Major depressive disorder

For other types of depression, seeMood disorder.

Not to be confused withDepression (mood).

Major depressive disorder
Other names	Clinical depression, major depression, unipolar depression, unipolar disorder, recurrent depression
Sorrowing Old Man (At Eternity's Gate),an 1890 portrait byVincent van Gogh
Specialty	Psychiatry,clinical psychology
Symptoms	Low mood,lowself-esteem,loss of interestin normally enjoyable activities,low energy,painwithout a clear cause,disturbed sleep pattern (insomniaorhypersomnia)
Complications	Self-harm,suicide
Usual onset	Age 20s
Duration	> 2 weeks
Causes	Environmental (e.g.adverse life experiences),genetic predisposition,psychological factors such asstress
Risk factors	Family history,major life changes, certainmedications,chronic health problems,substance use disorder
Differential diagnosis	Bipolar disorder,ADHD,sadness
Treatment	Psychotherapy,antidepressant medication,electroconvulsive therapy,transcranial magnetic stimulation,exercise
Medication	Antidepressants
Frequency	163 million (2017)

Major depressive disorder(MDD), also known asclinical depression,is amental disordercharacterized by at least two weeks of pervasivelow mood,lowself-esteem,andloss of interest or pleasurein normally enjoyable activities.Introduced by a group of US clinicians in the mid-1970s,the term was adopted by theAmerican Psychiatric Associationfor thissymptom clusterundermood disordersin the 1980 version of theDiagnostic and Statistical Manual of Mental Disorders(DSM-III), and has become widely used since. The disorder causes the second-mostyears lived with disability,afterlower back pain.

The diagnosis of major depressive disorder is based on the person's reported experiences, behavior reported by relatives or friends, and amental status examination.There is no laboratory test for the disorder, but testing may be done to rule out physical conditions that can cause similar symptoms.The most common time of onset is in a person's 20s,with females affected about twice as often as males.The course of the disorder varies widely, from one episode lasting months to a lifelong disorder with recurrentmajor depressive episodes.

Those with major depressive disorder are typically treated withpsychotherapyandantidepressant medication.Medication appears to be effective, but the effect may be significant only in the most severely depressed.Hospitalization (which may beinvoluntary) may be necessary in cases with associatedself-neglector a significant risk of harm to self or others.Electroconvulsive therapy(ECT) may be considered if other measures are not effective.

Major depressive disorder is believed to be caused by a combination ofgenetic,environmental, and psychological factors,with about 40% of the risk being genetic.Risk factors include afamily historyof the condition, major life changes, childhood traumas, certain medications,chronic health problems,andsubstance use disorders.It can negatively affect a person's personal life, work life, or education, and cause issues with a person's sleeping habits, eating habits, and general health.

Symptoms and signs

See also:Digital media use and mental health § Depression

An 1892lithographof a woman diagnosed withmelancholia

A person having amajor depressive episodeusually exhibits a low mood, which pervades all aspects of life, and an inability to experience pleasure in previously enjoyable activities.Depressed people may be preoccupied with orruminateover thoughts and feelings of worthlessness, inappropriate guilt or regret, helplessness or hopelessness.

Other symptoms of depression include poor concentration and memory,withdrawal from social situations and activities, reducedsex drive,irritability, and thoughts of death or suicide.Insomniais common; in the typical pattern, a person wakes very early and cannot get back to sleep.Hypersomnia,or oversleeping, can also happen,as well as day-night rhythm disturbances, such asdiurnal mood variation.Some antidepressants may also cause insomnia due to their stimulating effect.In severe cases, depressed people may havepsychoticsymptoms. These symptoms includedelusionsor, less commonly,hallucinations,usually unpleasant.People who have had previous episodes with psychotic symptoms are more likely to have them with future episodes.

A depressed person may report multiple physical symptoms such asfatigue,headaches, or digestive problems; physical complaints are the most common presenting problem in developing countries, according to theWorld Health Organization's criteria for depression.Appetiteoften decreases, resulting in weight loss, although increased appetite and weight gain occasionally occur.

Major depression significantly affects a person's family andpersonal relationships,work or school life, sleeping and eating habits, and general health.Family and friends may noticeagitationorlethargy.Older depressed people may havecognitivesymptoms of recent onset, such as forgetfulness,and a more noticeable slowing of movements.

Depressed children may often display an irritable rather than a depressed mood;most lose interest in school and show a steep decline in academic performance.Diagnosis may be delayed or missed when symptoms are interpreted as "normal moodiness".Elderly people may not present with classical depressive symptoms.Diagnosis and treatment is further complicated in that the elderly are often simultaneously treated with a number of other drugs, and often have other concurrent diseases.

Cause

Further information:Biology of depressionandEpigenetics of depression

A cup analogy demonstrating thediathesis–stress modelthat under the same amount of stressors, person 2 is more vulnerable than person 1, because of their predisposition

The etiology of depression is not yet fully understood.Thebiopsychosocial modelproposes that biological, psychological, and social factors all play a role in causing depression.Thediathesis–stress modelspecifies that depression results when a preexisting vulnerability, ordiathesis,is activated by stressful life events. The preexisting vulnerability can be eithergenetic,implying an interaction betweennature and nurture,orschematic,resulting from views of the world learned in childhood.American psychiatristAaron Becksuggested that atriadof automatic and spontaneous negative thoughts about theself,theworld or environment,and the future may lead to other depressive signs and symptoms.

Genetics

Genes play a major role in the development of depression.Family and twin studiesfind that nearly 40% of individual differences in risk for major depressive disorder can beexplained by genetic factors.Like most psychiatric disorders, major depressive disorder is likely influenced by many individual genetic changes.In 2018, agenome-wide association studydiscovered 44 genetic variants linked to risk for major depression;a 2019 study found 102 variants in the genome linked to depression.However, it appears that major depression is less heritable compared to bipolar disorder and schizophrenia.Research focusing on specific candidate genes has been criticized for its tendency to generate false positive findings.There are also other efforts to examine interactions between life stress and polygenic risk for depression.

Other health problems

Depression can also arise after a chronic or terminal medical condition, such asHIV/AIDSorasthma,and may be labeled "secondary depression".It is unknown whether the underlying diseases induce depression through effect on quality of life, or through shared etiologies (such as degeneration of thebasal gangliainParkinson's diseaseor immune dysregulation in asthma).Depression may also beiatrogenic(the result of healthcare), such as drug-induced depression. Therapies associated with depression includeinterferons,beta-blockers,isotretinoin,contraceptives,cardiac agents,anticonvulsants,antimigraine drugs,antipsychotics,andhormonal agentssuch asgonadotropin-releasing hormone agonist(GnRH agonist).Celiac diseaseis another possible contributing factor.

