Depression - Wikipedia
Major depressive disorder

(also known as clinical depression, major depression, unipolar depression, or unipolar disorder) is a mental disorder characterized by an all-encompassing low mood accompanied by low self-esteem, and loss of interest or pleasure in normally enjoyable activities. The term "major depressive disorder" was selected by the American Psychiatric Association to designate this symptom cluster as a mood disorder in the 1980 version of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III) classification, and has become widely used since. The general term depression is often used to describe the disorder, but as it can also be used to describe other types of psychological depression, more precise terminology is preferred for the disorder in clinical and research use. Major depression is a disabling condition which adversely affects a person's family, work or school life, sleeping and eating habits, and general health. In the United States, approximately 3.4% of people with major depression commit suicide, and up to 60% of people who commit suicide have depression or another mood disorder.

The diagnosis of major depressive disorder is based on the patient's self-reported experiences, behavior reported by relatives or friends, and a mental status exam. There is no laboratory test for major depression, although physicians generally request tests for physical conditions that may cause similar symptoms. The most common time of onset is between the ages of 30 and 40 years, with a later peak between 50 and 60 years. Major depression is reported about twice as frequently in women as in men, although men are at higher risk for committing suicide.

Most patients are treated in the community with antidepressant medication and some with psychotherapy or counseling. Hospitalization may be necessary in cases with associated self-neglect or a significant risk of harm to self or others. A minority are treated with electroconvulsive therapy (ECT), under a short-acting general anaesthetic. The course of the disorder varies widely, from one episode lasting months to a lifelong disorder with recurrent major depressive episodes. Depressed individuals have shorter life expectancies than those without depression, in part because of greater susceptibility to medical illnesses. Current and former patients may be stigmatized.

The understanding of the nature and causes of depression has evolved over the centuries, though many aspects of depression remain incompletely understood and are the subject of discussion and research. Psychological, psycho-social, hereditary, evolutionary and biological causes have been proposed. Psychological treatments are based on theories of personality, interpersonal communication, and learning. Most biological theories focus on the monoamine chemicals serotonin, norepinephrine, and dopamine that are naturally present in the brain and assist communication between nerve cells. Monoamines have been implicated in depression, and most antidepressants work to increase the active levels of at least one.

Contents [hide]
1 Symptoms and signs
2 Causes
2.1 Biological
2.1.1 Monoamine hypothesis
2.1.2 Other theories
2.2 Psychological
2.3 Social
2.4 Evolutionary
2.5 Drug use
3 Diagnosis
3.1 Clinical assessment
3.2 DSM-IV-TR and ICD-10 criteria
3.2.1 Major depressive episode
3.2.2 Subtypes
3.3 Differential diagnoses
4 Prevention
5 Management
5.1 Psychotherapy
5.2 Antidepressants
5.2.1 Pharmacological augmentation
5.2.2 Debated effectiveness
5.3 Electroconvulsive therapy
5.4 Physical exercise
5.5 Over-the-counter compounds
5.6 Other somatic treatments
6 Prognosis
7 Epidemiology
7.1 Comorbidity
8 History
9 Sociocultural aspects
10 See also
11 References
11.1 Cited texts
12 External links

[edit] Symptoms and signs
Major depression is a serious illness that affects a person's family, work or school life, sleeping and eating habits, and general health.[1] Its impact on functioning and well-being has been equated to that of chronic medical conditions such as diabetes.[2]

A person suffering a major depressive episode usually exhibits a very low mood that pervades all aspects of life and an inability to experience pleasure in activities that formerly were enjoyed. Depressed people may be preoccupied with, or ruminate over, thoughts and feelings of worthlessness, inappropriate guilt or regret, helplessness, hopelessness, and self-hatred.[3] Other symptoms include poor concentration and memory (especially in those with melancholic or psychotic features),[4] withdrawal from social situations and activities, reduced sex drive, and thoughts of death or suicide. Insomnia is common: in the typical pattern, a person wakes very early and is unable to get back to sleep.[5] Hypersomnia, or oversleeping, is less common.[5] Appetite often decreases, with resulting weight loss, although increased appetite and weight gain occasionally occur.[3] The person may report multiple physical symptoms such as fatigue, headaches, or digestive problems; physical complaints are the most common presenting problem in developing countries according to the World Health Organization's criteria of depression.[6] Family and friends may notice that the person's behavior is either agitated or lethargic.[5]

Older depressed persons may have cognitive symptoms of recent onset, such as forgetfulness,[4] and a more noticeable slowing of movements.[dead link][7] Depression often coexists with physical disorders common among the elderly, such as stroke, other cardiovascular diseases, Parkinson's disease, and chronic obstructive pulmonary disease.[8]

In severe cases, depressed people may have symptoms of psychosis such as delusions or, less commonly, hallucinations, usually of an unpleasant nature.[9]

Depressed children often display an irritable rather than a depressed mood,[3] and show varying symptoms depending on age and situation.[10] Most exhibit a loss of interest in school and a decline in academic performance. They may be described as clingy, demanding, dependent, or insecure.[5] Diagnosis may be delayed or missed when symptoms are interpreted as normal moodiness.[3] Depression may also coincide with attention-deficit hyperactivity disorder, complicating the diagnosis and treatment of both.[11]

[edit] Causes
The biopsychosocial model proposes that biological, psychological, and social factors all play a role to varying degrees in causing depression.[12] The diathesis–stress model posits that depression results when a preexisting vulnerability, or diathesis, is activated by stressful life events. The preexisting vulnerability can be either genetic,[13][14] implying an interaction between nature and nurture, or schematic, resulting from views of the world learned in childhood.[15] These interactive models have gained empirical support. For example, researchers in New Zealand took a prospective approach to studying depression, by documenting over time how depression emerged among an initially normal cohort of people. The researchers concluded that variation among the serotonin transporter (5-HTT) gene affects the chances that people who have dealt with very stressful life events will go on to experience depression. Specifically, depression may follow such events, but seems more likely to appear in people with one or two short alleles of the 5-HTT gene.[13]

A Swedish study estimated the heritability of depression—the degree to which individual differences in occurrence are associated with genetic differences—to be approximately 40% for women and 30% for men,[16] and evolutionary psychologists have proposed that the genetic basis for depression lies deep in the history of naturally selected adaptations. A substance-induced mood disorder resembling major depression has been causally linked to long-term drug use or abuse, or to withdrawal from certain sedative and hypnotic drugs.[17][18]

[edit] Biological
Main article: Biology of depression

[edit] Monoamine hypothesis
Most antidepressant medications work by increasing the levels of one or more of the monoamines—the neurotransmitters serotonin, norepinephrine and dopamine—in the synaptic cleft between neurons in the brain. Some medications affect the monoamine receptors directly.

