2.1 Neurological Factors in Psychological Disorders

Big Edie had always been unconventional. She didn’t seem to care what other people thought of her behavior. And although she loved performing—seemingly to the point of compulsion—she was a recluse for most of her adult life, seeing almost no one but her children. How did such a lifestyle arise? And what about Little Edie’s paranoid beliefs? Could neurological factors account for the odd beliefs and behaviors of this mother and daughter? In fact, accumulating research indicates that genes can contribute to the development of disorders by affecting both the structure and function of the brain (Gottesman, 1991; Greenwood & Kelsoe, 2003; Hasler et al., 2004).

Neurological factors that contribute to psychological disorders include abnormalities in the structure of the brain, in the operations of specific chemicals, and in specific genes. Researchers and clinicians sometimes focus on neurological factors when they explain psychopathology—noting, for example, that depression is correlated with abnormal levels of a particular chemical (serotonin) in the brain or that an irrational fear of spiders develops partly from an overly reactive brain structure involved in fear (the amygdala; Larson et al., 2006). However, as you know, the neuropsychosocial approach maintains that explanations based on neurological factors alone rarely provide the whole story. Each thought, feeling, and behavior, as well as each social experience and the environment in which we live and work, affects our neurological functioning. In other words, as noted above, the three types of factors typically interact with one another through feedback loops. Neurological factors contribute to psychopathology, but they must be considered in the context of the other factors.

To understand the role of neurological factors in explanations of psychopathology, we next consider brain structure and function, neurons and neurotransmitters, and genetics and the ways that genes interact with the environment.

Brain Structure and Brain Function

The brain is the organ of thinking, feeling, and behavior, and thus it must play a key role in psychopathology. In the following sections, we start our discussion with the big picture by considering the overall structure of the brain and its organization into large systems. Then we turn to increasingly more detailed components, considering how individual brain cells interact within these systems.

Psychopathology involves deficits in how a person thinks, feels, and behaves. The brain, of course, is ultimately responsible for all of these functions. Let’s briefly consider how different parts of the brain contribute to cognitive and emotional capacities when the brain is structured and functions normally. In later chapters, when we need to know more to understand a specific psychological disorder, we’ll look more closely at specific parts of the brain and how they can malfunction.

The Central Nervous System and the Peripheral Nervous System

The central nervous system (CNS) has two parts: the brain and the spinal cord. The CNS is the seat of memory and consciousness, as well as perception and voluntary action (Smith & Kosslyn, 2006). However, the CNS is not the only neurological foundation of our internal lives. The peripheral nervous system (PNS) also plays an important role and is of particular interest in the study of psychopathology.

The Peripheral Nervous System

Like the CNS, the PNS is divided into two parts, in this case the sensory-somatic nervous system and the autonomic nervous system (see Figure 2.1). The sensory-somatic nervous system is involved in connecting the brain to the world, via both the senses (inputs) and the muscles (outputs). The autonomic nervous system (ANS) is probably of greater relevance to psychopathology, in part because it plays a key role in how we respond to stress. The ANS controls many involuntary functions, such as those of the heart, digestive tract, and blood vessels (Goldstein, 2000; Hugdahl, 2001).

The ANS itself has two major components: the sympathetic nervous system and the parasympathetic nervous system. The sympathetic nervous system revs you up so that you can respond to an emergency: It speeds up the heart (providing more blood and oxygen to the limbs) and dilates the pupils of the eyes (making you more sensitive to light). The sympathetic system also slows down functions that are not essential in an emergency, such as those involved in digestion. The result of the sympathetic nervous system’s being activated is called the fight-or-flight response (or the stress response, because it occurs when people experience stress).

The other part of the ANS is the parasympathetic nervous system, which settles you down after a crisis is over: The parasympathetic nervous system slows the heart, contracts the pupils, and increases the activity of the digestive tract. The parasympathetic system typically counteracts the effects of the sympathetic nervous system, and psychopathology may arise if it fails to do so effectively. In fact, dysfunctional activity in the parasympathetic nervous system has been associated with various psychological problems, such as anxiety disorders, disruptive behavior, and hostility (Pine et al., 1998).

