Current Theories and Treatment of Depression
Definition and Description of Depression
Depression encompasses a wide range of clinical entities, from a mild mood disturbance commonly found in both normal and anxious persons to a serious, potentially lethal medical illness. Moreover, depression can be either a central or an associated feature of many types of mental disorders. Clinical depression can be defined as a condition characterized by a persistent and abnormal lowering of mood (feeling sad, blue, unhappy) and/or a loss of interest in usual activities, accompanied by a variety of characteristic signs and symptoms. The signs and symptoms of clinical depression are observed in five distinct, but related areas:
Negative affect: Characterized by low mood, loss of pleasure, and feelings of guilt, nervousness, irritability, and boredom.
Negative cognitions: Negative view of the self, the world and the future; indecisiveness, self-blame and feelings of worthlessness and hopelessness.
Negative motivations: Loss of interest, suicidal ideation, social withdrawal, and neglect of appearance and hygiene.
Behavioral changes: Reduction in activities or psychomotor retardation, and agitation.
Vegetative changes: Insomnia, loss of appetite and weight, reduced libido, vague aches and pains.
Since first described by Hippocrates as a medical illness, depression has undergone many transformations through the centuries. In the 1930s, Manfred Blueler classified depressive disorders under the term “affective” disorders. More recently, the revised fourth edition of the Diagnostic and Statistical Manual (DSM-IV-TR), published by the American Psychiatric Association (2000), replaced affective disorders by the term “mood” disorders in order to emphasize the gross deviation in mood. Although the DSM-IV-TR classification of mood disorders is not entirely satisfactory, it is the most widely used classification. Since no perfect system of classification exists, any classification of mood disorders is likely to be controversial. Because this book is confined to major depressive disorder (MDD), the terms depression, affective disorder, mood disorder, or unipolar depression are used interchangeably to denote nonbipolar depressions.
DSM-IV-TR divides mood disorders into bipolar and depressive disorders. Bipolar disorders are characterized by the presence of depressive symptoms and one or more episodes of mania (elevated mood, increased activity, and expansive and self-important ideas) or hypomania (mild mania). Depressive
disorders are subdivided into major depressive disorder (MDD), dysthymic disorder (DD), and depressive disorder not otherwise specified (DDNOS). These disorders exclude a history of manic, mixed, or hypomanic episodes, and they should not be due to the physiological effects of substances of abuse, other medications, or toxins (First & Tasman, 2004).
disorders are subdivided into major depressive disorder (MDD), dysthymic disorder (DD), and depressive disorder not otherwise specified (DDNOS). These disorders exclude a history of manic, mixed, or hypomanic episodes, and they should not be due to the physiological effects of substances of abuse, other medications, or toxins (First & Tasman, 2004).
DSM-IV-TR Criteria for Major Depressive Disorder
The formal diagnosis of MDD is made when five of the following symptoms are present for at least 2 weeks (either depressed mood or loss of interest and pleasure must be one of the five symptoms):
Sad or depressed mood most of the day, nearly every day (or irritable mood in children or adolescents).
Significant loss of interest and pleasure in all or almost all activities.
Poor appetite and marked weight loss, or increased appetite and weight gain.
Insomnia or hypersomnia nearly every day.
Fatigue or lack of energy nearly every day.
Psychomotor agitation or retardation nearly every day.
Diminished ability to think or concentrate, or indecisiveness.
Feelings of worthlessness and guilt, and negative self-concept, self-reproach and self-blame.
Recurrent thoughts of death or suicide.
DSM-IV-TR Criteria for Dysthymic Disorder
Dysthymic disorder (DD), previously known as depressive neurosis, is a chronic, mild-to-moderate form of clinical depression, prevalent for at least 2 years. Unlike MDD, DD has only one typical presentation and, because of its relatively constant course, there is some controversy whether dysthymia should be considered a specific disorder or a personality disorder (Arean & Chatav, 2003). The formal DSM-IV-TR diagnosis for DD is made when a person has been depressed most days, for most of the week for 2 years and presented two or more of these six symptoms: (i) poor appetite and overeating, (ii) insomnia or hypersomnia, (iii) low energy or fatigue, (iv) low self-esteem, (v) poor concentration or difficulty making decisions, and (vi) feelings of hopelessness. During the 2-year episode (1 year for children or adolescents), the symptoms of dysthymia must not be absent for more than 2 months at a time. Moreover, no major depressive episode must have been present during the first 2 years of the disturbance, and the symptoms must not be due to other nonaffective disorders such as schizophrenia or chronic medical conditions or to the direct physiological effects of a substance (including medication). In addition, the person must not have ever met criteria for manic episode, hypomanic episode, or cyclothymic disorder.