Substance use in early age is associated with increased risk of developing depression later in life.Depression occurring after giving birth is calledpostpartum depressionand is thought to be the result of hormonal changes associated withpregnancy.Seasonal affective disorder,a type of depression associated with seasonal changes in sunlight, is thought to be triggered by decreased sunlight. Vitamin B₂,B₆and B₁₂deficiency may cause depression in females.

Environmental

Adverse childhood experiences(incorporatingchildhood abuse,neglect andfamily dysfunction) markedly increase the risk of major depression, especially if more than one type.Childhood trauma also correlates with severity of depression, poor responsiveness to treatment and length of illness. Some are more susceptible than others to developing mental illness such as depression after trauma, and various genes have been suggested to control susceptibility.Couples in unhappy marriages have a higher risk of developing clinical depression.

There appears to be a link betweenair pollutionand depression and suicide. There may be an association between long-termPM2.5exposure and depression, and a possible association between short-termPM10exposure and suicide.

Pathophysiology

Further information:Biology of depressionandEpigenetics of depression

The pathophysiology of depression is not completely understood, but current theories center aroundmonoaminergicsystems, thecircadian rhythm,immunological dysfunction,HPA-axisdysfunction and structural or functional abnormalities of emotional circuits.

Derived from the effectiveness of monoaminergic drugs in treating depression, the monoamine theory posits that insufficient activity ofmonoamine neurotransmittersis the primary cause of depression. Evidence for the monoamine theory comes from multiple areas. First, acute depletion oftryptophan—a necessary precursor ofserotoninand a monoamine—can cause depression in those in remission or relatives of people who are depressed, suggesting that decreased serotonergic neurotransmission is important in depression.Second, the correlation between depression risk and polymorphisms in the5-HTTLPRgene, which codes for serotonin receptors, suggests a link. Third, decreased size of thelocus coeruleus,decreased activity oftyrosine hydroxylase,increased density ofAlpha -2 adrenergic receptor,and evidence from rat models suggest decreasedadrenergicneurotransmission in depression.Furthermore, decreased levels ofhomovanillic acid,altered response todextroamphetamine,responses of depressive symptoms todopamine receptoragonists, decreaseddopamine receptor D1binding in thestriatum,andpolymorphismofdopamine receptorgenes implicatedopamine,another monoamine, in depression.Lastly, increased activity ofmonoamine oxidase,which degrades monoamines, has been associated with depression.However, the monoamine theory is inconsistent with observations that serotonin depletion does not cause depression in healthy persons, that antidepressants instantly increase levels of monoamines but take weeks to work, and the existence of atypical antidepressants which can be effective despite not targeting this pathway.

One proposed explanation for the therapeutic lag, and further support for the deficiency of monoamines, is a desensitization of self-inhibition inraphe nucleiby the increased serotonin mediated by antidepressants.However, disinhibition of the dorsal raphe has been proposed to occur as a result ofdecreasedserotonergic activity in tryptophan depletion, resulting in a depressed state mediated by increased serotonin. Further countering the monoamine hypothesis is the fact that rats with lesions of the dorsal raphe are not more depressive than controls, the finding of increased jugular5-HIAAin people who are depressed that normalized withselective serotonin reuptake inhibitor(SSRI) treatment, and the preference forcarbohydratesin people who are depressed.Already limited, the monoamine hypothesis has been further oversimplified when presented to the general public.A 2022 review found no consistent evidence supporting the serotonin hypothesis, linking serotonin levels and depression.

HPA-axisabnormalities have been suggested in depression given the association ofCRHR1with depression and the increased frequency ofdexamethasone testnon-suppression in people who are depressed. However, this abnormality is not adequate as a diagnosis tool, because its sensitivity is only 44%.These stress-related abnormalities are thought to be the cause of hippocampal volume reductions seen in people who are depressed.Furthermore, ameta-analysisyielded decreased dexamethasone suppression, and increased response to psychological stressors.Further abnormal results have been obscured with thecortisol awakening response,with increased response being associated with depression.

There is also a connection between the gut microbiome and the central nervous system, otherwise known as theGut-Brain axis,which is a two-way communication system between the brain and the gut. Experiments have shown thatmicrobiotain the gut can play an important role in depression as people with MDD often have gut-brain dysfunction. One analysis showed that those with MDD have different bacteria living in their guts. BacteriaBacteroidetesandFirmicuteswere most affected in people with MDD, and they are also impacted in people with Irritable Bowel Syndrome.Another study showed that people with IBS have a higher chance of developing depression, which shows the two are connected.There is even evidence suggesting that altering the microbes in the gut can have regulatory effects on developing depression.

Theories unifyingneuroimagingfindings have been proposed. The first model proposed is the limbic-cortical model, which involves hyperactivity of the ventral paralimbic regions and hypoactivity of frontal regulatory regions in emotional processing.Another model, the cortico-striatal model, suggests that abnormalities of theprefrontal cortexin regulating striatal and subcortical structures result in depression.Another model proposes hyperactivity ofsalience structuresin identifying negative stimuli, and hypoactivity of cortical regulatory structures resulting in a negativeemotional biasand depression, consistent with emotional bias studies.

Immune Pathogenesis Theories on Depression

The newer field ofpsychoneuroimmunology,the study between the immune system and the nervous system and emotional state, suggests that cytokines may impact depression.

Immune system abnormalitieshave been observed, including increased levels ofcytokines-cells produced by immune cells that affect inflammation- involved in generatingsickness behavior,creating a pro-inflammatory profile in MDD.Some people with depression have increased levels of pro-inflammatory cytokines and some have decreased levels of anti-inflammatory cytokines.Research suggests that treatments can reduce pro-inflammatory cell production, like the experimental treatment of ketamine with treatment-resistant depression.With this, in MDD, people will more likely have a Th-1 dominant immune profile, which is a pro-inflammatory profile. This suggests that there are components of the immune system affecting the pathology of MDD.

Another waycytokinescan affect depression is in thekynurenine pathway,and when this is overactivated, it can cause depression. This can be due to too muchmicroglialactivation and too littleastrocyticactivity. When microglia get activated, they release pro-inflammatory cytokines that cause an increase in the production ofCOX₂.This, in turn, causes the production ofPGE₂,which is aprostaglandin,and this catalyzes the production ofindolamine,IDO. IDO causestryptophanto get converted intokynurenineand kynurenine becomesquinolinic acid.Quinolinic acid is an agonist forNMDAreceptors, so it activates the pathway. Studies have shown that the post-mortem brains of patients with MDD have higher levels of quinolinic acid than people who did not have MDD. With this, researchers have also seen that the concentration of quinolinic acid correlates to the severity of depressive symptoms.