Serotonin is hypothesized to help regulate other neurotransmitter systems; decreased serotonin activity may allow these systems to act in unusual and erratic ways.[19] According to this "permissive hypothesis", depression arises when low serotonin levels promote low levels of norepinephrine, another monoamine neurotransmitter.[20] Some antidepressants enhance the levels of norepinephrine directly, whereas others raise the levels of dopamine, a third monoamine neurotransmitter. These observations gave rise to the monoamine hypothesis of depression. In its contemporary formulation, the monoamine hypothesis postulates that a deficiency of certain neurotransmitters is responsible for the corresponding features of depression: "Norepinephrine may be related to alertness and energy as well as anxiety, attention, and interest in life; [lack of] serotonin to anxiety, obsessions, and compulsions; and dopamine to attention, motivation, pleasure, and reward, as well as interest in life."[21] The proponents of this theory recommend the choice of an antidepressant with mechanism of action that impacts the most prominent symptoms. Anxious and irritable patients should be treated with SSRIs or norepinephrine reuptake inhibitors, and those experiencing a loss of energy and enjoyment of life with norepinephrine- and dopamine-enhancing drugs.[21]

Schematic of a synapse between an axon of one neuron and a dendrite of another. Synapses are specialized gaps between neurons. Electrical impulses arriving at the axon terminal trigger release of packets of chemical messengers (neurotransmitters), which diffuse across the synaptic cleft to receptors on the adjacent dendrite temporarily affecting the likelihood that an electrical impulse will be triggered in the latter neuron. Once released the neurotransmitter is rapidly metabolised or pumped back into a neuron. Antidepressants influence the overall balance of these processes.In the past two decades, research has revealed multiple limitations of the monoamine hypothesis, and its explanatory inadequacy has been criticized within the psychiatric community.[22] Intensive investigation has failed to find convincing evidence of a primary dysfunction of a specific monoamine system in patients with major depressive disorders. The medications tianeptine and opipramol have long been known to have antidepressant properties despite the fact that the former is a serotonin reuptake enhancer and the latter has no effect on the monoamine system. Experiments with pharmacological agents that cause depletion of monoamines have shown that this depletion does not cause depression in healthy people nor does it worsen symptoms in depressed patients—although an intact monoamine system is necessary for antidepressants to achieve therapeutic effectiveness.[23] According to an essay published by the Public Library of Science (PLoS), the monoamine hypothesis, already limited, has been further oversimplified when presented to the general public as a mass marketing tool.[24]

[edit] Other theories
MRI scans of patients with depression have reported a number of differences in brain structure compared to those without the illness. Although there is some inconsistency in the results, meta-analyses have shown there is strong evidence for smaller hippocampal[25] volumes and increased numbers of hyperintensive lesions.[26] Hyperintensities have been associated with patients with a late age of onset, and have led to the development of the theory of vascular depression.[27]

There may be a link between depression and neurogenesis of the hippocampus,[28] a center for both mood and memory. Loss of hippocampal neurons is found in some depressed individuals and correlates with impaired memory and dysthymic mood. Drugs may increase serotonin levels in the brain, stimulating neurogenesis and thus increasing the total mass of the hippocampus. This increase may help to restore mood and memory.[29][30] Similar relationships have been observed between depression and an area of the anterior cingulate cortex implicated in the modulation of emotional behavior.[31] One of the neurotrophins responsible for neurogenesis is the brain-derived neurotrophic factor (BDNF). The level of BDNF in the blood plasma of depressed subjects is drastically reduced (more than threefold) as compared to the norm. Antidepressant treatment increases the blood level of BDNF. Although decreased plasma BDNF levels have been found in many other disorders, there is some evidence that BDNF is involved in the cause of depression and the mechanism of action of antidepressants.[32]

Major depression may also be caused in part by an overactive hypothalamic-pituitary-adrenal axis (HPA axis) that is similar to the neuro-endocrine response to stress. Investigations reveal increased levels of the hormone cortisol and enlarged pituitary and adrenal glands, suggesting disturbances of the endocrine system may play a role in some psychiatric disorders, including major depression. Oversecretion of corticotropin-releasing hormone from the hypothalamus is thought to drive this, and is implicated in the cognitive and arousal symptoms.[33]

Depression may be related to the same brain mechanisms that control the cycles of sleep and wakefulness.Depression may be related to abnormalities in the circadian rhythm, or biological clock. For example, the REM stage of sleep, the one in which dreaming occurs, may be quick to arrive, and intense, in depressed people. REM sleep depends on decreased serotonin levels in the brain stem,[34] and is impaired by compounds, such as antidepressants, that increase serotoninergic tone in brain stem structures.[34] Overall, the serotonergic system is least active during sleep and most active during wakefulness. Prolonged wakefulness due to sleep deprivation activates serotonergic neurons, leading to processes similar to the therapeutic effect of antidepressants, such as the selective serotonin reuptake inhibitors (SSRIs). Depressed individuals can exhibit a significant lift in mood after a night of sleep deprivation. SSRIs may directly depend on the increase of central serotonergic neurotransmission for their therapeutic effect, the same system that impacts cycles of sleep and wakefulness.[34]

Research on the effects of light therapy on treating seasonal affective disorder suggests that light deprivation is related to decreased activity in the serotonergic system and to abnormalities in the sleep cycle, particularly insomnia. Exposure to light also targets the serotonergic system, providing more support for the important role this system may play in depression.[35] Sleep deprivation and light therapy both target the same brain neurotransmitter system and brain areas as antidepressant drugs, and are now used clinically to treat depression.[36] Light therapy, sleep deprivation and sleep time displacement (sleep phase advance therapy) are being used in combination quickly to interrupt a deep depression in hospitalized patients.[35]

