MAJOR DEPRESSION

Major depressive disorder (MDD) (also known as clinical depression, major depression, unipolar depression, or unipolar disorder; or asrecurrent depression in the case of repeated episodes) is a mental disorderﾧ characterized by a pervasive and persistent low moodﾧ that is accompanied by low self-esteemﾧ and by a loss of interest or pleasureﾧ in normally enjoyable activities. This cluster of symptoms (syndromeﾧ) was named, described and classified as one of the mood disordersﾧ in the 1980 edition of the American Psychiatric Associationﾧ 's diagnostic manualﾧ. The term "depression" is ambiguous. It is often used to denote this syndrome but may refer to other mood disorders or to lower mood states lacking clinical significanceﾧ. Major depressive disorder is a disabling condition that adversely affects a person 's family, work or school life, sleeping and eating habits, and general health. In the United States, around 3.4% of people with major depression commit suicideﾧ, and up to 60% of people who commit suicide had depression or another mood disorder.[1]
The diagnosis of major depressive disorder is based on the patient 's self-reported experiences, behavior reported by relatives or friends, and amental status examinationﾧ. 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 20 and 30 years, with a later peak between 30 and 40 years.[2]
Typically, patients are treated with antidepressantﾧ medicationﾧ and, in many cases, also receive psychotherapyﾧ or counseling, although the effectiveness of medication for mild or moderate cases is questionable.[3] Hospitalization may be necessary in cases with associated self-neglectﾧor a significant risk of harm to self or others. A minority are treated with electroconvulsive therapyﾧ (ECT). The course of the disorder varies widely, from one episode lasting weeks to a lifelong disorder with recurrent major depressive episodesﾧ. Depressed individuals have shorter life expectanciesﾧthan those without depression, in part because of greater susceptibility to medical illnesses and suicide. It is unclear whether or not medications affect the risk of suicide. Current and former patients may be stigmatizedﾧ.
The understanding of the nature and causes of depression has evolved over the centuries, though this understanding is incomplete and has left many aspects of depression as the subject of discussion and research. Proposed causes include psychologicalﾧ, psycho-social, hereditaryﾧ,evolutionaryﾧ and biologicalﾧ factors. Long-term substance abuseﾧ may cause or worsen depressive symptoms. Psychological treatments are based on theories of personalityﾧ, interpersonal communicationﾧ, and learningﾧ. Most biological theories focus on the monoamineﾧ chemicals serotoninﾧ,norepinephrineﾧ and dopamineﾧ, which are naturally present in the brainﾧ and assist communication between nerve cellsﾧ.
Contents
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1 Symptoms and signsﾧ
1 1.1 Comorbidityﾧ
2 Causesﾧ
2 2.1 Biologicalﾧ
3 2.2 Psychologicalﾧ
4 2.3 Socialﾧ
5 2.4 Evolutionaryﾧ
6 2.5 Drug and alcohol useﾧ
3 Diagnosisﾧ
7 3.1 Clinical assessmentﾧ
8 3.2 DSM-IV-TR and ICD-10 criteriaﾧ
9 3.3 Differential diagnosesﾧ
2 4 Preventionﾧ
5 Managementﾧ
1 5.1 Psychotherapyﾧ
2 5.2 Antidepressantsﾧ
3 5.3 Electroconvulsive therapyﾧ
3 6 Prognosisﾧ
4 7 Epidemiologyﾧ
5 8 Historyﾧ
6 9 Society and cultureﾧ
7 10 In other animalsﾧ
11 Referencesﾧ
1 11.1 Selected cited worksﾧ
8 12 External linksﾧ
Symptoms and signs
Major depression significantly affects a person 's family and personal relationships, work or school life, sleeping and eating habits, and general health.[4] Its impact on functioning and well-being has been compared to that of chronic medical conditions such as diabetesﾧ.[5]
A person having a major depressive episodeﾧ usually exhibits a very low mood, which pervades all aspects of life, and an inability to experience pleasureﾧ in activities that were formerly enjoyed. Depressed people may be preoccupied with, or ruminateﾧ over, thoughts and feelings of worthlessness, inappropriate guilt or regret, helplessness, hopelessness, and self-hatred.[6] In severe cases, depressed people may have symptoms of psychosisﾧ. These symptoms include delusionsﾧ or, less commonly, hallucinationsﾧ, usually unpleasant.[7] Other symptoms of depression include poor concentration and memory (especially in those with melancholicﾧ or psychotic features),[8] withdrawal from social situations and activities, reduced sex driveﾧ, and thoughts of death or suicide.Insomniaﾧ is common among the depressed. In the typical pattern, a person wakes very early and cannot get back to sleep.[9] Insomnia affects at least 80% of depressed people.[medical citation needed] Hypersomniaﾧ, or oversleeping, can also happen.[9] Some antidepressants may also cause insomnia due to their stimulating effect.[10]
A depressed 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 'sﾧ criteria for depression.[11] Appetite often decreases, with resulting weight loss, although increased appetite and weight gain occasionally occur.[6] Family and friends may notice that the person 's behavior is either agitatedﾧ or lethargicﾧ.[9] Older depressed people may have cognitiveﾧ symptoms of recent onset, such as forgetfulness,[8]and a more noticeable slowing of movements.[12] Depression often coexists with physical disorders common among the elderly, such as strokeﾧ, other cardiovascular diseasesﾧ, Parkinson 's diseaseﾧ, and chronic obstructive pulmonary diseaseﾧ.[13]
Depressed children may often display an irritable mood rather than a depressed mood,[6] and show varying symptoms depending on age and situation.[14] Most lose interest in school and show a decline in academic performance. They may be described as clingy, demanding, dependent, or insecure.[9] Diagnosis may be delayed or missed when symptoms are interpreted as normal moodiness.[6] Depression may also coexist with attention-deficit hyperactivity disorderﾧ (ADHD), complicating the diagnosis and treatment of both.[15]
Comorbidity
Major depression frequently co-occursﾧ with other psychiatric problems. The 1990–92 National Comorbidity Surveyﾧ (US) reports that 51% of those with major depression also suffer from lifetimeanxietyﾧ.[16] 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.[17] American neuroendocrinologist Robert Sapolskyﾧ similarly argues that the relationship between stress, anxiety, and depression could be measured and demonstrated biologically.[18]There are increased rates of alcohol and drug abuse and particularly dependence,[19] and around a third of individuals diagnosed with ADHDﾧ develop comorbid depression.[20] Post-traumatic stress disorderﾧ and depression often co-occur.[4]
Depression and painﾧ often co-occur. One or more pain symptoms are present in 65% of depressed patients, and anywhere from 5 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. The outcome can also worsen if the depression is noticed but completely misunderstood.[21]
Depression is also associated with a 1.5- to 2-fold increased risk of cardiovascular diseaseﾧ, 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.[22]
Causes
The biopsychosocial modelﾧ proposes that biological, psychological, and social factors all play a role in causing depression.[23] The diathesis–stress modelﾧ specifies that depression results when a preexisting vulnerability, or diathesis, is activated by stressful life events. The preexisting vulnerability can be either geneticﾧ,[24][25] implying an interaction between nature and nurtureﾧ, orschematicﾧ, resulting from views of the world learned in childhood.[26]
Depression may be directly caused by damage to the cerebellumﾧ as is seen in cerebellar cognitive affective syndromeﾧ.[27][28][29]
These interactive models have gained empiricalﾧ support. For example, researchers in New Zealand took a prospective approachﾧ to studying depression, by documenting over timeﾧ how depression emerged among an initially normalﾧ cohortﾧ of people. The researchers concluded that variation among the serotonin transporterﾧ (5-HTT) gene affects the chancesﾧ that people who have dealt with very stressful life events will go on to experience depression. To be specific, depression may follow such events, but seems more likely to appear in people with one or two short allelesﾧ of the 5-HTT gene.[24] In addition, a Swedish study estimated the heritabilityﾧ of depression—the degree to which individual differences in occurrence are associated with genetic differences—to be around 40% for women and 30% for men,[30] and evolutionary psychologistsﾧ have proposed that the genetic basis for depression lies deep in the history of naturally selectedﾧ adaptationsﾧ. A substance-induced mood disorderﾧ resembling major depression has been causally linked to long-term drug useﾧ or drug abuseﾧ, or to withdrawalﾧ from certain sedativeﾧ and hypnotic drugsﾧ.[31][32]
Biological
Main article: Biology of depressionﾧ
Monoamine hypothesis
ﾧ
ﾧ
Of approx. 30 neurotransmittersﾧ that have been identified, researchers have discovered associations between clinical depression and the function of three major neurochemicalsﾧ. These substances are serotoninﾧ, norepinephrineﾧ, anddopamineﾧ. Antidepressants influence the overall balance of these three neurotransmitters within structures of the brain that regulate emotion, reactions to stress, and the physical drives of sleep, appetite, and sexuality.[medical citation needed]
Most antidepressantﾧ medications increase the levels of one or more of the monoamines — the neurotransmitters serotoninﾧ, norepinephrineﾧ anddopamineﾧ — in the synaptic cleftﾧ between neuronsﾧ in the brain. Some medications affect the monoamine receptors directly.