The Four Brain Lobes

Let’s now focus on one part of the CNS, the brain. As shown in Figure 2.2, the brain has four major lobes, back to front: occipital lobe, parietal lobe, temporal lobe, and frontal lobe. The brain is divided into two hemispheres (or half-spheres), left and right, and each hemisphere has all four lobes. We start with the back of the brain.

When the eyes are stimulated by light, they send neural impulses into the brain; the first area to process this information in detail is the occipital lobe, which is at the very back of the brain. This lobe is entirely dedicated to the function of vision.

Two major neural pathways lead forward from the occipital lobes. One extends up into the parietal lobe, at the top, back of the brain. This lobe processes spatial information, such as the relative location of objects. The parietal lobe also has other functions, including a role in self-awareness. The second neural pathway from the occipital lobe leads down to the temporal lobe (so named because it lies under the temple), which stores visual memories, processes auditory information, and decodes the meaning of speech; the temporal lobe also contributes to conscious experience. Abnormal functioning in the temporal lobe can produce intense emotions, such as elation when a person is manic (Gyulai et al., 1997).

Both the parietal lobe and the temporal lobe send information to the frontal lobe, which is located right behind the forehead. The frontal lobe plays crucial roles in feeling emotions and using emotional responses in decision making, as well as in thinking and problem solving more generally; it is also involved in programming actions and controlling body movements. Because these functions are so important to the vital activities of planning and reasoning, the frontal lobe is sometimes referred to as the seat of executive functioning; its role is much like that of the head of a successful company—an executive—who plans the company’s future and formulates responses to obstacles that arise. Abnormalities in the frontal lobe, and in executive functioning, are associated with a variety of disorders, including schizophrenia, a psychological disorder characterized by profoundly unusual and impaired behavior, expression of emotion, and mental processing (Bellgrove et al., 2006; Morey, Inan, et al., 2005).

The Cortex and Beneath the Cortex

The cerebral cortex is the outer layer of cells on the surface of the brain that overlays all four of the lobes. Contained in the cerebral cortex is the majority of the brain’s neurons, the cells that process information related to our physical, mental, and emotional functioning. Most of the brain functions just described are carried out primarily in the cortex of the corresponding lobes. But many important brain functions are carried out in subcortical areas, beneath the cortex, as shown in Figure 2.3.

The limbic system (key parts of which are shown in the left half of Figure 2.3) plays a key role in emotions; among its most important components are the hypothalamus, the hippocampus, and the amygdala:

• The hypothalamus governs bodily functions associated with eating, drinking, and controlling temperature, and it plays a key role in many aspects of our emotions and in our experience of pleasure (Swaab, 2003).
• The amygdala is central to producing and perceiving strong emotions, especially fear (LeDoux, 2000).
• The hippocampus works to store new information in memory of the sort that later can be voluntarily recalled (Squire, 2004).

In addition to components of the limbic system, other important subcortical structures include the thalamus, the basal ganglia, and the cerebellum. Both physical abnormalities and abnormal levels of activity in these subcortical brain areas can contribute to psychological disorders, as we will discuss in later chapters when relevant.

Now that you know essential functions that different parts of the brain perform, it’s time to discuss how these functions occur. All brain activity depends on neurons, and malfunctions of neurons often contribute to psychological disorders (Lambert & Kinsley, 2005). The brain contains numerous types of neurons, which have different functions, shapes, and sizes. Most neurons interact with other neurons. In some cases, neurons activate, or act to “turn on,” other neurons; in other cases, neurons inhibit, or act to “turn off,” other neurons. We can classify neurons into three main types:

• Sensory neurons receive input from the sense organs (eyes, ears, and so on).
• Motor neurons carry output that stimulates muscles and glands.
• Interneurons lie between other neurons—sensory neurons, motor neurons, and/or other interneurons—and make up most of the neurons in the brain.