The hormone estrogen has been implicated in depressive disorders due to the increase in risk of depressive episodes after puberty, the antenatal period, and reduced rates after menopause.[37] Conversely, the premenstrual and postpartum periods of low estrogen levels are also associated with increased risk.[37] The use of estrogen has been under-researched, and although some small trials show promise in its use to prevent or treat depression, the evidence for its effectiveness is not strong.[37] Estrogen replacement therapy has been shown to be beneficial in improving mood in perimenopause, but it is unclear if it is merely the menopausal symptoms that are being reversed.[37]

Other research has explored potential roles of molecules necessary for overall cellular functioning: cytokines and essential nutrients. The symptoms of major depressive disorder are nearly identical to those of sickness behavior, the response of the body when the immune system is fighting an infection.[38] This raises the possility that depression can result from a maladaptive manifestation of sickness behavior as a result of abnormalities in circulating cytokines.[39][40][41] Deficiencies in certain essential dietary nutrients, particularly vitamin B12 and folic acid, have been associated with depression;[42] other agents such as the elements copper and magnesium,[43] and vitamin A have also been implicated.[44]

[edit] Psychological
Various aspects of personality and its development appear to be integral to the occurrence and persistence of depression.[45] Although depressive episodes are strongly correlated with adverse events, a person's characteristic style of coping may be correlated with their resilience.[46] Additionally, low self-esteem and self-defeating or distorted thinking are related to depression. It is not always clear which factors are causes or which are effects of depression; however, depressed persons who are able to make corrections in their thinking patterns often show improved mood and self-esteem.[47]

American psychiatrist Aaron T. Beck developed what is now known as a cognitive model of depression in the early 1960s. He proposed that three concepts underlie depression: a triad of negative thoughts comprised of cognitive errors about oneself, one's world, and one's future; recurrent patterns of depressive thinking, or schemas; and distorted information processing.[48] From these principles, he developed the structured technique of cognitive behavioral therapy.[49] According to American psychologist Martin Seligman, depression in humans is similar to learned helplessness in laboratory animals, who remain in unpleasant situations when they are able to escape, but do not because they initially learned they had no control.[50]

Depressed individuals often blame themselves for negative events,[51] and—as reflected in a study of hospitalized adolescents with self-reported depression—those who do this may not take credit for positive outcomes.[52] This tendency is characteristic of a depressive attributional, or pessimistic explanatory style.[51] According to Albert Bandura, a Canadian social psychologist associated with social cognitive theory, depressed individuals have negative beliefs about themselves, based on experiences of failure, observing the failure of social models, a lack of social persuasion that they can succeed, and their own somatic and emotional states including tension and stress. These influences may result in a negative self-concept and a perceived lack of self-efficacy; that is, they do not believe they can influence events or achieve personal goals.[53]

An examination of depression in women indicates that vulnerability factors—such as early maternal loss, lack of a confiding relationship, responsibility for the care of several young children at home, and unemployment—can interact with life stressors to increase the risk of depression.[54] For older adults, the factors are often health problems, changes in relationships with a spouse or adult children due to the transition to a care-giving or care-needing role, the death of a significant other, or a change in the availability or quality of social relationships with older friends because of their own health-related life changes.[55]

The understanding of depression has also received contributions from the psychoanalytic, existential, and humanistic branches of psychology. From the classical psychoanalytic perspective of Austrian psychiatrist Sigmund Freud, depression, or melancholia, may be related to interpersonal loss[56][57] and early life experiences.[58] Existential psychologists have connected depression to the lack of both meaning in the present[59] and a vision of the future.[60] [61] The founder of humanistic psychology, American psychologist Abraham Maslow, suggested that depression could arise when people are unable to attain their needs or to self-actualize, to realize their full potential.[62][63]

[edit] Social
Poverty and social isolation are associated with increased risk of psychiatric problems in general.[45] Child abuse (physical, emotional, sexual, or neglect) is also associated with increased risk of developing depressive disorders later in life.[64] Disturbances in family functioning, such as parental (particularly maternal) depression, severe marital conflict or divorce, death of a parent, or other disturbances in parenting are additional risk factors.[45] In adulthood, stressful life events are strongly associated with the onset of major depressive episodes;[65] a first episode is more likely to be immediately preceded by stressful life events than are recurrent ones.[66]

The relationship between stressful life events and social support has been a matter of some debate; the lack of social support may increase the likelihood that life stress will lead to depression, or the absence of social support may constitute a form of strain that leads to depression directly.[67] There is evidence that neighborhood social disorder, for example, due to crime or illicit drugs, is a risk factor, and that a high neighborhood socioeconomic status, with better amenities, is a protective factor.[68] Adverse conditions at work, particularly demanding jobs with little scope for decision-making, are associated with depression, although diversity and confounding factors make it difficult to confirm that the relationship is causal.[69]

[edit] Evolutionary
Main article: Evolutionary approaches to depression
From the standpoint of evolutionary theory, major depression is hypothesized, in some instances, to increase an individual's ability to reproduce. Evolutionary approaches to depression and evolutionary psychology posit specific mechanisms by which depression may have been genetically incorporated into the human gene pool, accounting for the high heritability and prevalence of depression by proposing that certain components of depression are adaptations,[70] such as the behaviors relating to attachment and social rank.[71] Current behaviors can be explained as adaptations to regulate relationships or resources, although the result may be maladaptive in modern environments.[72]

From a counseling psychology viewpoint, the therapist may see depression, not as a biochemical illness or disorder, but as "a species-wide evolved suite of emotional programmes that are mostly activated by a perception, almost always over-negative, of a major decline in personal usefulness, that can sometimes be linked to guilt, shame or perceived rejection".[73] This suite may have manifested in aging hunters in humans' foraging past, who were marginalized by their declining skills, and may continue to appear in alienated members of today's society. The feelings of uselessness generated by such marginalization could hypothetically prompt support from friends and kin. Additionally, in a manner analogous to that in which physical pain has evolved to hinder actions that may cause further injury, "psychic misery" may have evolved to prevent hasty and maladaptive reactions to distressing situations.[74]

[edit] Drug use
See also: Substance induced mood disorder
The DSM precludes a diagnosis of major depressive disorder for those presenting with "the direct physiological effects of a substance" because sedative hypnotic drugs such as alcohol and benzodiazepines increase the risk of a syndrome that is similar to major depression. This increased risk may be due in part to the effects of drugs on neurochemistry, such as decreased levels of serotonin and norepinephrine.[18][75] Alcoholism or excessive alcohol consumption significantly increases the risk of developing this syndrome.[76][77][78] Chronic use of benzodiazepines, a class of medication that is commonly used to treat insomnia, anxiety and muscular spasms, also increases the risk.[79] Chronic, severe depression can develop as a result of chronic use of benzodiazepines or as part of a protracted withdrawal syndrome.[18][80][81][82]

