Major depressive disorder
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{{Infobox_Disease
| Name = Depression
| Image = Vincent Willem van Gogh 002.jpg
| Caption = [[Vincent van Gogh]]'s 1890 painting ''On the Threshold of Eternity'' may symbolize the despair and hopelessness of his depression; he committed [[suicide]] later that same year.
| Width = 200
| DiseasesDB = 3589
| ICD10 = {{ICD10|F|32||f|30}}, {{ICD10|F|33||f|30}}
| ICD9 = {{ICD9|296}}
| ICDO =
| OMIM = 608516
| MedlinePlus = 003213
| eMedicineSubj = med
| eMedicineTopic = 532
| MeshID =
}}
'''Major depressive disorder''', also known as '''major depression''', '''unipolar depression''', '''clinical depression''', or simply '''depression''', is a [[mental disorder]] characterized by a pervasive low mood, loss of interest in usual activities and diminished ability to experience pleasure. The diagnosis is made if a person has suffered one or more [[major depressive episode]]s. The onset is usually in early- to mid-adulthood. Diagnosis is based on the patient's self-reported experiences and observed behavior. There is no laboratory test for major depression, although physicians often test for physical conditions that may cause similar symptoms before arriving at a diagnosis. The course varies widely: it can be a once-in-a-lifetime event or have multiple recurrences; it can appear either gradually or suddenly; and can either last for a few months or be a life-long disorder.
The term "depression" is commonly used in the vernacular to describe a temporary [[depression (mood)|depressed mood]], when a person may feel sad or "down". Ideas about what causes and constitutes depression have [[Major_depressive_disorder#History|evolved over the centuries]]. Today, mental health professionals regard chronic and severe depression as a serious and often disabling condition that can significantly affect a person's work, family and school life, sleeping and eating habits, general health and ability to enjoy life.<ref name="NIMHPub">{{cite web
| last = Mayo Clinic Staff
| title = Depression
| publisher = [[National Institute of Mental Health]] (NIMH)
|date=2006-03-06
| url = http://www.nimh.nih.gov/health/publications/depression/nimhdepression.pdf
| accessdate = 2007-10-20 }}</ref> Depression is a major risk factor for [[suicide]]; in addition, people with depression suffer from higher [[mortality]] from other causes.<ref name="pmid17640152">{{cite journal |author=Rush AJ |title=The varied clinical presentations of major depressive disorder |journal=The Journal of clinical psychiatry |volume=68 Suppl 8 |issue= |pages=4–10 |year=2007 |pmid=17640152 |doi=}}</ref> When specific treatment is indicated, it usually consists of [[psychotherapy]] and [[antidepressant]]s.
==Signs and symptoms==
A [[major depressive episode]] can manifest with a variety of symptoms, but almost all who experience such an episode display a marked change in mood, a deep feeling of sadness, and a noticeable [[anhedonia|loss of interest or pleasure]] in favorite activities. The psychological, or mood change, symptoms may include persistent sad, anxious or "empty" moods, and feelings of worthlessness, inappropriate guilt, helplessness, hopelessness, or pessimism, a sense of restlessness or irritability, and difficulty thinking, concentrating, remembering, or making decisions. Physical symptoms associated with depression include increased or decreased appetite or weight; [[insomnia]], early morning awakening, or oversleeping; decreased energy, fatigue, feeling "slowed down" or sluggish; [[psychomotor agitation]] or [[psychomotor retardation]]; and persistent physical symptoms that do not respond to treatment, such as [[headache]]s, [[digestion|digestive]] problems, and [[chronic pain]].
Other symptoms include withdrawal from social situations, family gatherings and activities with friends; and thoughts of [[death]] or [[suicide]] or attempts at suicide. Not all people will suffer from every symptom. The severity of symptoms will vary widely among individuals. According to [[Major_depressive_disorder#DSM_IV-TR_Criteria|one diagnostic standard]], symptoms, with the exception of suicidal thoughts or attempts, must persist for at least two weeks before being considered a potential sign of depression.<ref name="APABrochure">{{cite web
| title = Let's Talk Facts About Depression
| publisher = American Psychiatric Association
|date=2006-11
| url = http://healthyminds.org/factsheets/LTF-Depression.pdf
| accessdate = 2007-10-21 }}</ref><ref name="NIMHPub" />
Diagnosis of an episode in children is more difficult than in adults. Depression in children is often undiagnosed, and thus untreated, because the symptoms in children are often dismissed as normal childhood moodiness. Children are more likely than adults to show different symptoms depending on the situation.<ref name="MedNetChildren">{{cite web
| title = Depression in Children
| publisher = MedicineNet.com and the Cleveland Clinic
|date=2005-01-31
| url = http://www.medicinenet.com/depression_in_children/article.htm
| accessdate = 2007-10-21 }}</ref> While some children still function reasonably well, most who are suffering from depression will exhibit a noticeable change in their social activities and life, a loss of interest in school and poor academic performance, and possibly drastic changes in appearance. They may also begin [[drug abuse|abusing drugs]] or [[alcohol abuse|alcohol]], particularly past the age of 12. Although much more rarely than adults, children with major depression may attempt suicide or have suicidal thoughts even before the age of 12.<ref name="MedNetChildren" />
===Comorbidity===
Depression and [[anxiety]] frequently co-occur; the National Comorbidity Survey (US) reports that 58 percent of those with major depression also suffer from lifetime anxiety. Even mild anxiety symptoms can have a major impact on the course of a depressive illness, and the commingling of any anxiety symptoms with the primary depression is important to consider. Ellen Frank ''et al''. found that depressed or bipolar patients with lifetime panic symptoms experienced significant delays in their remission.<ref>[http://archpsyc.ama-assn.org/cgi/content/abstract/48/9/851 Arch Gen Psychiatry - Abstract: Conceptualization and rationale for consensus definitions of terms in major depressive disorder. Remission, recovery, relapse, and recurrence, September 1991, Frank et al. 48 (9): 851<!-- Bot generated title -->]</ref> These patients also had higher levels of residual impairment. On a similar note, [[Robert Sapolsky]] argues that the relationship between stress, anxiety, and depression could be measured and demonstrated biologically.<ref>{{cite book | first = Robert M., Ph.D. | last = Sapolsky | year = 2004 | title = Why Zebras Don't Get Ulcers | chapter = | editor = | pages = 291-298 | publisher = Henry Holt and Company, LLC|id = ISBN 0-8050-7369-8 }}</ref>
About one-third of individuals diagnosed with [[attention-deficit hyperactivity disorder]] (ADHD) may develop [[comorbid]] depression.<ref>Hallowell, Edward M.; John J. Ratey (2005). ''Delivered from Distraction : Getting the Most out of Life with Attention Deficit Disorder''. New York: Ballantine Books, p. 253–5. ISBN 0-345-44231-8. </ref> [[Dysthymia]], a form of chronic, low-level depression, is particularly common in adults with undiagnosed ADHD who have encountered years of frustrating ADHD-related problems with education, employment, and interpersonal relationships.<ref>see Hallowell and Ratey, 2005</ref>
==Diagnosis==
Before a diagnosis of major depressive disorder is made, a [[physician]] may perform a medical examination to rule out a physical cause for the suspected depression. Although there are no biological tests which confirm major depression, tests are carried out to exclude medical illnesses. These include blood tests measuring [[Thyroid-stimulating hormone|TSH]] to exclude [[hypothyroidism|hypo-]] or [[hyperthyroidism]], [[Blood tests#Blood chemistry tests|basic electrolytes]] and serum [[calcium]] to rule out a [[Metabolic disorder|metabolic disturbance]], [[Complete blood count|full blood count]] including [[Erythrocyte sedimentation rate|ESR]] to rule out a [[systemic infection]] or chronic disease, and [[serology]] to exclude [[syphilis]] or [[HIV]] infection. Two commonly ordered investigations are [[Electroencephalography|EEG]] to exclude [[epilepsy]], and a [[Computed tomography|CT scan]] of the head to exclude brain lesions. Early dementia may present with depressive symptoms in older patients.
If no such cause is found, a [[psychological evaluation]] may be done by the physician or by referral to a [[psychiatrist]] or [[psychologist]].<ref name="NIMHPub" /> The evaluation will include a complete history of symptoms, a discussion of alcohol and drug use, and a determination of whether the patient has had or is having suicidal thoughts or thinking about [[death]]. The evaluation will also include a family medical history to see if other family members suffer from any form of depression or similar mood disorder.<ref name="NIMHPub" />
Investigations are not generally repeated for a recurrent episode unless there is a specific ''medical'' indication. These may include measuring serum sodium if the person presents with [[polyuria]] and is on a [[selective serotonin reuptake inhibitor]] (SSRI). Assessment and treatment are usually done on an [[outpatient]] basis; admission to an [[inpatient]] facility is considered for patients who pose a risk to themselves or to others.
===Rating scales===
There are several criteria lists and diagnostic tools that can also aid in the diagnosis of depression. Most are based on the [[Diagnostic and Statistical Manual of Mental Disorders]] (DSM-IV), a book published by the [[American Psychiatric Association]] that stipulates the criteria used to diagnose various mental disorders, including depression. Many are used in research or as screening tools, but not in the absence of review by a medical practitioner or a psychologist.
The [[Beck Depression Inventory]], originally designed by psychiatrist [[Aaron Temkin Beck|Aaron T. Beck]] in 1961, is a 21-question [[self-report inventory|patient-completed survey]] that covers items related to the basic symptoms of depression, such as hopelessness and irritability, [[cognition]]s such as guilt or feelings of being punished, as well as physical symptoms such as fatigue, weight loss, and lack of interest in sex.<ref>{{cite book
| last = Beck
| first = A. T.
| title = Depression: Causes and Treatment
| publisher = University of Pennsylvania Press
|date=1972
| location = Philadelphia
| isbn = 0-8122-1032-8 }}</ref> The Beck Inventory is one of the most widely used diagnostic tools for [[self-diagnosis]] of depression, although its main purpose is not the diagnosis of depression, but determining the severity and presence of symptoms.<ref>{{cite web
| title = Beck Depression Inventory - 2nd Edition
| publisher = Nova Southeastern University Center for Center for Psychological Studies
| url = http://www.cps.nova.edu/~cpphelp/BDI2.html
| accessdate = 2007-10-22 }}</ref>
There are also two Patient Health Questionnaires available that are also self-administered questionnaires. The PHQ-2 has only two questions that asks about the frequency of depressed mood and a loss of interest in doing things, with a positive to either question indicating the need for further testing.<ref name="pmid10568646">Spitzer RL, Kroenke K, Williams JB. Validation and utility of a self-report version of PRIME-MD: the PHQ primary care study. Primary Care Evaluation of Mental Disorders. Patient Health Questionnaire. JAMA. 1999;282:1737-44. PMID 10568646</ref> The PHQ-9 is a slightly more detailed nine question survey covering some of the major symptoms of depression and the frequency a person has experienced them. It is based directly on the diagnostic criteria listed in the DSM-IV and often used as a follow up to a positive PHQ-2 test.<ref>[http://www.depression-primarycare.org/clinicians/toolkits/materials/forms/phq9/ The MacArthur Initiative on Depression Primary Care - Resources for Clinicians: Patient Health Questionnaire]</ref>
Other scales commonly used include the [[Geriatric Depression Scale]], in older populations, the widely-used [[Hamilton Depression Rating Scale]] designed by psychiatrist [[Max Hamilton]] in 1960,<ref> Hamilton, M (1960) A rating scale for depression. ''Journal of Neurology, Neurosurgery and Psychiatry.'' '''23''': 56-62 PMID 14399272 (HRSD-21)</ref> and the [[Montgomery-Åsberg Depression Rating Scale]] (MADRS).
===DSM IV-TR Criteria===
The most widely used criteria for diagnosing depressive conditions are found in the [[American Psychiatric Association|American Psychiatric Association's]] [[Diagnostic and Statistical Manual of Mental Disorders]], the current version being DSM-IV-TR, and the [[World Health Organization|World Health Organization's]] [[ICD|International Statistical Classification of Diseases and Related Health Problems]], currently the ICD-10. The latter system is typically used in European countries, while the DSM criteria are used in the USA and many other non-European nations, and are frequently referenced in research studies.
The DSM IV-TR diagnosis hinges on the presence of a [[major depressive episode]], which may be either single or recurrent. Further qualifiers are used to classify both the episode itself and the course of the disorder. There is also a category of [[Depressive Disorder Not Otherwise Specified]]. The [[ICD-10]] system does not use the term ''Major depressive disorder'', but lists similar criteria for the diagnosis of a ''Depressive episode'' (mild, moderate or severe).
====Major depressive episode====
{{main|Major depressive episode}}
[[Image:Ivan Kramskoy- Unconsolable Grief.JPG|thumb|150px|left|At [[Bereavement#Normal_and_complicated_grief|what point]] does "Inconsolable Grief"—portrayed here by [[Ivan Kramskoy]]—become a psychological disorder?]]