Sets of connected neurons that work together to accomplish a basic process, such as making you recoil when you touch a hot stove, are called brain circuits; sets of brain circuits are organized into brain systems, which often can involve most of an entire lobe—or even large portions of several lobes. Many forms of psychopathology arise because specific brain circuits are not working properly, either alone or as part of a larger brain system.

To understand brain circuits, consider an analogy to a row of dominoes: When one domino falls, it causes the next in line to fall, and so on, down the line. Similarly, when a neuron within a brain circuit is activated, it in turn activates sequences of other neurons. However, unlike a domino in a row, the average neuron is connected to about 10,000 other neurons—and thus a complex pattern of spreading activity occurs when a brain circuit is activated, which usually ends up involving a large brain system. For each input, a brain system produces a specific output—for instance, an interpretation of the input, an association to it, or a response based on it. Ultimately, it is the pattern of activated neurons that is triggered—by a sight, smell, thought, memory, or other event—that gives rise to our cognitive and emotional lives. A pattern of neurons firing makes us desire that third piece of chocolate cake or causes us to recoil when a spider saunters out from behind it. Brain systems allow us to think, feel, and behave.

Psychopathology can arise when neurons fail to communicate appropriately, leading brain systems to produce incorrect outputs. For example, people with schizophrenia appear to have abnormal circuitry in key parts of their frontal lobes (Pantelis et al., 2003; Vidal et al., 2006). To understand such problems—and possible treatments for them—you need to know something about the structure and function of the neuron and its methods of communication.

The Cell Body

To see how neurons can fail to communicate appropriately, we must take a closer look at them. Figure 2.4 shows that a neuron has three parts: a receiving end, a sending end, and a middle part, called the cell body. When a neuron has been sufficiently stimulated (typically by signals from other neurons), very small holes in the cell’s outer covering (its “skin”) open, and the neuron’s internal balance of chemicals changes to the point where the neuron “fires.” It is this firing that sends information to other neurons (Lambert & Kinsley, 2005).

Each neuron registers the sum total of inputs, both those that try to stimulate it to fire and those that try to inhibit it from firing. The neuron, then, balances the two sorts of inputs against each other and only fires if the stimulating influences substantially outweigh the inhibiting ones (Kandel et al., 2007). To understand how firing occurs, we need to look at two other major parts of the neuron: the axon and the dendrites.

The Axon, Dendrites, and Glial Cells

The axon is the part of the neuron that sends signals to other neurons. The axon is a long, threadlike structure, some of which is covered by a layer of fatty material, known as the myelin sheath, that insulates it electrically; the axon includes the terminal buttons. Although each neuron has only a single axon, it often branches extensively, allowing signals to be sent simultaneously to many other neurons (Shepherd, 1999).

When a neuron has been stimulated to the point that it fires, a wave of chemical activity moves from the cell body down the axon very quickly. This wave is called an action potential. When the action potential reaches the end of the axon, it typically causes chemicals to be released. These chemicals are stored in structures called terminal buttons, and these chemicals affect other neurons, muscles, or glands. If stimulation does not cause a neuron to fire when it is supposed to, the circuit of which the neuron is a part will not function correctly—and psychopathology may result. Let’s consider why a neuron might not fire when stimulated appropriately.

We’ve seen that neurons fire after they are stimulated, but how are they stimulated? Two ways: First, they are stimulated at their dendrites, which receive signals from other neurons. Dendrites, like axons, are highly branched, so a single neuron can receive many different signals at the same time. Received signals move along the dendrites to the cell body (Kandel et al., 2007). Second, in some cases, neurons receive inputs directly on their cell bodies. Such inputs are produced not only by other neurons but also by glial cells. Glial cells are involved in the “care and feeding” of neurons, and act as a kind of support system (in fact, glial means “glue” in Greek; Lambert & Kinsley, 2005). The brain has about 10 times as many glial cells as neurons. Researchers have learned that glial cells do much more than provide support services; they can directly stimulate neurons, and they play a role in modulating input from other neurons (Parpura & Haydon, 2000).