Diagnosis

Assessment

Further information:Rating scales for depression

Caricature of a man with depression

A diagnostic assessment may be conducted by a suitably trainedgeneral practitioner,or by apsychiatristorpsychologist,whorecordsthe person's current circumstances, biographical history, current symptoms, family history, and alcohol and drug use. The assessment also includes amental state examination,which is an assessment of the person's current mood and thought content, in particular the presence of themes of hopelessness orpessimism,self-harmor suicide, and an absence of positive thoughts or plans.Specialist mental health services are rare in rural areas, and thus diagnosis and management is left largely toprimary-careclinicians.This issue is even more marked in developing countries.Rating scalesare not used to diagnose depression, but they provide an indication of the severity of symptoms for a time period, so a person who scores above a given cut-off point can be more thoroughly evaluated for a depressive disorder diagnosis. Several rating scales are used for this purpose;these include theHamilton Rating Scale for Depression,theBeck Depression Inventoryor theSuicide Behaviors Questionnaire-Revised.

Primary-care physicianshave more difficulty with underrecognition and undertreatment of depression compared to psychiatrists. These cases may be missed because for some people with depression,physical symptomsoften accompany depression. In addition, there may also be barriers related to the person, provider, and/or the medical system. Non-psychiatrist physicians have been shown to miss about two-thirds of cases, although there is some evidence of improvement in the number of missed cases.

A doctor generally performs a medical examination and selected investigations to rule out other causes of depressive symptoms. These include blood tests measuringTSHandthyroxineto excludehypothyroidism;basic electrolytesand serumcalciumto rule out ametabolic disturbance;and afull blood countincludingESRto rule out asystemic infectionor chronic disease.Adverse affective reactions to medications or alcohol misuse may be ruled out, as well.Testosteronelevels may be evaluated to diagnosehypogonadism,a cause of depression in men.Vitamin Dlevels might be evaluated, as low levels of vitamin D have been associated with greater risk for depression.Subjective cognitive complaints appear in older depressed people, but they can also be indicative of the onset of adementing disorder,such asAlzheimer's disease.Cognitive testingand brain imaging can help distinguish depression from dementia.ACT scancan exclude brain pathology in those with psychotic, rapid-onset or otherwise unusual symptoms.No biological tests confirm major depression.In general, investigations are not repeated for a subsequent episode unless there is a medicalindication.

DSM and ICD criteria

The most widely used criteria for diagnosing depressive conditions are found in theAmerican Psychiatric Association'sDiagnostic and Statistical Manual of Mental Disorders(DSM) and theWorld Health Organization'sInternational Statistical Classification of Diseases and Related Health Problems(ICD). The latter system is typically used in European countries, while the former is used in the US and many other non-European nations,and the authors of both have worked towards conforming one with the other.Both DSM and ICD mark out typical (main) depressive symptoms.The most recent edition of the DSM is the Fifth Edition, Text Revision (DSM-5-TR),and the most recent edition of the ICD is the Eleventh Edition (ICD-11).

Under mood disorders, ICD-11 classifies major depressive disorder as eithersingle episode depressive disorder(where there is no history of depressive episodes, or ofmania) orrecurrent depressive disorder(where there is a history of prior episodes, with no history of mania).ICD-11 symptoms, present nearly every day for at least two weeks, are a depressed mood oranhedonia,accompanied by other symptoms such as "difficulty concentrating, feelings of worthlessness or excessive or inappropriate guilt, hopelessness, recurrent thoughts of death or suicide, changes in appetite or sleep, psychomotor agitation or retardation, and reduced energy or fatigue."These symptoms must affect work, social, or domestic activities. The ICD-11 system allows further specifiers for the current depressive episode: the severity (mild, moderate, severe, unspecified); the presence of psychotic symptoms (with or without psychotic symptoms); and the degree of remission if relevant (currently in partial remission, currently in full remission).These two disorders are classified as "Depressive disorders", in the category of "Mood disorders".

According to DSM-5, at least one of the symptoms is either depressed mood or loss of interest or pleasure. Depressed mood occurs nearly every day as subjective feelings like sadness, emptiness, and hopelessness or observations made by others (e.g. appears tearful). Loss of interest or pleasure occurs in all, or almost all activities of the day, nearly every day. These symptoms, as well as five out of the nine more specific symptoms listed, must frequently occur for more than two weeks (to the extent in which it impairs functioning) for the diagnosis.Major depressive disorder is classified as a mood disorder in the DSM-5.The diagnosis hinges on the presence of single or recurrentmajor depressive episodes.Further qualifiers are used to classify both the episode itself and the course of the disorder. The categoryUnspecified Depressive Disorderis diagnosed if the depressive episode's manifestation does not meet the criteria for a major depressive episode.

Major depressive episode

Main article:Major depressive episode

A major depressive episode is characterized by the presence of a severely depressed mood that persists for at least two weeks.Episodes may be isolated or recurrent and are categorized as mild (few symptoms in excess of minimum criteria), moderate, or severe (marked impact on social or occupational functioning). An episode with psychotic features—commonly referred to aspsychotic depression—is automatically rated as severe.If the person has had an episode ofmaniaormarkedly elevated mood,a diagnosis ofbipolar disorderis made instead. Depression without mania is sometimes referred to asunipolarbecause the mood remains at one emotional state or "pole".

Bereavementis not an exclusion criterion in the DSM-5, and it is up to the clinician to distinguish between normal reactions to a loss and MDD. Excluded are a range of related diagnoses, includingdysthymia,which involves a chronic but milder mood disturbance;recurrent brief depression,consisting of briefer depressive episodes;minor depressive disorder,whereby only some symptoms of major depression are present;andadjustment disorder with depressed mood,which denotes low mood resulting from a psychological response to an identifiable event orstressor.

Subtypes

The DSM-5 recognizes six further subtypes of MDD, calledspecifiers,in addition to noting the length, severity and presence of psychotic features:

