fbpx
Wikipedia

Major depressive disorder

February 20, 2023

For other types of depression, see Mood disorder.
Not to be confused with Depression (mood).

Major depressive disorder (MDD), also known as clinical depression, is a mental disorder[9] characterized by at least two weeks of pervasive low mood, low self-esteem, and loss of interest or pleasure in normally enjoyable activities. Introduced by a group of US clinicians in the mid-1970s,[10] the term was adopted by the American Psychiatric Association for this symptom cluster under mood disorders in the 1980 version of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III), and has become widely used since.

Major depressive disorder
Other namesClinical depression, major depression, unipolar depression, unipolar disorder, recurrent depression
Sorrowing Old Man (At Eternity's Gate)
by Vincent van Gogh (1890)
SpecialtyPsychiatry, clinical psychology
SymptomsLow mood, low self-esteem, loss of interest in normally enjoyable activities, low energy, pain without a clear cause[1]
ComplicationsSelf-harm, suicide[2]
Usual onset20s[3][4]
Duration> 2 weeks[1]
CausesEnvironmental (adverse life experiences, stressful life events), genetic and psychological factors[5]
Risk factorsFamily history, major life changes, certain medications, chronic health problems, substance use disorder[1][5]
Differential diagnosisBipolar disorder, ADHD, sadness[6]
TreatmentPsychotherapy, antidepressant medication, electroconvulsive therapy, exercise[1][7]
MedicationAntidepressants
Frequency163 million (2017)[8]

The diagnosis of major depressive disorder is based on the person's reported experiences, behavior reported by relatives or friends, and a mental status examination.[11] There is no laboratory test for the disorder, but testing may be done to rule out physical conditions that can cause similar symptoms.[11] The most common time of onset is in a person's 20s,[3][4] with females affected about twice as often as males.[4] The course of the disorder varies widely, from one episode lasting months to a lifelong disorder with recurrent major depressive episodes.

Those with major depressive disorder are typically treated with psychotherapy and antidepressant medication.[1] Medication appears to be effective, but the effect may be significant only in the most severely depressed.[12][13] Hospitalization (which may be involuntary) may be necessary in cases with associated self-neglect or a significant risk of harm to self or others. Electroconvulsive therapy (ECT) may be considered if other measures are not effective.[1]

Major depressive disorder is believed to be caused by a combination of genetic, environmental, and psychological factors,[1] with about 40% of the risk being genetic.[5] Risk factors include a family history of the condition, major life changes, certain medications, chronic health problems, and substance use disorders.[1][5] 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.[1][5] Major depressive disorder affected approximately 163 million people (2% of the world's population) in 2017.[8] The percentage of people who are affected at one point in their life varies from 7% in Japan to 21% in France.[4] Lifetime rates are higher in the developed world (15%) compared to the developing world (11%).[4] The disorder causes the second-most years lived with disability, after lower back pain.[14]

Symptoms and signs

 
An 1892 lithograph of a woman diagnosed with melancholia

Major depression significantly affects a person's family and personal relationships, work or school life, sleeping and eating habits, and general health.[15] A person having a major depressive episode usually exhibits a low mood, which pervades all aspects of life, and an inability to experience pleasure in previously enjoyable activities.[16] Depressed people may be preoccupied with—or ruminate over—thoughts and feelings of worthlessness, inappropriate guilt or regret, helplessness or hopelessness.[17] Other symptoms of depression include poor concentration and memory, withdrawal from social situations and activities, reduced sex drive, irritability, and thoughts of death or suicide. Insomnia is common; in the typical pattern, a person wakes very early and cannot get back to sleep. Hypersomnia, or oversleeping, can also happen.[18] Some antidepressants may also cause insomnia due to their stimulating effect.[19] In severe cases, depressed people may have psychotic symptoms. These symptoms include delusions or, less commonly, hallucinations, usually unpleasant.[20] People who have had previous episodes with psychotic symptoms are more likely to have them with future episodes.[21]

A depressed person may report multiple physical symptoms such as fatigue, headaches, or digestive problems; physical complaints are the most common presenting problem in developing countries, according to the World Health Organization's criteria for depression.[22] Appetite often decreases, resulting in weight loss, although increased appetite and weight gain occasionally occur.[23] Family and friends may notice agitation or lethargy.[18] Older depressed people may have cognitive symptoms of recent onset, such as forgetfulness,[24] and a more noticeable slowing of movements.[25]

Depressed children may often display an irritable rather than a depressed mood;[18] most lose interest in school and show a steep decline in academic performance.[26] Diagnosis may be delayed or missed when symptoms are interpreted as "normal moodiness."[23] Elderly people may not present with classical depressive symptoms.[27] 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.[27]

Cause

Further information: Biology of depression and Epigenetics of depression
 
A cup analogy demonstrating the diathesis–stress model that under the same amount of stressors, person 2 is more vulnerable than person 1, because of their predisposition.[28]

The biopsychosocial model proposes that biological, psychological, and social factors all play a role in causing depression.[5][29] The diathesis–stress model specifies that depression results when a preexisting vulnerability, or diathesis, is activated by stressful life events. The preexisting vulnerability can be either genetic,[30][31] implying an interaction between nature and nurture, or schematic, resulting from views of the world learned in childhood.[32] American psychiatrist Aaron Beck suggested that a triad of automatic and spontaneous negative thoughts about the self, the world or environment, and the future may lead to other depressive signs and symptoms.[33][34]

Adverse childhood experiences (incorporating childhood abuse, neglect and family dysfunction) markedly increase the risk of major depression, especially if more than one type.[5] 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.[35]

Genetics

Family and twin studies find that nearly 40% of individual differences in risk for major depressive disorder can be explained by genetic factors.[36] Like most psychiatric disorders, major depressive disorder is likely influenced by many individual genetic changes. In 2018, a genome-wide association study discovered 44 genetic variants linked to risk for major depression;[37] a 2019 study found 102 variants in the genome linked to depression.[38] Research focusing on specific candidate genes has been criticized for its tendency to generate false positive findings.[39] There are also other efforts to examine interactions between life stress and polygenic risk for depression.[40]

Other health problems

Depression can also arise after a chronic or terminal medical condition, such as HIV/AIDS or asthma, and may be labeled "secondary depression."[41][42] It is unknown whether the underlying diseases induce depression through effect on quality of life, or through shared etiologies (such as degeneration of the basal ganglia in Parkinson's disease or immune dysregulation in asthma).[43] Depression may also be iatrogenic (the result of healthcare), such as drug-induced depression. Therapies associated with depression include interferons, beta-blockers, isotretinoin, contraceptives,[44] cardiac agents, anticonvulsants, antimigraine drugs, antipsychotics, and hormonal agents such as gonadotropin-releasing hormone agonist.[45] Substance use in early age is associated with increased risk of developing depression later in life.[46] Depression occurring after giving birth is called postpartum depression and is thought to be the result of hormonal changes associated with pregnancy.[47] Seasonal affective disorder, a type of depression associated with seasonal changes in sunlight, is thought to be triggered by decreased sunlight.[48] Vitamin B2, B6 and B12 deficiency may cause depression in females.[49]

Pathophysiology

Further information: Biology of depression and Epigenetics of depression

The pathophysiology of depression is not completely understood, but current theories center around monoaminergic systems, the circadian rhythm, immunological dysfunction, HPA-axis dysfunction 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 of monoamine neurotransmitters is the primary cause of depression. Evidence for the monoamine theory comes from multiple areas. First, acute depletion of tryptophan—a necessary precursor of serotonin and 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.[50] Second, the correlation between depression risk and polymorphisms in the 5-HTTLPR gene, which codes for serotonin receptors, suggests a link. Third, decreased size of the locus coeruleus, decreased activity of tyrosine hydroxylase, increased density of alpha-2 adrenergic receptor, and evidence from rat models suggest decreased adrenergic neurotransmission in depression.[51] Furthermore, decreased levels of homovanillic acid, altered response to dextroamphetamine, responses of depressive symptoms to dopamine receptor agonists, decreased dopamine receptor D1 binding in the striatum,[52] and polymorphism of dopamine receptor genes implicate dopamine, another monoamine, in depression.[53][54] Lastly, increased activity of monoamine oxidase, which degrades monoamines, has been associated with depression.[55] 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.[56] One proposed explanation for the therapeutic lag, and further support for the deficiency of monoamines, is a desensitization of self-inhibition in raphe nuclei by the increased serotonin mediated by antidepressants.[57] However, disinhibition of the dorsal raphe has been proposed to occur as a result of decreased serotonergic 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 jugular 5-HIAA in people who are depressed that normalized with selective serotonin reuptake inhibitor (SSRI) treatment, and the preference for carbohydrates in people who are depressed.[58] Already limited, the monoamine hypothesis has been further oversimplified when presented to the general public.[59] A 2022 review found no consistent evidence supporting the serotonin hypothesis, linking serotonin levels and depression.[60]