Given the roles of neurons and glial cells in brain function, it is not surprising that researchers have found that at least some patients with psychological disorders (specifically, the sorts of mood disorders we consider in Chapter 5) have abnormally low numbers of both types of cells. One possible reason for such deficits may be that stress early in childhood (and even to the mother, prior to a child’s birth) can disrupt the development of both neurons and glial cells (Zorumski, 2005).

The way neurons communicate is crucial for understanding psychopathology. In many cases, psychological disorders involve faulty signaling among neurons, and effective medications operate by altering the ways in which signals are produced or processed (Kelsey et al., 2006). Subsequent chapters of this book will describe how particular signaling problems contribute to some psychological disorders and how certain medications compensate for such problems. To understand these problems with chemical signaling, we now need to consider what happens at the synapse, what neurotransmitters do, the nature of receptors, and what can go wrong with chemical communication among neurons.

The Synapse

When a neuron fires, chemicals are released at the terminal button. Those chemicals usually contact another neuron at a synapse, which is the place where the tip of the axon of one neuron nestles against another neuron (usually at a dendrite) and sends signals to it. Most of the time, the sending neuron is not physically connected to the receiving neuron, though. Instead, the chemicals carry the signal across a gap, called the synaptic cleft, shown in Figure 2.5. Events at the synapses can go awry, which can underlie a variety of types of psychopathology.

Neurotransmitters

The chemicals that are released by the terminal buttons are called neurotransmitters. It is worth looking briefly at the major neurotransmitters that play roles in psychological disorders. However, keep in mind that no neurotransmitter works in isolation and that no psychological disorder can be traced solely to the function of a single neurotransmitter. Nevertheless, as shown in TABLE 2.1, imbalances in some of these substances have been linked, to some extent, with certain psychological disorders.

You may have noticed in TABLE 2.1 that the descriptions of what the neurotransmitters do are fairly general. There’s a reason for this: The effects of neurotransmitters depend in part on the nature of the receiving neurons. Thus, we must next look more closely at what’s on the receiving end of these chemical substances. The information in the following section is also crucial if we are to understand how various drugs work to treat psychopathology.

Chemical Receptors

A neuron receives chemical signals at its receptors, specialized sites that respond only to specific molecules (see Figure 2.5). Located on the dendrites or on the cell body, receptors work like locks into which only certain kinds of keys will fit (Kelsey et al., 2006; Lambert & Kinsley, 2005). However, instead of literally locking or unlocking the corresponding receptors, the neurotransmitter molecules bind to the receptors and affect them either by exciting them (making the receiving neuron more likely to fire) or by inhibiting them (making the receiving neuron less likely to fire). We noted earlier that a sending neuron can make a receiving neuron more or less likely to fire, and now we see how these effects occur: The sending neuron releases specific neurotransmitters.

Abnormal Communications Among Neurons

How can communications among neurons at the synaptic cleft go awry, and thereby lead to psychological disorders? Scientists point to at least three ways in which such communications can be disrupted.

First, neurons might have too many or too few dendrites or receptors, making the neurons more or less sensitive, respectively, to even normal amounts of neurotransmitters in the synaptic cleft (Meana et al., 1992). Second, the sending neurons might produce too much or too little of a neurotransmitter. Third, the events after a neuron fires may go awry (Kelsey et al., 2006). In particular, when a neuron fires and sends neurotransmitter chemicals to another neuron, not all of these molecules bind to receptors. Rather, some of the molecules linger in the synaptic cleft and need to be removed. Special chemical processes operate to reuptake these leftover neurotransmitters, moving them back into the sending neuron. Sometimes reuptake does not operate correctly, which may contribute to a psychological disorder.

Hormones are chemicals that are released directly into the bloodstream that activate or alter the activity of neurons. For example, some hormones play a key role in helping animals respond to stressful situations by altering the functioning of the ANS (Kandel et al., 2007). However, traumatic events can disrupt this often–helpful mechanism and contribute to psychological disorders such as depression (Claes, 2004).