Approximately 25% of patients with depressive disorders present the diagnosis of double depression (Keller & Shapiro, 1982) or concurrent presence of both major depression and DD. This is a chronic condition marked by episodes of MDD in dysthymic patients. The course of double depression has two notable characteristics compared to MDD. First, patients with double depression recover more rapidly from episodes of major depression
than do patients with MDD only (Boland & Keller, 2002). However, the recovery is not complete, but to a level of dysthymia. Second, patients with double depression are more likely to relapse than those patients with major depression alone.
than do patients with MDD only (Boland & Keller, 2002). However, the recovery is not complete, but to a level of dysthymia. Second, patients with double depression are more likely to relapse than those patients with major depression alone.
Depressive Disorder Not Otherwise Specified
Depressive disorder NOS (DDNOS) refers to a variety of conditions listed in DSM-IV-TR that do not meet formal criteria for MDD or DD. The conditions listed under this category include premenstrual dysphoric disorder, minor depressive disorder, recurrent brief depressive disorder, postpsychotic depressive disorder of schizophrenia, and depressive episode superimposed on delusional disorder or other psychotic disorder. It is important to note that DDNOS is associated with impairment in overall functioning and general health, and it affects 8% to 11% of the population (First & Tasman, 2004).
There has been considerable debate whether subtypes of depression should be classed as discrete illnesses or seen as dimensions of a single illness along a severity continuum (Arean & Chatav, 2003). However, as knowledge of depression advances, there is a strong movement toward considering both arguments in the diagnosis and treatment of depression. Since MDD has been most researched and understood, the rest of the chapter focuses on MDD when discussing the prevalence, course, etiology, and treatment of depression. Throughout the book, the words depression, mood disorder, or unipolar depression will be used to refer to MDD. However, the treatment techniques described are equally applicable to dysthymia and DDNOS.
Prevalence and Course of Depression
Depression is among one of the most common psychiatric disorders treated by psychiatrists and psychotherapists, and approximately one half of all psychiatric admissions are depressed patients. Both American and British statistics suggest that the lifetime expectancy of developing unipolar depression is approximately 20% in women and 10% in men. The prevalence rate of depression is higher among people from the lower socioeconomic group; divorced and separated persons (Smith & Weissman, 1992); primary care outpatients with chronic disease (ranging from 9% to 20%; Barry, et al., 1998); and medical inpatients (15% to 36%; Feldman, et al., 1987). However, the majority of depressed people do not seek or receive treatment. The estimated percentages of severely depressed patients receiving treatment range from 20% to 33% worldwide (Kaplan & Sardock, 1981).
Apart from being one of the most commonly diagnosed psychological disorders, major depressive disorder is reported to be on the increase (World Health Organization, 1998). It is estimated that out of every 100 people, approximately 13 men and 21 women are likely to develop the disorder at some point in life (Kessler, et al., 1994), and approximately one third of the population may suffer from mild depression at some point in their lives (Paykel & Priest, 1992). In fact, the rate of major depression is so high that the World Health Organization (WHO) Global Burden of Disease Study ranked depression as the single most burdensome disease in the world, in terms of total disability adjusted life years
among people during the middle years of life (Murray & Lopez, 1996). Major depression is also a very costly disorder in terms of lost productivity at work, industrial accidents, beds occupancy in hospitals, treatment, state benefits, and personal suffering. The disorder also adversely affects interpersonal relationships with spouses and children (Gotlib & Hammen, 2002), and the rate of divorce is higher among depressives than among nondepressed individuals (e.g., Wade & Cairney, 2000). The children of depressed parents are found to be at elevated risk of psychopathology (Gotlib & Goodman, 1999). According to WHO (1998), by 2020, clinical depression is likely to be second only to chronic heart disease as an international health burden, as measured by cause of death, disability, incapacity to work, and medical resources used.
among people during the middle years of life (Murray & Lopez, 1996). Major depression is also a very costly disorder in terms of lost productivity at work, industrial accidents, beds occupancy in hospitals, treatment, state benefits, and personal suffering. The disorder also adversely affects interpersonal relationships with spouses and children (Gotlib & Hammen, 2002), and the rate of divorce is higher among depressives than among nondepressed individuals (e.g., Wade & Cairney, 2000). The children of depressed parents are found to be at elevated risk of psychopathology (Gotlib & Goodman, 1999). According to WHO (1998), by 2020, clinical depression is likely to be second only to chronic heart disease as an international health burden, as measured by cause of death, disability, incapacity to work, and medical resources used.