• "Melancholic depression"is characterized by a loss of pleasure in most or all activities, a failure of reactivity to pleasurable stimuli, a quality of depressed mood more pronounced than that ofgriefor loss, a worsening of symptoms in the morning hours, early-morning waking,psychomotor retardation,excessive weight loss (not to be confused withanorexia nervosa), or excessive guilt.
• "Atypical depression"is characterized by mood reactivity (paradoxical anhedonia) and positivity, significantweight gainor increased appetite (comfort eating), excessive sleep or sleepiness (hypersomnia), a sensation of heaviness in limbs known as leaden paralysis, and significant long-term social impairment as a consequence of hypersensitivity to perceivedinterpersonal rejection.
• "Catatonic depression"is a rare and severe form of major depression involving disturbances of motor behavior and other symptoms. Here, the person is mute and almost stuporous, and either remains immobile or exhibits purposeless or even bizarre movements. Catatonic symptoms also occur inschizophreniaor in manic episodes, or may be caused byneuroleptic malignant syndrome.
• "Depression withanxiousdistress "was added into the DSM-5 as a means to emphasize the common co-occurrence between depression ormaniaand anxiety, as well as the risk of suicide of depressed individuals with anxiety. Specifying in such a way can also help with the prognosis of those diagnosed with a depressive or bipolar disorder.
• "psychotic depression"is a severe subtype of depression
• "Depression withperi-partumonset "refers to the intense, sustained and sometimes disabling depression experienced by women after giving birth or while a woman is pregnant. DSM-IV-TR used the classification" postpartum depression ", but this was changed to not exclude cases of depressed woman during pregnancy. Depression with peripartum onset has an incidence rate of 3–6% among new mothers. The DSM-5 mandates that to qualify as depression with peripartum onset, onset occurs during pregnancy or within one month of delivery.
• "Seasonal affective disorder"(SAD) is a form of depression in which depressive episodes come on in the autumn or winter, and resolve in spring. The diagnosis is made if at least two episodes have occurred in colder months with none at other times, over a two-year period or longer.

Differential diagnoses

Main article:Differential diagnoses of depression

To confirm major depressive disorder as the most likely diagnosis, otherpotential diagnosesmust be considered, includingdysthymia,adjustment disorderwith depressed mood, orbipolar disorder.Dysthymia is a chronic, milder mood disturbance in which a person reports a low mood almost daily over a span of at least two years. The symptoms are not as severe as those for major depression, although people with dysthymia are vulnerable to secondary episodes of major depression (sometimes referred to asdouble depression).Adjustment disorder with depressed moodis a mood disturbance appearing as a psychological response to an identifiable event or stressor, in which the resulting emotional or behavioral symptoms are significant but do not meet the criteria for a major depressive episode.

Other disorders need to be ruled out before diagnosing major depressive disorder. They include depressions due to physical illness,medications,andsubstance use disorders.Depression due to physical illness is diagnosed as amood disorder due to a general medical condition.This condition is determined based on history, laboratory findings, orphysical examination.When the depression is caused by a medication, non-medical use of a psychoactive substance, or exposure to atoxin,it is then diagnosed as a specific mood disorder (previously calledsubstance-induced mood disorder).

Screening and prevention

Preventive efforts may result in decreases in rates of the condition of between 22 and 38%.Since 2016, theUnited States Preventive Services Task Force(USPSTF) has recommended screening for depression among those over the age 12;though a 2005Cochrane reviewfound that the routine use of screening questionnaires has little effect on detection or treatment.Screening the general population is not recommended by authorities in the UK or Canada.

Behavioral interventions, such asinterpersonal therapyandcognitive-behavioral therapy,are effective at preventing new onset depression.Because such interventions appear to be most effective when delivered to individuals or small groups, it has been suggested that they may be able to reach their large target audience most efficiently through theInternet.

The Netherlands mental health care system provides preventive interventions, such as the "Coping with Depression" course (CWD) for people with sub-threshold depression. The course is claimed to be the most successful of psychoeducational interventions for the treatment and prevention of depression (both for its adaptability to various populations and its results), with a risk reduction of 38% in major depression and an efficacy as a treatment comparing favorably to other psychotherapies.

Management

Main article:Management of depression

The most common and effective treatments for depression are psychotherapy, medication, and electroconvulsive therapy (ECT); a combination of treatments is the most effective approach when depression is resistant to treatment.American Psychiatric Associationtreatment guidelines recommend that initial treatment should be individually tailored based on factors including severity of symptoms, co-existing disorders, prior treatment experience, and personal preference. Options may include pharmacotherapy, psychotherapy, exercise, ECT,transcranial magnetic stimulation(TMS) orlight therapy.Antidepressantmedication is recommended as an initial treatment choice in people with mild, moderate, or severe major depression, and should be given to all people with severe depression unless ECT is planned.There is evidence that collaborative care by a team of health care practitioners produces better results than routine single-practitioner care.

Psychotherapy is the treatment of choice (over medication) for people under 18,andcognitive behavioral therapy(CBT), third wave CBT andinterpersonal therapymay help prevent depression.The UKNational Institute for Health and Care Excellence(NICE) 2004 guidelines indicate that antidepressants should not be used for the initial treatment of mild depression because therisk-benefit ratiois poor. The guidelines recommend that antidepressants treatment in combination with psychosocial interventions should be considered for:

• People with a history of moderate or severe depression
• Those with mild depression that has been present for a long period
• As a second line treatment for mild depression that persists after other interventions
• As a first line treatment for moderate or severe depression.

The guidelines further note thatantidepressanttreatment should be continued for at least six months to reduce the risk ofrelapse,and thatSSRIsare better tolerated thantricyclic antidepressants.

Treatment options are more limited in developing countries, where access to mental health staff, medication, and psychotherapy is often difficult. Development of mental health services is minimal in many countries; depression is viewed as a phenomenon of the developed world despite evidence to the contrary, and not as an inherently life-threatening condition.There is insufficient evidence to determine the effectiveness of psychological versus medical therapy in children.

Lifestyle

Further information:Neurobiological effects of physical exercise § Major depressive disorder

Physical exercise is one recommended way to manage mild depression.

Physical exercisehas been found to be effective for major depression, and may be recommended to people who are willing, motivated, and healthy enough to participate in an exercise program as treatment.It is equivalent to the use of medications or psychological therapies in most people.In older people it does appear to decrease depression.Sleep and diet may also play a role in depression, and interventions in these areas may be an effective add-on to conventional methods.In observational studies,smoking cessationhas benefits in depression as large as or larger than those of medications.

Talking therapies

See also:Behavioral theories of depression

Talking therapy(psychotherapy) can be delivered to individuals, groups, or families by mental health professionals, including psychotherapists, psychiatrists, psychologists, clinicalsocial workers,counselors, and psychiatric nurses. A 2012 review found psychotherapy to be better than no treatment but not other treatments.With more complex and chronic forms of depression, a combination of medication and psychotherapy may be used.There is moderate-quality evidence that psychological therapies are a useful addition to standard antidepressant treatment oftreatment-resistant depressionin the short term.Psychotherapy has been shown to be effective in older people.Successful psychotherapy appears to reduce the recurrence of depression even after it has been stopped or replaced by occasional booster sessions.