[edit] Diagnosis

[edit] Clinical assessment
Further information: Rating scales for depression
A diagnostic assessment may be conducted by a general practitioner, or by a psychiatrist or psychologist,[1] who records the person's current circumstances, biographical history and current symptoms, and a family medical history to see if other family members have suffered from a mood disorder, and discuss the person's alcohol and drug use. The assessment also includes a mental state examination, which is an assessment of the person's current mood and thought content, in particular the presence of themes of hopelessness or pessimism, self-harm or suicide, and an absence of positive thoughts or plans.[1] Specialist mental health services are rare in rural areas, and thus diagnosis and management is largely left to primary care clinicians.[83] This issue is even more marked in developing countries.[84] The score on a rating scale alone is not sufficient to diagnose depression, but it provides an indication of the severity of symptoms for a time period, so a person who scores above a given cut-off point can be more thoroughly evaluated for a depressive disorder diagnosis.[85] Several rating scales are used for this purpose.[85] Screening programs have been advocated to improve detection of depression, but there is evidence that they do not improve detection rates, treatment, or outcome.[86]

Before diagnosing a major depressive disorder, a doctor generally performs a medical examination and selected investigations to rule out other causes of symptoms. These include blood tests measuring TSH and thyroxine to exclude hypothyroidism; basic electrolytes and serum calcium to rule out a metabolic disturbance; and a full blood count including ESR to rule out a systemic infection or chronic disease.[87] Adverse affective reactions to medications or alcohol misuse are often ruled out, as well. Testosterone levels may be evaluated to diagnose hypogonadism, a cause of depression in men.[88]

Subjective cognitive complaints appear in older depressed people, but they can also be indicative of the onset of a dementing disorder, such as Alzheimer's disease.[89] (See also Depression of Alzheimer disease.) Depression is also a common initial symptom of dementia.[90] Cognitive testing and brain imaging can help distinguish depression from dementia.[91] A CT scan can exclude brain pathology in those with psychotic, rapid-onset or otherwise unusual symptoms.[92] No biological tests confirm major depression.[93] Investigations are not generally repeated for a subsequent episode unless there is a medical indication.

[edit] DSM-IV-TR and ICD-10 criteria
The most widely used criteria for diagnosing depressive conditions are found in the American Psychiatric Association's revised fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), and the World Health Organization's International Statistical Classification of Diseases and Related Health Problems (ICD-10) which uses the name recurrent depressive disorder.[94] The latter system is typically used in European countries, while the former is used in the US and many other non-European nations,[95] and the authors of both have worked towards conforming one with the other.[96]

Major depressive disorder is classified as a mood disorder in DSM-IV-TR.[97] The diagnosis hinges on the presence of a single or recurrent major depressive episode.[3] Further qualifiers are used to classify both the episode itself and the course of the disorder. The category Depressive disorder not otherwise specified is diagnosed if the depressive episode's manifestation does not meet the criteria for a major depressive episode. The ICD-10 system does not use the term Major depressive disorder, but lists very similar criteria for the diagnosis of a depressive episode (mild, moderate or severe); the term recurrent may be added if there have been multiple episodes without mania.[98]

[edit] Major depressive episode
Main article: Major depressive episode
A major depressive episode is characterized by the presence of a severely depressed mood that persists for at least two weeks.[3] Episodes may be isolated or recurrent and are categorized as mild (few symptoms in excess of minimum criteria), moderate, or severe (marked impact on social or occupational functioning). An episode with psychotic features—commonly referred to as psychotic depression—is automatically rated as severe. If the patient has had an episode of mania or markedly elevated mood, a diagnosis of bipolar disorder is made instead.[99] Depression without mania is sometimes referred to as unipolar because the mood remains at one emotional state or "pole".[100]

DSM-IV-TR excludes cases where the symptoms are a result of bereavement, although it is possible for normal bereavement to evolve into a depressive episode if the mood persists and the characteristic features of a major depressive episode develop.[101] The criteria have been criticized because they do not take into account any other aspects of the personal and social context in which depression can occur.[102] In addition, some studies have found little empirical support for the DSM-IV cut-off criteria, indicating they are a diagnostic convention imposed on a continuum of depressive symptoms of varying severity and duration:[103] excluded are a range of related diagnoses, including dysthymia which involves a chronic but milder mood disturbance,[104] Recurrent brief depression which involves briefer depressive episodes,[105][106] minor depressive disorder which involves only some of the symptoms of major depression,[107] and adjustment disorder with depressed mood which involves low mood resulting from a psychological response to an identifiable event or stressor.[108]

[edit] Subtypes
The DSM-IV-TR recognizes five further subtypes of MDD, called specifiers, in addition to noting the length, severity and presence of psychotic features:

Melancholic depression is characterized by a loss of pleasure in most or all activities, a failure of reactivity to pleasurable stimuli, a quality of depressed mood more pronounced than that of grief or loss, a worsening of symptoms in the morning hours, early morning waking, psychomotor retardation, excessive weight loss (not to be confused with anorexia nervosa), or excessive guilt.[109]
Atypical depression is characterized by mood reactivity (paradoxical anhedonia) and positivity, significant weight gain or increased appetite (comfort eating), excessive sleep or sleepiness (hypersomnia), a sensation of heaviness in limbs known as leaden paralysis, and significant social impairment as a consequence of hypersensitivity to perceived interpersonal rejection.[110]
Catatonic depression is a rare and severe form of major depression involving disturbances of motor behavior and other symptoms. Here the person is mute and almost stuporose, and either remains immobile or exhibits purposeless or even bizarre movements. Catatonic symptoms also occur in schizophrenia or in manic episodes, or may be caused by neuroleptic malignant syndrome.[111]
Postpartum depression (Mild mental and behavioral disorders associated with the puerperium, not elsewhere classified in ICD-10[112]) refers to the intense, sustained and sometimes disabling depression experienced by women after giving birth. Postpartum depression, which has incidence rate of 10–15% among new mothers, typically sets in within three months of labor, and lasts as long as three months.[113]
Seasonal affective disorder (SAD) is a form of depression in which depressive episodes come on in the autumn or winter, and resolve in spring. The diagnosis is made if at least two episodes have occurred in colder months with none at other times, over a two-year period or longer.[114]