Immune system abnormalities have been observed, including increased levels of cytokines involved in generating sickness behavior (which shares overlap with depression).[61][62][63] The effectiveness of nonsteroidal anti-inflammatory drugs (NSAIDs) and cytokine inhibitors in treating depression,[64] and normalization of cytokine levels after successful treatment further suggest immune system abnormalities in depression.[65]

HPA-axis abnormalities have been suggested in depression given the association of CRHR1 with depression and the increased frequency of dexamethasone test non-suppression in people who are depressed. However, this abnormality is not adequate as a diagnosis tool, because its sensitivity is only 44%.[66] These stress-related abnormalities are thought to be the cause of hippocampal volume reductions seen in people who are depressed.[67] Furthermore, a meta-analysis yielded decreased dexamethasone suppression, and increased response to psychological stressors.[68] Further abnormal results have been obscured with the cortisol awakening response, with increased response being associated with depression.[69]

Theories unifying neuroimaging findings 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.[70] Another model, the cortico-striatal model, suggests that abnormalities of the prefrontal cortex in regulating striatal and subcortical structures result in depression.[71] Another model proposes hyperactivity of salience structures in identifying negative stimuli, and hypoactivity of cortical regulatory structures resulting in a negative emotional bias and depression, consistent with emotional bias studies.[72]

Diagnosis

Clinical assessment

Further information: Rating scales for depression
 
Caricature of a man with depression

A diagnostic assessment may be conducted by a suitably trained general practitioner, or by a psychiatrist or psychologist,[15] who records the person's current circumstances, biographical history, current symptoms, family history, and alcohol and drug use. The assessment also includes a mental state examination, which is an assessment of the person's current mood and thought content, in particular the presence of themes of hopelessness or pessimism, self-harm or suicide, and an absence of positive thoughts or plans.[15] Specialist mental health services are rare in rural areas, and thus diagnosis and management is left largely to primary-care clinicians.[73] This issue is even more marked in developing countries.[74] Rating scales are 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;[75] these include the Hamilton Rating Scale for Depression,[76] the Beck Depression Inventory[77] or the Suicide Behaviors Questionnaire-Revised.[78]

Primary-care physicians have more difficulty with underrecognition and undertreatment of depression compared to psychiatrists. These cases may be missed because for some people with depression, physical symptoms often 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.[79]

A doctor generally performs a medical examination and selected investigations to rule out other causes of depressive symptoms. These include blood tests measuring TSH and thyroxine to exclude hypothyroidism; basic electrolytes and serum calcium to rule out a metabolic disturbance; and a full blood count including ESR to rule out a systemic infection or chronic disease.[80] Adverse affective reactions to medications or alcohol misuse may be ruled out, as well. Testosterone levels may be evaluated to diagnose hypogonadism, a cause of depression in men.[81] Vitamin D levels might be evaluated, as low levels of vitamin D have been associated with greater risk for depression.[82] Subjective cognitive complaints appear in older depressed people, but they can also be indicative of the onset of a dementing disorder, such as Alzheimer's disease.[83][84] Cognitive testing and brain imaging can help distinguish depression from dementia.[85] A CT scan can exclude brain pathology in those with psychotic, rapid-onset or otherwise unusual symptoms.[86] No biological tests confirm major depression.[87] In general, investigations are not repeated for a subsequent episode unless there is a medical indication.

DSM and ICD criteria

The most widely used criteria for diagnosing depressive conditions are found in the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (DSM) and the World Health Organization's International 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,[88] and the authors of both have worked towards conforming one with the other.[89] Both DSM and ICD mark out typical (main) depressive symptoms.[90] The most recent edition of the DSM is the Fifth Edition, Text Revision (DSM-5-TR),[91] and the most recent edition of the ICD is the Eleventh Edition (ICD-11).[92]

Under mood disorders, ICD-11 classifies major depressive disorder as either single episode depressive disorder (where there is no history of depressive episodes, or of mania) or recurrent depressive disorder (where there is a history of prior episodes, with no history of mania).[93] ICD-11 symptoms, present nearly every day for at least two weeks, are a depressed mood or anhedonia, 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."[93] 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).[93] These two disorders are classified as "Depressive disorders", in the category of "Mood disorders".[93]

According to DSM-5, there are two main depressive symptoms: a depressed mood, and loss of interest/pleasure in activities (anhedonia). 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.[94][failed verification] Major depressive disorder is classified as a mood disorder in the DSM-5.[95] The diagnosis hinges on the presence of single or recurrent major depressive episodes.[96] Further qualifiers are used to classify both the episode itself and the course of the disorder. The category Unspecified Depressive Disorder is diagnosed if the depressive episode's manifestation does not meet the criteria for a major depressive episode.[95]

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.[23] Episodes may be isolated or recurrent and are categorized as mild (few symptoms in excess of minimum criteria), moderate, or severe (marked impact on social or occupational functioning). An episode with psychotic features—commonly referred to as psychotic depression—is automatically rated as severe.[95] If the person has had an episode of mania or markedly elevated mood, a diagnosis of bipolar disorder is made instead. Depression without mania is sometimes referred to as unipolar because the mood remains at one emotional state or "pole".[97]

Bereavement is 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, including dysthymia, which involves a chronic but milder mood disturbance;[98] recurrent brief depression, consisting of briefer depressive episodes;[99][100] minor depressive disorder, whereby only some symptoms of major depression are present;[101] and adjustment disorder with depressed mood, which denotes low mood resulting from a psychological response to an identifiable event or stressor.[102]

Subtypes

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

  • "Melancholic depression" is characterized by a loss of pleasure in most or all activities, a failure of reactivity to pleasurable stimuli, a quality of depressed mood more pronounced than that of grief or loss, a worsening of symptoms in the morning hours, early-morning waking, psychomotor retardation, excessive weight loss (not to be confused with anorexia nervosa), or excessive guilt.[103]
  • "Atypical depression" is characterized by mood reactivity (paradoxical anhedonia) and positivity, significant weight gain or increased appetite (comfort eating), excessive sleep or sleepiness (hypersomnia), a sensation of heaviness in limbs known as leaden paralysis, and significant long-term social impairment as a consequence of hypersensitivity to perceived interpersonal rejection.[104]
  • "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 in schizophrenia or in manic episodes, or may be caused by neuroleptic malignant syndrome.[105]
  • "Depression with anxious distress" was added into the DSM-5 as a means to emphasize the common co-occurrence between depression or mania and 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.[95]
  • "Depression with peri-partum onset" 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-V mandates that to qualify as depression with peripartum onset, onset occurs during pregnancy or within one month of delivery.[106]
  • "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.[107]

Differential diagnoses

Main article: Differential diagnoses of depression

To confirm major depressive disorder as the most likely diagnosis, other potential diagnoses must be considered, including dysthymia, adjustment disorder with depressed mood, or bipolar disorder. Dysthymia is a chronic, milder mood disturbance in which a person reports a low mood almost daily over a span of at least two years. The symptoms are not as severe as those for major depression, although people with dysthymia are vulnerable to secondary episodes of major depression (sometimes referred to as double depression).[98] Adjustment disorder with depressed mood is a mood disturbance appearing as a psychological response to an identifiable event or stressor, in which the resulting emotional or behavioral symptoms are significant but do not meet the criteria for a major depressive episode.[102]

Other disorders need to be ruled out before diagnosing major depressive disorder. They include depressions due to physical illness, medications, and substance use disorders. Depression due to physical illness is diagnosed as a mood disorder due to a general medical condition. This condition is determined based on history, laboratory findings, or physical examination. When the depression is caused by a medication, non-medical use of a psychoactive substance, or exposure to a toxin, it is then diagnosed as a specific mood disorder (previously called substance-induced mood disorder).[108]

Screening and prevention

Preventive efforts may result in decreases in rates of the condition of between 22 and 38%.[109] Since 2016, the United States Preventive Services Task Force (USPSTF) has recommended screening for depression among those over the age 12;[110][111] though a 2005 Cochrane review found that the routine use of screening questionnaires has little effect on detection or treatment.[112] Screening the general population is not recommended by authorities in the UK or Canada.[113]

Behavioral interventions, such as interpersonal therapy and cognitive-behavioral therapy, are effective at preventing new onset depression.[109][114][115] Because such interventions appear to be most effective when delivered to individuals or small groups, it has been suggested that they may be able to reach their large target audience most efficiently through the Internet.[116]

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.[114][117]

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.[118] American Psychiatric Association treatment 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) or light therapy. Antidepressant medication 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.[119] There is evidence that collaborative care by a team of health care practitioners produces better results than routine single-practitioner care.[120]

Psychotherapy is the treatment of choice (over medication) for people under 18,[121] and cognitive behavioral therapy (CBT), third wave CBT and interpersonal therapy may help prevent depression.[122] The UK National Institute for Health and Care Excellence (NICE) 2004 guidelines indicate that antidepressants should not be used for the initial treatment of mild depression because the risk-benefit ratio is poor. The guidelines recommend that antidepressants treatment in combination with psychosocial interventions should be considered for:[121]

  • 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 that antidepressant treatment should be continued for at least six months to reduce the risk of relapse, and that SSRIs are better tolerated than tricyclic antidepressants.[121]

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.[123] There is insufficient evidence to determine the effectiveness of psychological versus medical therapy in children.[124]

Lifestyle

Further information: Neurobiological effects of physical exercise § Major depressive disorder
 
Physical exercise is one recommended way to manage mild depression.