The most-studied form of psychotherapy for depression is CBT, which teaches clients to challenge self-defeating, but enduring ways of thinking (cognitions) and change counter-productive behaviors. CBT can perform as well as antidepressants in people with major depression.CBT has the most research evidence for the treatment of depression in children and adolescents, and CBT and interpersonal psychotherapy (IPT) are preferred therapies for adolescent depression.In people under 18, according to theNational Institute for Health and Clinical Excellence,medication should be offered only in conjunction with a psychological therapy, such asCBT,interpersonal therapy,orfamily therapy.Several variables predict success for cognitive behavioral therapy in adolescents: higher levels of rational thoughts, less hopelessness, fewer negative thoughts, and fewer cognitive distortions.CBT is particularly beneficial in preventing relapse.Cognitive behavioral therapy and occupational programs (including modification of work activities and assistance) have been shown to be effective in reducing sick days taken by workers with depression.Several variants of cognitive behavior therapy have been used in those with depression, the most notable beingrational emotive behavior therapy,andmindfulness-based cognitive therapy.Mindfulness-based stress reduction programs may reduce depression symptoms.Mindfulness programs also appear to be a promising intervention in youth.Problem solving therapy,cognitive behavioral therapy, and interpersonal therapy are effective interventions in the elderly.

Psychoanalysisis a school of thought, founded bySigmund Freud,which emphasizes the resolution ofunconsciousmental conflicts.Psychoanalytic techniques are used by some practitioners to treat clients presenting with major depression.A more widely practiced therapy, calledpsychodynamic psychotherapy,is in the tradition of psychoanalysis but less intensive, meeting once or twice a week. It also tends to focus more on the person's immediate problems, and has an additional social and interpersonal focus.In a meta-analysis of three controlled trials of Short Psychodynamic Supportive Psychotherapy, this modification was found to be as effective as medication for mild to moderate depression.

Antidepressants

Sertraline(Zoloft) is used primarily to treat major depression in adults.

Conflicting results have arisen from studies that look at the effectiveness of antidepressants in people with acute, mild to moderate depression.A review commissioned by theNational Institute for Health and Care Excellence(UK) concluded that there is strong evidence thatSSRIs,such asescitalopram,paroxetine,andsertraline,have greater efficacy thanplaceboon achieving a 50% reduction in depression scores in moderate and severe major depression, and that there is some evidence for a similar effect in mild depression.Similarly, a Cochrane systematic review of clinical trials of the generictricyclic antidepressantamitriptylineconcluded that there is strong evidence that its efficacy is superior to placebo.Antidepressants work less well for the elderly than for younger individuals with depression.

To find the most effective antidepressant medication with minimal side-effects, the dosages can be adjusted, and if necessary, combinations of different classes of antidepressants can be tried. Response rates to the first antidepressant administered range from 50 to 75%, and it can take at least six to eight weeks from the start of medication to improvement.Antidepressant medication treatment is usually continued for 16 to 20 weeks after remission, to minimize the chance of recurrence,and even up to one year of continuation is recommended.People with chronic depression may need to take medication indefinitely to avoid relapse.

SSRIsare the primary medications prescribed, owing to their relatively mild side-effects, and because they are less toxic in overdose than other antidepressants.People who do not respond to one SSRI can be switched toanother antidepressant,and this results in improvement in almost 50% of cases.Another option is to augment the atypical antidepressantbupropionto the SSRI as an adjunctive treatment.Venlafaxine,an antidepressant with a different mechanism of action, may be modestly more effective than SSRIs.However, venlafaxine is not recommended in the UK as a first-line treatment because of evidence suggesting its risks may outweigh benefits,and it is specifically discouraged in children and adolescents as it increases the risk of suicidal thoughts or attempts.

For children and adolescents with moderate-to-severe depressive disorder,fluoxetineseems to be the best treatment (either with or withoutcognitive behavioural therapy) but more research is needed to be certain.Sertraline,escitalopram,duloxetinemight also help in reducing symptoms. Some antidepressants have not been shown to be effective.Medications are not recommended in children with mild disease.

There is also insufficient evidence to determine effectiveness in those with depression complicated bydementia.Any antidepressant can causelow blood sodiumlevels;nevertheless, it has been reported more often with SSRIs.It is not uncommon for SSRIs to cause or worsen insomnia; the sedatingatypical antidepressantmirtazapinecan be used in such cases.

Irreversiblemonoamine oxidase inhibitors,an older class of antidepressants, have been plagued by potentially life-threatening dietary and drug interactions. They are still used only rarely, although newer and better-tolerated agents of this class have been developed.The safety profile is different with reversible monoamine oxidase inhibitors, such asmoclobemide,where the risk of serious dietary interactions is negligible and dietary restrictions are less strict.

It is unclear whether antidepressants affect a person's risk of suicide.For children, adolescents, and probably young adults between 18 and 24 years old, there is a higher risk of bothsuicidal ideationsandsuicidal behaviorin those treated with SSRIs.For adults, it is unclear whether SSRIs affect the risk of suicidality. One review found no connection;another an increased risk;and a third no risk in those 25–65 years old and a decreased risk in those more than 65.Ablack box warningwas introduced in the United States in 2007 on SSRIs and other antidepressant medications due to the increased risk of suicide in people younger than 24 years old.Similar precautionary notice revisions were implemented by the Japanese Ministry of Health.

Other medications and supplements

The combined use of antidepressants plusbenzodiazepinesdemonstrates improved effectiveness when compared to antidepressants alone, but these effects may not endure. The addition of a benzodiazepine is balanced against possible harms and other alternative treatment strategies when antidepressant mono-therapy is considered inadequate.

For treatment-resistant depression, adding on theatypical antipsychoticbrexpiprazolefor short-term or acute management may be considered.Brexpiprazole may be effective for some people, however, the evidence as of 2023 supporting its use is weak and this medication has potential adverse effects including weight gain andakathisia.Brexpiprazole has not been sufficiently studied in older people or children and the use and effectiveness of thisadjunctivetherapy for longer term management is not clear.

Ketaminemay have a rapid antidepressant effect lasting less than two weeks; there is limited evidence of any effect after that, common acute side effects, and longer-term studies of safety and adverse effects are needed.A nasal spray form ofesketaminewas approved by the FDA in March 2019 for use in treatment-resistant depression when combined with an oral antidepressant; risk of substance use disorder and concerns about its safety, serious adverse effects, tolerability, effect on suicidality, lack of information about dosage, whether the studies on it adequately represent broad populations, and escalating use of the product have been raised by an international panel of experts.

Nonsteroidal anti-inflammatory drugs(NSAIDs) and cytokine inhibitors are effective in treating depression. For instance,Celecoxib,an NSAID, is a selective COX-2 inhibitor– which is an enzyme that helps in the production of pain and inflammation.In recent clinical trials, this NSAID has been shown helpful with treatment-resistant depression as it helps inhibit proinflammatory signaling.

Statins,which are anti-inflammatory medications prescribed to lower cholesterol levels, have also been shown to have antidepressant effects. When prescribed for patients already taking SSRIs, this add-on treatment was shown to improve anti-depressant effects of SSRIs when compared to the placebo group. With this, statins have been shown to be effective in preventing depression in some cases too.