[edit] Differential diagnoses
To confer major depressive disorder as the most likely diagnosis, other potential diagnoses must be considered, including dysthymia, adjustment disorder with depressed mood or bipolar disorder. Dysthymia is a chronic, milder mood disturbance in which a person reports a low mood almost daily over a span of at least two years. The symptoms are not as severe as those for major depression, although people with dysthymia are vulnerable to secondary episodes of major depression (sometimes referred to as double depression).[104] Adjustment disorder with depressed mood is a mood disturbance appearing as a psychological response to an identifiable event or stressor, in which the resulting emotional or behavioral symptoms are significant but do not meet the criteria for a major depressive episode.[108] Bipolar disorder, previously known as manic-depressive disorder, is a condition in which depressive phases alternate with periods of mania or hypomania. Although depression is currently categorized as a separate disorder, there is ongoing debate because individuals diagnosed with major depression often experience some hypomanic symptoms, indicating a mood disorder continuum.[115]

[edit] Prevention
A 2008 meta-analysis found that behavioral interventions are effective at preventing new onset depression.[116] Because such interventions appear to be most effective when delivered to individuals or small groups, it has been suggested, they may be able to reach their large target audience most efficiently through the Internet.[117] However, an earlier meta-analysis found preventive programs with a competence-enhancing component to be superior to behaviorally oriented programs overall, and found behavioral programs to be particularly unhelpful for older people, for whom social support programs were uniquely beneficial. Additionally, the programs that best prevented depression comprised more than eight sessions, each lasting between 60 and 90 minutes; were provided by a combination of lay and professional workers; had a high-quality research design; reported attrition rates; and had a well-defined intervention.[118]

[edit] Management
For a fuller discussion of standard, rarely used, and more experimental treatments, see Treatment for depression.
The three most common treatments for depression are psychotherapy, medication, and electroconvulsive therapy. Psychotherapy is the treatment of choice for people under 18, while electroconvulsive therapy is only used as a last resort. Care is usually given on an outpatient basis, while treatment in an inpatient unit is considered if there is a significant risk to self or others. A significant number of recent studies have indicated that physical exercise has beneficial effects.

Treatment options are much more limited in developing countries, where access to mental health staff, medication, and psychotherapy is often difficult. Development of mental health services is minimal in many countries; depression is viewed as a phenomenon of the developed world despite evidence to the contrary, and not as an inherently life-threatening condition.[119]

[edit] Psychotherapy
Psychotherapy can be delivered, to individuals or groups, by mental health professionals, including psychotherapists, psychiatrists, psychologists, clinical social workers, counselors, and psychiatric nurses. With more complex and chronic forms of depression, a combination of medication and psychotherapy may be used.[120] In children and young people under 18, medication should only be offered in conjunction with a psychological therapy, such as CBT, interpersonal therapy, or family therapy.[121] Psychotherapy has been shown to be effective in older people.[122][123] Successful psychotherapy appears to reduce the recurrence of depression even after it has been terminated or replaced by occasional booster sessions.

The most studied form of psychotherapy for depression is cognitive behavioral therapy (CBT), thought to work by teaching clients to learn a set of useful cognitive and behavioral skills. Earlier research suggested that CBT was not as effective as antidepressant medication; however, research in 1996 suggests that it can perform as well as antidepressants in patients with moderate to severe depression.[124] Overall, evidence shows CBT to be effective in depressed adolescents,[125] although one systematic review noted there was insufficient evidence regarding severe episodes.[126] Combining fluoxetine with CBT appeared to bring no additional benefit,[127][128] or, at the most, only marginal benefit.[129] Several variables predict success for cognitive behavior therapy in adolescents: higher levels of rational thoughts, less hopelessness, fewer negative thoughts, and fewer cognitive distortions.[130]

Several variants of cognitive behavior therapy have been used in depressed patients, most notably rational emotive behavior therapy,[131] and more recently mindfulness-based cognitive therapy.[132]

Interpersonal psychotherapy focuses on the social and interpersonal triggers that may cause depression. The therapy takes a structured course with a set number of weekly sessions (often 12) that focus on relationships with others. Therapy can be used to foster interpersonal skills that allow people to communicate more effectively and to reduce stress.[133]

Psychoanalysis, a school of thought founded by Sigmund Freud that emphasizes the resolution of unconscious mental conflicts,[134] is used by its practitioners to treat clients presenting with major depression.[135] A more widely practiced, eclectic technique, called psychodynamic psychotherapy, is loosely based on psychoanalysis and has an additional social and interpersonal focus.[136] In a meta-analysis of three controlled trials of Short Psychodynamic Supportive Psychotherapy, this modification was found to be as effective as medication for mild to moderate depression.[137]

Logotherapy, a form of existential psychotherapy developed by Austrian psychiatrist Viktor Frankl, addresses the filling of an "existential vacuum" associated with feelings of futility and meaninglessness. This type of psychotherapy may be particularly useful for depressed adolescents.[138]

[edit] Antidepressants
The effects of prescription antidepressants can be comparable to those of psychotherapy, although more patients cease medication than cease psychotherapy, most likely due to side effects from the medication.[139]

To find the most effective antidepressant medication with tolerable or fewest side effects, the dosages can be adjusted, and if necessary, combinations of different classes of antidepressants can be tried. Response rates to the first antidepressant administered range from 50–75%, and it can take at least six to eight weeks from the start of medication to remission, when the patient is back to their normal self.[dead link][140] Antidepressant medication treatment is usually continued for 16 to 20 weeks after remission, to minimise the chance of recurrence.[dead link][140] People with chronic depression may need to take medication indefinitely to avoid relapse.[1]