Hormones are produced by glands in the endocrine system, which secretes substances into the bloodstream. Hormones affect various organs throughout the body. Cortisol is a particularly important hormone, which helps the body to cope with challenges by making more resources available; cortisol is produced by the adrenal glands (which are located right above the kidneys) and abnormal amounts of cortisol have been linked to anxiety and depression.

The Genetics of Psychopathology

Researchers knew about the inheritance of traits long before the discovery of DNA (deoxyribonucleic acid, the long molecule that contains many thousands of genes). Everyone knows that people “take after” their parents in some ways that have nothing to do with learning, and genes are responsible for this resemblance. Genes affect not only physical traits but also the brain and, through the brain, thinking, feeling, and behavior; moreover, genes can affect how vulnerable people are to particular psychological disorders (Plomin et al., 1997, 2003).

In the middle of the 20th century, James Watson and Francis Crick identified genes, which correspond to segments of DNA that control the production of particular proteins and other substances (see Figure 2.6). Genes are expressed when the information in them is used to produce proteins and other substances, which both produce biological structures (including the parts of the neurons) and affect biological processes (such as reputake). For many traits, gene variants—referred to as alleles—determine how the trait is manifested. The sum of an organism’s genes is called its genotype. In contrast, the sum of its observable traits is called its phenotype, which results from how the genotype is expressed in a particular environment.

For most traits, many genes work together to cause particular effects. Sets of genes give rise to traits, such as height, that are expressed along a continuum, and the joint actions of these genes produce complex inheritance (Plomin et al., 1997). Traits that arise from complex inheritance cannot be linked to a few distinct genes, but rather emerge from the interactions among the effects of numerous genes. Almost all psychological disorders that have a genetic component, such as schizophrenia and depression, arise in part through complex inheritance (Faraone et al., 2001; Plomin et al., 2003).

Studies that investigate the contributions of genes to mental illness rely on the methods of behavioral genetics, which is the field that investigates the degree to which the variability of characteristics in a population arises from genetic versus environmental factors (Plomin et al., 2003). With regard to psychopathology, behavioral geneticists consider these questions: What is the role of genetics in causing a particular mental disorder? What is the role of the environment? And what is the role of interactions between genes and the environment?

Throughout this book, we discuss the relative contributions of genes and the environment to the development of specific mental disorders. We must always keep in mind, however, that any conclusions about the relative contributions of the two influences are always tied to the specific environment in which the contributions are measured. To see why, consider the following example (based on Lewontin, 1976). Imagine three situations in which we plant two apple trees of the same variety, one of which has genes for large apples and one of which has genes for small apples.

In the first case, we keep the environment the same for the two trees. Unfortunately for them, however, it is not a very friendly environment: The soil is bad, the trees are in the shade, and there isn’t much water. Both trees produce small apples. In this case, the environment overshadows the genetic influence for large apples.

In the second case, the trees are luckier. For both trees, the soil is rich, the trees are in the sun, and they receive plenty of water. What happens? The tree with genes for large apples produces larger apples than the tree with genes for small apples.

In the third case, the tree with genes for large apples is planted in the impoverished environment, and the tree with genes for small apples is planted in the favorable environment. Now, the tree that has genes for small apples might produce bigger apples than the tree with genes for large apples because the environmental conditions have favored the former and acted against the latter.

As this example makes clear, for trees and other organisms—including humans—the influence of genes must be described in relation to the environment in which they function. In other words, genes and environment interact through feedback loops—and in fact, that’s why the phenotype depends on how genes function in a specific environment. The same genes can have different effects in different environments. A research finding of a certain degree of genetic influence on a disorder in one environment does not necessarily have any relationship to the degree of genetic influence on the disorder in other environments. For example, the fact that genes can predispose an individual to alcoholism has different effects in the alcohol-embracing culture of France and the alcohol-shunning culture of Pakistan.