There is insufficient high quality evidence to suggestOmega -3 fatty acidsare effective in depression.There is limited evidence that vitamin D supplementation is of value in alleviating the symptoms of depression in individuals who are vitamin D-deficient.Lithiumappears effective at lowering the risk of suicide in those with bipolar disorder and unipolar depression to nearly the same levels as the general population.There is a narrow range of effective and safe dosages of lithium thus close monitoring may be needed.Low-dosethyroid hormonemay be added to existing antidepressants to treat persistent depression symptoms in people who have tried multiple courses of medication.Limited evidence suggestsstimulants,such asamphetamineandmodafinil,may be effective in the short term, or asadjuvant therapy.Also, it is suggested thatfolatesupplements may have a role in depression management.There is tentative evidence for benefit fromtestosteronein males.

Electroconvulsive therapy

Electroconvulsive therapy(ECT) is a standardpsychiatrictreatment in whichseizuresare electrically induced in a person with depression to provide relief from psychiatric illnesses.ECT is used withinformed consentas a last line of intervention for major depressive disorder.A round of ECT is effective for about 50% of people with treatment-resistant major depressive disorder, whether it is unipolar orbipolar.Follow-up treatment is still poorly studied, but about half of people who respond relapse within twelve months.Aside from effects in the brain, the general physical risks of ECT are similar to those of briefgeneral anesthesia.Immediately following treatment, the most common adverse effects are confusion and memory loss.ECT is considered one of the least harmful treatment options available for severely depressed pregnant women.

A usual course of ECT involves multiple administrations, typically given two or three times per week, until the person no longer has symptoms. ECT is administered underanesthesiawith amuscle relaxant.Electroconvulsive therapy can differ in its application in three ways: electrode placement, frequency of treatments, and the electrical waveform of the stimulus. These three forms of application have significant differences in both adverse side effects and symptom remission. After treatment, drug therapy is usually continued, and some people receive maintenance ECT.

ECT appears to work in the short term via ananticonvulsanteffect mostly in thefrontal lobes,and longer term vianeurotrophiceffects primarily in themedial temporal lobe.

Other

Transcranial magnetic stimulation(TMS) ordeep transcranial magnetic stimulationis a noninvasive method used to stimulate small regions of the brain.TMS was approved by the FDA for treatment-resistant major depressive disorder (trMDD) in 2008and as of 2014 evidence supports that it is probably effective.The American Psychiatric Association,the Canadian Network for Mood and Anxiety Disorders,and the Royal Australia and New Zealand College of Psychiatrists have endorsed TMS for trMDD.Transcranial direct current stimulation(tDCS) is another noninvasive method used to stimulate small regions of the brain with a weak electric current. Several meta-analyses have concluded that active tDCS was useful for treating depression.

There is a small amount of evidence thatsleep deprivationmay improve depressive symptoms in some individuals,with the effects usually showing up within a day. This effect is usually temporary. Besides sleepiness, this method can cause a side effect ofmaniaorhypomania.There is insufficient evidence forReikianddance movement therapyin depression.Cannabisis specifically not recommended as a treatment.

Themicrobiomeof people with major depressive disorder differs from that of healthy people, andprobioticandsynbiotictreatment may achieve a modest depressive symptom reduction.With this,fecal microbiota transplants(FMT) are being researched as add-on therapy treatments for people who do not respond to typical therapies. It has been shown that the patient's depressive symptoms improved, with minor gastrointestinal issues, after a FMT, with improvements in symptoms lasting at least 4 weeks after the transplant.

Prognosis

Studies have shown that 80% of those with a first major depressive episode will have at least one more during their life,with a lifetime average of four episodes.Other general population studies indicate that around half those who have an episode recover (whether treated or not) and remain well, while the other half will have at least one more, and around 15% of those experience chronic recurrence.Studies recruiting from selective inpatient sources suggest lower recovery and higher chronicity, while studies of mostly outpatients show that nearly all recover, with a median episode duration of 11 months. Around 90% of those with severe or psychotic depression, most of whom also meet criteria for other mental disorders, experience recurrence.Cases when outcome is poor are associated with inappropriate treatment, severe initial symptoms including psychosis, early age of onset, previous episodes, incomplete recovery after one year of treatment, pre-existing severe mental or medical disorder, andfamily dysfunction.

A high proportion of people who experience full symptomatic remission still have at least one not fully resolved symptom after treatment.Recurrence or chronicity is more likely if symptoms have not fully resolved with treatment.Current guidelines recommend continuing antidepressants for four to six months after remission to prevent relapse. Evidence from manyrandomized controlled trialsindicates continuing antidepressant medications after recovery can reduce the chance of relapse by 70% (41% on placebo vs. 18% on antidepressant). The preventive effect probably lasts for at least the first 36 months of use.

Major depressive episodes often resolve over time, whether or not they are treated. Outpatients on a waiting list show a 10–15% reduction in symptoms within a few months, with approximately 20% no longer meeting the full criteria for a depressive disorder.Themedianduration of an episode has been estimated to be 23 weeks, with the highest rate of recovery in the first three months.According to a 2013 review, 23% of untreated adults with mild to moderate depression will remit within 3 months, 32% within 6 months and 53% within 12 months.

Ability to work

Depression may affect people's ability to work. The combination of usual clinical care and support with return to work (like working less hours or changing tasks) probably reduces sick leave by 15%, and leads to fewer depressive symptoms and improved work capacity, reducing sick leave by an annual average of 25 days per year.Helping depressed people return to work without a connection to clinical care has not been shown to have an effect on sick leave days. Additional psychological interventions (such as online cognitive behavioral therapy) lead to fewer sick days compared to standard management only. Streamlining care or adding specific providers for depression care may help to reduce sick leave.

Life expectancy and the risk of suicide

Depressed individuals have a shorterlife expectancythan those without depression, in part because people who are depressed are at risk of dying of suicide.About 50% of people who die of suicide have amood disordersuch as major depression, and the risk is especially high if a person has a marked sense of hopelessness or has both depression andborderline personality disorder.About 2–8% of adults with major depression die bysuicide.In the US, the lifetime risk of suicide associated with a diagnosis of major depression is estimated at 7% for men and 1% for women,even though suicide attempts are more frequent in women.

Depressed people also have a higherrate of dyingfrom other causes.There is a 1.5- to 2-fold increased risk ofcardiovascular disease,independent of other known risk factors, and is itself linked directly or indirectly to risk factors such as smoking and obesity. People with major depression are less likely to follow medical recommendations for treating and preventingcardiovascular disorders,further increasing their risk of medical complications.Cardiologistsmay not recognize underlying depression that complicates a cardiovascular problem under their care.