Selective serotonin reuptake inhibitors (SSRIs), such as sertraline, escitalopram, fluoxetine, paroxetine, and citalopram are the primary medications prescribed owing to their effectiveness, relatively mild side effects, and because they are less toxic in overdose than other antidepressants.[141] Patients who do not respond to one SSRI can be switched to another, and this results in improvement in almost 50% of cases.[142] Another option is to switch to the atypical antidepressant bupropion.[143][144][145] Venlafaxine, an antidepressant with a different mechanism of action, may be modestly more effective than SSRIs.[146] However, venlafaxine is not recommended in the UK as a first-line treatment because of evidence suggesting its risks may outweigh benefits,[147] and it is specifically discouraged in children and adolescents.[148][149] For adolescent depression, fluoxetine[148] and escitalopram[150] are the two recommended choices. Antidepressants have not been found to be beneficial in children.[151] Any antidepressant can cause low serum sodium levels (also called hyponatremia);[152] nevertheless, it has been reported more often with SSRIs.[141] It is not uncommon for SSRIs to cause or worsen insomnia; the sedating antidepressant mirtazapine can be used in such cases.[153][154]

Monoamine oxidase inhibitors, an older class of antidepressants, have been plagued by potentially life-threatening dietary and drug interactions. They are still used only rarely, although newer and better tolerated agents of this class have been developed.[155]

The terms refractory depression or treatment-resistant depression are used to describe cases that do not respond to adequate courses of least two antidepressants.[156] In many major studies, only about 35% of patients respond well to medical treatment. It may be difficult for a doctor to decide when someone has treatment-resistant depression or whether the problem is due to coexisting disorders, which are common among patients with major depression. [157]

[edit] Pharmacological augmentation
A doctor may add a medication with a different mode of action to bolster the effect of an antidepressant in cases of treatment resistance.[158] Medication with lithium salts has been used to augment antidepressant therapy in those who have failed to respond to antidepressants alone.[159] Furthermore, lithium dramatically decreases the suicide risk in recurrent depression.[160] Addition of a thyroid hormone, triiodothyronine may work as well as lithium, even in patients with normal thyroid function.[161] Addition of atypical antipsychotics when the patient has not responded to an antidepressant is also known to increase the effectiveness of antidepressant drugs, albeit offset by increased side effects.[162]

[edit] Debated effectiveness
The effectiveness of antidepressants continues to be questioned. Their effectiveness has been shown to increase with the severity of the depression, and to reach clinical significance only in studies involving the most severely depressed, perhaps because the very severely depressed had a decreased response to the placebo effect rather than an increased response to the medication.[163] An editorial in the BMJ drew attention to bias in the publication of studies showing antidepressant efficacy compared to unpublished studies where the data did not support efficacy. Though these unpublished studies might have suffered methodological or other problems, the article called attention to the possibility that sponsor or journal bias might have inflated or created the apparent efficacy of antidepressants over placebo.[164] A black box warning was introduced in the United States in 2007 on SSRI and other antidepressant medications due to increased risk of suicidality in patients younger than 24 years old.[165]

[edit] Electroconvulsive therapy
Main article: Electroconvulsive therapy
Electroconvulsive therapy (ECT) is a procedure whereby pulses of electricity are sent through the brain via two electrodes, usually one on each temple, to induce a seizure while the patient is under a short general anaesthetic. Hospital psychiatrists may recommend ECT for cases of severe major depression which have not responded to antidepressant medication or, less often, psychotherapy or supportive interventions.[166] ECT can have a quicker effect than antidepressant therapy and thus may be the treatment of choice in emergencies such as catatonic depression where the patient has stopped eating and drinking, or where a patient is severely suicidal.[166] ECT is probably more effective than pharmacotherapy for depression in the immediate short-term,[167] although a landmark community-based study found much lower remission rates in routine practice.[168] Used on its own the relapse rate within the first six months is very high; early studies put the rate at around 50%,[169] while a more recent controlled trial found rates of 84% even with placebos.[170] The early relapse rate may be reduced by the use of psychiatric medications or further ECT[171][172] (although the latter is not recommended by some authorities)[173] but remains high.[174] Common initial adverse effects from ECT include short and long-term memory loss, disorientation and headache.[175] Although objective psychological testing shows memory disturbance after ECT has mostly resolved by one month post treatment, ECT remains a controversial treatment, and debate on the extent of cognitive effects and safety continues.[176][177]

[edit] Physical exercise
Physical exercise is recommended by U.K. health authorities,[178] and a systematic review of 23 studies indicated a "large clinical effect". Among these, three studies employing intention to treat analysis and other bias-reducing measures were inconclusive.[179]

[edit] Over-the-counter compounds
St John's wort is available over-the-counter as a herbal remedy in some parts of the world;[141][180] however, the evidence of its effectiveness for the treatment of major depression is varying and confusing. Its safety can be compromised by inconsistency in pharmaceutical quality and in the amounts of active ingredient in different preparations.[181] Further, it interacts with numerous prescribed medicines including antidepressants, and it can reduce the effectiveness of hormonal contraception.[182]

The issue of efficacy of omega-3 fatty acids for major depression is controversial,[183] with controlled studies and meta-analyses supporting both positive[184][185] and negative conclusions.[186][187] Recent meta-analyses support their use as adjunctive treatments in major depressive disorder. Because side effects are minimal, they may prove a useful approach for pregnant women or children.[188]

Reviews of short-term clinical trials of S-adenosylmethionine (SAMe) indicate that it may be effective in treating major depression in adults.[189] A 2002 review reported that tryptophan and 5-hydroxytryptophan appear to be better than placebo, but it did not recommend their widespread use owing to lack of conclusive evidence on efficacy and safety, and generally preferred the use of safer antidepressants instead.[190]

[edit] Other somatic treatments
Repetitive transcranial magnetic stimulation (rTMS) applies powerful magnetic fields to the brain from outside the head. Multiple controlled studies support the use of this method in treatment-resistant depression; it has been approved for this indication in Europe, Canada, Australia, and the US.[191][192][193] rTMS appeared similarly effective for both uncomplicated depression and depression resistant to medication;[192] however, it was inferior to ECT in a side-by-side randomized trial.[194]

Vagus nerve stimulation was approved by the FDA in the United States in 2005 for use in treatment-resistant depression,[dead link][195] although it failed to show short-term benefit in the only large double-blind trial when used as an adjunct on treatment-resistant patients;[196] a 2008 systematic review concluded that despite the promising results reported mainly in open studies, further clinical trials are needed to confirm its efficacy in major depression.[197] Poor diet or medical disorders leading to deficiency in certain nutrients have been linked to major depression disorder. Thus improved diet or correction of nutritional deficiency may be of value in some cases of major depression.[198]

