Biological Explanation of Depression

9 Key excerpts on "Biological Explanation of Depression"

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  Depression

  • Chris Irons(Author)
  • 2014(Publication Date)
  • Bloomsbury Academic

    (Publisher)

  Chapter 3

  Biological Explanations

  Biological explanations seek to understand how a variety of factors – including genes, anatomical brain structures and neurotransmitters – may be involved in depression. As we will find out in this chapter, there is no single biological profile or signature of depression but rather a variety of processes that may play an important role. Whilst reading this chapter, it is also worth holding in mind an important point: Depression, like all other human experience, is biological in nature; without a particular set of physiological changes in the brain and body, we would not ‘feel’ depressed. However, whilst this is very important, it is difficult to say whether, in simple terms, depression is ‘caused’ by biological factors or whether certain types of experience (e.g. environmental stress) affect our biology in a way that leaves us feeling depressed. This of course relates to ‘nature–nurture’ and ‘cause and effect’ debates. It is therefore important to hold in mind that these biological factors are related to depression through a complex biopsychosocial interplay, in which an individual’s unique biological, psychological and social characteristics interact to lead to depression.

  Neurobiological factors

  For many, the brain is the starting point for exploration of mental health problems, including depression. For a long time, scientists and health professionals have been interested in whether there are particular changes in the brains of depressed people, in comparison with those who are not depressed. It turns out that there are a variety of neurophysiological and biological changes in depression, including changes in certain brain structures, neurotransmitters and neurohormones.

  Neurotransmitters

  A neuron is a type of nerve cell that helps to form our nervous system. It is similar in many ways to other cells in the human body but has a special ability to transmit information to other cells and thus communicate information throughout the body. Neurons can communicate this information in both electrical and chemical forms. When they communicate in chemical form, they do this via neurotransmitters . Neurotransmitters are chemicals that operate between neurons, facilitating the transmission of a message or signal from one neuron to another. Neurotransmitters are released at part of a neuron called the axon terminal, and travel across the synaptic gap (the gap between neurons) before reaching the ‘receptor site’ of another neuron. They are then ‘taken up’ by the same neuron – a process known as reuptake. This process is displayed in Figure 3.1

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  Depression

  • Constance Hammen, Ed Watkins(Authors)
  • 2018(Publication Date)
  • Routledge

    (Publisher)

  4 Biological aspects of depression        

  For decades many have characterised the causes of depression as fundamentally biological while others have emphasised primarily psychological causes. Those who have emphasised biological/genetic origins point to the fact that depression seems to run in families, the effectiveness of antidepressant medications and that depression often involves biological symptoms such as changes in sleep, appetite, energy and activity level. None of these arguments is necessarily logically or empirically compelling as evidence for biological causation. More than ever before, however, scientific breakthroughs in knowledge and technology in genetics and studies of the brain have powered much of the research in psychopathology. This chapter attempts to characterise the current state of the rapidly-evolving understanding of depression from the biological perspective.

  Conceptual issues in the biology of depressive disorders

  Before discussing the current understanding of the genetics and neurobiology of depression, several issues affect our understanding of the purpose, research design and interpretation of biological research. These are themes to employ when evaluating the quality and significance of research.

  Complexity

  Scientific advances in the past 25 years or so have opened the door to every level of analysis from intracellular and molecular genetic aspects of brain function to the activities of whole regions of the brain operating together as circuits. Research involves many levels of the workings of normal and impaired human emotional and behavioural functioning including genetic, hormonal, cellular and intracellular, structural and functional aspects of the brain. Further, it is understood that such activities interact with each other in unimaginably complex ways – and that those activities are strongly shaped by environmental (including cultural) factors as well as the unfolding of these processes and outcomes over the course of normal and aberrant development starting from gestation. The term ‘multiple levels of analysis’ has been promoted by many (Cicchetti and Dawson, 2002; Hankin, 2015) to attempt to capture genetic, neural, endocrinological and environmental processes at the individual, family and community level, and to explore their changing effects over the process of development. For some, the concept is a mandate for ‘team’ efforts linking environment, development and multiple biological/genetic factors, but clearly such efforts are extraordinarily complex, expensive and necessitate multidisciplinary groups of experts. Others are moved to go deeper into narrower topics. In this chapter and throughout the book we try to highlight some attempts at multiple levels of analysis but such efforts are clearly at a nascent stage.