Epidemiology

Main article:Epidemiology of depression

Disability-adjusted life yearfor unipolar depressive disorders per 100,000 inhabitants in 2004:

no data

<700

700–775

775–850

850–925

925–1,000

1,000–1,075

1,075–1,150

1,150–1,225

1,225–1,300

1,300–1,375

1,375–1,450

>1,450

Major depressive disorder affected approximately 163 million people in 2017 (2% of the global population).The percentage of people who are affected at one point in their life varies from 7% in Japan to 21% in France. In most countries the number of people who have depression during their lives falls within an 8–18% range. Lifetime rates are higher in thedeveloped world(15%) compared to thedeveloping world(11%).

In the United States, 8.4% of adults (21 million individuals) have at least one episode within a year-long period; the probability of having a major depressive episode is higher for females than males (10.5% to 6.2%), and highest for those aged 18 to 25 (17%).15% of adolescents, ages 12 to 17, in America are also affected by depression, which is equal to 3.7 million teenagers.Among individuals reporting two or more races, the US prevalence is highest.Out of all the people suffering from MDD, only about 35% seek help from a professional for their disorder.

Major depression is about twice as common in women as in men, although it is unclear why this is so, and whether factors unaccounted for are contributing to this.The relative increase in occurrence is related to pubertal development rather than chronological age, reaches adult ratios between the ages of 15 and 18, and appears associated with psychosocial more than hormonal factors.In 2019, major depressive disorder was identified (using either the DSM-IV-TR or ICD-10) in theGlobal Burden of Disease Studyas the fifth most common cause ofyears lived with disabilityand the 18th most common fordisability-adjusted life years.

People are most likely to develop their first depressive episode between the ages of 30 and 40, and there is a second, smaller peak of incidence between ages 50 and 60.The risk of major depression is increased with neurological conditions such asstroke,Parkinson's disease,ormultiple sclerosis,and during the first year after childbirth(Postpartum depression).It is also more common after cardiovascular illnesses, and is related more to those with a poor cardiacdisease outcomethan to a better one.Depressive disorders are more common in urban populations than in rural ones and the prevalence is increased in groups with poorer socioeconomic factors, e.g., homelessness.Depression is common among those over 65 years of age and increases in frequency beyond this age.The risk of depression increases in relation to the frailty of the individual.Depression is one of the most important factors which negatively impact quality of life in adults, as well as the elderly.Both symptoms and treatment among the elderly differ from those of the rest of the population.

Major depression was the leading cause ofdisease burdenin North America and other high-income countries, and the fourth-leading cause worldwide as of 2006. In the year 2030, it is predicted to be the second-leading cause of disease burden worldwide afterHIV,according to the WHO.Delay or failure in seeking treatment after relapse and the failure of health professionals to provide treatment are two barriers to reducing disability.

Comorbidity

Major depression frequentlyco-occurswith other psychiatric problems. The 1990–92National Comorbidity Survey(US) reported that half of those with major depression also have lifetimeanxietyand its associated disorders, such asgeneralized anxiety disorder.Anxiety symptoms can have a major impact on the course of a depressive illness, with delayed recovery, increased risk of relapse, greater disability and increased suicidal behavior.Depressed people have increased rates of alcohol and substance use, particularly dependence,and around a third of individuals diagnosed withattention deficit hyperactivity disorder(ADHD) develop comorbid depression.Post-traumatic stress disorderand depression often co-occur.Depression may also coexist with ADHD, complicating the diagnosis and treatment of both.Depression is also frequently comorbid withalcohol use disorderandpersonality disorders.Depression can also be exacerbated during particular months (usually winter) in those withseasonal affective disorder.Whileoveruse of digital mediahas been associated with depressive symptoms, using digital media may also improve mood in some situations.

Depression andpainoften co-occur. One or more pain symptoms are present in 65% of people who have depression, and anywhere from 5 to 85% of people who are experiencing pain will also have depression, depending on the setting—a lower prevalence in general practice, and higher in specialty clinics. Depression is often underrecognized, and therefore undertreated, in patients presenting with pain.Depression often coexists with physical disorders common among the elderly, such asstroke,othercardiovascular diseases,Parkinson's disease,andchronic obstructive pulmonary disease.

History

Main article:History of depression

The Ancient Greek physicianHippocratesdescribed a syndrome ofmelancholia(μελαγχολία,melankholía) as a distinct disease with particular mental and physical symptoms; he characterized all "fears and despondencies, if they last a long time" as being symptomatic of the ailment.It was a similar but far broader concept than today's depression; prominence was given to a clustering of the symptoms of sadness, dejection, and despondency, and often fear, anger, delusions and obsessions were included.

Diagnoses of depression go back at least as far asHippocrates.

The termdepressionitself was derived from the Latin verbdeprimere,meaning "to press down".From the 14th century, "to depress" meant to subjugate or to bring down in spirits. It was used in 1665 in English authorRichard Baker'sChronicleto refer to someone having "a great depression of spirit", and by English authorSamuel Johnsonin a similar sense in 1753.The term also came into use inphysiologyandeconomics.An early usage referring to a psychiatric symptom was by French psychiatristLouis Delasiauvein 1856, and by the 1860s it was appearing in medical dictionaries to refer to a physiological and metaphorical lowering of emotional function.SinceAristotle,melancholia had been associated with men of learning and intellectual brilliance, a hazard of contemplation and creativity. However, by the 19th century, this association has largely shifted and melancholia became more commonly linked with women.

Althoughmelancholiaremained the dominant diagnostic term,depressiongained increasing currency in medical treatises and was a synonym by the end of the century; German psychiatristEmil Kraepelinmay have been the first to use it as the overarching term, referring to different kinds of melancholia asdepressive states.Freud likened the state of melancholia to mourning in his 1917 paperMourning and Melancholia.He theorized thatobjectiveloss, such as the loss of a valued relationship through death or a romantic break-up, results insubjectiveloss as well; the depressed individual has identified with the object of affection through anunconscious,narcissisticprocess called thelibidinalcathexisof theego.Such loss results in severe melancholic symptoms more profound than mourning; not only is the outside world viewed negatively but the ego itself is compromised.The person's decline of self-perception is revealed in his belief of his own blame, inferiority, and unworthiness.He also emphasized early life experiences as a predisposing factor.Adolf Meyerput forward a mixed social and biological framework emphasizingreactionsin the context of an individual's life, and argued that the termdepressionshould be used instead ofmelancholia.The first version of theDSM(DSM-I,1952) containeddepressive reactionand theDSM-II(1968)depressive neurosis,defined as an excessive reaction to internal conflict or an identifiable event, and also included a depressive type of manic-depressive psychosis within Major affective disorders.