A ''major depressive episode'' has been defined as a severely depressed mood that persists for at least two weeks. Episodes may be isolated or recurrent and categorized as mild (few symptoms in excess of minimum criteria), moderate, or severe (marked impact on social or occupational functioning); any episode with psychotic features is automatically rated as severe. If the patient has already had an episode of [[mania]] or [[hypomania|markedly elevated mood]], a diagnosis of [[bipolar disorder]] is made instead. Depression without periods of elation or mania is sometimes referred to as ''unipolar depression'' because the mood remains at one emotional state or "pole". The DSM excludes cases in which the symptoms are a normal result of [[bereavement]] (though it is possible for normal bereavement to turn into a depressive episode). There is ongoing debate about whether the exclusion criteria should cover other social or financial losses.<ref>Wakefield, JC., Schmitz, MF., First, MB., Horwitz, AV. (2007) [http://archpsyc.ama-assn.org/cgi/content/abstract/64/4/433 Extending the Bereavement Exclusion for Major Depression to Other Losses: Evidence From the National Comorbidity Survey] Arch Gen Psychiatry. 2007;64(4):433-440.</ref><ref>Vedantam, S. (2007) [http://www.washingtonpost.com/wp-dyn/content/article/2007/04/02/AR2007040201693.html Criteria for Depression Are Too Broad, Researchers Say: Guidelines May Encompass Many Who Are Just Sad] Washington Post, April 3, P.A02</ref>
====Subtypes====
Diagnosticians recognize several possible subtypes or course specifiers:
* ''[[Melancholic depression]]'' – melancholia is characterized by a loss of pleasure (anhedonia) 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.
* ''[[Atypical depression]]'' – atypical depression is characterized by mood reactivity (paradoxical anhedonia) and positivity, significant [[weight gain]] or increased appetite ("comfort eating"),<ref>[http://www.depnet.com.au/universe1/depression/other_types_of_depression/ DepNet | Other types of depression<!-- Bot generated title -->]</ref> excessive sleep or somnolence ([[hypersomnia]]), leaden paralysis, or significant social impairment as a consequence of hypersensitivity to perceived [[social rejection|interpersonal rejection]]. Contrary to its name, atypical depression is the most common form of depression.<ref>[http://depression.about.com/cs/diagnosis/a/atypicaldepress.htm Atypical Depression Actually Very Typical]</ref>
* ''[[Psychotic depression]]'' – Some people with a major depressive episode, particularly of melancholic nature, may experience psychotic features. They may present with [[hallucination]]s or [[delusion]]s that are either mood-congruent (content coincident with depressive themes) or non-mood-congruent (content not coincident with depressive themes). It is clinically more common to encounter a delusional system as an adjunct to depression than to encounter hallucinations, whether visual or auditory.
*''[[Catatonia|Catatonic]] depression'' is a rare form of major depression involving disturbances of motor behavior and other symptoms.
*''[[Postpartum depression]]'' is listed as a course specifier in the DSM. It refers to the intense, sustained and sometimes disabling depression experienced by women after giving birth. Postpartum depression, which has incidence rate of 10-15%, typically sets in within three months of [[childbirth|labor]], and can last for as long as three months.<ref>[http://www.emedicine.com/med/topic3408.htm eMedicine - Postpartum Depression : Article by Ruta M Nonacs<!-- Bot generated title -->]</ref>
===Differential diagnoses===
* [[Dysthymia]] is a chronic, mild depression in which a person suffers from a depressive mood almost daily over a span of at least two years without episodes of major depression. The symptoms are not as severe as those for major depression, although people with dysthymia are vulnerable to co-occurring episodes of major depression (sometimes referred to as "double depression").<ref>[http://www.news-medical.net/?id=27964 Double depression<!-- Bot generated title -->]</ref>
*''[[Recurrent brief depression]]'' (RBD). This is distinguished from Major Depressive Disorder primarily by differences in duration. Patients with RBD have depressive episodes about once per month, with individual episodes lasting less than two weeks and typically less than 2–3 days. Diagnosis of RBD requires that the episodes occur over the span of at least one year and, in female patients, independently of the [[menstrual cycle]]. People with clinical depression can develop RBD, and vice versa, with both illnesses having similar risks.<ref> [http://www.gpnotebook.co.uk/simplepage.cfm?ID=1268383817 General Practice Notebook - Recurrent brief depression]</ref>
*''[[Minor Depressive Disorder|Minor depression]]'' refers to a depression that does not meet full criteria for major depression but in which at least two symptoms are present for two weeks.<ref>Rapaport MH, Judd LL, Schettler PJ, Yonkers KA, Thase ME, Kupfer DJ, Frank E, Plewes JM, Tollefson GD, Rush AJ. (2002) ''A descriptive analysis of minor depression.'' Am J Psychiatry. Apr;159(4):637-43. PMID 11925303</ref>
* [[Bipolar disorder]] is an episodic condition characterized by alternating states of [[mania]], [[hypomania]] and depression. In the United States, bipolar disorder has also been called "manic depression", but this term is no longer favored by the medical community.
* [[Adjustment disorder]] with depressed mood overlaps with what was previously known as ''reactive depression''.
==Epidemiology==
North American population studies have shown that 3-5% of males and 8-10% of females are suffering from a major depressive episode at any one time.<ref>{{cite journal |author=Kessler RC, Berglund P, Demler O, Jin R, Merikangas KR, Walters EE |year=2005|title=Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication |journal=Arch Gen Psychiatry |volume=62 |issue=6 |pages=617–27 |pmid=15939837|doi=10.1001/archpsyc.62.6.593}}</ref><ref>{{cite journal |author=Murphy JM, Laird NM, Monson RR, Sobol AM, Leighton AH |year=2000|title=A 40-year perspective on the prevalence of depression: the Stirling County Study|journal=Arch Gen Psychiatry |volume=57 |issue=3 |pages=209–15|pmid=10711905|doi=10.1001/archpsyc.57.3.209}}</ref> The National Comorbidity Survey Replication (NCS-R), conducted from 2001 through 2002, found that 16.2% of people had suffered a major depressive episode in their lives.<ref>{{cite journal |author=Kessler RC, Berglund P, Demler O, Jin R, Koretz D, Merikangas KR, Rush AJ, Walters EE, Wang PS |year=2003 |title=JAMA |journal= |volume=289|issue=203 |pages=3095–3105 |pmid=12813115 |url= |accessdate=}}</ref> Overall, major depression annually affects about 8.2% of the [[Canada|Canadian]] population and about 8.7% of the [[United States]] population. Researchers who compared epidemiological factors in Canada and the United States found the rate of major depression to be twice as high for Americans without medical insurance than either for Americans with insurance or for Canadians in general.<ref name="Prevalence">{{cite journal |author=Vasiliadis H-M, Lesage A, Adair C, Wang PS, Kessler RC |title=Do Canada and the United States differ in prevalence of depression and utilization of services? |journal=Psychiatric Services |volume=58 |issue=1 |pages=63-71 |year=2007 |month=January |pmid= |pmc= |doi= |url=http://psychservices.psychiatryonline.org/cgi/reprint/58/1/63}}</ref>
Major depressive disorder is often a recurring condition. The rate of recurrence depends on the severity of the first episode, with about a 90% recurrence rate over five years for the severerely depressed and a 70% rate for the average psychiatric patient with major depression.<ref name="pmid18251627">{{cite journal |author=Holma KM, Holma IA, Melartin TK, Rytsälä HJ, Isometsä ET |title=Long-term outcome of major depressive disorder in psychiatric patients is variable |journal=J Clin Psychiatry |volume=69 |issue=2 |pages=196–205 |year=2008 |month=February |pmid=18251627 |doi= |url=http://article.psychiatrist.com/?ContentType=START&ID=10003442}}</ref><ref name="pmid12877398">{{cite journal |author=Kanai T, Takeuchi H, Furukawa TA, ''et al'' |title=Time to recurrence after recovery from major depressive episodes and its predictors |journal=Psychol Med |volume=33 |issue=5 |pages=839–45 |year=2003 |month=July |pmid=12877398 |doi= |url=}}</ref> A comprehensive population-based study, which included persons who were never treated by a psychiatrist and likely had milder variant of major depression, put the 23-year recurrence rate at 50%. In 15% of the cases, the disorder had a chronic course and did not leave a single depression-free year out of the 23 examined.<ref name="pmid18458203">{{cite journal |author=Eaton WW, Shao H, Nestadt G, Lee BH, Bienvenu OJ, Zandi P |title=Population-based study of first onset and chronicity in major depressive disorder |journal=Arch. Gen. Psychiatry |volume=65 |issue=5 |pages=513–20 |year=2008 |month=May |pmid=18458203 |doi=10.1001/archpsyc.65.5.513 |url=}}</ref>
<!--Note: The following information appears to have been copy-pasted verbatim from a website (http://www.psychotherapy.ro/resources/mental-disorders/clinical-depression-epidemiology/), and then subjected to copy-edits here. The inclusion of various citations in this material is therefore baffling, although it may be promising in case editors would like to restore the section in a more appropriate form: "About twice as many females as males report or receive treatment for clinical depression, though this imbalance has recently shrunk, and the difference seems to disappear completely for those over the age of 50–55. Clinical depression is currently the leading cause of [[disability]] in North America, and is expected to become the second leading cause of disability worldwide (after [[heart disease]]) by the year 2020, according to the [[World Health Organization]].<ref>{{cite journal | last = Murray | first = C.J.L. | coauthors = Lopez, A.D. |date=1997 | title = Alternative projections of mortality and disability by cause 1990-2020: Global Burden of Disease Study | journal = Lancet | volume = 349 | pages = 1498?1504 | doi = 10.1016/S0140-6736(96)07492-2 }}</ref> The diagnostic criteria for depression may be too broad, resulting in diagnosis of major depression in people who are not truly suffering from the disorder, but who have shown normal responses to negative events.<ref>{{cite news |first=Shankar |last=Vedantam |title=Criteria for Depression Are Too Broad, Researchers Say |url=http://www.washingtonpost.com/wp-dyn/content/article/2007/04/02/AR2007040201693.html?hpid=topnews |publisher=''[[Washington Post]]'' |date=2007-04-03 |accessdate=2007-09-10 }}</ref>"-->
==Causes==
Current theories regarding the risk factors and causes of clinical depression can be broadly classified into two categories: psychological and biological.
===Psychological===
Events such as the death of a parent, issues with biological development, school related problems, [[Child abandonment|abandonment]] or rejection, [[neglect]], chronic illness, and [[physical abuse|physical]], [[psychological abuse|psychological]], or [[sexual abuse]] can increase the likelihood of depression later in life. [[Post-traumatic stress disorder]] (PTSD) and depression often co-occur, and both can result from childhood trauma.<ref>[http://www.upliftprogram.com/article_ptsd.html PTSD and Childhood Trauma<!-- Bot generated title -->]</ref>
Stressful or [[Psychological trauma|traumatic]] life experiences or circumstances, including [[rape]], [[assault]], or the death of a relative or friend, may trigger a depressive episode. A depressive episode may also be triggered by other major changes such as [[unemployment]], [[divorce]], or a loss of religious [[faith]].<ref>{{citation|title=The role of religion in depression|journal=Journal of Religion and Health|year=1972|publisher=Springer|author=NJC Andreasen}}</ref> Ongoing issues, such as financial difficulties or [[poverty]], ongoing major health problems (e.g., [[eating disorders]]), addictions (e.g., [[gambling addiction]] or drug addiction), [[Sexual dysfunction|sexual difficulties]], or [[Workplace stress|work-related stress]] can also contribute to depression.
