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17.1: Biological Factors in Psychological Disorders- An Introduction

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    130118
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    Learning Objectives
    • Identify 3 biological areas that contribute to psychological disorders.
    • Describe the role of neural structures in psychological disorders.
    • Identify 2 systems of chemical communication used by the brain.
    • Describe how genetics and epigenetics contribute to psychological disorders.

    Chapter Overview

    This chapter discusses the biological perspective on psychological disorders, exploring how our brain structures, neural systems, and genetics contribute to the etiology of such disorders as schizophrenia, depression, bipolar, anxiety, and obsessive/compulsion.

    Introduction

    by Amy E. Coren, Ph.D., Pasadena City College

    Although the term mental illness is often used when referring to disorders such as depression or anxiety, are these disorders really illnesses in the way that diabetes is an illness – that is a purely biological malfunction? Or are psychological disorders the product of something more intangible than a neurochemical imbalance or malfunctioning amygdala, something such as a conditioned response to stress learned in childhood? The answer is both.

    Within the field of psychology, it is generally acknowledged that psychological disorders develop out of a complex interaction of biological, social, and environmental factors. However, exactly how these factors interact with one another to produce a particular psychological disorder is still unclear. This is because diagnosing a psychological disorder is not like diagnosing other illnesses, such as diabetes or pneumonia.

    When making a diagnosis of diabetes, a doctor may use a blood test to determine blood glucose levels. Similarly, to diagnose pneumonia, a doctor may order a chest x-ray to look for evidence of the infection. However, when it comes to diagnosing psychological disorders, there is currently no x-ray for depression or blood test for anxiety. Diagnosing psychological disorders is a more subjective process, based on the current symptoms an individual is experiencing.

    The Diagnostic and Statistical Manual of Mental Disorders, 5th edition, (American Psychiatric Association, 2013) is the most widely accepted system used by clinicians and researchers for the classification of mental disorders, and outlines the diagnostic criteria for a specific mental disorder based on the symptoms an individual is experiencing. However, individuals suffering from the same disorder often display different symptoms while individuals suffering from different disorders may display many of the same symptoms, making the diagnosis of psychological disorders from outward symptoms alone, difficult.

    Note

    The American Psychological Association periodically updates the Diagnostic and Statistical Manual of Mental Disorders - also called the DSM - so that it will accurately reflect our current understanding of the symptoms, etiology, and treatment of psychological disorders. The revisions to the DSM-5 were released in early 2022, in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR).

    The remainder of this chapter focuses on the contributions of biological factors - such as brain structure abnormalities - to the development of psychological disorders.

    Biology of Psychological Disorders

    Research into the underlying biology of psychological disorders has primarily focused on the following three areas: (1) the structures of the brain, (2) the biochemistry of the brain, and (3) genetics and epigenetics.

    Structures of the Brain

    Research has shown that some psychological disorders appear to involve specific structures within the brain. For example, overactivity in an area of the brain known as Brodmann Area 25 (BA25), shown in Figure 17.1.1, is often present in individuals with clinical depression (also known as Major Depressive Disorder) (Mayberg et al., 2005). BA25 acts as a "junction box" that interacts, through the use of neurotransmitters such as dopamine, with other areas of the brain involved in mood, emotion and thinking. When the BA25 region is overactive, a person can experience an increased negative affect (e.g. sadness, anxiety) and decreased positive affect (e.g. happiness, joy) (Jumah & Dossani, 2021). We will explore the role of brain structures in more detail as we discuss specific disorders later in this chapter.

    Picture showing Brodman Area 25.png
    Figure \(\PageIndex{1}\): Brodmann Area 25 (BA25) is a narrow region of the brain located in the anterior cingulate cortex and is a part of the limbic system. BA25 is shown here colored in yellow. (Public Domain; By Brodmann; Colored by was_a_bee, via Wikimedia Commons)
    Dig Deeper

    Check out the following article from Harvard Health for more on the brain and the biological factors that play a role in depressive disorders:
    https://www.health.harvard.edu/mind-and-mood/what-causes-depression

    Biochemistry of the Brain

    In addition to the individual structures of the brain, researchers are also interested in what role our chemical communication systems – hormones and neurotransmitters –play in the development of psychological disorders.

    The primary communication in the brain occurs between neurons (neurotransmission) using chemicals known as neurotransmitters. When the levels of these neurotransmitters are out of balance, the communication between neurons can be altered or disrupted, resulting in a display of symptoms associated with various psychological disorders.

    For example, researchers believe that disruptions in the neurotransmitters, particularly dopamine, play an important role in schizophrenia (NIH, 2007). This link between dopamine and schizophrenia arose out of observations that individuals addicted to cocaine sometimes showed symptoms very similar to those seen in cases of schizophrenia. Cocaine works by reducing the amount of monoamine neurotransmitters (dopamine, norepinephrine, epinephrine, and serotonin) that are taken back into the presynaptic neuron (Richards & Laurin, 2021), as shown in Figure 2. When this happens, more monoamine neurotransmitters, crucially dopamine, are available in the synapse for binding to the receptors on the postsynaptic neuron. We will discuss the dopamine theory of schizophrenia in more detail later in this chapter.