Heritability

Behavioral genetics characterizes the relative influence of genetic factors in terms of the heritability of a characteristic. Heritability is an estimate of how much of the variation in that characteristic within a population (in a specific environment) can be attributed to genetics. For example, the heritability of generalized anxiety disorder (which is characterized by worry that is not associated with a particular situation or object, as we will discuss in detail in Chapter 6) is about .32 in citizens of Western countries (Hettema, Neale, & Kendler, 2001). This means that about one third of the variation in generalized anxiety disorder in this population is genetically determined.

There is no sure-fire research method for assessing heritability. Many variables can affect the results. For example, if researchers find a similar prevalence of a mental disorder in children and their parents, can they assume genetic inheritance? Not necessarily; they would have to rule out any effects of the environment that might be operating. It is difficult to assess “the environment” for a given person. The environment must be understood not in objective terms but rather in terms of how situations and events are perceived and understood. For instance, for siblings in a given family, does having divorced parents constitute the same environment? Not exactly: A child’s age at the time of parents’ divorce can influence how the child experiences the divorce. A preschooler might believe he or she somehow caused the divorce, whereas an older child—who is more mature cognitively, emotionally, and socially—is less likely to make that inference (Allison & Furstenberg, 1989; Hoffman, 1991). Researchers can entirely avoid such age effects between siblings by studying twins.

Twin and Adoption Studies

Twin studies compare some characteristic, or set of characteristics, in two groups of twins, identical and fraternal. Identical twins have basically the same genetic makeup, because they began life as a single fertilized egg (or zygote) that then divided to become two embryos. Such twins are monozygotic (mono- means “one”). Fraternal twins begin life as different fertilized eggs, and so are dizygotic (di- means “two”). Fraternal twins are like any other nonidentical siblings in terms of their genetic similarity: They have about 50% overlap in the genes that vary among humans. When researchers compare the characteristics of monozygotic twins and dizygotic twins, controlling as much as possible for the environment, they can attempt to draw conclusions about the relative contribution of genes to those characteristics in that environment. For instance, such studies have suggested that schizophrenia is about 50% heritable (Gottesman, 1991). However, we must be cautious about such estimates: Not only can identical twins have slightly different genetic makeups but they also begin to have different experiences before birth—in fact, one twin is usually heavier and larger at birth because of differences in the amounts of nutrients the two fetuses receive in the womb (Cheung et al., 1995; Hollier et al., 1999).

Sometimes researchers try to discover the roles of genes and the environment in mental disorders by conducting adoption studies: They study twins who were separated at birth and raised in different homes, then compare them to twins who were raised in the same home. In addition, researchers also study biologically unrelated children who were adopted and raised together, then compare them to unrelated children who were reared in different homes. But even in adoption studies, it’s not easy to disentangle the effects of genes and the environment. The reason is that genetic differences influence the environment—a relationship that is characterized by the reciprocal gene–environment model. For instance, suppose that a pair of twins has genes that lead them to be high-strung and very active. Even if these twins are raised apart in different environments, their parents may react similarly to them—trying to keep them calm and out of trouble, which might mean that they wouldn’t be taken on family outings as often as children who are less of a handful. The point is that even in different adopted households, genes can influence how twins are treated and what they experience. Thus, although twin and adoption studies can be fascinating, their findings must be interpreted cautiously.

The problems with twin and adoption studies have led many researchers to take advantage of recent technological advances in genetics: It is now possible to assess, inexpensively and quickly (for many genes), whether a particular person has a specific allele of a gene (Schena et al., 1995). Researchers have used such techniques to attempt to find associations between the presence or absence of specific alleles and psychological disorders. For example, Rasmussen and colleagues (2006) found that people who develop schizophrenia relatively late in life tend to have one particular allele of a certain gene.

Feedback Loops in Understanding Genes and the Environment

We’ve seen how genes can affect the environment, but—to the surprise of many—the genes themselves are also affected by the environment, including psychological and social factors (Slavich & Cole, 2013). We consider the feedback loops between the environment and the genes in the following two sections.