Low [[self-esteem]], [[learned helplessness]], and self-defeating or distorted thinking are connected with depression. There is debate as to whether these are causes or effects of depression. In either case, it is known that depressed persons who are able to make corrections in their thinking patterns can show improved mood and self-esteem.<ref name="urlNAMI Cognitive-Behavioral Therapy">{{cite web |url=http://www.nami.org/Template.cfm?Section=About_Treatments_and_Supports&template=/ContentManagement/ContentDisplay.cfm&ContentID=7952 |title=NAMI | Cognitive-Behavioral Therapy |format= |work= |accessdate=}}</ref> [[Psychology|Psychological]] factors related to depression include the complex development of one's [[personality]] and how one has learned to cope with external environmental factors, such as [[Stress (medicine)|stress]].<ref>[http://www.apa.org/monitor/feb00/depression.html Personality styles may predict susceptibility to depression<!-- Bot generated title -->]</ref>
[[Evolutionary psychology|Evolutionary psychologists]] have theorized that "psychic misery"<ref>{{cite journal | last = Mashman | first = RC | title = An evolutionary view of psychic misery | journal = Journal of Social Behaviour & Personality | volume = 12 | issue= | pages = 979–999 |date=1997 | url = | doi = }}</ref> and other components of major depression might be useful adaptations for [[Major_depressive_disorder#Sociocultural_aspects|our species]] in some situations.<ref name="pmid10632228">{{cite journal |author=Nesse RM |title=Is depression an adaptation? |journal=Arch. Gen. Psychiatry |volume=57 |issue=1 |pages=14–20 |year=2000 |month=January |pmid=10632228 |doi= |url=http://archpsyc.ama-assn.org/cgi/pmidlookup?view=long&pmid=10632228}}</ref> Some aspects of this theory have received empirical support and clinical application;<ref name="Gilbert">{{cite book |author=Gilbert, Paul |title=Overcoming Depression: A Self-Help Guide Using Cognitive Behavioral Techniques (2nd rev. ed.) |publisher=Robinson Publishing |location=London, UK |year=2000 |pages= |idbn= |oclc= |doi= |accessdate=}}</ref><ref>{{citation|title=Evolution, depression and counselling|journal=Counselling Psychology Quarterly|volume=Volume 18, Number 3|pages=215–222|url=http://www.ingentaconnect.com/content/routledg/ccpq/2005/00000018/00000003/art00005| date=September 2005|author=Tony J. Carey}}</ref> other components are still at a hypothetical stage.
[[Image:RolloMay.jpg|left|thumb|150px|[[Rollo May]] and other [[existential psychology|existential psychologists]] have argued that depression can stem from an inadequate grasp of personal [[free will|freedom]] and [[moral responsibility|responsibility]].]]
[[Existential psychology|Existential psychologists]] argue that "depression is the inability to construct a future."<ref>http://www.psychiatrictimes.com/display/article/10168/51281</ref><!--See epigraph.--> In order to construct a future, people must become acutely aware of both their mortality and their freedom, and they must exercise the latter within the explicit framework of the former. This awareness and responsibility produce "normal anxiety,"<ref name="Anxiety">{{cite book |author=May, Rollo |title=The Meaning Of Anxiety |publisher=W. W. Norton and Company |location=New York, NY, USA |year=1996 |pages= |isbn=0-393-31456-1 |oclc= |doi= |accessdate=}}</ref> whereas the lack of these things leads to "neurotic anxiety,"<ref name="Anxiety">{{cite book |author=May, Rollo |title=The Meaning Of Anxiety |publisher=W. W. Norton and Company |location=New York, NY, USA |year=1996 |pages= |isbn=0-393-31456-1 |oclc= |doi= |accessdate=}}</ref> "self-alienation,"<ref name="Escape">{{cite book |author=Fromm, Erich |title=Escape from Freedom |publisher=Holt, Rinehart, & Winston |location=New York, NY, USA |year=1941 |pages= |isbn= |oclc= |doi= |accessdate=}}</ref> "inauthentic" living,<ref name="Being">{{cite book |author=Heidegger, Martin |title=Being and Time |publisher=Niemeyer |location=Halle, Germany |year=1927 |pages= |isbn= |oclc= |doi= |accessdate=}}</ref> and depression. [[Humanistic psychology|Humanistic psychologists]] agree with many facets of existentialism, but argue that depression results from a specific incongruity between society on the one hand, and the individual's innate drive to [[self-actualization|self-actualize]] on the other.<ref name="History">{{cite book |author=Hergenhahn, B. R. |title=An Introduction to the History of Psychology (5th ed.) |publisher=Thomson Wadsworth |location=Belmont, CA, USA |year=2005 |pages=546-547 |isbn=0-534-55401-6 |oclc= |doi= |accessdate=}}</ref>
===Biological===
[[Image:Synapse Illustration2 tweaked.svg|thumb|250px|Illustration of the major elements in a prototypical '''synapse'''. Synapses are gaps between [[neuron|nerve cells]]. These cells convert their [[action potential|electrical impulses]] into bursts of neurochemical relayers, called [[neurotransmitter]]s, which travel across the synapses to receptors on the [[dendrite]]s of adjacent cells, thereby triggering further electrical impulses to travel down the latter cells.]]
Most experts believe that both [[Diathesis-stress model|biological and psychological factors]] play a role. The [[heritability]] of depression—the degree to which it is genetically determined—was estimated to be about 40% for women and about 30% for men.<ref name="pmid16390897">{{cite journal |author=Kendler KS, Gatz M, Gardner CO, Pedersen NL |title=A Swedish national twin study of lifetime major depression |journal=Am J Psychiatry |volume=163 |issue=1 |pages=109–14 |year=2006 |month=January |pmid=16390897 |doi=10.1176/appi.ajp.163.1.109 |url=}}</ref> From the [[evolution]]ary standpoint, major depression might be expected to reduce the [[Fitness (biology)|reproductive fitness]] of the individual suffering from it. One of the explanations for the apparent contradiction between this hypothesis and the high heritability and prevalence of major depression is that it results from the exaggeration and distortion of evolutionarily useful psychological defense mechanisms.<ref name="pmid12706512">{{cite journal |author=Sloman L, Gilbert P, Hasey G |title=Evolved mechanisms in depression: the role and interaction of attachment and social rank in depression |journal=J Affect Disord |volume=74 |issue=2 |pages=107–21 |year=2003 |month=April |pmid=12706512 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0165032702001167}}</ref>
Many modern [[antidepressant]] [[Psychoactive drug|drug]]s change [[Chemical synapse|synaptic]] levels of certain [[neurotransmitters]]—especially [[serotonin]] and [[norepinephrine]]—potentially implicating neurochemical factors as causally significant. However, the precise relationships among serotonin, [[Selective serotonin reuptake inhibitor|SSRIs]], and depression are largely unknown, and tend to be greatly oversimplified when presented to the public.<ref>http://medicine.plosjournals.org/archive/1549-1676/2/12/pdf/10.1371_journal.pmed.0020392-L.pdf</ref>
There may be a link between depression and [[neurogenesis]] of the [[hippocampus]],<ref>Dr Helen Mayberg, quoted in http://www.sciammind.com/article.cfm?&articleID=0002AD36-CF84-14C7-8DCC83414B7F0000 ''Scientific American'', volume 17, number 4, pp. 26-31</ref> a center for both mood and memory. Loss of [[neuron]]s in the [[hippocampus]] 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 thereby increasing the total mass of the hippocampus. This increase in mass may help to restore mood and memory.<ref>{{cite journal | last = Sheline | first = YI, ''et al''. | title = Untreated depression and hippocampal volume loss | journal = American Journal of Psychiatry | volume = 160 | issue= | pages = 1516–1518 |date=2003 | url = | doi = }}</ref><ref>{{cite journal | last = Duman | first = RS, ''et al''. | title = A molecular and cellular theory of depression | journal = Archives of General Psychiatry | volume = 54 | issue= | pages = 597–606 |date=1997 | url = | doi = }}</ref>
Depression may also be caused in part by an overactive [[hypothalamic-pituitary-adrenal axis]] (HPA axis) that resembles the neuro-endocrine response to [[stress]]. These HPA axis abnormalities participate in the development of depressive symptoms, and antidepressants serve to regulate HPA axis function.<ref> Carmine M. Pariante, Institute of Psychiatry, King’s College London [http://www.neuroendo.org.uk/content/view/31/11/ Depression, stress and the adrenal axis.] The British Society for Neuroendocrinology, 2003.</ref>
Many individuals with clinical depression exhibit markedly higher levels of [[monoamine oxidase A]] (MAO-A) in the brain compared to people without depression.<ref>Jeffrey H. Meyer, MD, PhD; Nathalie Ginovart, PhD; Anahita Boovariwala, BSc; Sandra Sagrati, BSc; Doug Hussey, BSc; Armando Garcia, BSc; Trevor Young, MD, PhD; Nicole Praschak-Rieder, MD; Alan A. Wilson, PhD; Sylvain Houle, MD, PhD, "Elevated Monoamine Oxidase A Levels in the Brain -- An Explanation for the Monoamine Imbalance of Major Depression," Arch Gen Psychiatry. 2006;63:1209-1216.[http://archpsyc.ama-assn.org/cgi/content/abstract/63/11/1209]</ref> MAO-A is an [[enzyme]] that reacts with and decreases the concentration of [[monoamine]]s such as serotonin, norepinephrine and dopamine.
==Treatment==
The three most commonly indicated treatments for depression are psychotherapy, medication, and electroconvulsive therapy.
===Psychotherapy===
{{main|Psychotherapy}}
[[Image:Albert_Ellis_2003_emocionalmente_sentado.jpg|left|thumb|150px|[[Albert Ellis]] invented [[Rational Emotive Behavior Therapy]], the earliest form of [[Cognitive Behavioral Therapy]].]]
There are a number of different psychotherapies for depression, which may be provided to individuals or groups. Psychotherapy can be delivered by a variety of mental health professionals, including psychotherapists, psychiatrists, psychologists, [[clinical social work]]ers, counselors, and psychiatric nurses. The most studied form of psychotherapy for depression is ''[[Cognitive behavioral therapy]]''. Several clinical trials have shown that CBT is as effective as antidepressant medications, even among more severely depressed clients. CBT is thought to work by teaching clients to learn a set of cognitive and behavioral skills, which they can employ on their own. This type of therapy attempts to teach people to learn healthier behaviors. Earlier research suggested that psychotherapy, specifically cognitive-behavioral therapy, was not as effective as medication in the treatment of depression; however, recent research suggests that CBT can perform as well as anti-depressant medication in the treatment of moderate to severe depression treated on an outpatient basis.<ref>[http://www.cedars-sinai.edu/6122.html Psychiatry and Behavioral Neurosciences - Outpatient Psychotherapy Groups<!-- Bot generated title -->]</ref> With more complex and chronic forms of depression the most effective treatment is often considered to be a combination of medication and psychotherapy.<ref>{{cite journal | last = Thase | first = ME | title = When are psychotherapy and pharmacotherapy combinations the treatment of choice for major depressive disorder? | journal = Psychiatr Q. | volume = 70 | issue=4 | pages = 333–346 |date=1999 | url = http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10587988&dopt=Abstract | doi = 10.1023/A:1022042316895}}</ref>
For the treatment of adolescent depression, CBT performed no better than placebo, and significantly worse than fluoxetine.<ref name="pmid15315995">{{cite journal |author=March J, Silva S, Petrycki S, ''et al'' |title=Fluoxetine, cognitive-behavioral therapy, and their combination for adolescents with depression: Treatment for Adolescents With Depression Study (TADS) randomized controlled trial |journal=JAMA |volume=292 |issue=7 |pages=807–20 |year=2004 |month=August |pmid=15315995 |doi=10.1001/jama.292.7.807 |url=}}</ref> Combining fluoxetine with CBT appeared to bring no additional benefit<ref name="pmid17556431">{{cite journal |author=Goodyer I, Dubicka B, Wilkinson P, ''et al'' |title=Selective serotonin reuptake inhibitors (SSRIs) and routine specialist care with and without cognitive behaviour therapy in adolescents with major depression: randomised controlled trial |journal=BMJ |volume=335 |issue=7611 |pages=142 |year=2007 |month=July |pmid=17556431 |pmc=1925185 |doi=10.1136/bmj.39224.494340.55 |url=}}</ref><ref name="pmid18462573">{{cite journal |author=Goodyer IM, Dubicka B, Wilkinson P, ''et al'' |title=A randomised controlled trial of cognitive behaviour therapy in adolescents with major depression treated by selective serotonin reuptake inhibitors. The ADAPT trial |journal=Health Technol Assess |volume=12 |issue=14 |pages=1–80 |year=2008 |month=May |pmid=18462573 |doi= |url=http://www.hta.ac.uk/execsumm/summ1214.htm}}</ref> or, at the most, only marginal benefit.<ref name="pmid18413703">{{cite journal |author=Domino ME, Burns BJ, Silva SG, ''et al'' |title=Cost-effectiveness of treatments for adolescent depression: results from TADS |journal=Am J Psychiatry |volume=165 |issue=5 |pages=588–96 |year=2008 |month=May |pmid=18413703 |doi=10.1176/appi.ajp.2008.07101610 |url=}}</ref>
Two randomized, controlled trials of mindfulness-based cognitive therapy (MBCT), which includes elements of [[meditation]], have been reviewed. MBCT was significantly more effective than "usual care" for the prevention of recurrent depression in patients who had had three or more depressive episodes. According to the review, the "usual care" did not include antidepressant treatment or any psychotherapy, and the improvement observed may have reflected the non-specific or placebo effects.<ref name="pmid18085916">{{cite journal |author=Coelho HF, Canter PH, Ernst E |title=Mindfulness-based cognitive therapy: evaluating current evidence and informing future research |journal=J Consult Clin Psychol |volume=75 |issue=6 |pages=1000–5 |year=2007 |month=December |pmid=18085916 |doi=10.1037/0022-006X.75.6.1000 |url=}}</ref>
''[[Interpersonal psychotherapy]]'' focuses on the social and interpersonal triggers that may cause depression. There is evidence that it is an effective treatment for depression. Here, the therapy takes a structured course with a set number of weekly sessions (often 12) as in the case of CBT, however the focus is on relationships with others. Therapy can be used to help a person develop or improve [[interpersonal skills]] in order to allow him or her to communicate more effectively and reduce stress.<ref>Weissman, M. M., Markowitz, J. C., & Klerman, G. L. (2000). ''Comprehensive guide to interpersonal psychotherapy''. New York: Basic Books.</ref>
''[[Psychoanalysis]]'', a school of thought founded by [[Sigmund Freud]] that emphasizes the resolution of unconscious mental conflicts,<ref name="isbn0-314-20412-1">{{cite book |author=Dworetzky, John |title=Psychology |publisher=Brooks/Cole Pub. Co |location=Pacific Grove, CA, USA |year=1997 |pages=602 |isbn=0-314-20412-1 |oclc= |doi= |accessdate=}}</ref> is used by its practitioners to treat clients presenting with major depression.<ref name="pmid12206545">{{cite journal |author=Doidge N, Simon B, Lancee WJ, ''et al'' |title=Psychoanalytic patients in the U.S., Canada, and Australia: II. A DSM-III-R validation study |journal=J Am Psychoanal Assoc |volume=50 |issue=2 |pages=615–27 |year=2002 |pmid=12206545 |doi= |url=}}</ref> A more widely practiced, eclectic technique, called ''[[psychodynamic psychotherapy]]'', is loosely based on psychoanalysis and has an additional social and interpersonal focus.<ref name="isbn0-534-34742-8">{{cite book |author=Durand, Vincent Mark; Barlow, David |title=Abnormal psychology: an integrative approach |publisher=Brooks/Cole Pub. Co |location=Pacific Grove, CA, USA |year=1999 |pages= |isbn=0-534-34742-8 |oclc= |doi= |accessdate=}}</ref> In a meta-analysis of three controlled trials, psychodynamic psychotherapy was found to be as effective as medication for mild to moderate depression.<ref name="pmid17557313">{{cite journal |author=de Maat S, Dekker J, Schoevers R, ''et al'' |title=Short Psychodynamic Supportive Psychotherapy, antidepressants, and their combination in the treatment of major depression: a mega-analysis based on three Randomized Clinical Trials |journal=Depress Anxiety |volume= |issue= |pages= |year=2007 |month=June |pmid=17557313 |doi=10.1002/da.20305 |url=}}</ref>
===Medication===
{{main|Antidepressant}}
A patient's doctor may change the antidepressant taken, adjust the dosages of medications, or try different combinations of antidepressants before finding the most effective option; response rates to the first agent administered may be as low as 50 percent.<ref>Depression Guideline Panel. Depression in primary care. Vol. 2. Treatment of major depression. Clinical practice guideline. No. 5. Rockville, MD: Agency for Health Care Policy and Research, 1999.</ref> It may take anywhere from three to eight weeks after the start of medication before its therapeutic effects can be fully discovered. Patients are generally advised not to stop taking an antidepressant suddenly and to continue its use for at least four months to prevent the chance of recurrence. For patients who have chronic depression, medication may be continued for the remainder of their lives.<ref name="NIMHPub" />
[[Image:S-fluoxetine-3D-vdW.png|thumb|200px|right|A [[molecule]] of [[fluoxetine]] (Prozac), the first [[FDA]]-approved [[SSRI]] and the most frequently prescribed antidepressant drug.]]