Serotonin is hypothesized to regulate other neurotransmitter systems; decreased serotonin activity may allow these systems to act in unusual and erratic ways.[33] According to this "permissive hypothesis", depression arises when low serotonin levels promote low levels of norepinephrine, another monoamine neurotransmitter.[34] 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 hypothesisﾧ 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."[35] 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 SSRIsﾧ or norepinephrine reuptake inhibitorsﾧ, and those experiencing a loss of energy and enjoyment of life with norepinephrine- and dopamine-enhancing drugs.[35]
Besides the clinical observations that drugs that increase the amount of available monoamines are effective antidepressants, recent advances inpsychiatric geneticsﾧ indicate that phenotypic variationﾧ in central monoamine function may be marginally associated with vulnerability to depression. Despite these findings, the cause of depression is not simply monoamine deficiency.[36] In the past two decades, research has revealed multiple limitations of the monoamine hypothesis, and its explanatory inadequacy has been highlighted within the psychiatric community.[37] A counterargument is that the mood-enhancing effect of MAO inhibitors and SSRIs takes weeks of treatment to develop, even though the boost in available monoamines occurs within hours. Another counterargument is based on experiments with pharmacological agents that cause depletion of monoamines; while deliberate reduction in the concentration of centrally available monoamines may slightly lower the mood of unmedicated depressed patients, this reduction does not affect the mood of healthy people.[36] The monoamine hypothesis, already limited, has been further oversimplified when presented to the general public as a mass marketing tool, usually phrased as a "chemical imbalanceﾧ".[38]
In 2003 a gene-environment interactionﾧ (GxE) was hypothesized to explain why life stress is a predictor for depressive episodes in some individuals, but not in others, depending on an allelic variation of the serotonin-transporter-linked promoter region (5-HTTLPRﾧ);[39] a 2009 meta-analysisﾧ showed stressful life events were associated with depression, but found no evidence for an association with the 5-HTTLPR genotype.[40] Another 2009 meta-analysis agreed with the latter finding.[41] A 2010 review of studies in this area found a systematic relationship between the method used to assess environmental adversity and the results of the studies; this review also found that both 2009 meta-analyses were significantly biased toward negative studies, which used self-report measures of adversity.[42]
Other hypotheses
MRIﾧ scans of patients with depression have revealed a number of differences in brain structure compared to those who are not depressed. Recent meta-analyses of neuroimaging studies in major depression, reported that compared to controls, depressed patients had increased volume of the lateral ventriclesﾧ and adrenal glandﾧ and smaller volumes of the basal gangliaﾧ, thalamusﾧ,hippocampusﾧ, and frontal lobeﾧ (including the orbitofrontal cortexﾧ and gyrus rectusﾧ).[43][44] Hyperintensities have been associated with patients with a late age of onset, and have led to the development of the theory of vascular depressionﾧ.[45]
There may be a link between depression and neurogenesisﾧ of the hippocampus,[46] 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.[47][48] Similar relationships have been observed between depression and an area of the anterior cingulate cortexﾧ implicated in the modulation of emotional behavior.[49] One of the neurotrophinsﾧ responsible for neurogenesis is brain-derived neurotrophic factorﾧ (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.[50]
There is some evidence that major depression may be caused in part by an overactive hypothalamic-pituitary-adrenal axisﾧ (HPA axis) that results in an effect similar to the neuro-endocrine response to stress. Investigations reveal increased levels of the hormone cortisolﾧ and enlarged pituitary and adrenal glands, suggesting disturbances of the endocrine systemﾧ may play a role in some psychiatric disorders, including major depression. Oversecretion of corticotropin-releasing hormoneﾧ from the hypothalamusﾧ is thought to drive this, and is implicated in the cognitive and arousal symptoms.[51]
The hormone estrogenﾧ has been implicated in depressive disorders due to the increase in risk of depressive episodes after puberty, the antenatal period, and reduced rates after menopauseﾧ.[52]On the converse, the premenstrual and postpartum periods of low estrogen levels are also associated with increased risk.[52] Sudden withdrawal of, fluctuations in or periods of sustained low levels of estrogen have been linked to significant mood lowering. Clinical recovery from depression postpartum, perimenopause, and postmenopause was shown to be effective after levels of estrogen were stabilized or restored.[53][54]
Other research has explored potential roles of molecules necessary for overall cellularﾧ functioning: cytokinesﾧ. The symptoms of major depressive disorder are nearly identical to those of sickness behaviorﾧ, the response of the body when the immune systemﾧ is fighting an infectionﾧ. This raises the possibility that depression can result from a maladaptive manifestation of sickness behavior as a result of abnormalities in circulating cytokines.[55] The involvement of pro-inflammatory cytokines in depression is strongly suggested by a meta-analysis of the clinical literature showing higher blood concentrations of IL-6ﾧ and TNF-αﾧ in depressed subjects compared to controls.[56] These immunological abnormalities may cause excessive prostaglandin E₂ production and likely excessive COX-2 expression. Abnormalities in how indoleamine 2,3-dioxygenaseﾧ enzyme activates as well as the metabolism of tryptophanﾧ-kynurenineﾧ may lead to excessive metabolism of tryptophan-kynurenine and lead to increased production of the neurotoxin quinolinic acidﾧ, contributing to major depression. NMDA activation leading to excessive glutamatergicﾧ neurotransmission, may also contribute.[57]
Finally, some relationships have been reported between specific subtypes of depression and climatic conditions. Thus, the incidence of psychotic depression has been found to increase when the barometric pressure is low, while the incidence of melancholic depression has been found to increase when the temperature and/or sunlight are low.[58]
Inflammatory processes can be triggered by negative cognitions or their consequences, such as stress, violence, or deprivation. Thus, negative cognitions can cause inflammation that can, in turn, lead to depression.[59]
Psychological
Various aspects of personalityﾧ and its developmentﾧ appear to be integral to the occurrence and persistence of depression,[60] with negative emotionalityﾧ as a common precursor.[61] Although depressive episodes are strongly correlated with adverse events, a person 's characteristic style of coping may be correlated with his or her resilience.[62] In addition, low self-esteemﾧ and self-defeating or distorted thinking are related to depression. Depression is less likely to occur, as well as quicker to remit, among those who are religious.[63][64][65] It is not always clear which factors are causes and which are effects of depression; however, depressed persons that are able to reflect upon and challenge their thinking patterns often show improved mood and self-esteem.[66]
American psychiatrist Aaron T. Beckﾧ, following on from the earlier work of George Kellyﾧ and Albert Ellisﾧ, developed what is now known as a cognitive model of depression in the early 1960s. He proposed that three concepts underlie depression: a triadﾧ of negative thoughts composed of cognitive errors about oneself, one 's world, and one 's future; recurrent patterns of depressive thinking, orschemas; and distorted information processingﾧ.[67] From these principles, he developed the structured technique of cognitive behavioral therapyﾧ (CBT).[68] According to American psychologistMartin Seligmanﾧ, depression in humans is similar to learned helplessnessﾧ 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.[69]
Attachment theoryﾧ, which was developed by English psychiatrist John Bowlbyﾧ in the 1960s, predicts a relationship between depressive disorder in adulthood and the quality of the earlier bond between the infant and the adult caregiver. In particular, it is thought that "the experiences of early loss, separation and rejection by the parent or caregiver (conveying the message that the child is unlovable) may all lead to insecure internal working models ... Internal cognitive representations of the self as unlovable and of attachment figures as unloving [or] untrustworthy would be consistent with parts of Beck 's cognitive triad".[70] While a wide variety of studies has upheld the basic tenets of attachment theory, research has been inconclusive as to whether self-reported early attachment and later depression are demonstrably related.[70]