    Image of how cocaine upregulates dopamine in the brain
    Figure \(\PageIndex{2}\): How cocaine increases the amount of dopamine in the synapse by reducing the activity of the dopamine reuptake transporter (DAT); (CC BY-SA 3.0; Hard-59 via Wikimedia Commons.)

    In addition to neurotransmitters, the brain also communicates via hormones, which are released by the endocrine system, and activate behaviors such as alertness or sleepiness, concentration, and reactions to stress. Elevated or depleted levels of certain hormones may be responsible for some of the symptoms seen in psychological disorders. For example, elevated levels of cortisol, a stress hormone, interfere with learning and memory as well as increase the risk of depression. High levels of cortisol have been shown to alter the function of serotonin receptors in the brain, leading to symptoms of depression (Qin et al., 2018).

    Genetics and Epigenetics

    Researchers have long recognized that many psychological disorders tend to run in families, suggesting a potential a genetic factor. In family and twin studies, schizophrenia is significantly more likely to be present in an identical twin than a fraternal twin (Coon & Miller, 2007) and in individuals with a first-degree relative (e.g. mother or father) with schizophrenia.

    Researchers have also linked several genetic variations, or mutations, to psychological disorders, including variations in two genes which code for the cellular machinery that helps regulate the flow of calcium into neurons (NIH, 2013). One of these calcium channel genes, CACNA1C, is known to affect the brain circuitry involved in emotion, thinking, attention and memory. Variations in this gene have been linked to disorder such as bipolar disorder, schizophrenia, and major depression.

    Figure \(\PageIndex{3}\): Dr. Bruce Cuthbert, Ph.D., director of NIMH's Division of Adult Translational Research, explains the significance of genetic findings for diagnosis and treatment of mental illnesses.

    Although individual genes, such as CACNA1C, have been linked to psychological disorders, most disorders are believed to be polygenic; that is linked to abnormalities in many genes, rather than just one. It is the complex interaction between multiple genes which may trigger a psychological disorder.

    Furthermore, while researchers currently believe that genetic factors are implicated in all psychological disorders, they are not believed to be the sole cause. There are important gene-environment interactions, also known as epigenetic factors, unique to each individual (even identical twins) which may explain why some individuals with a genetic predisposition toward a certain disorder develop that disorder while others do not (e.g., why one identical twin develops schizophrenia, but the other does not).

    References

    American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). https://doi.org/10.1176/appi.books.9780890425596

    Helen S. Mayberg, Andres M. Lozano, Valerie Voon, Heather E. McNeely, David Seminowicz, Clement Hamani, Jason M. Schwalb, and Sidney H. Kennedy (2005). Deep Brain Stimulation for Treatment-Resistant Depression. Neuron, 45(5), 651-660. https://doi.org/10.1016/j.neuron.2005.02.014

    Jumah FR, Dossani RH. (2021) Neuroanatomy, Cingulate Cortex. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK537077/

    National Institutes of Health (US); Biological Sciences Curriculum Study. NIH Curriculum Supplement Series [Internet]. Bethesda (MD): National Institutes of Health (US); 2007. Information about Mental Illness and the Brain. Available from: https://www.ncbi.nlm.nih.gov/books/NBK20369/

    Richards JR, Laurin EG. Cocaine. [Updated 2021 Jul 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430769/

    Qin, Dd., Rizak, J., Feng, Xl. et al. (2016). Prolonged secretion of cortisol as a possible mechanism underlying stress and depressive behavior. Sci Rep 6(30187). https://doi.org/10.1038/srep30187

    Cross-Disorder Group of the Psychiatric Genomics Consortium (2013). Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis. The Lancet, 381(9875), 1371-1379. https://doi.org/10.1016/S0140-6736(12)62129-1.

    Attributions

    Chapter 17, Biological Basis of Psychological Disorders, 17.1. Biological Basis of Psychological Disorders: An Introduction. Original material written by Amy E. Coren, PhD, Pasadena City College, is licensed under CC BY-NC-SA 4.0.

    Figure 17.1.1. Brodman Area 25. By Brodmann; Colured by was_a_bee; File:Brodmann_Cytoarchitectonics.PNG, Public Domain, via Wikimedia Commons.

    Figure 17.1.2. Cocaine and DAT. RicHard-59, CC BY-SA 3.0, via Wikimedia Commons.

    Figure 17.1.3 Dr. Bruce Cuthbert, Ph.D., director of NIMH's Division of Adult Translational Research, explains the significance of genetic findings for diagnosis and treatment of mental illnesses. (Video retrieved from https://youtu.be/8SDKV29NPaE).


    This page titled 17.1: Biological Factors in Psychological Disorders- An Introduction is shared under a mixed license and was authored, remixed, and/or curated by Multiple Authors (ASCCC Open Educational Resources Initiative (OERI)) .