Selective serotonin reuptake inhibitors, such as [[sertraline]] (Zoloft), [[escitalopram]] (Lexapro), [[fluoxetine]] (Prozac), [[paroxetine]] (Paxil) and [[citalopram]] (Celexa) are the primary medications considered for patients, due to their relatively mild side effects and broad effect on the symptoms of depression and anxiety. Those who do not respond to the first SSRI tried can be switched to another SSRI antidepressant. Such a switch results in improvement in almost 50% of cases.<ref name="pmid12620174">{{cite journal |author=Sutherland JE, Sutherland SJ, Hoehns JD |title=Achieving the best outcome in treatment of depression |journal=J Fam Pract |volume=52 |issue=3 |pages=201–9 |year=2003 |month=March |pmid=12620174 |doi= |url=http://www.jfponline.com/Pages.asp?AID=1406}}</ref> Another popular option is to switch the patient to the atypical antidepressant [[bupropion]] (Wellbutrin) or to add bupropion to the existing therapy<ref> For the most recent review, see: {{cite journal |author=Zisook S, Rush AJ, Haight BR, Clines DC, Rockett CB |title=Use of bupropion in combination with serotonin reuptake inhibitors |journal=Biol Psychiatry |volume=59 |issue=3 |pages=203–10 |year=2006 |pmid=16165100 |doi=10.1016/j.biopsych.2005.06.027}}</ref> with the latter strategy possibly more effective.<ref name="pmid16554525">{{cite journal |author=Rush AJ, Trivedi MH, Wisniewski SR, Stewart JW, Nierenberg AA, Thase ME, Ritz L, Biggs MM, Warden D, Luther JF, Shores-Wilson K, Niederehe G, Fava M |title=Bupropion-SR, sertraline, or venlafaxine-XR after failure of SSRIs for depression |journal=N. Engl. J. Med. |volume=354 |issue=12 |pages=1231–42 |year=2006 |pmid=16554525 |doi=10.1056/NEJMoa052963}}</ref><ref name="pmid16554526">{{cite journal |author=Trivedi MH, Fava M, Wisniewski SR, Thase ME, Quitkin F, Warden D, Ritz L, Nierenberg AA, Lebowitz BD, Biggs MM, Luther JF, Shores-Wilson K, Rush AJ |title=Medication augmentation after the failure of SSRIs for depression |journal=N. Engl. J. Med. |volume=354 |issue=12 |pages=1243–52 |year=2006 |pmid=16554526 |doi=10.1056/NEJMoa052964}}</ref> The causing or worsening of insomnia is not uncommon with SSRIs; a sedating antidepressant [[mirtazapine]] (Zispin, Remeron) can be used in such cases.<ref name="pmid16229049">{{cite journal |author=Mayers AG, Baldwin DS |title=Antidepressants and their effect on sleep |journal=Hum Psychopharmacol |volume=20 |issue=8 |pages=533–59 |year=2005 |month=December |pmid=16229049 |doi=10.1002/hup.726 |url=}}</ref><ref name="pmid14658972">{{cite journal |author=Winokur A, DeMartinis NA, McNally DP, Gary EM, Cormier JL, Gary KA |title=Comparative effects of mirtazapine and fluoxetine on sleep physiology measures in patients with major depression and insomnia |journal=J Clin Psychiatry |volume=64 |issue=10 |pages=1224–9 |year=2003 |month=October |pmid=14658972 |doi= |url=http://article.psychiatrist.com/?ContentType=START&ID=10000336}}</ref><ref name="pmid15323610">{{cite journal |author=Lawrence RW |title=Effect of mirtazapine versus fluoxetine on "sleep quality" |journal=J Clin Psychiatry |volume=65 |issue=8 |pages=1149–50 |year=2004 |month=August |pmid=15323610 |doi= |url=http://article.psychiatrist.com/?ContentType=START&ID=10001013}}</ref> [[Venlafaxine]] (Effexor) may be moderately more effective than SSRIs;<ref name="pmid17588546">{{cite journal |author=Papakostas GI, Thase ME, Fava M, Nelson JC, Shelton RC |title=Are antidepressant drugs that combine serotonergic and noradrenergic mechanisms of action more effective than the selective serotonin reuptake inhibitors in treating major depressive disorder? A meta-analysis of studies of newer agents |journal=Biol. Psychiatry |volume=62 |issue=11 |pages=1217–27 |year=2007 |month=December |pmid=17588546 |doi=10.1016/j.biopsych.2007.03.027 |url=}}</ref> however, it is not recommended as a first line treatment because of the high rate of side effects.<ref name="urlNeLM - MHRA issues updated prescribing advice for venlafaxine (Efexor/Efexor XL)">{{cite web |url=http://www.nelm.nhs.uk/Record%20Viewing/vR.aspx?id=565749 |title=NeLM - MHRA issues updated prescribing advice for venlafaxine (Efexor/Efexor XL) |format=htm |work= |accessdate=2008-06-07}}</ref>
Tricyclic antidepressants are less well tolerated than SSRIs and are usually reserved for the treatment of inpatients, for whom the tricyclic antidepressant [[amitriptyline]], in particular, appears to be more effective.<ref name="pmid9597346">{{cite journal |author=Anderson IM |title=SSRIS versus tricyclic antidepressants in depressed inpatients: a meta-analysis of efficacy and tolerability |journal=Depress Anxiety |volume=7 Suppl 1 |issue= |pages=11–7 |year=1998 |pmid=9597346|doi=10.1002/(SICI)1520-6394(1998)7:1 <11::AID-DA4>3.0.CO;2-I}}</ref><ref name="pmid10760555">{{cite journal |author=Anderson IM |title=Selective serotonin reuptake inhibitors versus tricyclic antidepressants: a meta-analysis of efficacy and tolerability |journal=J Affect Disord |volume=58 |issue=1 |pages=19–36 |year=2000 |month=April |pmid=10760555 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0165-0327(99)00092-0}}</ref> Their adverse side effect profile and toxicity in overdose limit their use. Monoamine oxidase inhibitors have historically been plagued by questionable efficacy and life-threatening adverse effects. They are still used only rarely, although newer agents of this class, with a better side effect profile, have been developed.<ref name="pmid17640156">{{cite journal |author=Krishnan KR |title=Revisiting monoamine oxidase inhibitors |journal=J Clin Psychiatry |volume=68 Suppl 8 |issue= |pages=35–41 |year=2007 |pmid=17640156 |doi= |url=http://article.psychiatrist.com/?ContentType=START&ID=10003141}}</ref>
In a [[meta-analysis]] of 35 clinical trials of four newer antidepressants, antidepressants were [[statistically]] superior to [[placebo]], but they often did not exceed the [[NICE]] criteria for a "clinically significant" effect. In particular, the effect size was very small for moderate depression but increased with severity reaching 'clinical significance' for very severe depression.<ref>{{cite web |url=http://medicine.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pmed.0050045 |title=Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration |accessdate=2008-02-26 |author=Kirsch I, Deacon BJ, Huedo-Medina TB, Scoboria A, Moore TJ, Johnson BT |authorlink= |coauthors= |date=February 2008 |format=htm |work= |publisher=PLoS Medicine |pages= |language= |archiveurl= |archivedate= |quote=}}</ref> This result is consistent with the earlier clinical studies in which only patients with severe depression benefited from the treatment with a tricyclic antidepressant, [[imipramine]], or from psychotherapy more than from the placebo treatment.<ref name="pmid2684085">{{cite journal |author=Elkin I, Shea MT, Watkins JT, Imber SD, Sotsky SM, Collins JF, Glass DR, Pilkonis PA, Leber WR, Docherty JP |title=National Institute of Mental Health Treatment of Depression Collaborative Research Program. General effectiveness of treatments |journal=Arch. Gen. Psychiatry |volume=46 |issue=11 |pages=971–82; discussion 983 |year=1989 |pmid=2684085 |doi=}}</ref><ref name="pmid7593878">{{cite journal |author=Elkin I, Gibbons RD, Shea MT, Sotsky SM, Watkins JT, Pilkonis PA, Hedeker D |title=Initial severity and differential treatment outcome in the National Institute of Mental Health Treatment of Depression Collaborative Research Program |journal=J Consult Clin Psychol |volume=63 |issue=5 |pages=841–7 |year=1995 |pmid=7593878 |doi=}}</ref><ref name="pmid1853989">{{cite journal |author=Sotsky SM, Glass DR, Shea MT, Pilkonis PA, Collins JF, Elkin I, Watkins JT, Imber SD, Leber WR, Moyer J |title=Patient predictors of response to psychotherapy and pharmacotherapy: findings in the NIMH Treatment of Depression Collaborative Research Program |journal=Am J Psychiatry |volume=148 |issue=8 |pages=997–1008 |year=1991 |pmid=1853989 |doi=}}</ref>
===Electroconvulsive therapy===
{{main|Electroconvulsive therapy}}
Electroconvulsive therapy (ECT), also known as electroshock, is a treatment in which [[seizure]]s are electrically induced in anesthetized patients for therapeutic effect. Today, ECT is a last resort, and is most often used as a treatment for severe [[clinical depression|major depression]] which has not responded to other treatment. An estimated 1 million people worldwide receive ECT every year<ref>{{cite web | title=Electroconvulsive therapy discussion hosted at the MGH | url=http://www.massgeneral.org/pubaffairs/Issues2006/101306ect.htm | accessdate=2007-06-05}}</ref> usually in a course of 6-12 treatments administered 2 or 3 times a week. In a study, ECT was shown clinically to be the most effective treatment for severe depression, and to result in improved [[quality of life]] in both short- and long-term.<ref>McCall WV, Prudic J, Olfson M, Sackeim H. Health-related quality of life following ECT in a large community sample. J Affect Disord. 2006 Feb;90(2-3):269-74. PMID 16412519</ref> After treatment, drug therapy can be continued, and some patients receive continuation/maintenance ECT. [[Short-term memory]] loss, disorientation, and headache are very common side effects. Detailed neuropsychological testing in clinical studies has not been able to prove permanent effects on memory.
