Читать книгу Introduction to Abnormal Child and Adolescent Psychology - Robert Weis - Страница 90

According to the diathesis–stress model, children will develop a disorder only if they have both a genetic risk for the disorder and an environmental stressor to trigger its onset. Moreover, gene–environment correlations show that our genotype and our environment are not independent; we sometimes select environments that are conducive to our genes. A new area of research called behavioral epigenetics shows that environmental factors can also directly affect the expression of our genes and our risk for mental health problems (Hill & Toth, 2016).

Recall that our genetic makeup consists of DNA, which is organized into genes and chromosomes in each of our cells. Genes direct the building of proteins that allow each cell to specialize and carry out its essential functions. These proteins influence our health, appearance, thoughts, feelings, and actions.

Epigenetic structures consist of chemical compounds and proteins that attach to our DNA and turn genes on or off. These compounds and proteins are not part of our genetic code; consequently, scientists call them epigenetic (i.e., above the genome). When these epigenetic structures attach to DNA and regulate its expression, scientists say they have “marked” the genome. Although these marks do not change the DNA itself, they do alter the way in which cells use the DNA’s instructions. These epigenetic marks can be passed on to new cells when they divide. Moreover, epigenetic marks can also be passed down from one generation to the next.

Epigenetic compounds can affect the expression of DNA in two ways (Image 2.4). In a process called DNA methylation, proteins attach chemical tags (called methyl groups) to certain portions of genes, turning them on or off. In another process called histone modification, DNA wraps either tightly or loosely around histones. Segments of DNA that are loosely wrapped can be expressed, whereas other segments that are tightly wrapped cannot (National Human Genome Research Institute, 2019).

Environmental experiences can change epigenetic structures. Certain environmental factors such as diet, smoking, and exposure to disease have been shown to alter structures, leading to different expressions of the genetic code. Epigenetic structures are heritable. Although much of the epigenome is reset when parents pass their genes to their children, some structures persist and affect the child’s phenotype (Cicchetti, 2019).

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Researchers at McGill University first demonstrated the effects of epigenetics on behavior in rats (Weaver et al., 2004). Rat pups have a certain gene that regulates their stress response. This gene is wrapped tightly around a histone that prevents it from becoming active. The researchers found that nurturing behaviors of the mother toward the pups (e.g., licking, grooming) caused this portion of the gene to unwind from the histone, allowing it to be expressed. When these pups reached adulthood, they were better able to cope with stress than rats whose mothers were less nurturing. Subsequent research showed that these epigenetic changes affected the care these rats gave to their own offspring, thus passing on this stress response to the next generation (Masterpasqua, 2009).

Researchers are only beginning to understand how epigenetics might help explain the development of disorders in children. In one recent study, researchers examined the caregiving behaviors of depressed and nondepressed mothers. As we might expect, depressed mothers expressed more negative emotions toward their infants than nondepressed mothers. Moreover, the infants of depressed mothers showed different epigenetic structures than the infants of nondepressed mothers, suggesting that these early caregiving experiences might affect children’s epigenetic activity. Longitudinal research is needed to determine whether these epigenetic changes, brought on by early experience, might affect children’s subsequent behavior (Moore, 2015).

Other research has begun to examine the epigenetic structure of children with existing behavior problems. In one of the largest studies so far, researchers examined children and adolescents referred to mental health clinics because of disruptive behavior. The researchers found that children’s stress hormones and their severity of behavior problems were associated with changes in their epigenetic structure, specifically, structures associated with the expression of the cortisol receptor gene. This finding is interesting because cortisol is the body’s main stress hormone; furthermore, the cortisol receptor gene plays a role in regulating the body’s stress response. Epigenetic changes to the expression of this gene might underlie some of the problems shown by these youths (Dadds, Moul, Hawes, Mendoza Diaz, & Brennan, 2016).

We are only beginning to appreciate how behavioral epigenetics can help us understand the emergence of childhood disorders. Perhaps equally as important, research might someday be helpful in developing medications that can affect epigenetic structures, genetic expression, and risk for mental health problems (Nigg, 2016b).

Review

 According to the diathesis–stress model, children must have both (1) a genetic risk and (2) an environmental stressor to develop a disorder. The model helps explain multifinality, that is, the tendency of children with similar genes or experiences to have different outcomes.

 The gene–environment correlation model assumes that our genes and environments are related. There are three types of gene–environment correlations: passive, evocative, and active. Their relative importance changes across development.

 Epigenetic structures (e.g., methyl tags and histones) can turn genes “on” or “off.” These structures, which are not part of children’s genotype, can be altered by environmental experiences and passed down from one generation to the next.