Depressed individuals often blame themselves for negative events,[71] and, as shown in a 1993 study of hospitalized adolescents with self-reported depression, those who blame themselves for negative occurrences may not take credit for positive outcomes.[72] This tendency is characteristic of a depressive attributionalﾧ, or pessimistic explanatory styleﾧ.[71] According to Albert Banduraﾧ, a Canadian social psychologistﾧ associated with social cognitive theoryﾧ, 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-conceptﾧ and a lack of self-efficacyﾧ; that is, they do not believe they can influence events or achieve personal goals.[73][74]
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.[75] 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-givingﾧ 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.[76]
The understanding of depression has also received contributions from the psychoanalyticﾧ and humanisticﾧ branches of psychology. From the classical psychoanalytic perspective of Austrian psychiatrist Sigmund Freudﾧ, depression, or melancholiaﾧ, may be related to interpersonal loss[77][78] and early life experiences.[79] Existential therapistsﾧ have connected depression to the lack of both meaningﾧ in the present[80] and a vision of the future.[81][82]
Social
Povertyﾧ and social isolationﾧ are associated with increased risk of mental health problems in general.[60] Child abuseﾧ (physicalﾧ, emotionalﾧ, sexualﾧ, or neglect) is also associated with increased risk of developing depressive disorders later in life.[83] Such a link has good face validity given that it is during the years of development that a child is learning how to become a social being. Abuse of the child by the caregiver is bound to distort the developing personality and create a much greater risk for depression and many other debilitating mental and emotional states. 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.[60] In adulthood, stressful life events are strongly associated with the onset of major depressive episodes.[84] In this context, life events connected to social rejection appear to be particularly related to depression.[85][86] Evidence that a first episode of depression is more likely to be immediately preceded by stressful life events than are recurrent ones is consistent with the hypothesis that people may become increasingly sensitized to life stress over successive recurrences of depression.[87][88]
The relationship between stressful life events and social supportﾧ 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.[89] 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 amenitiesﾧ, is a protective factor.[90] 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.[91]
Depression can be caused by prejudice. This can occur when people hold negative self-stereotypes about themselves. This "deprejudice" can be related to a group membership (e.g., Me-Gay-Bad) or not (Me-Bad). If someone has prejudicial beliefs about a stigmatized group and then becomes a member of that group, they may internalize their prejudice and develop depression. For example, a boy growing up in the United States may learn the negative stereotype that gay men are immoral. When he grows up and realizes he is gay, he may direct this prejudice inward on himself and become depressed. People may also show prejudice internalization through self-stereotyping because of negative childhood experiences such as verbal and physical abuse.[59]
Evolutionary
Main article: Evolutionary approaches to depressionﾧ
From the standpoint of evolutionary theory, major depression is hypothesized, in some instances, to increase an individual 's reproductiveﾧ fitnessﾧ. Evolutionary approaches to depressionﾧ andevolutionary psychologyﾧ posit specific mechanisms by which depression may have been genetically incorporated into the human gene pool, accounting for the high heritabilityﾧ and prevalence of depression by proposing that certain components of depression are adaptations,[92] such as the behaviors relating to attachmentﾧ and social rankﾧ.[93] Current behaviors can be explained as adaptations to regulate relationships or resources, although the result may be maladaptive in modern environments.[94]
From another viewpoint, a counseling therapist may see depression not as a biochemical illness or disorder but as "a species-wide evolved suite of emotional programs 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".[95] This suite may have manifested in aging hunters in humans ' foragingﾧ past, who were marginalized by their declining skills, and may continue to appear in alienated membersﾧ of today 's society. The feelings of uselessness generated by such marginalization could in theory prompt support from friends and kin. In addition, in a manner analogous to that in which physical painﾧ has evolved to hinder actions that may cause further injury, "psychic miseryﾧ" may have evolved to prevent hasty and maladaptive reactions to distressing situations.[96]
Drug and alcohol use
See also: Substance-induced mood disordersﾧ
Very high levels of substance abuse occur in the psychiatric population, especially alcohol, sedatives and cannabis. Depression and other mental health problems can have a substance induced cause; making a differential or dual diagnosisﾧ regarding whether mental ill-health is substance related or not or co-occurring is an important part of a psychiatric evaluation.[97] According to the DSM-IV, a diagnosis of mood disorder cannot be made if the cause is believed to be due to "the direct physiological effects of a substance"; when a syndrome resembling major depression is believed to be caused immediately by substance abuse or by an adverse drug reaction, it is referred to as, "substance-induced mood disturbance". Alcoholismﾧ or excessive alcohol consumption significantly increases the risk of developing major depression.[98][99] Like alcoholﾧ, the benzodiazepinesﾧ are central nervous systemﾧ depressantsﾧ; this class of medication is commonly used to treat insomniaﾧ, anxietyﾧ, and muscular spasmsﾧ. Similar to alcohol, benzodiazepines increase the risk of developing major depression. This increased risk of depression may be due in part to the adverse or toxic effects of sedative-hypnotic drugs including alcohol on neurochemistryﾧ,[99] such as decreased levels of serotonin and norepinephrine,[32] or activation of immune mediated inflammatory pathways in the brain.[100] Chronic use of benzodiazepines also can cause or worsen depression,[101] or depression may be part of a protracted withdrawal syndromeﾧ.[102][103] About a quarter of people recovering from alcoholismﾧ experience anxiety and depression, which can persist for up to 2 years.[104] Methamphetamineﾧ abuse is also commonly associated with depression.[105]
Diagnosis
Clinical assessment
Further information: Rating scales for depressionﾧ
A diagnostic assessment may be conducted by a suitably trained general practitionerﾧ, or by a psychiatristﾧ or psychologistﾧ,[4] who recordsﾧ the person 's current circumstances, biographical history, current symptoms, and family history. The broad clinical aim is to formulate the relevant biological, psychological, and social factors that may be impacting on the individual 's mood. The assessor may also discuss the person 's current ways of regulating mood (healthy or otherwise) such as alcohol and drug use. The assessment also includes a mental state examinationﾧ, which is an assessment of the person 's current mood and thought content, in particular the presence of themes of hopelessness or pessimism, self-harmﾧ or suicide, and an absence of positive thoughts or plans.[4] Specialist mental health services are rare in rural areas, and thus diagnosis and management is left largely to primary-careﾧ clinicians.[106] This issue is even more marked in developing countries.[107] The mental health examination may include the use of a rating scaleﾧ such as the Hamilton Rating Scale for Depressionﾧ[108] or the Beck Depression Inventoryﾧ.[109] The score on a rating scale alone is insufficient to diagnose depression to the satisfaction of the DSM or ICD, 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.[110] Several rating scales are used for this purpose.[110] Screeningﾧ programs have been advocated to improve detection of depression, but there is evidence that they do not improve detection rates, treatment, or outcome.[111]
Primary-care physiciansﾧ and other non-psychiatrist physicians have difficulty diagnosing depression, in part because they are trained to recognize and treat physical symptoms, and depression can cause myriad physical (psychosomaticﾧ) symptoms. Non-psychiatrists miss two-thirds of cases and unnecessarily treat other patients.[112][113]