Physical exercise has 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.[125] It is equivalent to the use of medications or psychological therapies in most people.[7] In older people it does appear to decrease depression.[126] Sleep and diet may also play a role in depression, and interventions in these areas may be an effective add-on to conventional methods.[127] In observational studies, smoking cessation has benefits in depression as large as or larger than those of medications.[128]

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, clinical social workers, counselors, and psychiatric nurses. A 2012 review found psychotherapy to be better than no treatment but not other treatments.[129] With more complex and chronic forms of depression, a combination of medication and psychotherapy may be used.[130][131] There is moderate-quality evidence that psychological therapies are a useful addition to standard antidepressant treatment of treatment-resistant depression in the short term.[132] Psychotherapy has been shown to be effective in older people.[133][134] 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.[135] 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.[136] In people under 18, according to the National Institute for Health and Clinical Excellence, medication should be offered only in conjunction with a psychological therapy, such as CBT, interpersonal therapy, or family therapy.[137] Several variables predict success for cognitive behavioral therapy in adolescents: higher levels of rational thoughts, less hopelessness, fewer negative thoughts, and fewer cognitive distortions.[138] CBT is particularly beneficial in preventing relapse.[139][140] 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.[141] Several variants of cognitive behavior therapy have been used in those with depression, the most notable being rational emotive behavior therapy,[142] and mindfulness-based cognitive therapy.[143] Mindfulness-based stress reduction programs may reduce depression symptoms.[144][145] Mindfulness programs also appear to be a promising intervention in youth.[146] Problem solving therapy, cognitive behavioral therapy, and interpersonal therapy are effective interventions in the elderly.[147]

Psychoanalysis is a school of thought, founded by Sigmund Freud, which emphasizes the resolution of unconscious mental conflicts.[148] Psychoanalytic techniques are used by some practitioners to treat clients presenting with major depression.[149] A more widely practiced therapy, called psychodynamic 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.[150] 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.[151]

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.[152] A review commissioned by the National Institute for Health and Care Excellence (UK) concluded that there is strong evidence that SSRIs, such as escitalopram, paroxetine, and sertraline, have greater efficacy than placebo on 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.[153] Similarly, a Cochrane systematic review of clinical trials of the generic tricyclic antidepressant amitriptyline concluded that there is strong evidence that its efficacy is superior to placebo.[154] Antidepressants work less well for the elderly than for younger individuals with depression.[147]

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.[119][155] Antidepressant medication treatment is usually continued for 16 to 20 weeks after remission, to minimize the chance of recurrence,[119] and even up to one year of continuation is recommended.[156] People with chronic depression may need to take medication indefinitely to avoid relapse.[15]

SSRIs are the primary medications prescribed, owing to their relatively mild side-effects, and because they are less toxic in overdose than other antidepressants.[157] People who do not respond to one SSRI can be switched to another antidepressant, and this results in improvement in almost 50% of cases.[158] Another option is to switch to the atypical antidepressant bupropion.[159] Venlafaxine, an antidepressant with a different mechanism of action, may be modestly more effective than SSRIs.[160] However, venlafaxine is not recommended in the UK as a first-line treatment because of evidence suggesting its risks may outweigh benefits,[161] and it is specifically discouraged in children and adolescents as it increases the risk of suicidal thoughts or attempts.[162][163][164][165][166][167][168]

For children and adolescents with moderate-to-severe depressive disorder, fluoxetine seems to be the best treatment (either with or without cognitive behavioural therapy) but more research is needed to be certain.[169][163][170][164] Sertraline, escitalopram, duloxetine might also help in reducing symptoms. Some antidepressants have not been shown to be effective.[171][163] Medications are not recommended in children with mild disease.[172]

There is also insufficient evidence to determine effectiveness in those with depression complicated by dementia.[173] Any antidepressant can cause low blood sodium levels;[174] nevertheless, it has been reported more often with SSRIs.[157] It is not uncommon for SSRIs to cause or worsen insomnia; the sedating atypical antidepressant mirtazapine can be used in such cases.[175][176]

Irreversible monoamine oxidase inhibitors, an older class of antidepressants, have been plagued by potentially life-threatening dietary and drug interactions. They are still used only rarely, although newer and better-tolerated agents of this class have been developed.[177] The safety profile is different with reversible monoamine oxidase inhibitors, such as moclobemide, where the risk of serious dietary interactions is negligible and dietary restrictions are less strict.[178]

It is unclear whether antidepressants affect a person's risk of suicide.[179] For children, adolescents, and probably young adults between 18 and 24 years old, there is a higher risk of both suicidal ideations and suicidal behavior in those treated with SSRIs.[180][181] For adults, it is unclear whether SSRIs affect the risk of suicidality. One review found no connection;[182] another an increased risk;[183] and a third no risk in those 25–65 years old and a decreased risk in those more than 65.[184] A black box warning was 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.[185] Similar precautionary notice revisions were implemented by the Japanese Ministry of Health.[186]

Other medications and supplements

The combined use of antidepressants plus benzodiazepines demonstrates 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.[187]

Ketamine may 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.[188][189] A nasal spray form of esketamine was 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.[190][191]

There is insufficient high quality evidence to suggest omega-3 fatty acids are effective in depression.[192] There is limited evidence that vitamin D supplementation is of value in alleviating the symptoms of depression in individuals who are vitamin D-deficient.[82] Lithium appears effective at lowering the risk of suicide in those with bipolar disorder and unipolar depression to nearly the same levels as the general population.[193] There is a narrow range of effective and safe dosages of lithium thus close monitoring may be needed.[194] Low-dose thyroid hormone may be added to existing antidepressants to treat persistent depression symptoms in people who have tried multiple courses of medication.[195] Limited evidence suggests stimulants, such as amphetamine and modafinil, may be effective in the short term, or as adjuvant therapy.[196][197] Also, it is suggested that folate supplements may have a role in depression management.[198] There is tentative evidence for benefit from testosterone in males.[199]

Electroconvulsive therapy

Electroconvulsive therapy (ECT) is a standard psychiatric treatment in which seizures are electrically induced in a person with depression to provide relief from psychiatric illnesses.[200]: 1880  ECT is used with informed consent[201] as a last line of intervention for major depressive disorder.[202] A round of ECT is effective for about 50% of people with treatment-resistant major depressive disorder, whether it is unipolar or bipolar.[203] Follow-up treatment is still poorly studied, but about half of people who respond relapse within twelve months.[204] Aside from effects in the brain, the general physical risks of ECT are similar to those of brief general anesthesia.[205]: 259  Immediately following treatment, the most common adverse effects are confusion and memory loss.[202][206] ECT is considered one of the least harmful treatment options available for severely depressed pregnant women.[207]

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 under anesthesia with a muscle relaxant.[208] 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.[202]

ECT appears to work in the short term via an anticonvulsant effect mostly in the frontal lobes, and longer term via neurotrophic effects primarily in the medial temporal lobe.[209]

Other

Transcranial magnetic stimulation (TMS) or deep transcranial magnetic stimulation is a noninvasive method used to stimulate small regions of the brain.[210] TMS was approved by the FDA for treatment-resistant major depressive disorder (trMDD) in 2008[211] and as of 2014 evidence supports that it is probably effective.[212] The American Psychiatric Association,[213] the Canadian Network for Mood and Anxiety Disorders,[214] and the Royal Australia and New Zealand College of Psychiatrists have endorsed TMS for trMDD.[215] 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.[216][217]

There is a small amount of evidence that sleep deprivation may improve depressive symptoms in some individuals,[218] with the effects usually showing up within a day. This effect is usually temporary. Besides sleepiness, this method can cause a side effect of mania or hypomania.[219] There is insufficient evidence for Reiki[220] and dance movement therapy in depression.[221] Cannabis is specifically not recommended as a treatment.[222]

Prognosis

Studies have shown that 80% of those with a first major depressive episode will have at least one more during their life,[223] with a lifetime average of four episodes.[224] 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.[225] 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.[226][227] 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, and family dysfunction.[228]

A high proportion of people who experience full symptomatic remission still have at least one not fully resolved symptom after treatment.[229] Recurrence or chronicity is more likely if symptoms have not fully resolved with treatment.[229] Current guidelines recommend continuing antidepressants for four to six months after remission to prevent relapse. Evidence from many randomized controlled trials indicates continuing antidepressant medications after recovery can reduce the chance of relapse by 70% (41% on placebo vs. 18% on antidepressant). The preventive effect probably lasts for at least the first 36 months of use.[230]

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.[231] The median duration of an episode has been estimated to be 23 weeks, with the highest rate of recovery in the first three months.[232] 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.[233]

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.[141] 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.[141]