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  Depression And The Medically Ill

  An Integrated Approach

  • Gary Gary Rodin(Author)
  • 2017(Publication Date)
  • Routledge

    (Publisher)

  8

  Biological Factors

  The two previous chapters in this section review the psychological and social mechanisms that may contribute to the development of depression in persons with a physical illness. This chapter focuses on a variety of biological mechanisms that have also been implicated in the production of depression in some patients. To a large extent, systematic research into the role of biological mechanisms in the development of depression in medical patients is still in its infancy. A decade after research in this area began, there is still need for the type of coordinated, disorder-by-disorder investigation called for by Klerman in 1981. Such research might help to elucidate the etiology of depression, not only in the medically ill, but also in the general population. For example, identifying the mechanisms by which viral diseases produce depression may provide valuable clues to the pathways and biochemistry involved in the production of depressive disorders in other circumstances.

  In the first section of this chapter, we focus on the difficulties involved in isolating biological from other depressogenic mechanisms. Following this, we summarize the evidence to support a direct relationship between specific physical illnesses and depression and consider the biological mechanisms that have been implicated. We do not provide a comprehensive list of all physical conditions that have been postulated to cause depression. The interested reader is referred to reviews of this topic for a more detailed listing (e.g., Hall, 1980). We emphasize those illnesses in which specific mechanisms have been postulated to account for their association with depression. Biological mechanisms that have been implicated in the production of depression in the medically ill include the effects of pharmacologic agents (e.g., the antihypertensive agent reserpine) and metabolic disturbances associated with specific medical disorders (e.g., depressive symptoms with Cushing’s syndrome). The term organic mood disorder is most applicable in these cases. It may be argued that symptoms of depression that are an inherent component of a medical disease should not be assigned a distinct psychiatric diagnosis. However, identifying the factors involved in the development of depression in these conditions may help to elucidate biological mechanisms responsible for depression generally. We do not assume that psychological factors are necessarily inconsequential when depression can be linked to a direct physical cause.

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  Patterns of Emotions

  A New Analysis of Anxiety and Depression

  • Carrolle E. Izard(Author)
  • 2013(Publication Date)
  • Academic Press

    (Publisher)

  CHAPTER SEVEN Neurophysiologica! and Biochemical Factors in Depression I have taken the position that neurophysiology and bio-chemistry can contribute to our understanding of the emotions and emotion processes. These disciplines may tell us more about how emotion processes work than why they occur. But the how of the emotion process has immediate implications for the management of emotions and behavior. The evidence reviewed in Chapter One indicated that dis-tress (sadness, dejection), the most prominent fundamental emotion in depression, was accompanied primarily by parasympathetic ac-tivity rather than by sympathetic activity. If distress were the only emotion involved in depression, its neurophysiological and biochem-ical study would be greatly simplified. As we shall see, depression involves other emotions. It involves anger, which apparently is ac-companied by both parasympathetic and sympathetic activity. If there are emotion-specific neurophysiological and biochemical pat-terns, the biological study of depression is obviously highly complex. Most of the physiologically oriented studies in this area have been inspired by clinical problems and conducted by clinically oriented investigators. As a consequence, the studies have focused on the clinical syndrome or unitary concept of depression, rather than on discrete fundamental emotions. This has created some confusion and difficulty and may well have contributed to the fairly frequent contradictory or unreplicated findings in this field. 175 7. Neurophysiological and Biochemical Factors in Depression I. NEUROPHYSIOLOGICAL CONSIDERATIONS The neurophysiology of depression is highly complex be-cause it involves a number of fundamental emotions and their inter-actions. In view of the complex nature of depression, it is necessary to approach the search for consistency in neurophysiological func-tioning with caution.