Before diagnosing a major depressive disorder, in general a doctor performs a medical examination and selected investigations to rule out other causes of symptoms. These include blood tests measuring TSHﾧ and thyroxineﾧ to exclude hypothyroidismﾧ; basic electrolytesﾧ and serum calciumﾧ to rule out a metabolic disturbanceﾧ; and a full blood countﾧ including ESRﾧ to rule out a systemic infectionﾧ or chronic disease.[113][114] Adverse affective reactions to medications or alcohol misuse are often ruled out, as well. Testosteroneﾧ levels may be evaluated to diagnose hypogonadismﾧ, a cause of depression in men.[115]
Subjective cognitive complaints appear in older depressed people, but they can also be indicative of the onset of a dementing disorderﾧ, such as Alzheimer 's diseaseﾧ.[116][117] Cognitive testingﾧ and brain imaging can help distinguish depression from dementia.[118] A CT scanﾧ can exclude brain pathology in those with psychotic, rapid-onset or otherwise unusual symptoms.[119] In general, investigations are not repeated for a subsequent episode unless there is a medical indication.
No biological tests confirm major depression.[120] Biomarkers of depression have been sought to provide an objective method of diagnosis. There are several potential biomarkers, including Brain-Derived Neurotrophic Factor and various functional MRI techniques. One study developed a decision tree model of interpreting a series of fMRI scans taken during various activities. In their subjects, the authors of that study were able to achieve a sensitivity of 80% and a sensitivity of 87%, corresponding to a negative predictive value of 98% and a positive predictive value of 32% (positive and negative likelihood ratios were 6.15, 0.23, respectively). However, much more research is needed before these tests could be used clinically.[121]
DSM-IV-TR and ICD-10 criteria
The most widely used criteria for diagnosing depressive conditions are found in the American Psychiatric Associationﾧ 's revised fourth edition of the Diagnostic and Statistical Manual of Mental Disordersﾧ (DSM-IV-TR), and the World Health Organizationﾧ 's International Statistical Classification of Diseases and Related Health Problemsﾧ (ICD-10), which uses the name depressive episodefor a single episode and recurrent depressive disorder for repeated episodes.[122] The latter system is typically used in European countries, while the former is used in the US and many other non-European nations,[123] and the authors of both have worked towards conforming one with the other.[124]
Both DSM-IV-TR and ICD-10 mark out typical (main) depressive symptoms. ICD-10 defines three typical depressive symptoms (depressed mood, anhedonia, and reduced energy), two of which should be present to determine depressive disorder diagnosis.[125] According to DSM-IV-TR, there are two main depressive symptoms—depressed mood and anhedonia. At least one of these must be present to make a diagnosis of major depressive episode.[126]
Major depressive disorder is classified as a mood disorder in DSM-IV-TR.[127] The diagnosis hinges on the presence of single or recurrent major depressive episodesﾧ.[6] Further qualifiers are used to classify both the episode itself and the course of the disorder. The category Depressive Disorder Not Otherwise Specifiedﾧ is diagnosed if the depressive episode 's manifestation does not meet the criteria for a major depressive episode. The ICD-10ﾧ 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.[128]
Major depressive episode
Main article: Major depressive episodeﾧ
A major depressive episode is characterized by the presence of a severely depressed mood that persists for at least two weeks.[6] 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 aspsychotic depressionﾧ — is automatically rated as severe. If the patient has had an episode of maniaﾧ or markedly elevated moodﾧ, a diagnosis of bipolar disorderﾧ is made instead.[129] Depression without mania is sometimes referred to as unipolar because the mood remains at one emotional state or "pole".[130]
DSM-IV-TR excludes cases where the symptoms are a result of bereavementﾧ, 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.[131] 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.[132] 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:[133] Excluded are a range of related diagnoses, including dysthymiaﾧ, which involves a chronic but milder mood disturbance;[134] recurrent brief depressionﾧ, consisting of briefer depressive episodes;[135][136] minor depressive disorderﾧ, whereby only some of the symptoms of major depression are present;[137] and adjustment disorder with depressed moodﾧ, which denotes low mood resulting from a psychological response to an identifiable event or stressorﾧ.[138]
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:
9 Melancholic depressionﾧ 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 ofgriefﾧ or loss, a worsening of symptoms in the morning hours, early-morning waking, psychomotor retardationﾧ, excessive weight loss (not to be confused with anorexia nervosaﾧ), or excessive guilt.[139]
10 Atypical depressionﾧ is characterized by mood reactivity (paradoxical anhedonia) and positivity, significant weight gainﾧ or increased appetite (comfort eating), excessive sleep or sleepiness (hypersomniaﾧ), a sensation of heaviness in limbs known as leaden paralysis, and significant social impairment as a consequence of hypersensitivity to perceived interpersonal rejectionﾧ.[140]
11 Catatonicﾧ 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 stuporous, and either remains immobile or exhibits purposeless or even bizarre movements. Catatonic symptoms also occur in schizophreniaﾧ or in manic episodes, or may be caused by neuroleptic malignant syndromeﾧ.[141]
12 Postpartum depressionﾧ, or mental and behavioral disorders associated with the puerperiumﾧ, not elsewhere classified,[142] refers to the intense, sustained and sometimes disabling depression experienced by women after giving birth. Postpartum depression has an incidence rate of 10–15% among new mothers. The DSM-IV mandates that, in order to qualify as postpartum depression, onset occur within one month of delivery. It has been said that postpartum depression can last as long as three months.[143]
13 Seasonal affective disorderﾧ (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.[144]
Differential diagnoses
Main article: Depression (differential diagnoses)ﾧ
To confer major depressive disorder as the most likely diagnosis, other potential diagnosesﾧ must be considered, including dysthymia, adjustment disorder with depressed mood, or bipolar disorder. Dysthymiaﾧ 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).[134] Adjustment disorder with depressed moodﾧ 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.[138] Bipolar disorderﾧ, also known as manic–depressive disorder, is a condition in which depressive phases alternate with periods of mania or hypomaniaﾧ. 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.[145]
Other disorders need to be ruled out before diagnosing major depressive disorder. They include depressions due to physical illness, medicationsﾧ, and substance abuseﾧ. Depression due to physical illness is diagnosed as a mood disorderﾧ due to a general medical condition. This condition is determined based on history, laboratory findings, or physical examinationﾧ. When the depression is caused by a substance abused including a drug of abuse, a medication, or exposure to a toxinﾧ, it is then diagnosed as a substance-induced mood disorder.[146]
Prevention
Behavioral interventions, such as interpersonal therapyﾧ and cognitive-behavioral therapyﾧ, are effective at preventing new onset depression.[147][148][149] Because such interventions appear to be most effective when delivered to individuals or small groups, it has been suggested that they may be able to reach their large target audience most efficiently through the Internetﾧ.[150]
However, an earlier meta-analysis found preventive programs with a competence-enhancing component to be superior to behavior-oriented programs overall, and found behavioral programs to be particularly unhelpful for older people, for whom social support programs were uniquely beneficial. In addition, 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 ratesﾧ, and had a well-defined intervention.[151]
The Netherlands mental health care system provides preventive interventions, such as the "Coping with Depression" course (CWD) for people with sub-threshold depression. The course is claimed to be the most successful of psychoeducational interventions for the treatment and prevention of depression (both for its adaptability to various populations and its results), with a risk reduction of 38% in major depression and an efficacy as a treatment comparing favorably to other psychotherapies.[147][152] Preventative efforts may result in a decreases in rates of the condition of between 22 and 38%.[149] A stepped-care intervention (watchful waiting, Cognitive behavioral therapyﾧ (CBT) and medication for some) achieved a 50% lower incidence rate in a patient group aged 75 or older.[153]