Life expectancy and the risk of suicide

Depressed individuals have a shorter life expectancy than those without depression, in part because people who are depressed are at risk of dying of suicide.[234] About 50% of people who die of suicide have a mood disorder such as major depression, and the risk is especially high if a person has a marked sense of hopelessness or has both depression and borderline personality disorder.[235][236] About 2–8% of adults with major depression die by suicide.[2][237] 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,[238] even though suicide attempts are more frequent in women.[239]

Depressed people have a higher rate of dying from other causes.[240] There is a 1.5- to 2-fold increased risk of cardiovascular disease, independent of other known risk factors, and is itself linked directly or indirectly to risk factors such as smoking and obesity. People with major depression are less likely to follow medical recommendations for treating and preventing cardiovascular disorders, further increasing their risk of medical complications.[241] Cardiologists may not recognize underlying depression that complicates a cardiovascular problem under their care.[242]

Epidemiology

Main article: Epidemiology of depression
 
Disability-adjusted life year for unipolar depressive disorders per 100,000 inhabitants in 2004.[243]
  no data
  <700
  700–775
  775–850
  850–925
  925–1000
  1000–1075
  1075–1150
  1150–1225
  1225–1300
  1300–1375
  1375–1450
  >1450

Major depressive disorder affected approximately 163 million people in 2017 (2% of the global population).[8] The percentage of people who are affected at one point in their life varies from 7% in Japan to 21% in France.[4] In most countries the number of people who have depression during their lives falls within an 8–18% range.[4]

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%).[244] Among adolescents between the ages of 12 and 17, 17% of the U.S. population (4.1 million individuals) had a major depressive episode in 2020 (females 25.2%, males 9.2%).[244] Among individuals reporting two or more races, the US prevalence is highest.[244]

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.[245] 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.[245] In 2019, major depressive disorder was identified (using either the DSM-IV-TR or ICD-10) in the Global Burden of Disease Study as the fifth most common cause of years lived with disability and the 18th most common for disability-adjusted life years.[246]

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.[247] The risk of major depression is increased with neurological conditions such as stroke, Parkinson's disease, or multiple sclerosis, and during the first year after childbirth.[248] It is also more common after cardiovascular illnesses, and is related more to those with a poor cardiac disease outcome than to a better one.[249][250] 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.[251] Depression is common among those over 65 years of age and increases in frequency beyond this age.[27] The risk of depression increases in relation to the frailty of the individual.[252] Depression is one of the most important factors which negatively impact quality of life in adults, as well as the elderly.[27] Both symptoms and treatment among the elderly differ from those of the rest of the population.[27]

Major depression was the leading cause of disease burden in 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 after HIV, according to the WHO.[253] Delay or failure in seeking treatment after relapse and the failure of health professionals to provide treatment are two barriers to reducing disability.[254]

Comorbidity

Major depression frequently co-occurs with other psychiatric problems. The 1990–92 National Comorbidity Survey (US) reported that half of those with major depression also have lifetime anxiety and its associated disorders, such as generalized anxiety disorder.[255] 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.[256] Depressed people have increased rates of alcohol and substance use, particularly dependence,[257][258] and around a third of individuals diagnosed with attention deficit hyperactivity disorder (ADHD) develop comorbid depression.[259] Post-traumatic stress disorder and depression often co-occur.[15] Depression may also coexist with ADHD, complicating the diagnosis and treatment of both.[260] Depression is also frequently comorbid with alcohol use disorder and personality disorders.[261] Depression can also be exacerbated during particular months (usually winter) in those with seasonal affective disorder. While overuse of digital media has been associated with depressive symptoms, using digital media may also improve mood in some situations.[262][263]

Depression and pain often 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.[264] Depression often coexists with physical disorders common among the elderly, such as stroke, other cardiovascular diseases, Parkinson's disease, and chronic obstructive pulmonary disease.[265]

History

Main article: History of depression

The Ancient Greek physician Hippocrates described a syndrome of melancholia (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.[266] 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.[267]

 
Diagnoses of depression go back at least as far as Hippocrates.

The term depression itself was derived from the Latin verb deprimere, meaning "to press down".[268] From the 14th century, "to depress" meant to subjugate or to bring down in spirits. It was used in 1665 in English author Richard Baker's Chronicle to refer to someone having "a great depression of spirit", and by English author Samuel Johnson in a similar sense in 1753.[269] The term also came into use in physiology and economics. An early usage referring to a psychiatric symptom was by French psychiatrist Louis Delasiauve in 1856, and by the 1860s it was appearing in medical dictionaries to refer to a physiological and metaphorical lowering of emotional function.[270] 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.[267]

Although melancholia remained the dominant diagnostic term, depression gained increasing currency in medical treatises and was a synonym by the end of the century; German psychiatrist Emil Kraepelin may have been the first to use it as the overarching term, referring to different kinds of melancholia as depressive states.[271] Freud likened the state of melancholia to mourning in his 1917 paper Mourning and Melancholia. He theorized that objective loss, such as the loss of a valued relationship through death or a romantic break-up, results in subjective loss as well; the depressed individual has identified with the object of affection through an unconscious, narcissistic process called the libidinal cathexis of the ego. Such loss results in severe melancholic symptoms more profound than mourning; not only is the outside world viewed negatively but the ego itself is compromised.[272] The person's decline of self-perception is revealed in his belief of his own blame, inferiority, and unworthiness.[273] He also emphasized early life experiences as a predisposing factor.[267] 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.[274] The first version of the DSM (DSM-I, 1952) contained depressive reaction and the DSM-II (1968) depressive neurosis, defined as an excessive reaction to internal conflict or an identifiable event, and also included a depressive type of manic-depressive psychosis within Major affective disorders.[275]

The term unipolar (along with the related term bipolar) was coined by the neurologist and psychiatrist Karl Kleist, and subsequently used by his disciples Edda Neele and Karl Leonhard.[276]

The term Major depressive disorder was introduced by a group of US clinicians in the mid-1970s as part of proposals for diagnostic criteria based on patterns of symptoms (called the "Research Diagnostic Criteria", building on earlier Feighner Criteria),[10] and was incorporated into the DSM-III in 1980.[277] The American Psychiatric Association added "major depressive disorder" to the Diagnostic and Statistical Manual of Mental Disorders (DSM-III),[278] as a split of the previous depressive neurosis in the DSM-II, which also encompassed the conditions now known as dysthymia and adjustment disorder with depressed mood.[278] 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.[90][277] The ancient idea of melancholia still survives in the notion of a melancholic subtype.

The new definitions of depression were widely accepted, albeit with some conflicting findings and views. There have been some continued empirically based arguments for a return to the diagnosis of melancholia.[279][280] 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.[281]

Society and culture

Further information: Depression and culture

Terminology

 
The 16th American president, Abraham Lincoln, had "melancholy", a condition that now may be referred to as clinical depression.[282]

The term "depression" is used in a number of different ways. It is often used to mean this syndrome but may refer to other mood disorders or 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."[283] 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.[284][285]

Stigma

Historical figures were often reluctant to discuss or seek treatment for depression due to social stigma about the condition, or due to ignorance of diagnosis or treatments. Nevertheless, analysis or interpretation of letters, journals, artwork, writings, or statements of family and friends of some historical personalities has led to the presumption that they may have had some form of depression. People who may have had depression include English author Mary Shelley,[286] American-British writer Henry James,[287] and American president Abraham Lincoln.[288] Some well-known contemporary people with possible depression include Canadian songwriter Leonard Cohen[289] and American playwright and novelist Tennessee Williams.[290] Some pioneering psychologists, such as Americans William James[291][292] and John B. Watson,[293] dealt with their own depression.

There has been a continuing discussion of whether neurological disorders and mood disorders may be linked to creativity, a discussion that goes back to Aristotelian times.[294][295] British literature gives many examples of reflections on depression.[296] English philosopher John Stuart Mill experienced a several-months-long period of what he called "a dull state of nerves", when one is "unsusceptible to enjoyment or pleasurable excitement; one of those moods when what is pleasure at other times, becomes insipid or indifferent". He quoted English poet Samuel Taylor Coleridge's "Dejection" as a perfect description of his case: "A grief without a pang, void, dark and drear, / A drowsy, stifled, unimpassioned grief, / Which finds no natural outlet or relief / In word, or sigh, or tear."[297][298] English writer Samuel Johnson used the term "the black dog" in the 1780s to describe his own depression,[299] and it was subsequently popularized by British Prime Minister Sir Winston Churchill, who also had the disorder.[299] Johann Wolfgang von Goethe in his Faust, Part I, published in 1808, has Mephistopheles assume the form of a black dog, specifically a poodle.

