Depression

Integrating Science, Culture, and Humanities

Bradley Lewis

• Publisher: Routledge
• Year: 2012
• ISBN:
  9781136598135
• Edition: 1
• Topic: Sciences sociales
• Subtopic: Sociologie

We live in an era of depression, a condition that causes extensive suffering for individuals and families and saps our collective productivity. Yet there remains considerable confusion about how to understand depression. Depression: Integrating Science, Culture, and Humanities looks at the varied and multiple models through which depression is understood. Highlighting how depression is increasingly seen through models of biomedicine—and through biomedical catch-alls such as "broken brains" and "chemical imbalances"—psychiatrist and cultural studies scholar Bradley Lewis shows how depression is also understood through a variety of other contemporary models. Furthermore, Lewis explores the different ways that depression has been categorized, described, and experienced across history and across cultures.

PART I

THE FACTS

1 What We Teach Our Doctors

Depression, we can say for certain, has become the subject of extensive scientific research. This research is the mainstay of contemporary medical and psychiatric understandings of depression, and it makes up the vast bulk of what we teach our doctors about depression. We need a thorough understanding of this scientific research because when we go to the doctor with complaints of depression our doctor will use it to make sense of our concerns. In addition, although this research can be controversial, it contains invaluable insights and information on depression.

To access contemporary medical and psychiatric approaches to depression, some of the best places to turn to are psychiatric textbooks—which distill a vast amount of scientific research for medical students, general physicians, and psychiatric specialists (as well as psychologists, social workers, nurses, and counselors). This does not mean there is a one-to-one relationship between psychiatric textbooks and what particular clinicians may think. Textbook knowledge is further developed and refined by clinical experience, mentorship with senior clinicians, conference meetings, seminars, continuing education, and further reading of books and journals. But, nonetheless, psychiatric text-books do provide the basic frame from which our healthcare workers think about depression. For this reason, we start our study of depression with an overview of contemporary psychiatric textbook presentations. Along the way, we will also discuss some of the scientific controversies surrounding this material.

Textbooks of psychiatry generally organize their presentation of depression with sections devoted to diagnosis, epidemiology, pathophysiology, and treatment.¹ We follow this outline and our focus will be on “major depressive disorder”—or as it is often called “major depression” or more simply “depression.” Major depression is a subset of a broader class of conditions known as “mood disorders.” As a group, mood disorders share a “disturbance of mood” (or sustained emotion) as their most prominent feature. Major depression is the mood disorder characterized by episodes of depressive mood that may occur one or more times during a person’s life.

Diagnosis

In the United States, psychiatry has strived to produce a rigorously descriptive criterion for depression. The Diagnostic and Statistical Manual IV-TR (DSM IV-TR), psychiatry’s primary diagnostic guide, provides the following classification for a major depressive episode:

DSM-IV-TR Diagnostic Criteria

Major Depressive Episode

A. Five (or more) of the following symptoms have been present during the same 2-week period and represent a change from previous functioning; at least one of the symptoms is either (1) depressed mood or (2) loss of interest or pleasure.

(1) depressed mood;

(2) markedly diminished interest or pleasure;

(3) significant weight loss when not dieting or weight gain, or decrease or increase in appetite;

(4) insomnia or hypersomnia;

(5) psychomotor agitation or retardation;

(6) fatigue or loss of energy;

(7) feelings of worthlessness or excessive or inappropriate guilt;

(8) diminished ability to think or concentrate, or indecisiveness;

(9) recurrent thoughts of death or suicide.

B. The symptoms do not meet criteria for a Mixed Episode (of manic and depressive symptoms).

C. The symptoms cause significant distress or impairment in social, occupational, or other important areas of functioning.

D. The symptoms are not due to the direct physiological effects of a substance (e.g. a drug of abuse, a medication) or a general medical condition (e.g. hypothyroidism).

E. The symptoms are not better accounted for by bereavement, i.e., after the loss of a loved one, the symptoms persist for longer than two months and are characterized by marked functional impairment, morbid preoccupation with worthlessness, suicidal ideation, psychotic symptoms, or psychomotor retardation.

Adapted from Diagnostic and Statistical Manual of Mental Disorders (American Psychiatric Association 2000)

Textbooks of psychiatry use these criteria, and they organize their descriptions of DSM-IV symptoms by dividing them into three categories: 1) emotional symptoms; 2) cognitive symptoms; and 3) vegetative symptoms.

The cardinal emotional symptoms are depressed mood and loss of pleasure. These emotional symptoms are so important to the criteria of major depression that without at least one of these symptoms the diagnosis cannot be made. Depressed mood is a profound sadness that goes beyond everyday blues in longevity (greater than two weeks) and intensity (severe enough to interfere with functioning). This sadness is often accompanied by irritability, anxiety, discouragement, or an overall feeling or lassitude and heaviness. In clear cases, people will bemoan their situation on interview, and they will seem sad and tearful as well. They may cry profusely, their facial musculature may sag, they may have a pained look on their face with a furrowed or pinched brow, and they may be slouched or hunched over in the chair. All of this can make others, including the psychiatrist, feel sad as well.