ECT produces a very fast response in the client; however, this response has been shown not always to last unless maintenance electroshock or maintenance medication is used. Whereas antidepressants usually take around a month to take effect, the results of ECT have been shown to be much faster. For this reason, it is the treatment of choice in emergencies (e.g., in catatonic depression in which the patient has ceased oral intake of fluid or nutrients). The [[American Psychiatric Association]] and the [[National Institute for Health and Clinical Excellence]] have concluded that the procedure does not cause brain damage.<ref name=brain>{{cite web | url = http://www.psych.org/research/apire/training_fund/clin_res/index.cfm | author = American Psychiatric Association | title=Electroconvulsive Therapy (ECT) | accessdate=2007-12-29}}</ref><ref name='ECT_NICE'>{{cite book | last = National Institute for Clinical Excellence | first = | authorlink = National Institute for Health and Clinical Excellence | coauthors = | title = Guidance on the use of electrocunvulsive therapy | publisher = | date = 2003-04 | location = London | pages = | url = http://www.nice.org.uk/nicemedia/pdf/59ectfullguidance.pdf | doi = | id = | isbn = 1-84257-282-2 }}</ref> Whether or not ECT can be given without a patient's consent is subject to legal conditions in the pertinent jurisdiction. In the U.S. state of [[Oregon]], patient consent is necessary by statute.<ref>[http://www.oflikeminds.com/Crisisplanning.htm Being prepared for a crisis with a psychiatric advance directive<!-- Bot generated title -->]</ref>
===Other conventional methods of treatment===
[[Image:Saint johns wart flowers.jpg|left|200px|thumb|[[St. John's wort]] may be an effective naturally growing antidepressant.]]
* [[St John's wort]] extract is used extensively in Europe to treat mild and moderate depression. It is a prescription [[antidepressant]] in several European countries but is classified as [[herbal supplement]] and sold over the counter in the U.S. The opinions on its efficacy for major depression differ. A systematic [[meta-analysis]] of 37 trials conducted by [[Cochrane Collaboration]] indicated [[statistically significant]] weak-to-moderate effect as compared to [[placebo]]. The same meta-analysis found that St John's wort efficacy for major depression is not different from prescription antidepressants.<ref name="linde_mulrow_2003">{{cite journal |author=Linde K, Mulrow CD, Berner M, Egger M |title=St John's wort for depression |journal=Cochrane Database Syst Rev |volume= |issue=2 |pages=CD000448 |year=2005 |pmid=15846605 |doi=10.1002/14651858.CD000448.pub2}}</ref> [[National Center for Complementary and Alternative Medicine|NCCAM]] and other [[NIH]]-affiliated organizations hold that St John's wort has minimal or no effects beyond placebo in the treatment of major depression, based primarily on one study with negative outcome conducted by NCCAM.<ref>[http://nccam.nih.gov/health/stjohnswort/sjwataglance.htm St. John's Wort and Depression] [[National Center for Complementary and Alternative Medicine|NCCAM]] on St John's wort and depression]</ref><ref>[http://www.nimh.nih.gov/health/publications/depression/treatment.shtml How is depression detected and treated?] [[National Institute of Mental Health|NIMH]] on depression, including a section on St John's wort</ref>
* [[S-Adenosyl methionine]] (SAM-e) is available as a prescription antidepressant in [[Europe]] and an over-the-counter [[dietary supplement]] in the United States. A fairly strong evidence, based on 16 clinical trials, suggests it to be more effective than placebo and as effective as standard antidepressant medication for the treatment of major depression.<ref name="pmid12420702">{{cite journal |author=Mischoulon D, Fava M |title=Role of S-adenosyl-L-methionine in the treatment of depression: a review of the evidence |journal=Am. J. Clin. Nutr. |volume=76 |issue=5 |pages=1158S–61S |year=2002 |month=November |pmid=12420702 |doi= |url=http://www.ajcn.org/cgi/pmidlookup?view=long&pmid=12420702}}</ref><ref name="pmid7941964">{{cite journal |author=Bressa GM |title=S-adenosyl-l-methionine (SAMe) as antidepressant: meta-analysis of clinical studies |journal=Acta Neurol. Scand., Suppl. |volume=154 |issue= |pages=7–14 |year=1994 |pmid=7941964 |doi= |url=}}</ref>
* [[Repetitive transcranial magnetic stimulation]] (rTMS) use in treatment-resistant depression is supported by multiple controlled studies, and it has been approved for this indication in Europe, Canada and Australia, but not in the U.S.<ref name="pmid17655558"/> A 2008 meta-analysis based on 32 trials found a robust effect of this method on depression, and it appeared similarly effective for both uncomplicated depression and depression resistant to medication.<ref name="pmid18447962">{{cite journal |author=Schutter DJ |title=Antidepressant efficacy of high-frequency transcranial magnetic stimulation over the left dorsolateral prefrontal cortex in double-blind sham-controlled designs: a meta-analysis |journal=Psychol Med |volume= |issue= |pages=1–11 |year=2008 |month=April |pmid=18447962 |doi=10.1017/S0033291708003462 |url=}}</ref> However, in a side-by-side randomized trial rTMS was inferior to [[electroconvulsive therapy]].<ref name="pmid17202547">{{cite journal |author=Eranti S, Mogg A, Pluck G, ''et al'' |title=A randomized, controlled trial with 6-month follow-up of repetitive transcranial magnetic stimulation and electroconvulsive therapy for severe depression |journal=Am J Psychiatry |volume=164 |issue=1 |pages=73–81 |year=2007 |month=January |pmid=17202547 |doi=10.1176/appi.ajp.164.1.73 |url=}}</ref>
* [[Vagus nerve stimulation]] (VNS) is an approved therapy for treatment-resistant depression and is used as an adjunct to existing antidepressant treatment. The support for this method comes primarily from open-label trials, which indicate that a several month period may be necessary for the therapy to become effective.<ref name="pmid17655558"/> The only large double-blind trial conducted lasted only 10 weeks and yielded inconclusive results. VNS failed to show superiority over a sham treatment on the primary efficacy outcome but the result were more favorable for the secondary outcome.<ref name="pmid16139580">{{cite journal |author=Rush AJ, Marangell LB, Sackeim HA, ''et al'' |title=Vagus nerve stimulation for treatment-resistant depression: a randomized, controlled acute phase trial |journal=Biol. Psychiatry |volume=58 |issue=5 |pages=347–54 |year=2005 |month=September |pmid=16139580 |doi=10.1016/j.biopsych.2005.05.025 |url=}}</ref>
===Alternative treatment methods===
[[Image:Bright light lamp.jpg|thumb|200px|right|Bright light therapy is sometimes used to treat depression, especially in its [[seasonal affective disorder|seasonal form]].]]
* A meta-analysis of bright [[light therapy]] commissioned by the [[American Psychiatric Association]] found it to be more effective than placebo—usually, dim light—for both [[seasonal affective disorder]] and for nonseasonal depression, with effect sizes similar to those for conventional antidepressants. For non-seasonal depression, adding light therapy to the standard antidepressant treatment was not effective.<ref name="pmid15800134">{{cite journal |author=Golden RN, Gaynes BN, Ekstrom RD, ''et al'' |title=The efficacy of light therapy in the treatment of mood disorders: a review and meta-analysis of the evidence |journal=Am J Psychiatry |volume=162 |issue=4 |pages=656–62 |year=2005 |month=April |pmid=15800134 |doi=10.1176/appi.ajp.162.4.656 |url=}}</ref> A meta-analysis of light therapy for non-seasonal depression conducted by Cochrane Collaboration, studied a different set of trials, where light was used mostly as an addition to medication or [[sleep deprivation]]. A moderate statistically significant effect of light therapy was found; however, it disappeared if a different statistical technique was used.<ref name="pmid15106233">{{cite journal |author=Tuunainen A, Kripke DF, Endo T |title=Light therapy for non-seasonal depression |journal=Cochrane Database Syst Rev |volume= |issue=2 |pages=CD004050 |year=2004 |pmid=15106233 |doi=10.1002/14651858.CD004050.pub2 |url=}}</ref> Both analyses noted poor quality of most studies and their small size, and urged caution in the interpretation of their results. The short 1-2 weeks duration of most trials makes it unclear whether the effect of light therapy could be sustained in the longer term.
* A 2004 [[Cochrane Review]] concluded that there was insufficient evidence to judge the efficacy of [[acupuncture]] in the management of depression. Although acupuncture showed no difference in the improvement of depression compared with conventional medication, the methodological quality of the evidence base was found to be poor.<ref name='Acupuncture_Cochrane'> {{cite journal|title=Acupuncture for Depression|journal=Cochrane Database of Systematic Reviews|date=2005|first=CA|last=Smith|coauthors=PPJ Hay|volume=2005|issue=2|pages=CD004046|doi= 10.1002/14651858.CD004046.pub2|url=|format=|accessdate= }}</ref>
* [[Exercise]], when used in conjunction with medication by non-suicidal patients, can have beneficial effects in preventing the return of depression. Patients who completed 30 minutes of brisk exercise at least three times a week were found to have a significantly lower incidence of relapse.<ref name="DukeExerciseStudy">{{cite web
| last = Merritt
| first = Richard
| title = Study: Exercise Has Long-Lasting Effect on Depression
| publisher = Duke University News
|date=2000-09-22
| url = http://dukenews.duke.edu/2000/09/exercise922.html
| accessdate = 2007-10-20 }}</ref>
* The support for the use of [[deep brain stimulation]] in [[treatment-resistant depression]] comes from a handful of case studies, and this treatment is still in a very early investigational stage.<ref name="pmid17655558">{{cite journal |author=Marangell LB, Martinez M, Jurdi RA, Zboyan H |title=Neurostimulation therapies in depression: a review of new modalities |journal=Acta Psychiatr Scand |volume=116 |issue=3 |pages=174–81 |year=2007 |month=September |pmid=17655558 |doi=10.1111/j.1600-0447.2007.01033.x |url=}}</ref>
* [[Insulin shock therapy]] is an old and largely abandoned treatment for severe depression, [[psychosis]], [[catatonia]], and other [[mental disorders]]. It consists of induction of [[hypoglycemia|hypoglycemic]] [[coma]] by [[intravenous infusion]] of [[insulin]].