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.[300] In the UK, the Royal College of Psychiatrists and the Royal College of General Practitioners conducted a joint Five-year Defeat Depression campaign to educate and reduce stigma from 1992 to 1996;[301] a MORI study conducted afterwards showed a small positive change in public attitudes to depression and treatment.[302]

References

  1. ^ a b c d e f g h i "Depression". U.S. National Institute of Mental Health (NIMH). May 2016. from the original on 5 August 2016. Retrieved 31 July 2016.
  2. ^ a b Richards CS, O'Hara MW (2014). The Oxford Handbook of Depression and Comorbidity. Oxford University Press. p. 254. ISBN 978-0-19-979704-2.
  3. ^ a b American Psychiatric Association 2013, p. 165.
  4. ^ a b c d e f g Kessler RC, Bromet EJ (2013). "The epidemiology of depression across cultures". Annual Review of Public Health. 34: 119–38. doi:10.1146/annurev-publhealth-031912-114409. PMC 4100461. PMID 23514317.
  5. ^ a b c d e f g American Psychiatric Association 2013, p. 166.
  6. ^ American Psychiatric Association 2013, pp. 167–168.
  7. ^ a b Cooney GM, Dwan K, Greig CA, Lawlor DA, Rimer J, Waugh FR, McMurdo M, Mead GE (September 2013). Mead GE (ed.). "Exercise for depression". The Cochrane Database of Systematic Reviews. 2013 (9): CD004366. doi:10.1002/14651858.CD004366.pub6. PMC 9721454. PMID 24026850.
  8. ^ a b c GBD 2017 Disease and Injury Incidence and Prevalence Collaborators (10 November 2018). "Global, regional, and national incidence, prevalence, and years lived with disability for 354 diseases and injuries for 195 countries and territories, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017". Lancet. 392 (10159): 1789–1858. doi:10.1016/S0140-6736(18)32279-7. PMC 6227754. PMID 30496104.
  9. ^ Sartorius N, Henderson AS, Strotzka H, et al. "The ICD-10 Classification of Mental and Behavioural Disorders Clinical descriptions and diagnostic guidelines" (PDF). World Health Organization. (PDF) from the original on 5 February 2022. Retrieved 23 June 2021.
  10. ^ a b Spitzer RL, Endicott J, Robins E (1975). "The development of diagnostic criteria in psychiatry" (PDF). (PDF) from the original on 14 December 2005. Retrieved 8 November 2008.
  11. ^ a b Patton LL (2015). The ADA Practical Guide to Patients with Medical Conditions (2nd ed.). John Wiley & Sons. p. 339. ISBN 978-1-118-92928-5.
  12. ^ Fournier JC, DeRubeis RJ, Hollon SD, Dimidjian S, Amsterdam JD, Shelton RC, Fawcett J (January 2010). "Antidepressant drug effects and depression severity: a patient-level meta-analysis". JAMA. 303 (1): 47–53. doi:10.1001/jama.2009.1943. PMC 3712503. PMID 20051569.
  13. ^ Kirsch I, Deacon BJ, Huedo-Medina TB, Scoboria A, Moore TJ, Johnson BT (February 2008). "Initial severity and antidepressant benefits: a meta-analysis of data submitted to the Food and Drug Administration". PLOS Medicine. 5 (2): e45. doi:10.1371/journal.pmed.0050045. PMC 2253608. PMID 18303940.
  14. ^ Global Burden of Disease Study 2013 Collaborators (August 2015). "Global, regional, and national incidence, prevalence, and years lived with disability for 301 acute and chronic diseases and injuries in 188 countries, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013". Lancet. 386 (9995): 743–800. doi:10.1016/S0140-6736(15)60692-4. PMC 4561509. PMID 26063472.
  15. ^ a b c d e Depression (PDF). National Institute of Mental Health (NIMH). (PDF) from the original on 28 August 2021. Retrieved 13 October 2021.
  16. ^ American Psychiatric Association 2013, p. 160.
  17. ^ American_Psychiatric_Association 2013, p. 161.
  18. ^ a b c American Psychiatric Association 2013, p. 163.
  19. ^ "Insomnia: Assessment and Management in Primary Care". American Family Physician. 59 (11): 3029–3038. 1999. from the original on 26 July 2011. Retrieved 12 November 2014.
  20. ^ American Psychiatric Association 2000a, p. 412
  21. ^ Nelson JC, Bickford D, Delucchi K, Fiedorowicz JG, Coryell WH (2018). "Risk of Psychosis in Recurrent Episodes of Psychotic and Nonpsychotic Major Depressive Disorder: A Systematic Review and Meta-Analysis". Am J Psychiatry. 175 (9): 897–904. doi:10.1176/appi.ajp.2018.17101138. PMID 29792050. S2CID 43951278.
  22. ^ Fisher JC, Powers WE, Tuerk DB, Edgerton MT (March 1975). "Development of a plastic surgical teaching service in a women's correctional institution". American Journal of Surgery. 129 (3): 269–72. doi:10.1136/bmj.322.7284.482. PMC 1119689. PMID 11222428.
  23. ^ a b c American Psychiatric Association 2000a, p. 349
  24. ^ Delgado PL, Schillerstrom J (2009). "Cognitive Difficulties Associated With Depression: What Are the Implications for Treatment?". Psychiatric Times. 26 (3). from the original on 22 July 2009.
  25. ^ Faculty of Psychiatry of Old Age, NSW Branch, RANZCP, Kitching D, Raphael B (2001). Consensus Guidelines for Assessment and Management of Depression in the Elderly (PDF). North Sydney, New South Wales: NSW Health Department. p. 2. ISBN 978-0-7347-3341-2. (PDF) from the original on 1 April 2015.
  26. ^ American Psychiatric Association 2013, p. 164.
  27. ^ a b c d e Swedish Agency for Health Technology Assessment and Assessment of Social Services (SBU) (27 January 2015). "Depression treatment for the elderly". sbu.se. from the original on 18 June 2016. Retrieved 16 June 2016.
  28. ^ Hankin BL, Abela JR (2005). Development of Psychopathology: A Vulnerability-Stress Perspective. SAGE Publications. pp. 32–34. ISBN 9781412904902.
  29. ^ Department of Health and Human Services (1999). "The fundamentals of mental health and mental illness" (PDF). Mental Health: A Report of the Surgeon General. (PDF) from the original on 17 December 2008. Retrieved 11 November 2008.
  30. ^ Caspi A, Sugden K, Moffitt TE, Taylor A, Craig IW, Harrington H, McClay J, Mill J, Martin J, Braithwaite A, Poulton R (July 2003). "Influence of life stress on depression: moderation by a polymorphism in the 5-HTT gene". Science. 301 (5631): 386–89. Bibcode:2003Sci...301..386C. doi:10.1126/science.1083968. PMID 12869766. S2CID 146500484.
  31. ^ Haeffel GJ, Getchell M, Koposov RA, Yrigollen CM, Deyoung CG, Klinteberg BA, Oreland L, Ruchkin VV, Grigorenko EL (January 2008). "Association between polymorphisms in the dopamine transporter gene and depression: evidence for a gene-environment interaction in a sample of juvenile detainees" (PDF). Psychological Science. 19 (1): 62–69. doi:10.1111/j.1467-9280.2008.02047.x. PMID 18181793. S2CID 15520723. (PDF) from the original on 17 December 2008.
  32. ^ Slavich GM (2004). "Deconstructing depression: A diathesis-stress perspective (Opinion)". APS Observer. from the original on 11 May 2011. Retrieved 11 November 2008.
  33. ^ Beck AT, Rush AJ, Shaw BF, Emery G (1979). Cognitive therapy of depression. New York: The Guilford Press. pp. 11–12. ISBN 0-89862-000-7. Retrieved 26 February 2022.
  34. ^ Nieto I, Robles E, Vasquez C (1 November 2020). "Self-reported cognitive biases in depression: A meta-analysis". Clinical Psychology Review. ScienceDirect. 82: 101934. doi:10.1016/j.cpr.2020.101934. PMID 33137610. S2CID 226243519. Retrieved 26 February 2022.
  35. ^ Saveanu RV, Nemeroff CB (March 2012). "Etiology of depression: genetic and environmental factors". The Psychiatric Clinics of North America. 35 (1): 51–71. doi:10.1016/j.psc.2011.12.001. PMID 22370490.
  36. ^ Sullivan PF, Neale MC, Kendler KS (October 2000). "Genetic epidemiology of major depression: review and meta-analysis". The American Journal of Psychiatry. 157 (10): 1552–62. doi:10.1176/appi.ajp.157.10.1552. PMID 11007705.
  37. ^ Wray NR (May 2018). "Genome-wide association analyses identify 44 risk variants and refine the genetic architecture of major depression". Nature Genetics. 50 (5): 668–681. doi:10.1038/s41588-018-0090-3. hdl:11370/3a0e2468-99e7-40c3-80f4-9d25adfae485. PMC 5934326. PMID 29700475.