[edit] Prognosis
Major depressive episodes often resolve over time whether or not they are treated. Outpatients on a waiting list show a 10–15% reduction in symptoms within a few months, with approximately 20% no longer meeting the full criteria for a depressive disorder.[199] The median duration of an episode has been estimated to be 23 weeks, with the highest rate of recovery in the first three months.[200]

General population studies indicate around half those who have a major depressive episode (whether treated or not) recover and remain well, while 35% will have at least one more, and around 15% experience chronic recurrence.[201] Studies recruiting from selective inpatient sources suggest lower recovery and higher chronicity, while studies of mostly outpatients show that nearly all recover, with a median episode duration of 11 months. Around 90% of those with severe or psychotic depression, most of whom also meet criteria for other mental disorders, experience recurrence.[202][203]

Recurrence is more likely if symptoms have not fully resolved with treatment. Current guidelines recommend continuing antidepressants for four to six months after remission to prevent relapse. Evidence from many randomized controlled trials indicates continuing antidepressant medications after recovery can reduce the chance of relapse by 70% (41% on placebo vs. 18% on antidepressant). The preventive effect probably lasts for at least the first 36 months of use. [204]

Depressed individuals have a shorter life expectancy than those without depression, in part because depressed patients are at risk of dying by suicide.[205] However, they also have a higher rate of dying from other causes,[206] being more susceptible to medical conditions such as heart disease.[207] Up to 60% of people who commit suicide have a mood disorder such as major depression, and the risk is especially high if a person has a marked sense of hopelessness or has both depression and borderline personality disorder.[208] The lifetime risk of suicide associated with a diagnosis of major depression in the US is estimated at 3.4%, which averages two highly disparate figures of almost 7% for men and 1% for women[209] (although suicide attempts are more frequent in women).[210] The estimate is substantially lower than a previously accepted figure of 15% which had been derived from older studies of hospitalized patients.[211]

[edit] Epidemiology
Depression is a major cause of morbidity worldwide.[212] Lifetime prevalence varies widely, from 3% in Japan to 17% in the US. In most countries the number of people who would suffer from depression during their lives falls within an 8–12% range.[213][214] In North America the probability of having a major depressive episode within a year-long period is 3–5% for males and 8–10% for females.[215][216] Population studies have consistently shown major depression to be about twice as common in women as in men, although it is unclear why this is so, and whether factors unaccounted for are contributing to this.[217] The relative increase in occurrence is related to pubertal development rather than chronological age, reaches adult ratios between the ages of 15 and 18, and appears associated with psychosocial more than hormonal factors.[217]

People are most likely to suffer their first depressive episode between the ages of 30 and 40, and there is a second, smaller peak of incidence between ages 50 and 60.[218] The risk of major depression is increased with neurological conditions such as stroke, Parkinson's disease, or multiple sclerosis and during the first year after childbirth.[219] It is also more common after cardiovascular illnesses, and is related more to a poor outcome than to a better one.[207][220] Studies conflict on the prevalence of depression in the elderly, but most data suggest there is a reduction in this age group.[221]

Depression is often associated with unemployment and poverty.[222] Major depression is currently the leading cause of disease burden in North America and other high-income countries, and the fourth-leading cause worldwide. In the year 2030, it is predicted to be the second-leading cause of disease burden worldwide after HIV, according to the World Health Organization.[223] Delay or failure in seeking treatment after relapse, and the failure of health professionals to provide treatment, are two barriers to reducing disability.[224]

The World Health Organization updated its report The global burden of disease in 2004. Their "Years Lost due to Disability", or YLD, is a measurement of the equivalent years of healthy life lost through time spent in states of less than full health, and they state that in all regions, "neuropsychiatric conditions are the most important causes of disability, accounting for around one third of YLD among adults aged 15 and over." Specifically, unipolar depressive disorders are the leading cause in both males and females, in high-income countries and in low- and middle-income countries.[225]

[edit] Comorbidity
Major depression frequently co-occurs with other psychiatric problems. The 1990–92 National Comorbidity Survey (US) reports that 51% of those with major depression also suffer from lifetime anxiety.[226] Anxiety symptoms can have a major impact on the course of a depressive illness, with delayed recovery, increased risk of relapse, greater disability and increased suicide attempts.[227] American neuroendocrinologist Robert Sapolsky similarly argues that the relationship between stress, anxiety, and depression could be measured and demonstrated biologically.[228] There are increased rates of alcohol and drug abuse and particularly dependence,[229] and around a third of individuals diagnosed with attention-deficit hyperactivity disorder develop comorbid depression.[230] Post-traumatic stress disorder and depression often co-occur.[1]

Depression and pain often co-occur. One or more pain symptoms is present in 65% of depressed patients, and anywhere from five to 85% of patients with pain will be suffering from depression, depending on the setting; there is a lower prevalence in general practice, and higher in specialty clinics. The diagnosis of depression is often delayed or missed, and the outcome worsens.[231]

Depression is also associated with a 1.5- to 2-fold increased risk of cardiovascular disease, independent of other known risk factors, and is itself linked directly or indirectly to risk factors such as smoking and obesity. People with major depression are less likely to follow medical recommendations for treating cardiovascular disorders, which further increases their risk. In addition, cardiologists may not recognize underlying depression that complicates a cardiovascular problem under their care. [232]

[edit] History
Main article: History of depression
The Ancient Greek physician Hippocrates described a syndrome of melancholia as a distinct disease with particular mental and physical symptoms; he characterized all "fears and despondencies, if they last a long time" as being symptomatic of the ailment.[233] It was a similar but far broader concept than today's depression; prominence was given to a clustering of the symptoms of sadness, dejection, and despondency, and often fear, anger, delusions and obsessions were included.[58]

The term depression itself was derived from the Latin verb deprimere, "to press down".[234] From the 14th century, "to depress" meant to subjugate or to bring down in spirits. It was used in 1665 in English author Richard Baker's Chronicle to refer to someone having "a great depression of spirit", and by English author Samuel Johnson in a similar sense in 1753.[235] The term also came in to use in physiology and economics. An early usage referring to a psychiatric symptom was by French psychiatrist Louis Delasiauve in 1856, and by the 1860s it was appearing in medical dictionaries to refer to a physiological and metaphorical lowering of emotional function.[236] Since Aristotle, melancholia had been associated with men of learning and intellectual brilliance, a hazard of contemplation and creativity. The newer concept abandoned these associations and through the 19th century, became more associated with women.[58]