Management
Main article: Management of depressionﾧ
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 used only as a last resort. Care is usually given on an outpatientﾧ basis, whereas treatment in an inpatientﾧ unit is considered if there is a significant risk to self or others.
Physical exerciseﾧ is recommended for management of mild depression,[154] and has a moderate effect on symptoms.[155] It is equivalent to the use of medications or psychological therapies in most people.[155] In the older people it does appear to decrease depression.[156] Stopping smoking has benefits in depression as large as or larger than those of medications.[157]
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.[158]
Psychotherapy
Psychotherapyﾧ can be delivered, to individuals, groups, or families by mental health professionals, including psychotherapists, psychiatristsﾧ, psychologistsﾧ, clinical social workersﾧ, counselors, and suitably trained psychiatric nurses. With more complex and chronic forms of depression, a combination of medication and psychotherapy may be used.[159][160]
Cognitive behavioral therapyﾧ (CBT) currently has the most research evidence for the treatment of depression in children and adolescents, and CBT and interpersonal psychotherapy (IPT) are preferred therapies for adolescent depression.[161] In people under 18, according to the National Institute for Health and Clinical Excellenceﾧ, medication should be offered only in conjunction with a psychological therapy, such as CBTﾧ, interpersonal therapyﾧ, or family therapy.[162]
Psychotherapy has been shown to be effective in older people.[163][164] 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 CBT, which teaches clients to challenge self-defeating, but enduring ways of thinking (cognitions) and change counter-productive behaviors. Research beginning in the mid-1990s suggested that CBT could perform as well or better than antidepressants in patients with moderate to severe depression.[165][166] CBT may be effective in depressed adolescents,[167] although its effects on severe episodes are not definitively known.[168] Several variables predict success for cognitive behavioral therapy in adolescents: higher levels of rational thoughts, less hopelessness, fewer negative thoughts, and fewer cognitive distortions.[169] CBT is particularly beneficial in preventing relapse.[170][171] Several variants of cognitive behavior therapy have been used in depressed patients, the most notable being rational emotive behavior therapyﾧ,[172] and more recently mindfulness-based cognitive therapyﾧ.[173]
Psychoanalysisﾧ is a school of thought, founded by Sigmund Freudﾧ, which emphasizes the resolution of unconsciousﾧ mental conflicts.[174] Psychoanalytic techniques are used by some practitioners to treat clients presenting with major depression.[175] A more widely practiced, eclecticﾧ technique, called psychodynamic psychotherapyﾧ, is loosely based on psychoanalysis and has an additional social and interpersonal focus.[176] 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.[177]
Logotherapyﾧ, a form of existential psychotherapy developed by Austrian psychiatrist Viktor Franklﾧ, addresses the filling of an "existential vacuum"ﾧ associated with feelings of futility and meaninglessness. It is posited that this type of psychotherapy may be useful for depression in older adolescents.[178]
Antidepressants
ﾧ
ﾧ
Zoloft (sertralineﾧ) is used primarily to treat major depression in adult outpatientsﾧ. In 2007, it was the most prescribed antidepressant on the U.S. retail market, with 29,652,000 prescriptions.[179]
The effectiveness of antidepressantsﾧ is none to minimal in those with mild or moderate depression but significant in those with very severe disease.[180]The effects of antidepressants are somewhat superior to those of psychotherapy, especially in cases of chronic major depression, although in short-term trials more patients—especially those with less serious forms of depression—cease medication than cease psychotherapy, most likely due to adverse effectsﾧ from the medication and to patients ' preferences for psychological therapies over pharmacological treatments.[181][182]
To find the most effective antidepressant medication with minimal 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 remissionﾧ.[183] Antidepressant medication treatment is usually continued for 16 to 20 weeks after remission, to minimize the chance of recurrence,[183] and even up to one year of continuation is recommended.[184] People with chronic depression may need to take medication indefinitely to avoid relapse.[4]
Selective serotonin reuptake inhibitorsﾧ (SSRIs) are the primary medications prescribed, owing to their relatively mild side-effects, and because they are less toxic in overdose than other antidepressants.[185] Patients who do not respond to one SSRI can be switched to another antidepressantﾧ, and this results in improvement in almost 50% of cases.[186] Another option is to switch to the atypical antidepressant bupropionﾧ.[187] Venlafaxineﾧ, an antidepressant with a different mechanism of action, may be modestly more effective than SSRIs.[188] However, venlafaxine is not recommended in the UK as a first-line treatment because of evidence suggesting its risks may outweigh benefits,[189] and it is specifically discouraged in children and adolescents.[190][191] For adolescent depression, fluoxetine[190] and escitalopram[192] are the two recommended choices. Antidepressants have not been found to be beneficial in children.[193] There is also insufficient evidence to determine effectiveness in those with depression complicated bydementiaﾧ.[194] Any antidepressant can cause low serum sodiumﾧ levels (also called hyponatremiaﾧ);[195] nevertheless, it has been reported more often with SSRIs.[185] It is not uncommon for SSRIs to cause or worsen insomnia; the sedating antidepressant mirtazapineﾧ can be used in such cases.[196][197]
Irreversible monoamine oxidase inhibitorsﾧ, 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.[198] The safety profile is different with reversible monoamine oxidase inhibitors such as moclobemideﾧ where the risk of serious dietary interactions is negligible and dietary restrictions are less strict.[199]
For children, adolescents, and probably young adults between 18 and 24 years old, there is a higher risk of both suicidal ideations and suicidal behavior in those treated with SSRIs.[200][201] For adults, it is unclear whether or not SSRIs affect the risk of suicidality.[201] One review found no connection;[202] another an increased risk;[203] and a third no risk in those 25–65 years old and a decrease risk in those more than 65.[204] Epidemiological data has found that the widespread use of antidepressants in the new "SSRI-era" is associated with a significant decline in suicide rates in most countries with traditionally high baseline suicide rates.[205] The causality of the relationship is inconclusive.[206] A black box warningﾧ was introduced in the United States in 2007 on SSRI and other antidepressant medications due to increased risk of suicide in patients younger than 24 years old.[207] Similar precautionary notice revisions were implemented by the Japanese Ministry of Health.[208]
There is some evidence that fish oil supplements containing high levels of eicosapentaenoic acidﾧ (EPA) to docosahexaenoic acidﾧ (DHA) may be effective in major depression,[209] but other meta-analysis of the research conclude that positive effects may be due to publication bias.[210] There is some preliminary evidence that COX-2 inhibitorsﾧ have a beneficial effect on major depression.[57]
Lithiumﾧ appears effective at lowering the risk of suicide in those with bipolar disorderﾧ and unipolar depression to nearly the same levels as the general population.[211]
Electroconvulsive therapy
Electroconvulsive therapyﾧ (ECT) is a procedure whereby pulses of electricity are sent through the brain via two electrodes, usually one on each templeﾧ, to induce a seizureﾧ while the person is under a brief period of general anesthesiaﾧ. Hospital psychiatrists may recommend ECT for cases of severe major depression that have not responded to antidepressant medication or, less often, psychotherapy or supportive interventions.[212] 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 person has stopped eating and drinking, or where a person is severely suicidal.[212] ECT is probably more effective than pharmacotherapy for depression in the immediate short-term,[213] although a landmark community-based study found much lower remission rates in routine practice.[214] When ECT is used on its own, the relapse rate within the first six months is very high; early studies put the rate at around 50%,[215] while a more recent controlled trial found rates of 84% even with placebosﾧ.[216] The early relapse rate may be reduced by the use of psychiatric medications or further ECT[217][218] (although the latter is not recommended by some authorities)[219] but remains high.[220] Common initial adverse effectsﾧ from ECT include shortﾧ and long-term memoryﾧ loss, disorientation and headache.[221] Although memory disturbance after ECTﾧ usually resolves within one month, ECT remains a controversial treatment, and debate on its efficacy and safety continues.[222][223]