  38. ^ Howard DM, Adams MJ, Clarke TK, Hafferty JD, Gibson J, Shirali M, et al. (March 2019). "Genome-wide meta-analysis of depression identifies 102 independent variants and highlights the importance of the prefrontal brain regions". Nature Neuroscience. 22 (3): 343–352. doi:10.1038/s41593-018-0326-7. PMC 6522363. PMID 30718901.
  39. ^ Duncan LE, Keller MC (October 2011). "A critical review of the first 10 years of candidate gene-by-environment interaction research in psychiatry". The American Journal of Psychiatry. 168 (10): 1041–9. doi:10.1176/appi.ajp.2011.11020191. PMC 3222234. PMID 21890791.
  40. ^ Peyrot WJ, Van der Auwera S, Milaneschi Y, Dolan CV, Madden PA, Sullivan PF, Strohmaier J, Ripke S, Rietschel M, Nivard MG, Mullins N, Montgomery GW, Henders AK, Heat AC, Fisher HL, Dunn EC, Byrne EM, et al. (July 2018). "Does Childhood Trauma Moderate Polygenic Risk for Depression? A Meta-analysis of 5765 Subjects From the Psychiatric Genomics Consortium". Biological Psychiatry. 84 (2): 138–147. doi:10.1016/j.biopsych.2017.09.009. PMC 5862738. PMID 29129318.
  41. ^ Simon GE (November 2001). "Treating depression in patients with chronic disease: recognition and treatment are crucial; depression worsens the course of a chronic illness". The Western Journal of Medicine. 175 (5): 292–93. doi:10.1136/ewjm.175.5.292. PMC 1071593. PMID 11694462.
  42. ^ Clayton PJ, Lewis CE (March 1981). "The significance of secondary depression". Journal of Affective Disorders. 3 (1): 25–35. doi:10.1016/0165-0327(81)90016-1. PMID 6455456.
  43. ^ Kewalramani A, Bollinger ME, Postolache TT (1 January 2008). "Asthma and Mood Disorders". International Journal of Child Health and Human Development. 1 (2): 115–23. PMC 2631932. PMID 19180246.
  44. ^ Rogers D, Pies R (December 2008). "General medical with depression drugs associated". Psychiatry. 5 (12): 28–41. PMC 2729620. PMID 19724774.
  45. ^ Botts S, Ryan M. . pp. 1–23. Archived from the original on 23 December 2010.
  46. ^ Brook DW, Brook JS, Zhang C, Cohen P, Whiteman M (November 2002). "Drug use and the risk of major depressive disorder, alcohol dependence, and substance use disorders". Archives of General Psychiatry. 59 (11): 1039–44. doi:10.1001/archpsyc.59.11.1039. PMID 12418937.
  47. ^ Meltzer-Brody S (9 January 2017). "New insights into perinatal depression: pathogenesis and treatment during pregnancy and postpartum". Dialogues in Clinical Neuroscience. 13 (1): 89–100. doi:10.31887/DCNS.2011.13.1/smbrody. PMC 3181972. PMID 21485749.
  48. ^ Melrose S (1 January 2015). "Seasonal Affective Disorder: An Overview of Assessment and Treatment Approaches". Depression Research and Treatment. 2015: 178564. doi:10.1155/2015/178564. PMC 4673349. PMID 26688752.
  49. ^ Wu Y, Zhang L, Li S, Zhang D (29 April 2021). "Associations of dietary vitamin B1, vitamin B2, vitamin B6, and vitamin B12 with the risk of depression: a systematic review and meta-analysis". Nutrition Reviews. Oxford University Press (OUP). 80 (3): 351–366. doi:10.1093/nutrit/nuab014. ISSN 0029-6643. PMID 33912967.
  50. ^ Ruhé HG, Mason NS, Schene AH (April 2007). "Mood is indirectly related to serotonin, norepinephrine and dopamine levels in humans: a meta-analysis of monoamine depletion studies". Molecular Psychiatry. 12 (4): 331–59. doi:10.1038/sj.mp.4001949. PMID 17389902.
  51. ^ Delgado PL, Moreno FA (2000). "Role of norepinephrine in depression". The Journal of Clinical Psychiatry. 61 (Suppl 1): 5–12. PMID 10703757.
  52. ^ Savitz JB, Drevets WC (April 2013). "Neuroreceptor imaging in depression". Neurobiology of Disease. 52: 49–65. doi:10.1016/j.nbd.2012.06.001. PMID 22691454.
  53. ^ Hasler G (October 2010). "Pathophysiology of depression: do we have any solid evidence of interest to clinicians?". World Psychiatry. 9 (3): 155–61. doi:10.1002/j.2051-5545.2010.tb00298.x. PMC 2950973. PMID 20975857.
  54. ^ Dunlop BW, Nemeroff CB (March 2007). "The role of dopamine in the pathophysiology of depression". Archives of General Psychiatry. 64 (3): 327–37. doi:10.1001/archpsyc.64.3.327. PMID 17339521.
  55. ^ Meyer JH, Ginovart N, Boovariwala A, et al. (November 2006). "Elevated monoamine oxidase a levels in the brain: an explanation for the monoamine imbalance of major depression". Archives of General Psychiatry. 63 (11): 1209–16. doi:10.1001/archpsyc.63.11.1209. PMID 17088501.
  56. ^ Davis KL, Charney D, Coyle JT, Nemeroff C, eds. (2002). Neuropsychopharmacology: the fifth generation of progress: an official publication of the American College of Neuropsychopharmacology (5th ed.). Philadelphia: Lippincott Williams & Wilkins. pp. 1139–63. ISBN 978-0-7817-2837-9.
  57. ^ Adell A (April 2015). "Revisiting the role of raphe and serotonin in neuropsychiatric disorders". The Journal of General Physiology. 145 (4): 257–59. doi:10.1085/jgp.201511389. PMC 4380212. PMID 25825168.
  58. ^ Andrews PW, Bharwani A, Lee KR, Fox M, Thomson JA (April 2015). "Is serotonin an upper or a downer? The evolution of the serotonergic system and its role in depression and the antidepressant response". Neuroscience and Biobehavioral Reviews. 51: 164–88. doi:10.1016/j.neubiorev.2015.01.018. PMID 25625874. S2CID 23980182.
  59. ^ Lacasse JR, Leo J (December 2005). "Serotonin and depression: a disconnect between the advertisements and the scientific literature". PLOS Medicine. 2 (12): e392. doi:10.1371/journal.pmed.0020392. PMC 1277931. PMID 16268734.
  60. ^ Moncrieff J, Cooper RE, Stockman T, et al. (July 2022). "The serotonin theory of depression: a systematic umbrella review of the evidence". Mol Psychiatry. doi:10.1038/s41380-022-01661-0. PMID 35854107. S2CID 250646781. Lay source Medicalxpress
  61. ^ Krishnadas R, Cavanagh J (May 2012). "Depression: an inflammatory illness?". Journal of Neurology, Neurosurgery, and Psychiatry. 83 (5): 495–502. doi:10.1136/jnnp-2011-301779. PMID 22423117.
  62. ^ Patel A (September 2013). "Review: the role of inflammation in depression". Psychiatria Danubina. 25 (Suppl 2): S216–23. PMID 23995180.
  63. ^ Dowlati Y, Herrmann N, Swardfager W, Liu H, Sham L, Reim EK, Lanctôt KL (March 2010). "A meta-analysis of cytokines in major depression". Biological Psychiatry. 67 (5): 446–57. doi:10.1016/j.biopsych.2009.09.033. PMID 20015486. S2CID 230209.
  64. ^ Köhler O, Benros ME, Nordentoft M, Farkouh ME, Iyengar RL, Mors O, Krogh J (December 2014). "Effect of anti-inflammatory treatment on depression, depressive symptoms, and adverse effects: a systematic review and meta-analysis of randomized clinical trials" (PDF). JAMA Psychiatry. 71 (12): 1381–91. doi:10.1001/jamapsychiatry.2014.1611. PMID 25322082. (PDF) from the original on 20 July 2018.
  65. ^ Raedler TJ (November 2011). "Inflammatory mechanisms in major depressive disorder". Current Opinion in Psychiatry. 24 (6): 519–25. doi:10.1097/YCO.0b013e32834b9db6. PMID 21897249. S2CID 24215407.
  66. ^ Arana GW, Baldessarini RJ, Ornsteen M (December 1985). "The dexamethasone suppression test for diagnosis and prognosis in psychiatry. Commentary and review". Archives of General Psychiatry. 42 (12): 1193–204. doi:10.1001/archpsyc.1985.01790350067012. PMID 3000317.
  67. ^ Varghese FP, Brown ES (August 2001). "The Hypothalamic-Pituitary-Adrenal Axis in Major Depressive Disorder: A Brief Primer for Primary Care Physicians". Primary Care Companion to the Journal of Clinical Psychiatry. 3 (4): 151–55. doi:10.4088/pcc.v03n0401. PMC 181180. PMID 15014598.
  68. ^ Lopez-Duran NL, Kovacs M, George CJ (2009). "Hypothalamic-pituitary-adrenal axis dysregulation in depressed children and adolescents: a meta-analysis". Psychoneuroendocrinology. 34 (9): 1272–1283. doi:10.1016/j.psyneuen.2009.03.016. PMC 2796553. PMID 19406581.
  69. ^ Dedovic K, Ngiam J (2015). "The cortisol awakening response and major depression: examining the evidence". Neuropsychiatric Disease and Treatment. 11: 1181–1189. doi:10.2147/NDT.S62289. PMC 4437603. PMID 25999722.