Moreover, depression has significant impact on mortality. The link between depression and mortality is most noticeable in patients with cardiovascular disease. A twofold elevated risk of mortality is noted in patients with depression recovering from myocardial infarction (Frasure, Smith, Lesperance, & Talajic, 1995). Similarly, the mortality rate for depressive older adults residing in nursing homes is twice of those without depression (Rovner, 1993). Furthermore, about 15% of patients suffering from primary mood disorder ultimately take their own lives (Stolberg, Clark, & Bongar, 2002).
A major depressive episode is the most common form of depression diagnosed in clinical practice. If two or more major depressive episodes occur, separated by a period of at least 2 months, during which the individual was not depressed, major depressive disorder, recurrence, is diagnosed. Approximately 60% of people who have a major depressive episode will have a second episode. Among those who have experienced two episodes, 70% will have a third, and among those who have had three episodes, 90% will have a fourth (American Psychiatric Association, 2000). Recurrence is very important in predicting the future course of the disorder, as well as in choosing appropriate treatments. As many as 85% of single-episode cases later experience a second episode. The median lifetime number of major depressive episodes is four, and 25% of depressed patients experience six or more episodes (Angst & Preizig, 1996). Depression therefore is considered to be a chronic condition that waxes and wanes over time but seldom disappears (Solomon, et al., 2000). The median duration of recurrent depression is 5 months. Episodes of MDD are often triggered by severe psychosocial stressors, such as the death of a loved one or divorce. Studies indicate, however, that psychosocial stressors play a more significant role in the precipitation of the first or second episodes than in the onset of subsequent episodes (American Psychiatric Association, 2000).
Over 50% of depressed patients have their first episode of depression before the age of 40. An untreated episode of depression may last 6 to 13 months, whereas most treated episodes last about 3 months. Approximately 50% to 85% of patients have a second depressive episode within the next 4 to 6 months. The risk of recurrence is usually increased by coexisting dysthymia, alcohol or drug abuse, anxiety symptoms, older age at onset, and a history of more than one previous depressive episode. Approximately 50% of all depressed patients recover completely, but in 20% to 35% of
cases, a chronic course ensues, with considerable residual symptomatic and social impairment (DSM-IV-TR, 2000).
cases, a chronic course ensues, with considerable residual symptomatic and social impairment (DSM-IV-TR, 2000).
In trying to define the course of major depressive disorder, researchers have come to realize that depression is a heterogeneous disorder, with many possible courses. Moreover, people with the same diagnosis may vary greatly from one another. For example, some depressed patients may be diagnosed as having psychotic features, such as delusions and hallucinations. Such distinction among unipolar depressives is important because it has implications both for treating and recognizing the severity of the illness. It has been proved that depressed patients with delusions do not generally respond well to antidepressants, but show better response when an antipsychotic drug is combined with the antidepressant. It is also known that depression with psychotic features tends to be more severe than depression without delusions, and it involves more social impairment and less time between episodes (Coryell, et al., 1996).