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  Psychiatry

  • Allan Tasman, Jerald Kay, Jeffrey A. Lieberman, Michael B. First, Mario Maj, Allan Tasman, Jerald Kay, Jeffrey A. Lieberman, Michael B. First, Mario Maj(Authors)
  • 2011(Publication Date)
  • Wiley

    (Publisher)

  CHAPTER 21 Neurobiologic Foundations of Mood Disorders

  Ronald Duman1

  H. Jonathan Polan2

  Alan Schatzberg3

  1 Department of Psychiatry, Yale University, New Haven, CT, USA

  2 Department of Psychiatry, Columbia University College of Physicians and Surgeons, New York, NY, USA

  3 Department of Psychiatry, Stanford University, Stanford, CA, USA

  In his classic paper, Mourning and Melancholia, Freud provided a vivid clinical description of what we now call major depression, as well as a pscyhodynamic formulation. Freud acknowledged that some forms of depression were biological in origin. The past 40 years have witnessed a major effort to understand the biology of depression and the major affective disorder, manic depression. This chapter highlights the history of biological approaches to mood disorders and then reviews recent advances in understanding the neurobiology of these complex disorders.

  Perhaps the major development in the past decade has been a shift from a view of depression as a relatively straightforward disorder of monoaminergic function to a more nuanced view of multiple causal steps ranging from alterations in neuronal second messenger systems to dysregulation of growth factor, peptide, and transmitter systems. These approaches have led to the investigation of decreased activity of neurotrophins and neurogenesis in specific brain regions and to altered activity in novel circuits. In each of these areas, available technology has generated new findings, which have spurred new theories of etiology.

  Nomenclature

  The modern era of biological research on affective disorders depended on the development of a reliable classification. Investigators in the United Kingdom and Germany took the lead in classifying depressions. Three major distinctions were made. The first distinguished endogenous from nonendogenous depression. Endogenous depression referred either to a depression that was not precipitated by external events or to depression with prominent biological symptoms akin to melancholia. Over time it was recognized that some patients developed severe melancholic depressions that were clearly precipitated, so that the diagnostic significance of external precipitation for major depression was dropped in the American Psychiatric Association’s Diagnostic and Statisti cal Manual of Mental Disorders

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  Mood Disorders

  • Nese Kocabasoglu(Author)
  • 2013(Publication Date)
  • IntechOpen

    (Publisher)

  So, the research for biological markers of depressive disorders is helpful for finding diagnostic method and useful to distinguish the effectiveness and early improvement after antidepressant administration. Although work in this area has been inconclusive, many animal, post-mortem, clinical, and genetic studies have produced results implicating at least 3 neurobiological systems in the © 2013 Lee and Kim; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. pathogenesis in major depression: dysfunction in the serotonergic system, hyperactivity of the hypothalamic-pituitary-adrenal axis, and decreased neuroplasticity. Additionally, other neurotransmitters, biochemical factors including inflammatory markers, neurophysiologic markers and neuroimaging markers may be associated with MDD. In this chapter, we discuss biological markers involved in the pathogenesis of major depres‐ sive disorder. 2. Biological marker and genetic factor 2.1. Neurotransmitters 2.1.1. Serotonergic system It has been hypothesized that a deficit in serotonin may be a crucial determinant in the path‐ ophysiology of major depression. The serotonin system has been widely investigated in studies of major depression. The innervations of the serotonin system project from the dor‐ sal raphe nucleus to all of the regions of the brain, including the cerebral cortex and hippo‐ campus.

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  Handbook of Depression and Anxiety

  A Biological Approach, Second Edition

  • Siegfried Kasper, Johan A. den Boer, J.M. Ad Sitsen(Authors)
  • 2003(Publication Date)
  • CRC Press

    (Publisher)