  70. ^ Mayberg HS (1997). "Limbic-cortical dysregulation: a proposed model of depression". The Journal of Neuropsychiatry and Clinical Neurosciences. 9 (3): 471–81. doi:10.1176/jnp.9.3.471. PMID 9276848.
  71. ^ Graham J, Salimi-Khorshidi G, Hagan C, Walsh N, Goodyer I, Lennox B, Suckling J (2013). "Meta-analytic evidence for neuroimaging models of depression: state or trait?". Journal of Affective Disorders. 151 (2): 423–431. doi:10.1016/j.jad.2013.07.002. PMID 23890584.
  72. ^ Hamilton JP, Etkin A, Furman DJ, Lemus MG, Johnson RF, Gotlib IH (July 2012). "Functional neuroimaging of major depressive disorder: a meta-analysis and new integration of base line activation and neural response data". The American Journal of Psychiatry. 169 (7): 693–703. doi:10.1176/appi.ajp.2012.11071105. PMID 22535198.
  73. ^ Kaufmann IM (1993). "Rural psychiatric services. A collaborative model". Canadian Family Physician. 39: 1957–1961. PMC 2379905. PMID 8219844.
  74. ^ "Call for action over Third World depression". BBC News (Health). British Broadcasting Corporation (BBC). 1 November 1999. from the original on 13 May 2008. Retrieved 11 October 2008.
  75. ^ Sharp LK, Lipsky MS (September 2002). "Screening for depression across the lifespan: a review of measures for use in primary care settings". American Family Physician. 66 (6): 1001–08. PMID 12358212.
  76. ^ Zimmerman M, Chelminski I, Posternak M (September 2004). "A review of studies of the Hamilton depression rating scale in healthy controls: implications for the definition of remission in treatment studies of depression". The Journal of Nervous and Mental Disease. 192 (9): 595–601. doi:10.1097/01.nmd.0000138226.22761.39. PMID 15348975. S2CID 24291799.
  77. ^ McPherson A, Martin CR (February 2010). "A narrative review of the Beck Depression Inventory (BDI) and implications for its use in an alcohol-dependent population". Journal of Psychiatric and Mental Health Nursing. 17 (1): 19–30. doi:10.1111/j.1365-2850.2009.01469.x. PMID 20100303.
  78. ^ Osman A, Bagge CL, Gutierrez PM, Konick LC, Kopper BA, Barrios FX (December 2001). "The Suicidal Behaviors Questionnaire-Revised (SBQ-R): validation with clinical and nonclinical samples". Assessment. 8 (4): 443–54. doi:10.1177/107319110100800409. PMID 11785588. S2CID 11477277.
  79. ^ Cepoiu M, McCusker J, Cole MG, Sewitch M, Belzile E, Ciampi A (January 2008). "Recognition of depression by non-psychiatric physicians—a systematic literature review and meta-analysis". Journal of General Internal Medicine. 23 (1): 25–36. doi:10.1007/s11606-007-0428-5. PMC 2173927. PMID 17968628.
  80. ^ Dale J, Sorour E, Milner G (2008). "Do psychiatrists perform appropriate physical investigations for their patients? A review of current practices in a general psychiatric inpatient and outpatient setting". Journal of Mental Health. 17 (3): 293–98. doi:10.1080/09638230701498325. S2CID 72755878.
  81. ^ Orengo CA, Fullerton G, Tan R (October 2004). "Male depression: a review of gender concerns and testosterone therapy". Geriatrics. 59 (10): 24–30. PMID 15508552.
  82. ^ a b Parker GB, Brotchie H, Graham RK (January 2017). "Vitamin D and depression". Journal of Affective Disorders. 208: 56–61. doi:10.1016/j.jad.2016.08.082. PMID 27750060.
  83. ^ Reid LM, Maclullich AM (2006). "Subjective memory complaints and cognitive impairment in older people". Dementia and Geriatric Cognitive Disorders. 22 (5–6): 471–85. doi:10.1159/000096295. PMID 17047326. S2CID 9328852.
  84. ^ Katz IR (1998). "Diagnosis and treatment of depression in patients with Alzheimer's disease and other dementias". The Journal of Clinical Psychiatry. 59 (Suppl 9): 38–44. PMID 9720486.
  85. ^ Wright SL, Persad C (December 2007). "Distinguishing between depression and dementia in older persons: neuropsychological and neuropathological correlates". Journal of Geriatric Psychiatry and Neurology. 20 (4): 189–98. doi:10.1177/0891988707308801. PMID 18004006. S2CID 33714179.
  86. ^ Sadock 2002, p. 108
  87. ^ Sadock 2002, p. 260
  88. ^ Sadock 2002, p. 288
  89. ^ American Psychiatric Association 2013, p. xii.
  90. ^ a b Gruenberg AM, Goldstein RD, Pincus HA (2005). "Classification of Depression: Research and Diagnostic Criteria: DSM-IV and ICD-10" (PDF). In Licinio J, Wong ML (eds.). Biology of Depression. Biology of Depression: From Novel Insights to Therapeutic Strategies. Wiley-VCH Verlag GmbH. pp. 1–12. doi:10.1002/9783527619672.ch1. ISBN 978-3-527-61967-2. (PDF) from the original on 3 May 2005. Retrieved 30 October 2008.
  91. ^ "Diagnostic and Statistical Manual of Mental Disorders (DSM-5-TR)". American Psychiatric Association. Retrieved 9 July 2022. The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR) features the most current text updates based on scientific literature with contributions from more than 200 subject matter experts.
  92. ^ "International Statistical Classification of Diseases and Related Health Problems (ICD)". World Health Organization. Retrieved 9 July 2022. ... the latest version of the ICD, ICD-11, was adopted by the 72nd World Health Assembly in 2019 and came into effect on 1st January 2022.
  93. ^ a b c d ICD-11, 6A70 Single episode depressive disorder and 6A71 Recurrent depressive disorder
  94. ^ (PDF). City of Palo Alto Project Safety Net. Archived from the original (PDF) on 3 August 2020. Retrieved 21 February 2019.
  95. ^ a b c d Parker GF (1 June 2014). "DSM-5 and Psychotic and Mood Disorders". Journal of the American Academy of Psychiatry and the Law Online. 42 (2): 182–190. ISSN 1093-6793. PMID 24986345.
  96. ^ American Psychiatric Association 2013, p. 162
  97. ^ Parker 1996, p. 173
  98. ^ a b Sadock 2002, p. 552
  99. ^ American Psychiatric Association 2013, p. 183.
  100. ^ Carta MG, Altamura AC, Hardoy MC, Pinna F, Medda S, Dell'Osso L, Carpiniello B, Angst J (June 2003). "Is recurrent brief depression an expression of mood spectrum disorders in young people? Results of a large community sample". European Archives of Psychiatry and Clinical Neuroscience. 253 (3): 149–53. doi:10.1007/s00406-003-0418-5. hdl:2434/521599. PMID 12904979. S2CID 26860606.
  101. ^ Rapaport MH, Judd LL, Schettler PJ, Yonkers KA, Thase ME, Kupfer DJ, Frank E, Plewes JM, Tollefson GD, Rush AJ (April 2002). "A descriptive analysis of minor depression". The American Journal of Psychiatry. 159 (4): 637–43. doi:10.1176/appi.ajp.159.4.637. PMID 11925303.
  102. ^ a b American Psychiatric Association 2013, p. 168.
  103. ^ American Psychiatric Association 2013, p. 185.
  104. ^ American Psychiatric Association 2013, pp. 185–186.
  105. ^ American Psychiatric Association 2013, pp. 119–120.
  106. ^ American Psychiatric Association 2013, pp. 186–187.
  107. ^ American Psychiatric Association 2013, p. 187.
  108. ^ American_Psychiatric_Association 2013, p. 167.
  109. ^ a b Cuijpers P, van Straten A, Smit F, Mihalopoulos C, Beekman A (October 2008). "Preventing the onset of depressive disorders: a meta-analytic review of psychological interventions". The American Journal of Psychiatry. 165 (10): 1272–80. doi:10.1176/appi.ajp.2008.07091422. hdl:1871/16952. PMID 18765483.
  110. ^ Siu AL, Bibbins-Domingo K, Grossman DC, et al. (January 2016). "Screening for Depression in Adults: US Preventive Services Task Force Recommendation Statement". JAMA. 315 (4): 380–87. doi:10.1001/jama.2015.18392. PMID 26813211.
  111. ^ Siu AL (March 2016). "Screening for Depression in Children and Adolescents: U.S. Preventive Services Task Force Recommendation Statement". Annals of Internal Medicine. 164 (5): 360–66. doi:10.7326/M15-2957. PMID 26858097.
  112. ^ Gilbody S, House AO, Sheldon TA (October 2005). "Screening and case finding instruments for depression". The Cochrane Database of Systematic Reviews. 2005 (4): CD002792. doi:10.1002/14651858.CD002792.pub2. PMC 6769050. PMID 16235301.
