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While sadness and depressed mood may be indicative of an underlying depression, they may also be part of a normal response to the anticipation of one's own death. While periodic sadness is to be expected in these circumstances, such a normal mood state must be distinguished from the entity of clinical depression. The term depression can be used in a variety of ways. In its colloquial form, it is used as a synonym for the affect of sadness. It can also refer to a symptom associated with a wide variety of physical and psychological states. Finally, it also refers to a very specific group of psychiatric syndromes. Given that the latter may represent a highly remediable source of suffering in this patient population, the ability to distinguish these different entities, measure or quantify depression, and make a psychiatric diagnosis when appropriate is critical.

This chapter examines three different approaches—the moral, medical, and social/political—as they apply to the study of affective disorders (mood disorders). It focuses on clinical depression because of its relation to the historical category of melancholia, which once included almost all known psychiatric categories of illness that presently exist, including cognitive disorders, volitional disorders, and psychotic disorders. It considers a particularly entrenched debate between advocates of the moral and the medical perspectives regarding clinical depression, illustrating this debate by highlighting the current moral and political issues surrounding psychopharmacology. It demonstrates how the social/political approach offers an interesting change of perspective on the significance of melancholia, by moving away from positing personhood and personal identity as the locus of philosophical analyses of psychiatric illness.

Affective disorders are described with respect to a model of positive and negative affect, which suggests that clinical depression may result both from an impairment of reward anticipation and experience as well as from an increase in negative affect, which correlates with increased activation of limbic circuits associated with fear and anxiety. Dopamine and serotonin dysfunction interacting with such functional alterations are described, and stress effects on these neurotransmitter systems are discussed. The dimensional approach to affective disorders is explained with respect to different syndrome clusters reflecting negative affect and clinical depression.

Understanding and explanation are not innocent terms used interchangeably in psychiatric discourse. They are technical terms that represent two opposed approaches to a comprehension of human behavior. This chapter begins with a preliminary explication of the terms. It then offers a case history to exemplify their application in psychiatry—that involving Mrs. D. who suffers from clinical depression—and reviews the further development of the terms since their initial articulation.

This chapter describes the main drugs used in affective disorders. Many drugs produce euphoria in normal subjects and some of these, at least temporarily, lighten mood in depressed patients. However, a characteristic of antidepressant drugs is that they have little effect on mood in normal subjects, yet restore normal mood in patients with clinical depression. Similarly, some drugs which are effective in mania (lithium, carbamazepine) have little effect on mood in normal subjects.

The general strategy of Part 2 of the book is to test the plausibility of the tripartite theory of responsibility by investigating its predictions about the responsibility-status of several marginal agents, once the relevant empirical details are filled in. Chapter 4 discusses two such cases and how they bear primarily on attributability: clinical depression (alongside its polar opposite mania) and scrupulosity. Are their attitudes generally attributable to them? The complicated answer is that there are several possible volitional and attitudinal objects, some of which are attributable while some are not, and so many of these agents have mitigated or exempt attributability for some attitudes but not others. The chapter also explores their answerability and accountability to a limited extent.

This chapter highlights clinical depression and anxiety. What seemed like a major step forward both in the understanding of depression, and how to treat it, occurred in the 1950s, when evidence emerged that depression might be due to low levels of the neurochemical serotonin. In particular, neuroscientists discovered that certain chemicals that alleviated the symptoms of depression appeared to work by inhibiting the reuptake of serotonin into certain neurons in the brain. The chapter then looks at the selective serotonin reuptake inhibitors (SSRIs), which are now used to treat far more conditions than clinical depression. Recently, doubts have surfaced about the appropriateness of doctors prescribing SSRIs for such different conditions, the effectiveness of these drugs, and the mechanisms by which they affect brain function. One problem in determining the true effectiveness of SSRIs for the treatment of depression is how little is understood about the biological basis of this disorder and how drugs like SSRIs alleviate it. A complicating factor for any attempt to identify a biological basis to depression, or for that matter any mental disorder, is the important role that the social environment plays in the genesis of such disorders.

What’s the difference between being very shy and having social phobia? Or between a “neat freak” and a person who suffers from obsessive-compulsive disorder? Or a particularly fidgety schoolboy and a child with attention-deficit hyperactivity disorder? Distinctions between the outer bounds of “normal” and “pathological” are ubiquitous in modern life and not easy to make. People who experience loss respond in different ways, with varying degrees of intensity, and for different lengths of time. Mental health professionals find these responses difficult to predict. For example, leaders in the bereavement field have disagreed sharply and for a long time about how to define normal and abnormal grief. This professional disagreement about grief and bereavement made headlines when the American Psychiatric Association (APA) considered changing its Diagnostic and Statistical Manual of Mental Disorders (DSM). Every fifteen to twenty years, the APA revises the DSM—which establishes the criteria clinicians use to diagnose psychiatric disorders—to incorporate the latest scientific research and contemporary expert opinion. Before the most recent edition (DSM-5) came out, the APA considered two grief-related proposals that sparked very heated debate. The most controversial proposal suggested modifying how professionals diagnose major depression. The previous edition of the DSM specified that clinicians could not consider someone to have major depression if that person had lost a loved one less than two months earlier. The APA intended this “bereavement exclusion” to keep mental health professionals from mistaking grief for clinical depression. Clinical researchers Sidney Zisook, MD, at the University of California at San Diego and Katherine Shear, MD, at the Columbia University School of Social Work led one side of the debate. They argued that professionals should diagnose clinical depression even in the context of bereavement as they would following any other stressful life event such as divorce or the loss of a job. Zisook and Shear thought that people could experience both grief and depression simultaneously. Perhaps most importantly, they said, people who had clinical depression during early bereavement were no less deserving of treatment for their depression.

This chapter details the story of how eleven-year old Tim brought a gun to school, prompting the principal to call the police and suspend Tim for ten days. Upon entering sixth grade, Tim had already been diagnosed with attention deficit disorder, clinical depression, and language-based learning disabilities, and was in reciept of help via the Individualized Education Program (IEP). Tim fitted the profile of an unbalanced young man who might be harmful to others. However, the fact is that people with mental illness are more likely to be victims of violence than perpetrators. The principal's view of Tim's illness as a police matter instead of a mental health issue provoked Tim's father to blame the people making the rules. Despite clear relations between mental illness and chronic diseases, there is but little administrative progress in securing mental health services in different states.

This chapter describes the symptoms Kendra Hamilton developed during her younger years, which her parents attributed to adolescent growing pains. Her parents were alarmed because Hamilton hardly spoke and retreated into her books and daydreams. Every single day after school, she would suffer from intense migraines that made her thrash on her narrow twin bed. Hamilton would later discover that the cause of her symptoms was not physical. The symptoms corresponded to those of clinical depression—a depression caused by the fact that she had ceased to be part of a large extended family and had become a social experiment. Hamilton saw the “integration” that children had to endure during the 1960s and 1970s in the South as a violent severing from which some had never recovered.