* [[Tryptophan]] and [[5-hydroxytryptophan]] may be more effective than placebo in alleviating depression according to the Cochrane Collaboration meta-analysis. However, only two out of 108 trials were of sufficient quality to be included in this analysis.<ref name="pmid11869656">{{cite journal |author=Shaw K, Turner J, Del Mar C |title=Tryptophan and 5-hydroxytryptophan for depression |journal=Cochrane Database Syst Rev |volume= |issue=1 |pages=CD003198 |year=2002 |pmid=11869656 |doi=10.1002/14651858.CD003198 |url=}}</ref>
* [[Omega-3 fatty acid]]s have been studied in clinical trials for major depression primarily as an adjunctive to antidepressant therapy. A meta-analysis of eight such trials indicated a statistically significant superiority of combinations with omega-3 fatty acids over single antidepressants; however, the authors warned that, due to multiple problems with these trials, a reliable conclusion is difficult to achieve.<ref name="pmid17158410">{{cite journal |author=Appleton KM, Hayward RC, Gunnell D, ''et al'' |title=Effects of n-3 long-chain polyunsaturated fatty acids on depressed mood: systematic review of published trials |journal=Am. J. Clin. Nutr. |volume=84 |issue=6 |pages=1308–16 |year=2006 |month=December |pmid=17158410 |doi= |url=http://www.ajcn.org/cgi/pmidlookup?view=long&pmid=17158410}}</ref>
* [[Dehydroepiandrosterone]] (DHEA), available as a supplement in the U.S., has been shown to be more effective than placebo for major depression in two small double-blind trials: in one—as an adjunctive to antidepressant treatment<ref name="pmid10200751">{{cite journal |author=Wolkowitz OM, Reus VI, Keebler A, ''et al'' |title=Double-blind treatment of major depression with dehydroepiandrosterone |journal=Am J Psychiatry |volume=156 |issue=4 |pages=646–9 |year=1999 |month=April |pmid=10200751 |doi= |url=http://ajp.psychiatryonline.org/cgi/pmidlookup?view=long&pmid=10200751}}</ref>, in another—as monotherapy.<ref name="pmid15699292">{{cite journal |author=Schmidt PJ, Daly RC, Bloch M, ''et al'' |title=Dehydroepiandrosterone monotherapy in midlife-onset major and minor depression |journal=Arch. Gen. Psychiatry |volume=62 |issue=2 |pages=154–62 |year=2005 |month=February |pmid=15699292 |doi=10.1001/archpsyc.62.2.154 |url=}}</ref>
* [[Chromium picolinate]] was found to be equivalent to placebo for [[atypical depression]] overall but possibly efficacious in the sub-group of patients with severe carbohydrate craving.<ref name="pmid16184071">{{cite journal |author=Docherty JP, Sack DA, Roffman M, Finch M, Komorowski JR |title=A double-blind, placebo-controlled, exploratory trial of chromium picolinate in atypical depression: effect on carbohydrate craving |journal=J Psychiatr Pract |volume=11 |issue=5 |pages=302–14 |year=2005 |month=September |pmid=16184071 |doi= |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=1527-4160&volume=11&issue=5&spage=302}}</ref>
* [[Zinc]] supplementation was found in a small study to augment the effect of antidepressants.<ref name="pmid14730113">{{cite journal |author=Nowak G, Siwek M, Dudek D, Zieba A, Pilc A |title=Effect of zinc supplementation on antidepressant therapy in unipolar depression: a preliminary placebo-controlled study |journal=Pol J Pharmacol |volume=55 |issue=6 |pages=1143–7 |year=2003 |pmid=14730113 |doi= |url=http://www.if-pan.krakow.pl/pjp/pdf/2003/6_1143.pdf}}</ref>
*[[Cranial electrotherapy stimulation]] (CES, electrosleep) devices currently on the market have been granted marketing authorization by the FDA based on the legacy waver, that is because a sufficiently similar device had been marketed before 1976, when the new regulations requiring controlled testing were introduced.<ref name=CES_FDA>[http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfCFR/CFRSearch.cfm?FR=882.5800 FDA > CDRH > CFR Title 21 Database Search<!-- Bot generated title -->]</ref> The FDA considers them to be the class III devices—"devices for which insufficient information exists to ... provide reasonable assurance of safety and effectiveness"<ref>[http://www.fda.gov/cdrh/ode/515iltr.html FDA 515(i) Reclassification Letter to Manufacturers]</ref> The effects of CES on depression were inconclusive or negative in multiple double-blind studies of psychiatric patients.<ref name="pmid769773">{{cite journal |author=Levitt EA, James NM, Flavell P |title=A clinical trial of electrosleep therapy with a psychiatric inpatient sample |journal=Aust N Z J Psychiatry |volume=9 |issue=4 |pages=287–90 |year=1975 |month=December |pmid=769773 |doi= |url=}}</ref><ref name="pmid972328">{{cite journal |author=Passini FG, Watson CG, Herder J |title=The effects of cerebral electric therapy (electrosleep) on anxiety, depression, and hostility in psychiatric patients |journal=J. Nerv. Ment. Dis. |volume=163 |issue=4 |pages=263–6 |year=1976 |month=October |pmid=972328 |doi= |url=}}</ref><ref name="pmid2018818">{{cite journal |author=Philip P, Demotes-Mainard J, Bourgeois M, Vincent JD |title=Efficiency of transcranial electrostimulation on anxiety and insomnia symptoms during a washout period in depressed patients. A double-blind study |journal=Biol. Psychiatry |volume=29 |issue=5 |pages=451–6 |year=1991 |month=March |pmid=2018818 |doi= |url=}}</ref><ref name="pmid1091305">{{cite journal |author=Moore JA, Mellor CS, Standage KF, Strong H |title=A double-blind study of electrosleep for anxiety and insomnia |journal=Biol. Psychiatry |volume=10 |issue=1 |pages=59–63 |year=1975 |pmid=1091305 |doi=}}</ref><ref name="pmid972328">{{cite journal |author=Passini FG, Watson CG, Herder J |title=The effects of cerebral electric therapy (electrosleep) on anxiety, depression, and hostility in psychiatric patients |journal=J. Nerv. Ment. Dis. |volume=163 |issue=4 |pages=263–6 |year=1976 |pmid=972328 |doi=}}</ref><ref name="pmid4724809">{{cite journal |author=Feighner JP, Brown SL, Olivier JE |title=Electrosleep therapy. A controlled double blind study |journal=J. Nerv. Ment. Dis. |volume=157 |issue=2 |pages=121–8 |year=1973 |pmid=4724809 |doi=}}</ref> In one of them, four out of six clinically depressed patients dropped out of the study because of the massive worsening of depressive symptoms, with two of them becoming actively suicidal.<ref name="pmid4724809"/> One of the authors of the latter study cautioned that CES “should not be used as a treatment of choice” for the patients with the primary diagnosis of depression, “and should be used with caution if this diagnosis is suspected.”<ref>{{cite journal |author=Feighner JP |title=Electrosleep Therapy: Current Usage in Psychiatry |journal=Calif. Med. |volume=115 |issue=3 |pages=44 |year=1971|url=http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1518073|accessdate=2007-12-02}}</ref> Nevertheless, the CES practitioners continue to employ it as a treatment of choice for depression.<ref name="pmid14629839">{{cite journal |author=Shealy CN |title=Transcutaneous electrical nerve stimulation: the treatment of choice for pain and depression |journal=J Altern Complement Med |volume=9 |issue=5 |pages=619–23 |year=2003 |month=October |pmid=14629839 |doi=10.1089/107555303322524463 |url=}}</ref><ref>{{cite journal |author=Shealy CN, Thomlinson P |title= Safe Effective Nondrug Treatment of Chronic Depression: A Review of Research on Low-Voltage Cranial Electrical Stimulation and Other Adjunctive Therapies |journal=Complementary Health Practice Review |volume=13 |issue=2 |pages=92–99 |year=2008 |doi=10.1177/1533210108317232 |url=http://chp.sagepub.com/cgi/content/abstract/13/2/92}}</ref>
==Prognosis==
Recurrence is more likely if treatment has not resulted in full remission of symptoms. Current guidelines for antidepressant use recommend 4 to 6 months of continuing treatment after symptom resolution to prevent relapse. Combined evidence from many [[randomized controlled trials]] indicates that continuing antidepressant medications after recovery can reduce the odds 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. Thus, in a significant minority of patients depression [[tachyphylaxis|recurs despite the prolonged treatment]] with antidepressants.<ref name="pmid12606176">{{cite journal |author=Geddes JR, Carney SM, Davies C, ''et al'' |title=Relapse prevention with antidepressant drug treatment in depressive disorders: a systematic review |journal=Lancet |volume=361 |issue=9358 |pages=653–61 |year=2003 |month=February |pmid=12606176 |doi=10.1016/S0140-6736(03)12599-8 |url=}}</ref> The reason for recurrence in these cases is as poorly understood and could be a "true pharmacologic failure or a worsening of the disease, a relapse that overrides medication." Because of the difficulties of carrying out controlled clinical trials of longer duration, the approval of most antidepressants for the prevention of recurrence is based on up to a year-long trials.<ref>[http://cms.psychologytoday.com/articles/pto-19990301-000032.html Psychology Today: Skirmish or Siege?<!-- Bot generated title -->]</ref>
==History==
{{seealso|History of mental disorders}}
===Prehistory to antiquity===
Archaeologists have found human skulls from prehistoric eras, with large holes cut into them through a process called [[trepanation]]. Cave paintings suggest that people believed the practice would cure a range of ailments including mental disorders.<ref>{{cite book |author=Brothwell, Don R. |year=1963 |title=Digging up Bones; the Excavation, Treatment and Study of Human Skeletal Remains |location=London |publisher=British Museum (Natural History) |oclc=14615536 |pages=126}}</ref> Out of 120 prehistoric skulls found at one burial site in [[France]] dated to 6500 BC, 40 had trepanation holes.<ref name="restak2000">{{cite book |author=Restak, Richard|chapter=Fixing the Brain |title=Mysteries of the Mind |publisher=National Geographic Society |location=Washington, D.C. |year=2000 |isbn=0-792-27941-7 |oclc=43662032}}</ref>
[[Image:Lavater1.jpg|left|thumb|200px|The four temperaments (clockwise from top right; choleric; melancholic; sanguine; phlegmatic), according to an [[Humorism|ancient theory of mental states]]. The melancholic temperament, associated with black bile, is most similar to what is now known as major depression.]]
The Greek scholar [[Empedocles]] (490-430 BC), who proposed disease was caused by an imbalance of the [[four humours]], influenced [[Hippocrates]] (460-377 BC), who is credited with being the first physician to reject supernatural or divine explanations of illness. He believed that disease was the product of environmental factors, diet and living habits, not a punishment inflicted by the [[Greek gods|gods]]. Hippocrates believed that the appropriate treatment for a mental disorder depended on which bodily fluid, or humour, had caused the problem.
[[Image:Hippocrates rubens.jpg|right|thumb|150px|[[Hippocrates]], depicted here by [[Peter Paul Rubens]], was an early Western proponent of the [[Philosophy_of_mind#The_mind-body_problem|mind-body connection]] and helped to advance the proto-psychological theory of [[humourism]].]]
The modern idea of depression appears similar to the much older concept of [[melancholia]], which derives its name from the [[theory]] of ''the four [[humorism|humours]]'': disease being caused by an imbalance in one or other of the four basic bodily fluids, or humours. Personality types were similarly determined by the dominant humour in a particular person. Melancholia was caused by an excess of black [[bile]]; hence the name, which means 'black bile' ([[Ancient Greek]] μέλας, ''melas'', "black", + χολή, ''kholé'', "bile"); a person whose constitution tended to have a preponderance of black bile had a ''melancholic'' disposition. Melancholia was described as a distinct [[disease]] with particular mental and physical symptoms in the [[5th century BC|fifth]] and [[4th century BC|fourth centuries BC]]. [[Hippocrates]], in his ''Aphorisms'', characterized all "fears and despondencies, if they last a long time" as being symptomatic of melancholia.<ref>Hippocrates, ''Aphorisms'', Section 6.23</ref>
[[Plato]] (427-347 BC) argued that there were two types of mental illness: "divinely inspired" mental illness that gave the person prophetic powers, and a second type that was caused by a physical disease.<ref name="Ackerknecht">{{cite book |author=Ackerknecht, EH |title=A Short History of Psychiatry |publisher=Hafner |location=New York, NY, USA |year=1959 |pages= |isbn= |oclc= |doi= |accessdate=}}</ref> [[Aristotle]] (384-322 BC), who studied under Plato, abandoned the divinely-caused mental illness theory, and proposed instead that all mental illness was caused by physical problems.
Through long contact with Greek culture, and their eventual conquest of Greece, the [[Roman Empire|Romans]] absorbed many of the Greek ideas on medicine.<ref>von Staden, "Liminal Perils: Early Roman Receptions of Greek Medicine," in ''Tradition, Transmission, Transformation'', ed. F. Jamil Ragep and Sally P. Ragep with Steven Livesey (Leiden: Brill, 1996), pp. 369-418.</ref> The Greek physician [[Asclepiades]] (c. 124 – 40 BC), who practiced in Rome, discarded the humoral doctrine of Hippocrates. He advocated humane treatment of mental disorders, and had insane persons freed from confinement and treated them with natural therapy, such as diet and massages. While [[Arateus]] (ca AD 30-90) argued that it is hard to pinpoint where a mental illness comes from, [[Galen]] (AD 129 –ca. 200) revived the Greek theories of the "four humours" and proposed that melancholy is caused by "animal spirits". In the [[Old Testament]], which was composed and compiled between the 12th and the 2nd century BC, the description of [[King Saul]] includes symptoms that resemble some elements in the modern diagnosis of depression; eventually the King commits suicide.