Lack of pleasure, or anhedonia, is the other cardinal mood symptom of depression. Anhedonic patients lose interest in former attachments and curiosity for new possibilities in life. They take limited pleasure in their activities; little arouses them—even sexual attraction can lose its appeal—and in general they must force themselves to do things they previously enjoyed. As a result, they often go about their day lifeless and desolate.

Prominent cognitive symptoms of major depression include difficulty concentrating, indecision, and memory problems. People with depression often find it hard to focus and complain of confusion, dullness, and forgetfulness. They describe themselves as being in a fog or like they are under water. They have trouble remembering where they put things or what they are planning to do. Simple tasks such as reading can be excruciating, and they are often forced to read the same page over and over again to understand it. Decision making can also be difficult, and even basic choices can become overwhelming. For example, in severe cases people experiencing a depressive episode find it impossible to decide what to wear or what to do in the day.

Other cognitive symptoms include negative thoughts centering on themes of worthlessness, guilt, and shame. People with depression often blame themselves for their problems, the problems of others, and even the woes of the world. They may loudly berate themselves, confessing and accusing themselves of the worst sins and derelictions. Their self-esteem and self-worth is often very low, and they may see themselves as having never done anything of value. When they look over their lives, they may seem blind to accomplishments and aware only of misdeeds and shortcomings. This can become magnified to heinous proportions, even to the point that the person feels evil or somehow rotten to the core. They may ruminate about their failings and defects, and they may repeat their gloomy predictions for the future in an interminable litany.

For many, suicidal thoughts can be a constant preoccupation. Suicidal thoughts may be passive in that people may wish to die of some disease or accident without any intent to bring their own demise. Or they may be active, in that people may make conscious plans to hang or shoot themselves, jump from tall buildings, or overdose on dangerous medicines. These thoughts come partly from the pain of depression and partly because of deep pessimism about the future. The risk of a suicide may be highest when the depressive episode starts to lift. In early recovery, while still feeling worthless and hopeless, people may have enough energy to carry out suicidal plans that they only thought about before.

In a small percentage of cases, cognitive disturbances become so severe that psychiatrists use the term “psychotic depression” to describe them. The most common psychotic depression involves extreme negative thoughts that devolve into frank delusions or hallucinations. A delusion is a fixed unshakeable belief that others find improbable or fantastic. Commonly, delusions in depression magnify other symptoms. Guilt may become extreme, and people may confess to unspeakable, impossible sins. For example, they may believe that they have poisoned their children, or that they have caused world pollution, hunger, and war. They may believe they are condemned to hell, or that they are possessed by Satan. They may feel deservedly persecuted, that their neighbors or co-workers talk about them, or that the police survey them with hidden cameras. They may have delusions of poverty and destitution or may believe themselves to have a terminal disease or be near death. Auditory hallucinations, when they occur, generally reflect delusions. Voices may accuse people of evil deeds or may announce their execution. Visual or olfactory hallucinations, though rare, can also occur.

Psychiatrists refer to vegetative symptoms as those disturbances that seem most embodied, such as disturbances of sleep, appetite, energy level, and sexuality. All of these can increase or decrease, but for the most part they go down in depression. Decreased sleep, or insomnia, is a common sleep problem in depression. People have trouble falling asleep, or more typically, they wake up in the middle of the night or early in the morning and having trouble getting back to sleep. During these waking hours people can experience depressive ruminations and worries that they cannot escape. On the other hand, some people with depression complain of hypersomnia, with a tendency to sleep much longer than usual, or to take naps throughout the day.

Energy levels in depression are often very low, with people complaining of feeling tired, fatigued, lifeless, or drained. But for some people, energy levels go up—with an excess of nervous energy, mild agitation, restlessness, and hand wringing. Appetite can also go up or down. Most commonly people lose their appetite, and for many this means significant weight loss. In these cases, food may lose its taste and may even leave people feeling nauseated when they try to eat. By contrast, some people find themselves hungry all the time, using food in an attempt to soothe themselves to the point that they can put on considerable weight. Finally, libido is usually much diminished, with people losing most, if not all, interest in sex. But occasionally, it goes the other way around and people find themselves constantly turning to sex or masturbation for comfort.

Epidemiology

Psychiatric epidemiologists study the rates of psychiatric conditions in populations. Epidemiologic research helps us understand the extent and burden of depression as well as social and demographic factors that may cause or contribute to depression. Psychiatric epidemiologists commonly report rates in terms of prevalence—which is a percentage calculated by dividing the number of cases (per unit of time) by the population.

Influential studies of major depression in the U.S., Europe, and Australia find a one-year prevalence of depression somewhere between 3% and 10% of the population. Over a lifetime, the prevalence ranges from 5% to 17% of the population (Rihmer and Angst 2009, 1648). The wide range in these numbers comes from the variability of populations along with the diagnostic reliability of the instruments used. Still, if we take an average of these numbers, we can get a fair approximation of the epidemiology of depression in Western countries—7% one-year prevalence and 12% lifetime prevalence.