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.[224] The medianﾧ duration of an episode has been estimated to be 23 weeks, with the highest rate of recovery in the first three months.[225]
Studies have shown that 80% of those suffering from their first major depressive episode will suffer from at least 1 more during their life,[226] with a lifetime average of 4 episodes.[227] Other general population studies indicate that around half those that have an episode (whether treated or not) recover and remain well, while the other half will have at least one more, and around 15% of those experience chronic recurrence.[228] 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 meeting criteria for other mental disorders, experience recurrence.[229][230]
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 trialsﾧ 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.[231]
Those people experiencing repeated episodes of depression require ongoing treatment in order to prevent more severe, long-term depression. In some cases, people must take medications for long periods of time or for the rest of their lives.[232]
Cases when outcome is poor are associated with inappropriate treatment, severe initial symptoms that may include psychosis, early age of onset, more previous episodes, incomplete recovery after 1 year, pre-existing severe mental or medical disorder, and family dysfunctionﾧ as well.[233]
Depressed individuals have a shorter life expectancyﾧ than those without depression, in part because depressed patients are at risk of dying by suicide.[234] However, they also have a higher rate of dyingﾧ from other causes,[235] being more susceptible to medical conditions such as heart disease.[236] 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 disorderﾧ.[1] 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[237] (although suicide attempts are more frequent in women).[238] The estimate is substantially lower than a previously accepted figure of 15%, which had been derived from older studies of hospitalized patients.[239]
Depression is often associated with unemployment and poverty.[240] Major depression is currently the leading cause of disease burdenﾧ 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 HIVﾧ, according to the World Health Organization.[241] Delay or failure in seeking treatment after relapse, and the failure of health professionals to provide treatment, are two barriers to reducing disability.[242]
Epidemiology
Main article: Epidemiology of depressionﾧ
ﾧ
ﾧ
Disability-adjusted life yearﾧ for unipolar depressive disorders per 100,000 inhabitants in 2004.[243] no data 1450

Depression is a major cause of morbidityﾧ worldwide.[244] It is believed to currently affect approximately 298 million people as of 2010 (4.3% of the global population).[245] Lifetime prevalence varies widely, from 3% in Japan to 17% in the US.[246] In most countries the number of people who have depression during their lives falls within an 8–12% range.[246] 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.[247][248] 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.[249] 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.[249]
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.[250] The risk of major depression is increased with neurological conditions such as strokeﾧ, Parkinson 's diseaseﾧ, ormultiple sclerosisﾧ, and during the first year after childbirth.[251] It is also more common after cardiovascular illnesses, and is related more to a poor outcome than to a better one.[236][252] Studies conflict on the prevalence of depression in the elderly, but most data suggest there is a reduction in this age group.[253] Depressive disorders are more common to observe in urban than in rural population and the prevalence is in groups with stronger socioeconomic factors i.e. homelessness.[254]
History
ﾧ
ﾧ
Diagnoses of depression go back at least as far as Hippocratesﾧ
Main article: History of depressionﾧ
The Ancient Greek physician Hippocratesﾧ 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.[255] 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.[79]
The term depression itself was derived from the Latin verb deprimere, "to press down".[256] 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 'sﾧ Chronicle to refer to someone having "a great depression of spirit", and by English author Samuel Johnsonﾧ in a similar sense in 1753.[257] The term also came into use in physiologyﾧ and economicsﾧ. An early usage referring to a psychiatric symptom was by French psychiatrist Louis Delasiauveﾧ in 1856, and by the 1860s it was appearing in medical dictionaries to refer to a physiological and metaphorical lowering of emotional function.[258] Since Aristotleﾧ, 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.[79]
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 Kraepelinﾧ may have been the first to use it as the overarching term, referring to different kinds of melancholia as depressive states.[259]
Sigmund Freud likened the state of melancholia to mourning in his 1917 paper Mourning and Melancholia. He theorized that objectiveﾧ loss, such as the loss of a valued relationship through death or a romantic break-up, results in subjectiveﾧ loss as well; the depressed individual has identified with the object of affection through an unconsciousﾧ, narcissisticﾧ process called the libidinal cathexisﾧ of the egoﾧ. 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.[77] The patient 's decline of self-perception is revealed in his belief of his own blame, inferiority, and unworthiness.[78] He also emphasized early life experiences as a predisposing factor.[79] 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 ofmelancholia.[260] 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.[261]
In the mid-20th century, researchers theorized that depression was caused by a chemical imbalanceﾧ in neurotransmitters in the brain, a theory based on observations made in the 1950s of the effects of reserpineﾧ and isoniazidﾧ in altering monoamine neurotransmitter levels and affecting depressive symptoms.[262]
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 Criteriaﾧ),[263] and was incorporated into the DSM-III in 1980.[264] 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.[264][265] The ancient idea ofmelancholia 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.[266][267] 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.[268]
Society and culture
ﾧ
ﾧ
The 16th American presidentﾧ Abraham Lincolnﾧ suffered from "melancholyﾧ", a condition that now may be referred to as clinical depression.[269]
See also: List of people with major depressive disorderﾧ
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."[270] 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.[271][272]
The diagnosis is less common in some countries, such as Chinaﾧ. It has been argued that the Chinese traditionally deny or somatizeﾧ emotional depression (although since the early 1980s, the Chinese denial of depression may have modified drastically).[273] Alternatively, it may be that Western cultures reframe and elevate some expressions of human distress to disorder status. Australian professor Gordon Parkerﾧ and others have argued that the Western concept of depression "medicalizes" sadness or misery.[274][275] Similarly, Hungarian-American psychiatrist Thomas Szaszﾧ and others argue that depression is a metaphorical illness that is inappropriately regarded as an actual disease.[276] There has also been concern that the DSM, as well as the field of descriptive psychiatryﾧ that employs it, tends to reifyﾧ abstract phenomena such as depression, which may in fact be social constructsﾧ.[277] American archetypal psychologistﾧ James Hillmanﾧ writes that depression can be healthy for the soulﾧ, insofar as "it brings refuge, limitation, focus, gravity, weight, and humble powerlessness."[278] Hillman argues that therapeutic attempts to eliminate depression echo the Christian theme of resurrectionﾧ, 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 stigmaﾧ 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 Shelleyﾧ,[279] American-British writer Henry Jamesﾧ,[280] and American president Abraham Lincolnﾧ.[281] Some well-known contemporary people with possible depression include Canadian songwriter Leonard Cohenﾧ[282] and American playwright and novelist Tennessee Williamsﾧ.[283] Some pioneering psychologists, such as Americans William Jamesﾧ[284][285] and John B. Watsonﾧ,[286] dealt with their own depression.