Although melancholia remained the dominant diagnostic term, depression gained increasing currency in medical treatises and was a synonym by the end of the century; German psychiatrist Emil Kraepelin may have been the first to use it as the overarching term, referring to different kinds of melancholia as depressive states.[237]

Sigmund Freud likened the state of melancholia to mourning in his 1917 paper Mourning and Melancholia. He theorized that objective loss, such as the loss of a valued relationship through death or a romantic break-up, results in subjective loss as well; the depressed individual has identified with the object of affection through an unconscious, narcissistic process called the libidinal cathexis of the ego. Such loss results in severe melancholic symptoms more profound than mourning; not only is the outside world viewed negatively, but the ego itself is compromised.[56] The patient's decline of self-perception is revealed in his belief of his own blame, inferiority, and unworthiness.[57] He also emphasized early life experiences as a predisposing factor.[58] Meyer put forward a mixed social and biological framework emphasizing reactions in the context of an individual's life, and argued that the term depression should be used instead of melancholia.[238] The first version of the DSM (DSM-I, 1952) contained depressive reaction and the DSM-II (1968) depressive neurosis, defined as an excessive reaction to internal conflict or an identifiable event, and also included a depressive type of manic-depressive psychosis within Major affective disorders.[239]

In the mid-20th century, researchers theorized that depression was caused by a chemical imbalance in neurotransmitters in the brain, a theory based on observations made in the 1950s of the effects of reserpine and isoniazid in altering monoamine neurotransmitter levels and affecting depressive symptoms.[240]

The term Major depressive disorder was introduced by a group of US clinicians in the mid-1970s as part of proposals for diagnostic criteria based on patterns of symptoms (called the "Research Diagnostic Criteria", building on earlier Feighner Criteria),[241] and was incorporated in to the DSM-III in 1980.[242] To maintain consistency the ICD-10 used the same criteria, with only minor alterations, but using the DSM diagnostic threshold to mark a mild depressive episode, adding higher threshold categories for moderate and severe episodes.[242][243] The ancient idea of melancholia still survives in the notion of a melancholic subtype.

The new definitions of depression were widely accepted, albeit with some conflicting findings and views. There have been some continued empirically based arguments for a return to the diagnosis of melancholia.[244][245] There has been some criticism of the expansion of coverage of the diagnosis, related to the development and promotion of antidepressants and the biological model since the late 1950s.[246]

[edit] Sociocultural aspects
See also: List of people with depression

American president Abraham Lincoln appears to have had at least two major depressive episodes.[247]Even today, people's conceptualizations of depression vary widely, both within and among cultures. "Because of the lack of scientific certainty," one commentator has observed, "the debate over depression turns on questions of language. What we call it—'disease,' 'disorder,' 'state of mind'—affects how we view, diagnose, and treat it."[248] There are cultural differences in the extent to which serious depression is considered an illness requiring personal professional treatment, or is an indicator of something else, such as the need to address social or moral problems, the result of biological imbalances, or a reflection of individual differences in the understanding of distress that may reinforce feelings of powerlessness, and emotional struggle.[249][250]

The diagnosis is less common in some countries, such as China. It has been argued that the Chinese traditionally deny or somatize emotional depression (although since the early 1980s the Chinese denial of depression may have modified drastically).[251] Alternatively, it may be that Western cultures reframe and elevate some expressions of human distress to disorder status. Australian professor Gordon Parker and others have argued that the Western concept of depression "medicalizes" sadness or misery.[252][253] Similarly, Hungarian-American psychiatrist Thomas Szasz and others argue that depression is a metaphorical illness that is inappropriately regarded as an actual disease.[254] There has also been concern that the DSM, as well as the field of descriptive psychiatry that employs it, tends to reify abstract phenomena such as depression, which may in fact be social constructs.[255] American archetypal psychologist James Hillman writes that depression can be healthy for the soul, insofar as "it brings refuge, limitation, focus, gravity, weight, and humble powerlessness."[256] Hillman argues that therapeutic attempts to eliminate depression echo the Christian theme of resurrection, but have the unfortunate effect of demonizing a soulful state of being.

Historical figures were often reluctant to discuss or seek treatment for depression due to social stigma about the condition, or due to ignorance of diagnosis or treatments. Nevertheless, analysis or interpretation of letters, journals, artwork, writings or statements of family and friends of some historical personalities has led to the presumption that they may have had some form of depression. People who may have had depression include English author Mary Shelley,[257] American-British writer Henry James,[258] and American president Abraham Lincoln.[259] Some well-known contemporary people with possible depression include Canadian songwriter Leonard Cohen[260] and American playwright and novelist Tennessee Williams.[261] Some pioneering psychologists, such as Americans William James[262][263] and John B. Watson,[264] dealt with their own depression.

There has been a continuing discussion of whether neurological disorders and mood disorders may be linked to creativity, a discussion that goes back to Aristotelian times.[265][266] British literature gives many examples of reflections on depression.[267] English philosopher John Stuart Mill experienced a several-months-long period of what he called "a dull state of nerves", when one is "unsusceptible to enjoyment or pleasurable excitement; one of those moods when what is pleasure at other times, becomes insipid or indifferent". He quoted English poet Samuel Taylor Coleridge's "Dejection" as a perfect description of his case: "A grief without a pang, void, dark and drear, / A drowsy, stifled, unimpassioned grief, / Which finds no natural outlet or relief / In word, or sigh, or tear."[268][269] English writer Samuel Johnson used the term "the black dog" in the 1780s to describe his own depression,[270] and it was subsequently popularized by depression sufferer former British Prime Minister Sir Winston Churchill.[270]

Social stigma of major depression is widespread, and contact with mental health services reduces this only slightly. Public opinions on treatment differ markedly to those of health professionals; alternative treatments are held to be more helpful than pharmacological ones, which are viewed poorly.[271] In the UK, the Royal College of Psychiatrists and the Royal College of General Practitioners conducted a joint Five-year Defeat Depression campaign to educate and reduce stigma from 1992 to 1996;[272] a MORI study conducted afterwards showed a small positive change in public attitudes to depression and treatment.[273]

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