Many people seem to think of genes as instructions for building the brain and the body, guiding the construction process and then ceasing to function. For many genes, this is not so. Even in adulthood, a person’s genes are regulated by the environment (Hyman & Nestler, 1993). Consider a simple example: Did you ever try to learn to play piano? If you did, your fingers were probably sore after even a half-hour of practice. But if you stuck with it, you could play for longer and longer periods with no discomfort. What happened? Your muscles got stronger. But how? When you first began, the stress of using your fingers in new ways actually damaged the muscles (which is why they felt sore). Then, a series of chemical events inside the muscle cells of your fingers turned on genes in the nuclei of these cells. These genes directed the cells to produce more proteins, to build up the muscles, which made them stronger. If you stopped playing for a period of time, those genes would turn off, and the muscles would become weaker. This is why your fingers might be sore when you first resumed playing after having taken a long break.

The point is that some genes are activated, or turned on, as a result of experience, of interacting with the world (Kandel et al., 2007; South & Krueger, 2011). This is true of genes in the brain that produce neurotransmitters and that cause new synapses to form. In fact, when you learn something, genes in your brain are turned on, which causes new connections among neurons to be formed. This is true even when you learn maladaptive behaviors, which can produce, among other problems, a phobia—an intense, irrational fear of an object or situation. Moreover, genetic factors can contribute to a neurological vulnerability for a psychological disorder. For example, genetic factors can lead a person to be prone to learning maladaptive behaviors. However, researchers have found that the same genes are associated with a number of different mental disorders. This probably occurs because these genes affect shared neural functions that have been disrupted (Cross-Disorder Group of the Psychiatric Genomics Consortium, 2013). It seems likely that if a person inherits genes that can underlie such fundamental dysfunctions, different environmental stressors can trigger the dysfunction in different contexts, leading to different disorders.

However, genes are not destiny. More often than not, having specific genes does not determine behavior but rather predisposes a person to be affected by the environment in certain ways. That is, genes can predispose a person for a specific disorder, but those genes may have that effect only when triggered by psychological or social factors.

We’ve just seen that the environment affects the genes, and we’ve already noted that the reverse also occurs. Let’s now look in more detail at ways in which the genes affect the environment. Many researchers (e.g., Plomin et al., 1997; Scarr & McCartney, 1983) distinguish three ways in which genes affect the environment—passive interaction, evocative interaction, and active interaction:

1. Passive interaction. The parents’ genes affect the child’s environment—and the child passively receives these influences. For instance, some parents avoid social groups because they are shy, which is in part a result of their genes; this means that their child has relatively few social experiences. The child may not have inherited the parents’ shy temperament, but the parents’ genes nonetheless act through the environment to affect the child.
2. Evocative interaction (also called reactive interaction). A person’s inherited traits encourage other people to behave in particular ways, and hence the person’s social environment will be affected by his or her genes. For example, if you are very tall and heavy-set, others may respond to you somewhat cautiously—in a way they would not if you were short and frail. Similarly, others may approach or avoid you (fairly or not!) in response to your temperament (e.g., shy, calm, high-strung); any specific temperament will appeal to some and not to others. Thus, even your circle of friends will be somewhat determined by your genes, and those friends will then affect you in certain ways, depending on their own characteristics.
3. Active interaction. Each of us actively seeks out some environments and avoids others, and our genes influence which environments feel most comfortable to us. For example, a person who is sensitive to environmental stimulation might prefer spending a quiet evening at home curled up with a good book instead of going to a loud, crowded party at a friend’s house.

The interactions between genes and the environment involve all the factors considered by the neuropsychosocial approach and hence create complex feedback loops. Once the environment (including social factors, such as one’s choice of friends) has been influenced by genes, the environment in turn affects the genes (as well as one’s knowledge, beliefs, attitudes, and so on).

Again, the import of these observations for psychological disorders is clear. Genes can put a person at risk for a particular psychological disorder, but other factors—psychological and social—can influence the expression of the genes. And the specific psychological and social factors that affect a person arise, in part, from that person’s genes (which affect, for example, aspects of his or her appearance). Thus, even though genes may make some people vulnerable to specific kinds of mental illness, the path from genes to illness is neither straight nor inevitable.