the quality of our early environmental experiences. Our genes and early experiences are related. For example, parents with high intelligence may pass on this genetic predisposition to their children. At the same time, because of their high intelligence and (perhaps) income, these parents have access to higher-quality medical care, nutrition, childcare, and schools. Intelligent parents speak and read to their children frequently, provide stimulating educational toys, and take their children on outings. In this manner, their children passively receive genotypes and early environmental experiences conducive to high intelligence.
As children develop, their phenotype gradually emerges from the interaction between their genotype and early environment. Like their parents, they may begin to show signs of above-average intelligence. They show well-developed verbal skills, learn more quickly than their peers, perform more tasks independently, and are curious about a wide range of topics. These behaviors evoke certain responses in others. School personnel may identify these children as gifted and provide them with more enriched educational experiences. They may be admitted into accelerated classes in high school and gain academic scholarships to selective colleges.
As children continue to develop, they actively select environmental experiences conducive to their genotype. For example, they might develop friendships with other bright children with similar interests and hobbies; seek out extracurricular activities that satisfy their curiosity in science, music, or art; and select challenging and rewarding majors in college. In a sense, youths select their own environments based on the cumulative influence of their genes and early experiences.
Now that you know the basics of gene–environment correlation, consider Kirby (From Science to Practice). Can you explain the emergence of Kirby’s problems using the concept of passive, evocative, and active gene–environment correlation?
From Science to Practice: Understanding Gene–Environment Correlation
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Kirby is a 10-year-old boy who attends the third grade at a local public school. Kirby failed first grade and will likely fail again this year. Kirby’s reading is well below average, and he makes frequent mistakes in math. His writing skills are also poor. The school psychologist did not find evidence of a learning disability; however, psychological testing revealed below-average intelligence.
Kirby is frequently disruptive and inattentive during class. His teacher stated that Kirby’s parents “just don’t care.” She has tried to contact his mother by telephone, but she usually does not return her calls and rarely follows through with her suggestions for home tutoring. Kirby will likely be sent to a remedial “special ed” class next year if improvements are not made.
Socially, Kirby is awkward. He is larger and taller than his classmates. He is teased because of his size, his poor grades, and the frequent reprimands he receives from teachers. Classmates also make fun of Kirby because of his name, his old “Walmart clothes,” his poorly cut hair, and the fact that he always “smells like hot dogs”—due to his family’s wood burning stove.
Kirby has few friends in his class. After school, he often hangs around with older kids at the junior high school. Kirby has been caught smoking on a few occasions and teachers also suspect some alcohol use. He is also beginning to pick on younger children after school.
Kirby’s problems include poor academic skills, disruptive behavior at school, and rejection by peers. They can be explained using the three types of gene–environment correlation.
1 Kirby’s parents pass their genes on to him—genes that may have placed him at risk for low academic achievement. Furthermore, his parents also provide him with an early environment that is not conducive to good grades. They may not be able to afford high-quality schools and do not seem involved in his education. Consequently, Kirby struggles with reading and acts out in class.
2 Kirby’s poor academic skills and appearance evoke negative