There has been a continuing discussion of whether neurological disorders and mood disorders may be linked to creativityﾧ, a discussion that goes back to Aristotelian times.[287][288] British literature gives many examples of reflections on depression.[289] English philosopher John Stuart Millﾧ 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 Coleridgeﾧ '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."[290][291] English writer Samuel Johnsonﾧ used the term "the black dog" in the 1780s to describe his own depression,[292] and it was subsequently popularized by depression sufferer former British Prime Minister Sir Winston Churchillﾧ.[292]
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.[293] In the UK, the Royal College of Psychiatristsﾧ and the Royal College of General Practitionersﾧ conducted a joint Five-year Defeat Depression campaign to educate and reduce stigma from 1992 to 1996;[294] a MORIﾧ study conducted afterwards showed a small positive change in public attitudes to depression and treatment.[295]
In other animals
Further information: animal psychopathology#Depressionﾧ
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66 Jump up^ﾧ Hippocrates, Aphorisms, Section 6.23
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68 Jump up^ﾧ Wolpert, L. Malignant Sadness: The Anatomy of Depressionﾧ; 1999 [Retrieved 30 October 2008].
69 Jump up^ﾧ Berrios GE. Melancholia and depression during the 19th century: A conceptual history. British Journal of Psychiatry. 1988;153:298–304.doiﾧ:10.1192/bjp.153.3.298ﾧ. PMID 3074848ﾧ.
70 Jump up^ﾧ Historical aspects of mood disorders. Psychiatry. 2006;5(4):115–18. doiﾧ:10.1383/psyt.2006.5.4.115ﾧ.
71 Jump up^ﾧ Lewis, AJ. Melancholia: A historical review. Journal of Mental Science. 1934;80:1–42. doiﾧ:10.1192/bjp.80.328.1ﾧ.
72 Jump up^ﾧ American Psychiatric Association. Diagnostic and statistical manual of mental disorders: DSM-IIﾧ [PDF]. Washington, DC: American Psychiatric Publishing, Inc.; 1968 [Retrieved 3 August 2008]. Schizophrenia. p. 36–37, 40.
73 Jump up^ﾧ Schildkraut, JJ. The catecholamine hypothesis of affective disorders: A review of supporting evidence. American Journal of Psychiatry. 1965;122(5):509–22.doiﾧ:10.1176/appi.ajp.122.5.509ﾧ. PMID 5319766ﾧ.
74 Jump up^ﾧ Spitzer RL, Endicott J, Robins E. The development of diagnostic criteria in psychiatryﾧ [PDF]; 1975 [Retrieved 8 November 2008].
75 ^ Jump up to:aﾧ bﾧ Philipp M, Maier W, Delmo CD. The concept of major depression. I. Descriptive comparison of six competing operational definitions including ICD-10 and DSM-III-Rﾧ.European Archives of Psychiatry and Clinical Neuroscience. 1991;240(4–5):258–65. doiﾧ:10.1007/BF02189537ﾧ. PMID 1829000ﾧ.
76 Jump up^ﾧ Gruenberg, A.M., Goldstein, R.D., Pincus, H.A. (2005)."Classification of Depression: Research and Diagnostic Criteria: DSM-IV and ICD-10"ﾧ. wiley.com. Retrieved 30 October 2008.
77 Jump up^ﾧ Bolwig, Tom G.. Melancholia: Beyond DSM, beyond neurotransmitters. Proceedings of a conference, May 2006, Copenhagen, Denmark. Acta Psychiatrica Scandinavica Suppl. 2007;115(433):4–183. doiﾧ:10.1111/j.1600-0447.2007.00956.xﾧ. PMID 17280564ﾧ.
78 Jump up^ﾧ Fink M, Bolwig TG, Parker G, Shorter E. Melancholia: Restoration in psychiatric classification recommended. Acta Psychiatrica Scandinavica. 2007;115(2):89–92.doiﾧ:10.1111/j.1600-0447.2006.00943.xﾧ. PMID 17244171ﾧ.
79 Jump up^ﾧ The Antidepressant Era. Cambridge, MA: Harvard University Press; 1999. ISBN 0-674-03958-0ﾧ. p. 42.
80 Jump up^ﾧ Wolf, Joshua "Lincoln 's Great Depression"ﾧ, The Atlantic, October 2005, Retrieved 10 October 2009
81 Jump up^ﾧ Maloney F. Washington Post. The Depression Wars: Would Honest Abe Have Written the Gettysburg Address on Prozac?ﾧ; 3 November 2005 [Retrieved 3 October 2008].
82 Jump up^ﾧ Karasz A. Cultural differences in conceptual models of depression. Social Science in Medicine. 2005;60(7):1625–35. doiﾧ:10.1016/j.socscimed.2004.08.011ﾧ. PMID 15652693ﾧ.
83 Jump up^ﾧ Tilbury, F. There are orphans in Africa still looking for my hands ': African women refugees and the sources of emotional distressﾧ. Health Sociology Review. 2004 [Retrieved 3 October 2008];13(1):54–64.doiﾧ:10.5555/hesr.2004.13.1.54ﾧ.
84 Jump up^ﾧ Parker Gﾧ, Gladstone G, Chee KT. Depression in the planet 's largest ethnic group: The Chinese. American Journal of Psychiatry. 2001;158(6):857–64.doiﾧ:10.1176/appi.ajp.158.6.857ﾧ. PMID 11384889ﾧ.