A well-respected study in the U.S. found that major depression was the most common psychiatric condition causing significant morbidity. Major depression tied with phobia in terms of one-year prevalence (at 7.1%) and was significantly higher than the next most common disorder, which was alcohol abuse (4.7%) (Narrow and Rubio-Stipec 2009, 767). The extent and severity of depression was made particularly poignant by the Global Burden of Disease study, sponsored by the World Health Organization (WHO) and the World Bank. This study looked not only at disease prevalence but also at the extent to which disease caused disability. For developed regions, the study found that major depression was the leading psychiatric cause of disability. Furthermore, the study found that major depression caused more years lived with disability than any other disease—including medical diseases such as diabetes, cerebrovascular disease, cancer, and traffic accidents (p. 769).

Epidemiologic studies also reveal consistent sociodemographic patterns for depression. The mean age of onset for major depression is generally in the late 20s. After that depression tends to be recurrent across the life span. Occurrence with other psychiatric conditions is common. Women are twice as likely as men to suffer from depression. Married people suffer depression less often than their single or divorced cohorts. People who are unemployed or have low socioeconomic status have increased rates of depression, and low-income single mothers have an especially high risk. Race and ethnicity are thought to be risk factors particularly when combined with socioeconomic factors. In addition, several studies have found increasing prevalence of depression over the last half century. However, this finding is controversial, and others argue that the increase is due to heightened cultural awareness and preoccupation with depression as a condition (see Chapter 4 for further discussion of this concern).

Epidemiological studies of risk factors have focused extensively on familial patterns and stress. A family history of major depression increases the risk for depression, and a family history also increases the risk of more severe depression. Twin studies and adoption studies point to an at least partial genetic component to these family trends. Estimates of the monozygotic-to-dizygotic ratio have found as high as increased prevalence in monozygotic compared to dizygotic twins. Stress is also a well-documented epidemiological risk factor for depression. Early childhood traumas and negative life events increase the risk of depression—particularly child abuse (physical, sexual, and neglect) and the loss of significant other. In adults, too, stressful life events in family, work, health, and finances increase the risk of depression.

The link between loss, negative life events, and stress is the leading explanation for increased depression among women and lower socioeconomic groups. Increased prejudice, disadvantage, and hardship faced by lower status groups yield considerably increased stress and therefore increased depression. However, there is also evidence that those with a family history of depression are more vulnerable to stressful events than others. It seems from this evidence that there is a spiraling, and bidirectional, effect of depression and stress. Persons who are depressed for whatever reason have increased difficulty managing life challenges—obtaining and maintaining work, relationships, self-care, etc. These can all lead to increased stress, loss, negative life events, and lower socioeconomic status (Williams and Neighbors 2006). This same spiraling relationship between stress and vulnerability shows up in recent pathophysiological studies of depression, which suggests that individual genetic predisposition interacts with psychological and social factors.

Pathophysiology

In recent years, the vast bulk of causal research in psychiatry has focused on a search for biological abnormalities in depression. Genetic vulnerabilities were discussed in the last section. In this section research on neurochemical and neuroanatomical pathology will be considered.

Extensive neurochemical research has centered on the “monoamine theory” of depression. The term monoamine refers to the neurotransmitters (chemical messengers) norepinephrine, serotonin, and dopamine. The theory evolved because of the effects of medications on depression. By the 1950s, there were several medications observed either to trigger depressive symptoms or to reduce them. For example, iproniazid (first used for tuberculosis) was found to decrease depressive symptoms and was known to be a monoamine oxidase inhibitor. By inhibiting the oxidation (or breakdown) of monamines, iproniazid effectively increased the amount of monoamines available for neuro-transmission. Similarly, imipramine, the first antidepressant widely used, also worked on the monoamines. Julius Axelrod won the Nobel prize for his research showing that imipramine and similar medications blocked the reuptake of monoamines in the synapse (the space between nerve endings). Blocking the reuptake of monoamines also effectively increases their availability in the synapse. By the 1960s and 1970s studies such as these led to a wide consensus known as “the monoamine hypothesis” that depression was caused by a deficit of norepinephrine and serotonin.

This period of consensus around the monoamine hypothesis is the scientific background for the popular use of the phrase “chemical imbalance” to explain depression. But over the past 15 years the monoamine hypothesis has lost ground in scientific circles. Studies of norepinephrine and serotonin have not reliably shown depleted levels, and evidence for a primary neurochemical dysfunction has been lacking (Delgado and Moreno 2006, 111).

Increasingly, research into depression has moved from the neurochemical level to the neuroanatomical level. Neurochemical factors may be important, but many argue they must be understoo...

Table of contents

• Cover Page
• Half Title Page
• Series
• Title Page
• Copyright Page
• Contents
• Series Foreword
• Preface
• Acknowledgements
• Introduction
• Part I The Facts
• 1 What We Teach Our Doctors
• 2 What We Also Know
• Part II Historical and Cultural Perspectives
• 3 Western History
• 4 Cultural Context
• Part III Theoretical and Clinical Concerns
• 5 What We May Never Know
• 6 Clinical Encounters
• Notes
• References
• Index