The termunipolar(along with the related termbipolar) was coined by the neurologist and psychiatristKarl Kleist,and subsequently used by his disciplesEdda NeeleandKarl Leonhard.

The termMajor depressive disorderwas introduced by a group of US clinicians in the mid-1970s as part of proposals for diagnostic criteria based on patterns of symptoms (called the "Research Diagnostic Criteria", building on earlierFeighner Criteria),and was incorporated into theDSM-IIIin 1980.TheAmerican Psychiatric Associationadded "major depressive disorder" to theDiagnostic and Statistical Manual of Mental Disorders(DSM-III),as a split of the previousdepressive neurosisin theDSM-II,which also encompassed the conditions now known as dysthymia andadjustment disorder with depressed mood.To maintain consistency the ICD-10 used the same criteria, with only minor alterations, but using theDSMdiagnostic threshold to mark amild depressive episode,adding higher threshold categories for moderate and severe episodes.The ancient idea ofmelancholiastill survives in the notion of a melancholic subtype.

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

Society and culture

Further information:Depression and culture

Terminology

The 16thAmerican president,Abraham Lincoln,had "melancholy",a condition that now may be referred to as clinical depression.

The term "depression" is used in a number of different ways. It is often used to mean this syndrome but may refer to othermood disordersor simply to a low mood. People's conceptualizations of depression vary widely, both within and among cultures. "Because of the lack of scientific certainty," one commentator has observed, "the debate over depression turns on questions of language. What we call it—'disease,' 'disorder,' 'state of mind'—affects how we view, diagnose, and treat it."There are cultural differences in the extent to which serious depression is considered an illness requiring personal professional treatment, or an indicator of something else, such as the need to address social or moral problems, the result of biological imbalances, or a reflection of individual differences in the understanding of distress that may reinforce feelings of powerlessness, and emotional struggle.

Cultural dimension

Cultural differences contribute to different prevalence of symptoms. "Do the Chinesesomatizedepression? A cross-cultural study "by Parkeret al.discusses the cultural differences in prevalent symptoms of depression betweenindividualisticandcollectivistic cultures.The authors reveal that individuals with depression in collectivistic cultures tend to present more somatic symptoms and less affective symptoms compared to those in individualistic cultures. The finding suggests that individualistic cultures 'warranting' orvalidatingone's expression of emotions explains this cultural difference since collectivistic cultures see this as a taboo against the social cooperation it deems one of the most significant values.

Stigma

Historical figures were often reluctant to discuss or seek treatment for depression due tosocial stigmaabout the condition, or due to ignorance of diagnosis or treatments. Nevertheless, analysis or interpretation of letters, journals, artwork, writings, or statements of family and friends of some historical personalities has led to the presumption that they may have had some form of depression. People who may have had depression include English authorMary Shelley,American-British writerHenry James,and American presidentAbraham Lincoln.Some well-known contemporary people with possible depression include Canadian songwriterLeonard Cohenand American playwright and novelistTennessee Williams.Some pioneering psychologists, such as AmericansWilliam JamesandJohn B. Watson,dealt with their own depression.

There has been a continuing discussion of whether neurological disorders and mood disorders may be linked tocreativity,a discussion that goes back toAristoteliantimes.British literature gives many examples of reflections on depression.English philosopherJohn Stuart Millexperienced a several-months-long period of what he called "a dull state of nerves", when one is "unsusceptible to enjoyment or pleasurable excitement; one of those moods when what is pleasure at other times, becomes insipid or indifferent". He quoted English poetSamuel Taylor Coleridge's "Dejection" as a perfect description of his case: "A grief without a pang, void, dark and drear, / A drowsy, stifled, unimpassioned grief, / Which finds no natural outlet or relief / In word, or sigh, or tear."English writerSamuel Johnsonused the term "the black dog" in the 1780s to describe his own depression,and it was subsequently popularized by British Prime Minister SirWinston Churchill,who also had the disorder.Johann Wolfgang von Goethein hisFaust, Part I,published in 1808, hasMephistophelesassume the form of a black dog, specifically apoodle.

In 1998, the Norwegian PMKjell Magne Bondevikpublicly announced he will take a break in order to recover from a depressive episode.

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

While serving his first term as Prime Minister of Norway,Kjell Magne Bondevikattracted international attention in August 1998 when he announced that he was suffering from a depressive episode, becoming the highest ranking worldleaderto admit to suffering from a mental illness while in office. Upon this revelation,Anne Engerbecame acting Prime Minister for three weeks, from 30 August to 23 September, while he recovered from the depressive episode. Bondevik then returned to office. Bondevik received thousands of supportive letters, and said that the experience had been positive overall, both for himself and because it made mental illness more publicly acceptable.

References

Cited works

• American Psychiatric Association (2000a).Diagnostic and statistical manual of mental disorders(Fourth Edition, Text Revision: DSM-IV-TR ed.). Washington, DC: American Psychiatric Publishing, Inc.ISBN978-0-89042-025-6.
• American Psychiatric Association (2013).Diagnostic and statistical manual of mental disorders(Fifth Edition: DSM-5 ed.). Washington, DC: American Psychiatric Publishing, Inc.ISBN978-0-89042-555-8.
• Barlow DH, Durand VM (2005).Abnormal psychology: An integrative approach(5th ed.). Belmont, CA: Thomson Wadsworth.ISBN978-0-534-63356-1.
• Beck AT, Rush J, Shaw BF, Emery G (1987) [1979].Cognitive therapy of depression.New York: Guilford Press.ISBN978-0-89862-919-4.
• Hergenhahn BR (2005).An Introduction to the History of Psychology(5th ed.). Belmont, CA: Thomson Wadsworth.ISBN978-0-534-55401-9.
• Parker G, Hadzi-Pavlovic D, eds. (1996).Melancholia: a disorder of movement and mood: a phenomenological and neurobiological review.Cambridge: Cambridge University Press.ISBN978-0-521-47275-3.
• Royal Pharmaceutical Society of Great Britain (2008).British National Formulary (BNF 56).UK: BMJ Group and RPS Publishing.ISBN978-0-85369-778-7.
• Sadock VA, Sadock BJ, Kaplan HI (2003).Kaplan & Sadock's synopsis of psychiatry: behavioral sciences/clinical psychiatry.Philadelphia: Lippincott Williams & Wilkins.ISBN978-0-7817-3183-6.
• "6A70 Single episode depressive disorder".International Classification of Diseases 11th Revision.World Health Organization. February 2022 [adopted in 2019].Retrieved9 July2022.
• "6A71 Recurrent depressive disorder".International Classification of Diseases 11th Revision.World Health Organization. February 2022 [adopted in 2019].Retrieved9 July2022.