85 Jump up^ﾧ Parker, Gﾧ. Is depression overdiagnosed? Yesﾧ. BMJﾧ. 2007;335(7615):328. doiﾧ:10.1136/bmj.39268.475799.ADﾧ.PMID 17703040ﾧ. PMCﾧ 1949440ﾧ.
86 Jump up^ﾧ Pilgrim D, Bentall R. The medicalisation of misery: A critical realist analysis of the concept of depressionﾧ.Journal of Mental Health. 1999;8(3):261–74.doiﾧ:10.1080/09638239917580ﾧ.
87 Jump up^ﾧ Steibel W (Producer). Is depression a disease?ﾧ; 1998 [Retrieved 16 November 2008].
88 Jump up^ﾧ Blazer DG. The age of melancholy: "Major depression" and its social origins. New York, NY, USA: Routledge; 2005. ISBN 978-0-415-95188-3ﾧ.
89 Jump up^ﾧ Hillman J (T Moore, Ed.). A blue fire: Selected writings by James Hillman. New York, NY, USA: Harper & Row; 1989.ISBN 0-06-016132-9ﾧ. p. 152–53.
90 Jump up^ﾧ Mary Shelley. Grove Press; 2002. ISBN 0-8021-3948-5ﾧ. p. 560–61.
91 Jump up^ﾧ pbs.orgﾧ. Biography of Henry Jamesﾧ [Retrieved 19 August 2008].
92 Jump up^ﾧ Burlingame, Michael. The Inner World of Abraham Lincoln. Urbana: University of Illinois Press; 1997. ISBN 0-252-06667-7ﾧ.[page needed]
93 Jump up^ﾧ Pita E. An Intimate Conversation with...Leonard Cohenﾧ; 26 September 2001 [Retrieved 3 October 2008].
94 Jump up^ﾧ Jeste ND, Palmer BW, Jeste DV. Tennessee Williams.American Journal of Geriatric Psychiatry. 2004;12(4):370–75. doiﾧ:10.1176/appi.ajgp.12.4.370ﾧ. PMID 15249274ﾧ.
95 Jump up^ﾧ James H (Ed.). Letters of William James (Vols. 1 and 2). Montana USA: Kessinger Publishing Co; 1920. ISBN 978-0-7661-7566-2ﾧ. p. 147–48.
96 Jump up^ﾧ Hergenhahn 2005ﾧ, p. 311
97 Jump up^ﾧ Cohen D. J. B. Watson: The Founder of Behaviourism. London, UK: Routledge & Kegan Paul; 1979. ISBN 0-7100-0054-5ﾧ. p. 7.
98 Jump up^ﾧ Andreasen NC. The relationship between creativity and mood disorders. Dialogues in clinical neuroscience. 2008;10(2):251–5. PMID 18689294ﾧ.
99 Jump up^ﾧ Simonton, DK. Are genius and madness related? Contemporary answers to an ancient questionﾧ.Psychiatric Times. 2005;22(7).
100 Jump up^ﾧ Heffernan CF. The melancholy muse: Chaucer, Shakespeare and early medicine. Pittsburgh, PA, USA: Duquesne University Press; 1996. ISBN 0-8207-0262-5ﾧ.
101 Jump up^ﾧ Mill JSﾧ. Autobiographyﾧ [txt]. Project Gutenberg EBook; 2003 [Retrieved 9 August 2008]. ISBN 1-4212-4200-1ﾧ. A crisis in my mental history: One stage onward. p. 1826–32.
102 Jump up^ﾧ Sterba R. The 'Mental Crisis ' of John Stuart Millﾧ.Psychoanalytic Quarterly. 1947 [Retrieved 5 November 2008];16(2):271–72.
103 ^ Jump up to:aﾧ bﾧ Black Dog Institute. Churchill’s Black Dog?: The History of the ‘Black Dog’ as a Metaphor for Depressionﾧ [PDF]; 2005 [Retrieved 18 August 2008].
104 Jump up^ﾧ Jorm AF, Angermeyer M, Katschnig H. Public knowledge of and attitudes to mental disorders: a limiting factor in the optimal use of treatment services. In: Andrews G, Henderson S (eds). Unmet Need in Psychiatry:Problems, Resources, Responses. Cambridge University Press; 2000.ISBN 0-521-66229-Xﾧ. p. 409.
105 Jump up^ﾧ Paykel ES, Tylee A, Wright A, Priest RG, Rix S, Hart D. The Defeat Depression Campaign: psychiatry in the public arena. American Journal of Psychiatry. 1997;154(6 Suppl):59–65. PMID 9167546ﾧ.
106 Jump up^ﾧ Paykel ES, Hart D, Priest RG. Changes in public attitudes to depression during the Defeat Depression Campaign.British Journal of Psychiatry. 1998;173:519–22.doiﾧ:10.1192/bjp.173.6.519ﾧ. PMID 9926082ﾧ.
Selected cited works
American Psychiatric Association. Diagnostic and statistical manual of mental disorders, Fourth Edition, Text Revision: DSM-IV-TR. Washington, DC: American Psychiatric Publishing, Inc.; 2000a. ISBN 0-89042-025-4ﾧ.
Barlow DH. Abnormal psychology: An integrative approach (5th ed.). Belmont, CA, USA: Thomson Wadsworth; 2005. ISBN 0-534-63356-0ﾧ.
Beck AT, Rush J, Shaw BF, Emery G. Cognitive Therapy of depression. New York, NY, USA: Guilford Press; 1987. ISBN 0-89862-919-5ﾧ.
Hergenhahn BR. An Introduction to the History of Psychology. 5th ed. Belmont, CA, USA: Thomson Wadsworth; 2005. ISBN 0-534-55401-6ﾧ.
May R. The discovery of being: Writings in existential psychology. New York, NY, USA: W. W. Norton & Company; 1994. ISBN 0-393-31240-2ﾧ.
Hadzi-Pavlovic, Dusan; Parker, Gordon. Melancholia: a disorder of movement and mood: a phenomenological and neurobiological review. Cambridge, UK: Cambridge University Press; 1996.ISBN 0-521-47275-Xﾧ.
Royal Pharmaceutical Society of Great Britain. British National Formularyﾧ (BNF 56). UK: BMJ Group and RPS Publishing; 2008. ISBN 978-0-85369-778-7ﾧ.
Sadock, Virginia A.; Sadock, Benjamin J.; Kaplan, Harold I.. Kaplan & Sadock 's synopsis of psychiatry: behavioral sciences/clinical psychiatry. Philadelphia: Lippincott Williams & Wilkins; 2003. ISBN 0-7817-3183-6ﾧ.
External links
Depressionﾧ on the Open Directory Projectﾧ
[showﾧ]
vﾧ tﾧ eﾧ
Mentalﾧ and behavioral disordersﾧ (Fﾧ 290–319ﾧ)

[showﾧ] vﾧ tﾧ eﾧ Mood disorderﾧ (F30–F39ﾧ, 296ﾧ)

ﾧ

Categoriesﾧ:
Abnormal psychologyﾧ
Bipolar spectrumﾧ
History of medicineﾧ
Mood disordersﾧ
Depression (psychology)ﾧ
Psychiatric diagnosisﾧ

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