  Despite the devastating impact that these diseases have on the lives of millions worldwide, there is still a dearth of knowl-edge concerning their underlying etiology and pathophysiology. This dearth of knowledge regarding the cellular underpinnings of depression has undoubtedly contributed to the lack of development of new treatments for depression. Studies on pathophysiology of mood disorders involve genetics, neurotransmitter systems, intracellular signal transduction pathways, neurotrophic factors, neuroimaging, endocrine abnormalities, neurodegenera-tion, vascular disease and increased platelet aggregability, pineal function and circadian rhythm, and immunological function. This chapter will review studies on the pathophysiol-ogy of major depression. II. GENETICS OF MOOD DISORDERS Genetics undoubtedly plays a major role in the etiology of mood disorders. By determining the rates of illness in different types of relatives, genetic epidemiological studies can pro-vide information about the familial and genetic nature of a disorder (e.g., depression). The probability that a person will develop a mood disorder is influenced by a number of factors, including premature death of a parent, a history of traumatic event, inadequate rearing by parents, poverty, malnutrition, medical illness (e.g., diabetes), personal or fam-ily history of affective episodes, extent of psychosocial support, and recent stressful life events [152]. In terms of the genetic component of major depression, such studies have been conducted and provide much information about the genetic transmission of mood disorders. Three types of studies have been used to determine the role of genetic factors in mood disorders: (1) family studies; (2) twin studies; (3) adoption studies. A. Family Studies Family studies address the question of whether a disorder is familial.

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  Biological Child Psychiatry

  Recent Trends and Developments

  • T. Banaschewski, L. A. Rohde, W. P. Kaschka, W. F. Gattaz(Authors)
  • 2008(Publication Date)
  • S. Karger

    (Publisher)

  Banaschewski T, Rohde LA (eds): Biological Child Psychiatry. Recent Trends and Developments. Adv Biol Psychiatry. Basel, Karger, 2008, vol 24, pp 53–66 Neurobiology of Depression in Childhood and Adolescence Christine Bark Franz Resch Klinik für Kinder- und Jugendpsychiatrie, Universität Heidelberg, Heidelberg, Germany Abstract In the past decade a great deal of success has been achieved in our understanding of the neurobiological basis of depressive syndromes. Genetic factors, structural changes and neuronal networks, which are impor-tant in generating pathological cognitive processes, emotional and behavioral patterns have been identified and characterized. These findings have lead to an improvement in therapeutic interventions and drug ther-apy. Risk factors have been described thus allowing the early detection of affective disorders. At present the main focus of research is to gain greater understanding of the functional polymorphism in the serotonin transporter promoter region. Furthermore, the genetic basis of neurotoxic and neuroprotective processes (neurotrophic factors) and their relation to anatomical changes are being examined. The functional polymor-phism in the serotonin transporter promoter region increases stress-related vulnerability which has been found to be associated with a higher risk for affective disorders. Structural and functional neuroimaging of the amygdala, hippocampus and the prefrontal cortex allow detailed descriptions of morphological changes. Imbalances in different neurotransmitter systems and factors modulating monoamine receptor sensitivity have been characterized and their correlations with genetic, structural and psychosocial factors influencing depressive syndromes are being studied.

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  Depression Sourcebook, 5th Ed.

  • Angela L. Williams(Author)
  • 2019(Publication Date)
  • Omnigraphics

    (Publisher)

  You might have heard of the glass half-full or glass-half-empty test that is, a person may get upset quickly and see the glass as half-empty while others let setbacks slide off easily and see the glass as half-full. The ways in which a person thinks, responds, and reacts to given situations may contribute to depression. “Why Do People Get Depressed?” © 2020 Omnigraphics. Reviewed October 2019. 30 Depression Sourcebook, Fifth Edition Genes Could Be a Reason for Depression Studies show that depression may run in families and that some peo-ple inherit genes that put them at greater risk of becoming depressed. However, not all who acquire these genes get depressed (whereas all people whose ancestors suffer from diabetes are affected). Also, studies indicate that people who do not have any family history of depression can still get depressed. Hence, although genes may be one of the causes of depression, they are not a stand-alone factor to the disorder. Brain Chemistry Could Be a Leading Cause of Depression Depression primarily affects the brain s fragile chemistry involving neurotransmitter signaling. Neurotransmitters send communications between the nerve cells in the brain. They help control the mood of a person. However, when a person is depressed, these neurotransmitters are low in secretion or are imbalanced. Genes and brain chemistry can be interrelated since people who are genetically susceptible to depression are more prone to developing the neurotransmitter activity imbalance, which leads to depression. It s a vicious circle. Various factors can affect the secretion and stability of the neurotrans-mitters, including stress and exposure to daylight. The use of alcohol and drugs can also cause chemical alterations in the brain that influence the mood. However, an imbalance of the neurotransmitters can be completely restored with appropriate medications prescribed by a doctor.

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