Moreover, depression co-occurs with other disorders, both medical and psychiatric. Kessler (2002), from his review of the epidemiology of depression, concludes that comorbidity is the norm among people with depression. For example, the Epidemiologic Catchment Area Study (Robins & Regier, 1991) found that 75% of respondents with lifetime depressive disorder also met criteria for at least one of the other DSM-III disorders assessed in that survey. Anxiety is the most frequent comorbid condition with depression. Approximately 50% to 76% of depressed patients experience anxiety (Dozois & Westra, 2004). In fact, considerable symptom overlap occurs between these two conditions. The presence of poor concentration, irritability, hypervigilance, fatigue, guilt, memory loss, sleep difficulties, and worry may suggest a diagnosis of either disorder. The symptom overlap between the two conditions may be indicative of similar neurobiologic correlates. At a psychologic level, it seems reasonable to assume that depression can result from the demoralization caused by anxiety, for example in a case of an agoraphobic who becomes withdrawn because of the fear of going out. Conversely, a person with depression may become anxious due to worry about being unable to hold gainful employment. Although there is an apparent overlap between anxiety and depression, it is common clinical practice to focus on treating one disorder at a time. Lack of an integrated approach to treatment may mean that a patient is treated only for depression while still suffering from anxiety. One of the rationales for combining hypnosis with cognitive behavior therapy, as described in this book, is to address symptoms of anxiety.
Theories of Depression
Despite the well-known fact that many types of depression exist, each involving multiple factors in the genesis of the disorders, researchers have expended a great deal of energy finding a single cause of depression. Some of the well-known biological and psychological theories of depression are briefly and selectively reviewed here to underline the limitation of searching for a single cause of depression. The cognitive theory of depression is described in greater details in the next chapter, because it forms
part of the integrated model of depression (Cognitive-Dissociative Model of Depression) described in Chapter 4.
part of the integrated model of depression (Cognitive-Dissociative Model of Depression) described in Chapter 4.
Biological Theories
The biological theories of depression have mainly focused on genetic predisposition, neurochemistry, the neuroendocrine system, and structural changes in the brain.
Research on the role of genetic transmission in depression has focused on family, twin, and adoption studies. The genetic information available indicates that unipolar depression clusters in first-degree relatives of individuals with depression. But this observation does not address the issue of whether the familial aggregation is due to genetic or familial environmental factors. As multiple psychosocial risk factors such as gender, early parental loss, parental separation, rearing patterns, trauma and abuse, personality factors, prior major depression, low social class, and stressful recent life events are associated with depression (Kendler, et al., 1993), it would appear that environmental risk factors not shared by relatives are clearly important in the etiology of depression. Although specific life events can trigger the initial episode of depression, it is not known whether they have a similar impact on the subsequent precipitation of depressive episodes. Post (1992) argues that, while adverse life events are associated with the initial or second episode of depression, subsequent recurrent episodes are associated with neurobiological factors. Post further asserts that sensitization to stressors and episodes may become encoded at the level of gene expression, underscoring the role of neurobiological factors in the progression of depressive illness. An individual’s social support and effective treatment can, however, protect the individual from the vulnerability of recurrent episodes (First & Tasman, 2004).
Since the advent of effective antidepressant drugs in the 1950s, the past 40 years have seen active research into the biological determinants of depression. From this area of research, several biochemical theories of depression have been proposed, including the hypotheses that (a) a deficiency of important neurotransmitters (such as norepinephrine and serotonin) occurs in certain areas of the brain; (b) an abnormality is present in the functioning of the neuroendocrine system that regulates hormonal secretion and other important biological activities; and (c) some structural changes occur in the brains of depressed individuals.
It was initially believed that depression was caused, in part, by lack of the neurotransmitters norepinephrine and serotonin. Recent studies have challenged this simple paradigm, and it is now known that it is the dysregulation rather than the deficiency of these neurotransmitters that cause depression (Moore & Bona, 2001). Recently, researchers have focused on the postsynaptic effects of antidepressants and are beginning to develop theories of depression that implicate postsynaptic mechanisms (Veenstra-VanderWeele, Anderson, & Cook, 2000). The neurotransmitter theory of depression, although important, provides only a partial picture of the biological origin of depression. Moreover, abnormalities in neurotransmitter regulation do not always lead to depression.
The contribution of endocrine system alterations in depression has been studied extensively. Both hypothyroidism and hypercortisolism may result in depression. Although some depressed patients may have a thyroid dysfunction, the role of thyroid in depression is unclear (First & Tasman, 2004). The evidence for the role of the hypothalamic-pituitary-adrenocortical axis (HPA) in depression is much stronger. Various findings support the hypothesis that an overabundance of cortisol (an adrenocortical hormone) is present in the systems of depressed patients, resulting from oversecretion of thyrotropin-releasing hormone by the hypothalamus (Garbutt, et al., 1994


Stay updated, free articles. Join our Telegram channel

Full access? Get Clinical Tree