===Medieval to Renaissance eras===
Galen's ideas about medicine dominated Western medical thinking from the medieval era until the [[Renaissance]], in part because the Catholic church supported them. In addition to viewing mental illness through the lens of Galen's "four humours", medieval Europeans viewed mental illness as the entry of demons or evil spirits into the body.<ref>Deborah Kent. Snake Pits, Talking Cures & Magic Bullets: A History of Mental Illness. 2003, Twenty-First Century
Books. ISBN 0761327045, page 34</ref> [[Arnaldus de Villanova]] (1235-1313) even combined the "evil spirit" and Galen-oriented "four humours" theories. Despite his familiarity with Arabic treatises (he translated a number of medical texts from Arabic, including works by [[Avicenna|Ibn Sina]] and Galen), he suggested that people with mental illness could be cured by trepanning a cross-shaped hole in their head to let the demons and excess humours excape. In the 13th and 14th centuries, the treatment of people with mental illness varied. While some people with mental illnesses were treated at hospitals such as [[Bethlem Royal Hospital]] (better known by its nickname, “Bedlam”), which was founded in 1329,<ref>Deborah Kent. Snake Pits, Talking Cures & Magic Bullets: A History of Mental Illness. 2003, Twenty-First Century
Books. ISBN 0761327045, page 47</ref> others were persecuted as witches.<ref>http://72.14.205.104/search?q=cache:-6640GTpnZUJ:www.mind.org.uk/Information/Factsheets/History%2Bof%2Bmental%2Bhealth/Notes%2Bon%2Bthe%2BHistory%2Bof%2BMental%2BHealth%2BCare.htm </ref> For people deemed to be witches, a common treatment was exorcism, often in the form of physical punishments that aimed to drive out the devil and save the person’s soul. The [[witch hunt|witch-hunting]] attitude was not held in all quarters.<ref>http://72.14.205.104/search?q=cache:-6640GTpnZUJ:www.mind.org.uk/Information/Factsheets/History%2Bof%2Bmental%2Bhealth/Notes%2Bon%2Bthe%2BHistory%2Bof%2BMental%2BHealth%2BCare.htm </ref> The Franciscan monk [[Bartholomeus Anglicus]] (ca. 1203 - 1272) described a condition which resembles depression in his encyclopedia, ''De Proprietatibis Rerum'', and he suggested that music would help people with this condition.
In the [[Islamic Golden Age|medieval Islamic world]], the [[Islamic psychology|Muslim psychologist]] Ishaq ibn Imran (d. 908), known as "Isaac" in the West, wrote an [[essay]] entitled ''Maqala fi-l-Malikhuliya'', in which discovered a type of melancholia: the "cerebral type" or "[[phrenitis]]". In [[Arabic language|Arabic]], he referred to this [[mood disorder]] as "''malikhuliya''", which [[Constantine the African]] translated into [[Latin]] as "''melancolia''", from which the English term "melancholia" is derived.<ref>{{citation|last=Jacquart|first=Danielle|contribution=The Influence of Arabic Medicine in the Medieval West|pages=980}} in {{Harv|Morrison|Rashed|1996|pp=963-84}}</ref> In ''[[The Canon of Medicine]]'' (1020s), [[Avicenna]] described a number of [[neuropsychiatry|neuropsychiatric]] conditions, including melancholia.<ref>S Safavi-Abbasi, LBC Brasiliense, RK Workman (2007), "The fate of medical knowledge and the neurosciences during the time of Genghis Khan and the Mongolian Empire", ''Neurosurgical Focus'' '''23''' (1), E13, p. 3.</ref> He described melancholia as a [[Depression (mood)|depressive]] type of [[mood disorder]] in which the person may become suspicious and develop certain types of [[phobia]]s.<ref name=Amber-366>Amber Haque (2004), "Psychology from Islamic Perspective: Contributions of Early Muslim Scholars and Challenges to Contemporary Muslim Psychologists", ''Journal of Religion and Health'' '''43''' (4): 357-377 [366].</ref> ''The Canon of Medicine'' was also translated into Latin in the 12th century.
In Larry Merkel's lectures on the history of Western psychiatry, he argues that "medieval concepts of mental illness stressed that individuals had free will and were responsible for their actions, but that illness (including mental illness) came from sin and resulting punishment from God or possession by the devil."<ref>THE HISTORY OF PSYCHIATRY PGY II Lecture 9/18/03 Larry Merkel M.D., Ph.D. http://72.14.205.104/search?q=cache:11HPtrRHi9QJ:www.healthsystem.virginia.edu/internet/psych-training/seminars/history-of-psychiatry-8-04.pdf</ref> As a result, "[m]ental illness was seen as either the result of sin or as a test of faith". <ref>THE HISTORY OF PSYCHIATRY PGY II Lecture 9/18/03 Larry Merkel M.D., Ph.D. http://72.14.205.104/search?q=cache:11HPtrRHi9QJ:www.healthsystem.virginia.edu/internet/psych-training/seminars/history-of-psychiatry-8-04.pdf</ref> "[M]elancholia was seen as a trial of faith", and one of the "seven deadly sins...sloth (acedia) had a clinical profile, presenting with boredom, depression, obsessions, anxiety, and a variety of psychosomatic symptoms."<ref>THE HISTORY OF PSYCHIATRY PGY II Lecture 9/18/03 Larry Merkel M.D., Ph.D. http://72.14.205.104/search?q=cache:11HPtrRHi9QJ:www.healthsystem.virginia.edu/internet/psych-training/seminars/history-of-psychiatry-8-04.pdf</ref> In Robert Daly's article ''Before Depression: The Medieval Vice of Acedia'', he argues that in medieval Europe, "phenomena akin to the symptoms and signs of modern depression", were interpreted as "acedia", a "spiritual disease", vice, or "undesirable trait of character." He also claims that "acedia was a vice that could be distinguished from melancholia" and notes that while acedia is similar to the modern concept of depression, it "should not be identified with depression."<ref>Robert W. Daly Before Depression: The Medieval Vice of Acedia. 10.1521/psyc.2007.70.1.30 Volume: 70 | Issue: 1 Spring 2007 Page(s): 30-51. Available at: http://www.atypon-link.com/GPI/doi/abs/10.1521/psyc.2007.70.1.30 </ref>
From the 11th century onwards, as medieval Europeans had increasing contact with Islamic culture, the "classical Greek and other Hellenistic ideas...of Hippocrates, Galen, and the philosophy of Aristotle were combined to create an advanced level of science and medicine."<ref>THE HISTORY OF PSYCHIATRY PGY II Lecture 9/18/03 Larry Merkel M.D., Ph.D. http://72.14.205.104/search?q=cache:11HPtrRHi9QJ:www.healthsystem.virginia.edu/internet/psych-training/seminars/history-of-psychiatry-8-04.pdf</ref> In Islamic countries, physicians treated the mentally ill with "a calm and relaxed environment, with fountains, gardens, and the use of soothing baths, perfumes, music and special diets."<ref>THE HISTORY OF PSYCHIATRY PGY II Lecture 9/18/03 Larry Merkel M.D., Ph.D. http://72.14.205.104/search?q=cache:11HPtrRHi9QJ:www.healthsystem.virginia.edu/internet/psych-training/seminars/history-of-psychiatry-8-04.pdf</reF>
In the 16th century, the physician and alchemist [[Paracelsus]] (1493-1541) argued that sickness and health in the body relied on the harmony of man, the microcosm, and nature. Since he believed that illnesses could be cured by chemical remedies, he rejected the witch-hunt and demonology approach to mental illness.<ref>http://72.14.205.104/search?q=cache:-6640GTpnZUJ:www.mind.org.uk/Information/Factsheets/History%2Bof%2Bmental%2Bhealth/Notes%2Bon%2Bthe%2BHistory%2Bof%2BMental%2BHealth%2BCare.htm </ref> In the 16th century, the physician [[Johann Weyer]] (1515-1588) also argued against the witchcraft and demon-possession theories, proposing instead that mental illnesses had natural causes.<ref>http://72.14.205.104/search?q=cache:-6640GTpnZUJ:www.mind.org.uk/Information/Factsheets/History%2Bof%2Bmental%2Bhealth/Notes%2Bon%2Bthe%2BHistory%2Bof%2BMental%2BHealth%2BCare.htm </ref> However, the Catholic church banned Weyer’s book, ''De Praestigiis Daemonum'', and he was accused of being a sorcerer.<ref>http://72.14.205.104/search?q=cache:-6640GTpnZUJ:www.mind.org.uk/Information/Factsheets/History%2Bof%2Bmental%2Bhealth/Notes%2Bon%2Bthe%2BHistory%2Bof%2BMental%2BHealth%2BCare.htm </ref> [[Juan Luis Vives]] (1492-1540) exemplifies the more humane approach to dealing with the mentally ill; he founded hospitals where mentally ill people could be treated.
===17th to 19th centuries===
The seminal scholarly work of the 17th century was [[Robert Burton (scholar)|Robert Burton's]] ''[[The Anatomy of Melancholy]]'', drawing on numerous theories and the author's own experiences. Burton suggested that melancholy could be combated with a healthy diet, sufficient sleep, music, and "meaningful work", along with talking about the problem with a friend.<ref>Deborah Kent. Snake Pits, Talking Cures & Magic Bullets: A History of Mental Illness. 2003, Twenty-First Century Books. ISBN 0761327045, page 55</ref><ref>http://www.gutenberg.org/files/10800/10800-8.txt</ref> [[William Shakespeare|Shakespeare's]] plays, such as ''[[Hamlet]]'' and ''[[King Lear]]'', described characters with deep melancholy.
There was increasing medical dissatisfaction with the concept of melancholia. During the 18th century its connections to humoral theory were increasingly challenged by mechanical and electrical explanations; references to dark and gloomy states gave way to ideas of slowed circulation and depleted energy.<ref>Jackson SW. (1983) Melancholia and mechanical explanation in eighteenth-century medicine. J Hist Med Allied Sci. Jul;38(3):298-319. PMID 6350428</ref> The German physician [[Johann Christian August Heinroth|Johann Christian Heinroth]] (1773 - 1843), however, argued that melancholia was a disturbance of the soul due to moral conflict within the patient. French physician [[Phillipe Pinel]] (1745 - 1826) introduced a new classification scheme, with melancholia as one of four main categories of mental illness. Eventually various authors proposed up to 30 different subtypes of melancholia, and alternative terms were suggested and discarded. [[Hypochondria]] came to be seen as a separate disorder. The German psychiatrist [[Wilhelm Griesinger]] (1817-1868) argued for a unitary view, with different forms of melancholia (and other mental illnesses) due to a single disease process in the brain.<ref name="Davison2006"/>
The term "depression" was derived from the [[Latin]] "deprimere", meaning "to press down".<ref>depress. (n.d.). Online Etymology Dictionary. Retrieved June 30, 2008, from Dictionary.com website: http://dictionary.reference.com/browse/depress</ref> From the 14th century, "to depress" meant to subjugate or to bring down in spirits. An early published instance of a psychological usage of the noun was in 1665 in [[Richard Baker (chronicler)|Richard Baker's]] "Chronicle", referring to someone having "a great depression of spirit", and [[Samuel Johnson]] used the term in a similar sense in 1753.<ref>Wolpert, L. (2001) [http://www.nytimes.com/glogin?URI=http://www.nytimes.com/books/first/w/wolpert-sadness.html Malignant Sadness: The Anatomy of Depression.] Faber and Faber. New Edition, introduction. ISBN 0571207278</ref> The term also came in to use in [[depression (physiology)|physiology]] and [[depression (economics)|economics]]. One of the earliest uses to refer to a psychiatric symptom was by [[Louis Delasiauve]] in 1856; by the 1860s it was appearing in medical dictionaries to refer to a physiological and metaphorical lowering of emotional function.<ref>Berrios GE. (1988) Melancholia and depression during the 19th century: a conceptual history. Br J Psychiatry. Sep;153:298-304. PMID 3074848</ref> 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.<ref name="Radden2003">Jennifer Radden (2003) [http://muse.jhu.edu/journals/philosophy_psychiatry_and_psychology/v010/10.1radden01.html Is This Dame Melancholy?: Equating Today's Depression and Past Melancholia.] Philosophy, Psychiatry, & Psychology 10.1 (2003) 37-52</ref>
Although melancholia remained the dominant diagnostic term, "depression" gained increasing currency in medical treatises and by the end of the century it had become a synonym of melancholia; the German psychiatrist [[Emil Kraepelin]] (1855-1926) may have been the first to use it as the overarching term, referring to different kinds of melancholia as "depressive states".<ref name="Davison2006">Davison, K. (2006) [http://linkinghub.elsevier.com/retrieve/pii/S1476179306700246 Historical aspects of mood disorders.] Psychiatry, Vol 5, Issue 4, 1 April, P 115-118</ref> English psychiatrist [[Henry Maudsley]] proposed an overarching category of "affective disorder".<ref name="Lewis1934">Lewis, A.J. (1934) [http://bjp.rcpsych.org/cgi/content/citation/80/328/1 Melancholia: A Historical Review.] Journal of Mental Science.1934; 80: 1-42</ref>
===20th century-present===
[[Image:Emil Kraepelin.png|left|thumb|150px|[[Emil Kraepelin]] helped to distinguish [[mood disorder]]s from [[psychosis|psychoses]].]]
The influential system put forward by [[Emil Kraepelin]] unified nearly all types of mood disorder into "manic–depressive insanity", with a separate category of [[Dementia praecox]] ([[Schizophrenia]]). Kraepelin worked from an assumption of underlying brain pathology, but also promoted a distinction between [[endogenous]] and [[exogenous]] (which came to be known as "reactive") types.<ref name="Davison2006"/> [[Sigmund Freud]], on the other hand, emphasized early life experiences and conflicting psychological drives; he influentially associated melancholia with psychological loss and self-criticism.<ref name="Radden2003"/> In the United States, [[Adolf Meyer (psychiatrist)|Adolf 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".<ref name="Lewis1934"/> The 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, as well as including a depressive type of manic-depressive "psychosis" under "Major affective disorders".
In the mid-20th century, researchers theorized that clinical depression was a [[chemical imbalance theory|chemical imbalance]] in transmitters 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.<ref>{{cite journal | last = Schildkraut | first = J.J. |date=1965 | title = The catecholamine hypothesis of affective disorders: a review of supporting evidence | journal = Am J Psychiatry | volume = 122 | issue = 5 | pages = 509–22}}</ref> During the 1960s and 70s, manic-depression came to refer to just one type of mood disorder (now most commonly known as [[bipolar disorder]]) which was distinguished from (unipolar) depression. The terms unipolar and bipolar had been coined by [[Karl Kleist]].<ref name="Davison2006"/>
The term "Major depression" or depressive disorder was introduced by a group of US psychiatrists in the mid-70s as part of proposals for diagnostic criteria based on symptom lists (called the "Research Diagnostic Criteria", building on earlier [[Feighner Criteria]]), and was incorporated in to the DSM-III in 1980.<ref name="Philipp1991">Philipp M, Maier W, Delmo CD. (1991) [http://www.springerlink.com/content/y2460650rm747035/ The concept of major depression. I. Descriptive comparison of six competing operational definitions including ICD-10 and DSM-III-R.] Eur Arch Psychiatry Clin Neurosci. 240(4-5):258-65. PMID 1829000</ref> In order 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.<ref name="Philipp1991"/><ref>Gruenberg, A.M., Goldstein, R.D., Pincus, H.A. (2005) [http://media.wiley.com/product_data/excerpt/50/35273078/3527307850.pdf Classification of Depression: Research and Diagnostic Criteria:DSM-IV and ICD-10]</ref> The ancient idea of ''melancholia'' still survives in the notion of a "melancholic depression" subtype.
Subsequently, many causes for clinical depression have been proposed.<ref name="chem">Castren, E. (2005). Is Mood Chemistry? Nat Rev Neurosci, : p6(3):241-6 PMID 15738959.</ref> [[Biological psychiatry|Biological psychiatrists]], for example, explored the biological substrates of depression; psychiatrist [[David Healy (psychiatrist)|David Healy]] wrote about the growth of the diagnosis, along with perspectives on the development and promotion of antidepressants and the biological model since the late 1950s.<ref>[[David Healy (psychiatrist)|Healy, David]]. (1999). ''The Antidepressant Era'', Paperback Edition, Harvard University Press. ISBN 0-674-03958-0</ref>
==Sociocultural aspects==
There are cultural differences in the extent to which serious depression is considered an illness requiring personal professional treatment, or an indicator of the need to address social problems, structural determinants of powerlessness, and emotional struggle.<ref>Karasz A. (2005) Cultural differences in conceptual models of depression. Soc Sci Med. 2005 Apr;60(7):1625-35. PMID 15652693</ref><ref>Tilbury, F., Rapley, M. (2004) [http://www.atypon-link.com/EMP/doi/abs/10.5555/hesr.2004.13.1.54 'There are orphans in Africa still looking for my hands': African women refugees and the sources of emotional distress] Health Sociology Review. Vol 13, Issue 1, pp 54-64</ref> The diagnosis is less common in some countries, such as [[China]]. It has been argued that the Chinese traditionally deny or [[Somatization|somatize]] emotional depression, or alternatively that Western cultures reframe and elevate some expressions of human distress to disorder status.<ref>Parker G, Gladstone G, Chee KT. (2001) Depression in the planet's largest ethnic group: the Chinese. Am J Psychiatry. Jun;158(6):857-64. PMID 11384889</ref> The validity of the medical concept of depression has also been challenged from within the Western social sciences.<ref>Pilgrim D.; Bentall R. (1999) [http://www.ingentaconnect.com/content/apl/cjmh/1999/00000008/00000003/art00007 The medicalisation of misery: A critical realist analysis of the concept of depression] Journal of Mental Health, Volume 8, Number 3, 1 June, pp. 261-274(14)</ref>
[[Image:wm_james.jpg|right|thumb|150px|The influential psychologist [[William James]] was nearly driven to suicide during his depression. His choice to believe in [[free will]] was instrumental in helping him to overcome this condition.<ref name="James">{{cite book |author=James, Henry (Ed.) |title=Letters of William James (Vols. 1 and 2) |publisher=Atlantinc Monthly Press |location=Boston, MA, USA |year=1920 |pages= |isbn= |oclc= |doi= |accessdate=}}</ref>]]
Evolutionary theorists may view depression as an [[adaptation]] to regulate relationships or resources, although it may be unwanted or disordered in modern environments.<ref name="Klein07">Klein, J.M. (2007) [http://articles.latimes.com/2007/feb/12/health/he-evpsych12 The mind, as it evolves.] Los Angeles Times, Health, February 12.</ref> From an evolutionary perspective, depression can be seen 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."<ref>{{citation|title=Evolution, depression and counselling|journal=Counselling Psychology Quarterly|volume=Volume 18, Number 3|pages=215–222|url=http://www.ingentaconnect.com/content/routledg/ccpq/2005/00000018/00000003/art00005| date=September 2005|author=Tony J. Carey}}</ref> Like an ageing hunter in our foraging past, an alienated member of today's society may feel and act in ways that 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.<ref>{{cite journal | last = Mashman | first = RC | title = An evolutionary view of psychic misery | journal = Journal of Social Behaviour & Personality | volume = 12 | issue= | pages = 979–999 |date=1997 | url = | doi = }}</ref> These insights may be helpful in counselling therapy.<ref>{{citation|title=Evolution, depression and counselling|journal=Counselling Psychology Quarterly|volume= Volume 18, Number 3|pages=215–222|url=http://www.ingentaconnect.com/content/routledg/ccpq/2005/00000018/00000003/art00005| date=September 2005|author=Tony J. Carey}}</ref><ref>{{citation|title=Is depression good for you?|url=http://news.bbc.co.uk/1/hi/magazine/7268496.stm|date=Thursday, 28 February 2008|author=Tom Geoghegan}}</ref>
There is ongoing debate about the extent to which even serious depression may be linked to [[creativity]], [[depressive realism]], and [[moral]] struggle. Because of a lack of scientific certainty, the public debate often turns on questions of how depression is labeled (e.g., as "disorder" vs. "disease") or on political, religious and scientific leanings.<ref>Maloney, F. (2005) [http://www.slate.com/id/2129377/ The Depression Wars: Would Honest Abe have written the Gettysburg Address on Prozac?] Slate, Culturebox, Nov 3rd.</ref> The relationship between depression and creativity appears to be especially strong among female [[poet]]s.<ref>{{cite journal | last = Kaufman | first = JC | title = The Sylvia Plath effect: Mental illness in eminent creative writers | journal = Journal of Creative Behavior | volume = 35 | issue=1 | pages = 37–50 |date=2001 | url = | doi = }}</ref> Conversely, [[John Stuart Mill]] implicated poetry—namely that of [[William Wordsworth]]—in the ''curing'' of his depression, albeit in part because he could identify with a poet who "also had felt that the first freshness of youthful enjoyment of life was not lasting."<ref>http://www.gutenberg.org/files/10378/10378-8.txt</ref> Important to Mill was Wordsworth's ability to compensate for these feelings through "tranquil contemplation." English essayist and wit [[Samuel Johnson]] (1709 – 1784) coined the term "the black dog" to describe his own battles with depression.<ref>{{cite book |title=Oxford Concise Dictionary of Quotations, 5th Edition |publisher=Oxford University Press |year=2006 |isbn=13: 978-0-19-861417-3}}</ref> This phrase was subsequently popularised by former British Prime Minister Sir [[Winston Churchill]], who also faced depression.<ref> [http://www.biographybase.com/biography/Churchill_Winston_Spencer.html Churchill's Black Dog]</ref>
<!--Note: Reputable sources are needed for all new additions to this section, especially for living people. This section is not intended to grow into a long list; there is already a "List of people with depression" article-->
While depression was often stigmatized until recent decades, since then, society has begun discussing depression more openly. Earlier 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. Historical figures who may have had depression include the Dutch [[painter]] [[Vincent Van Gogh]];<ref> [http://www.philosophicalsociety.com/Archives/Philosophy%20And%20Depression.htm ety] Philosophical Society, USA, June 2005 </ref> British writer [[Henry James]];<ref>[http://psychology.about.com/od/profilesofmajorthinkers/p/jamesbio.htm William James - Biography of William James<!-- Bot generated title -->]</ref> American president [[Abraham Lincoln]]<ref> Burlingame, Michael : The inner world of Abraham Lincoln ISBN 0-252-06667-7 </ref>; German [[composer]] [[Robert Schumann]];<ref> [http://www.classicalarchives.com/bios/schumann_bio.html Schumann Biography]</ref> and German [[philosopher]] [[Friedrich Nietzsche]].<ref> [http://www.philosophicalsociety.com/Archives/Philosophy%20And%20Depression.htm Source] Philosophical Society, USA, June 2005 </ref> Some well-known people with depression from the contemporary era include American [[film director]] [[Woody Allen]];<ref> {{cite news | url= http://news.bbc.co.uk/2/hi/entertainment/4539493.stm | title= Allen uses films to avoid anxiety | work=[[BBC]] | date=[[12 May]] [[2005]] | accessdate= 2006-11-06}}</ref> <ref> [http://www.biogs.com/famous/allenwoody.html Woody Allen] biogs.com </ref> Canadian [[songwriter]] [[Leonard Cohen]];<ref> Pita, Elena [http://www.webheights.net/10newsongs/press/elmunmag.htm An Intimate Conversation with...Leonard Cohen], El Mundo September 26, 2001 (translated from Spanish)</ref> British [[music]]ian [[Nick Drake]];<ref> [http://www.nickdrake.com/nick_life_in_quotes.html www.nickdrake.com Nick Drake]</ref> American poet [[T. S. Eliot]];<ref> [http://www.philosophicalsociety.com/Archives/Philosophy%20And%20Depression.htm ety] Philosophical Society, USA, June 2005 </ref> American writer [[Ernest Hemingway]];<ref>[http://www.philosophicalsociety.com/Archives/Philosophy%20And%20Depression.htm ety] Philosophical Society, USA, June 2005</ref> and American playwright and novelist [[Tennessee Williams]].<ref>Jeste ND, Palmer BW, Jeste DV. Tennessee Williams. Am J Geriatr Psychiatry. 2004 Jul-Aug;12(4):370-5. PMID: 15249274 [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=search&term=15249274]</ref> Even some pioneering psychologists, such as [[William James]]<ref name="James">{{cite book |author=James, Henry (Ed.) |title=Letters of William James (Vols. 1 and 2) |publisher=Atlantinc Monthly Press |location=Boston, MA, USA |year=1920 |pages= |isbn= |oclc= |doi= |accessdate=}}</ref> and [[John B. Watson]],<ref name="Cohen">{{cite book |author=Cohen, David |title=J. B. Watson: The Founder of Behaviourism |publisher=Routledge & Kegan Paul |location=London, UK |year=1979 |pages= |isbn= |oclc= |doi= |accessdate=}}</ref> dealt with depression in their adulthoods. For more information on historical and contemporary public figures who faced depression, see the ''[[List of people with depression]]''.
==References==
<!-- Dead note "oldref_4": {{cite journal | url = http://jama.ama-assn.org/cgi/content/full/289/23/3152 | last = Keller | first = M.B. | date = 2003 | title = Past, Present, and Future Directions for Defining Optimal Treatment Outcome in Depression | journal = JAMA | volume = 289 | pages = 3152?3160 | doi = 10.1001/jama.289.23.3152 | pmid = 12813121 }} -->
{{reflist|2}}
==See also==
* [[Obsessive-compulsive_disorder]]
* [[Social Anxiety]]
==External links==
* [http://www.mindsite.com/dsm_iv/major_depressive_disorder DSM-IV Diagnostic Criteria for Major Depressive Disorder] - DSM-IV-TR text from mindsite.com
* [http://www.blackdoginstitute.org.au/ Black Dog Institute] – Depression and Bipolar Disorder Information Australia
* {{dmoz|Health/Mental_Health/Disorders/Mood/Depression|Depression}}
* [http://www.nami.org National Alliance on Mental Illness] – Depression support, advocacy, and education
* [http://www.ndmda.org National Depressive and Manic Depressive Association] - National Depressive and Manic Depressive Association
{{Mental and behavioural disorders}}
[[Category:Medical emergencies]]
[[Category:Mood disorders]]
[[Category:Abnormal psychology]]
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