  113. ^ Ferenchick EK, Ramanuj P, Pincus HA (2019). "Depression in primary care: part 1—screening and diagnosis". British Medical Journal. 365: l794. doi:10.1136/bmj.l794. PMID 30962184. S2CID 104296515.
  114. ^ a b Muñoz RF, Beardslee WR, Leykin Y (May–June 2012). "Major depression can be prevented". The American Psychologist. 67 (4): 285–95. doi:10.1037/a0027666. PMC 4533896. PMID 22583342.
  115. ^ Cuijpers P (20 September 2012). (PDF). Psychology for Health: Contributions to Policy Making, Brussels. Archived from the original (PDF) on 12 May 2013. Retrieved 16 June 2013.
  116. ^ Griffiths KM, Farrer L, Christensen H (2010). "The efficacy of internet interventions for depression and anxiety disorders: a review of randomised controlled trials" (PDF). Medical Journal of Australia. 192 (11): 4–11. doi:10.5694/j.1326-5377.2010.tb03685.x. PMID 20528707. S2CID 1948009. (PDF) from the original on 12 November 2014. Retrieved 12 November 2014.
  117. ^ Cuijpers P, Muñoz RF, Clarke GN, Lewinsohn PM (July 2009). "Psychoeducational treatment and prevention of depression: the "Coping with Depression" course thirty years later". Clinical Psychology Review. 29 (5): 449–58. doi:10.1016/j.cpr.2009.04.005. PMID 19450912.
  118. ^ Karrouri R, Hammani Z, Benjelloun R, Otheman Y (November 2021). "Major depressive disorder: Validated treatments and future challenges". World J Clin Cases (Review). 9 (31): 9350–9367. doi:10.12998/wjcc.v9.i31.9350. PMC 8610877. PMID 34877271.
  119. ^ a b c "Practice guideline for the treatment of patients with major depressive disorder (revision). American Psychiatric Association". The American Journal of Psychiatry. 157 (4 Suppl): 1–45. April 2000. PMID 10767867.; Third edition doi:10.1176/appi.books.9780890423363.48690
  120. ^ Archer J, Bower P, Gilbody S, et al. (October 2012). "Collaborative care for depression and anxiety problems". The Cochrane Database of Systematic Reviews. 10: CD006525. doi:10.1002/14651858.CD006525.pub2. hdl:10871/13751. PMID 23076925.
  121. ^ a b c "Depression". National Institute for Health and Care Excellence. December 2004. from the original on 15 November 2008. Retrieved 20 March 2013.
  122. ^ Hetrick SE, Cox GR, Witt KG, Bir JJ, Merry SN (August 2016). "Cognitive behavioural therapy (CBT), third-wave CBT and interpersonal therapy (IPT) based interventions for preventing depression in children and adolescents". The Cochrane Database of Systematic Reviews. 2016 (8): CD003380. doi:10.1002/14651858.CD003380.pub4. PMC 8407360. PMID 27501438.
  123. ^ Patel V, Araya R, Bolton P (May 2004). "Treating depression in the developing world". Tropical Medicine & International Health. 9 (5): 539–41. doi:10.1111/j.1365-3156.2004.01243.x. PMID 15117296. S2CID 73073889.
  124. ^ Cox GR, Callahan P, Churchill R, et al. (November 2014). "Psychological therapies versus antidepressant medication, alone and in combination for depression in children and adolescents". The Cochrane Database of Systematic Reviews. 2014 (11): CD008324. doi:10.1002/14651858.CD008324.pub3. PMC 8556660. PMID 25433518.
  125. ^ Josefsson T, Lindwall M, Archer T (April 2014). "Physical exercise intervention in depressive disorders: meta-analysis and systematic review". Scandinavian Journal of Medicine & Science in Sports. 24 (2): 259–72. doi:10.1111/sms.12050. PMID 23362828. S2CID 29351791.
  126. ^ Bridle C, Spanjers K, Patel S, Atherton NM, Lamb SE (September 2012). "Effect of exercise on depression severity in older people: systematic review and meta-analysis of randomised controlled trials". The British Journal of Psychiatry. 201 (3): 180–85. doi:10.1192/bjp.bp.111.095174. PMID 22945926.
  127. ^ Lopresti AL, Hood SD, Drummond PD (May 2013). "A review of lifestyle factors that contribute to important pathways associated with major depression: diet, sleep and exercise" (PDF). Journal of Affective Disorders. 148 (1): 12–27. doi:10.1016/j.jad.2013.01.014. PMID 23415826. (PDF) from the original on 9 January 2017.
  128. ^ Taylor G, McNeill A, Girling A, et al. (February 2014). "Change in mental health after smoking cessation: systematic review and meta-analysis". BMJ. 348 (feb13 1): g1151. doi:10.1136/bmj.g1151. PMC 3923980. PMID 24524926.
  129. ^ Khan A, Faucett J, Lichtenberg P, Kirsch I, Brown WA (30 July 2012). "A systematic review of comparative efficacy of treatments and controls for depression". PLOS ONE. 7 (7): e41778. Bibcode:2012PLoSO...741778K. doi:10.1371/journal.pone.0041778. PMC 3408478. PMID 22860015.
  130. ^ Thase ME (1999). "When are psychotherapy and pharmacotherapy combinations the treatment of choice for major depressive disorder?". The Psychiatric Quarterly. 70 (4): 333–46. doi:10.1023/A:1022042316895. PMID 10587988. S2CID 45091134.
  131. ^ Cordes J (2013). "Depression". Encyclopedia of Sciences and Religions. pp. 610–16. doi:10.1007/978-1-4020-8265-8_301. ISBN 978-1-4020-8264-1.
  132. ^ Ijaz S, Davies P, Williams CJ, et al. (May 2018). "Psychological therapies for treatment-resistant depression in adults". The Cochrane Database of Systematic Reviews. 5 (8): CD010558. doi:10.1002/14651858.CD010558.pub2. PMC 6494651. PMID 29761488.
  133. ^ Wilson KC, Mottram PG, Vassilas CA (January 2008). "Psychotherapeutic treatments for older depressed people". The Cochrane Database of Systematic Reviews. 23 (1): CD004853. doi:10.1002/14651858.CD004853.pub2. PMID 18254062.
  134. ^ Cuijpers P, van Straten A, Smit F (December 2006). "Psychological treatment of late-life depression: a meta-analysis of randomized controlled trials". International Journal of Geriatric Psychiatry. 21 (12): 1139–49. doi:10.1002/gps.1620. hdl:1871/16894. PMID 16955421. S2CID 14778731.
  135. ^ Gartlehner G, Wagner G, Matyas N, et al. (June 2017). "Pharmacological and non-pharmacological treatments for major depressive disorder: review of systematic reviews". BMJ Open. 7 (6): e014912. doi:10.1136/bmjopen-2016-014912. PMC 5623437. PMID 28615268.
  136. ^ . abct.org. Last updated: 30 July 2010
  137. ^ NICE guidelines: Depression in children and adolescents. London: NICE. 2005. p. 5. ISBN 978-1-84629-074-9. from the original on 24 September 2008. Retrieved 16 August 2008.
  138. ^ Becker SJ (2008). "Cognitive-Behavioral Therapy for Adolescent Depression: Processes of Cognitive Change". Psychiatric Times. 25 (14).
  139. ^ Almeida AM, Lotufo Neto F (October 2003). "[Cognitive-behavioral therapy in prevention of depression relapses and recurrences: a review]". Revista Brasileira de Psiquiatria. 25 (4): 239–44. doi:10.1590/S1516-44462003000400011. PMID 15328551.
  140. ^ Paykel ES (February 2007). "Cognitive therapy in relapse prevention in depression". The International Journal of Neuropsychopharmacology. 10 (1): 131–36. doi:10.1017/S1461145706006912. PMID 16787553.
  141. ^ a b c Nieuwenhuijsen K, Verbeek JH, Neumeyer-Gromen A, et al. (October 2020). "Interventions to improve return to work in depressed people". Cochrane Database Syst Rev. 10 (12): CD006237. doi:10.1002/14651858.CD006237.pub4. PMC 8094165. PMID 33052607.
  142. ^ Beck et al. 1987, p. 10.
  143. ^ Coelho HF, Canter PH, Ernst E (December 2007). "Mindfulness-based cognitive therapy: evaluating current evidence and informing future research". Journal of Consulting and Clinical Psychology. 75 (6): 1000–05. doi:10.1037/0022-006X.75.6.1000. PMID 18085916.
  144. ^ Khoury B, Lecomte T, Fortin G, et al. (August 2013). "Mindfulness-based therapy: a comprehensive meta-analysis". Clinical Psychology Review. 33 (6): 763–71. doi:10.1016/j.cpr.2013.05.005. PMID 23796855.
  145. ^ Jain FA, Walsh RN, Eisendrath SJ, Christensen S, Rael Cahn B (2014). "Critical analysis of the efficacy of meditation therapies for acute and subacute phase treatment of depressive disorders: a systematic review". Psychosomatics. 56 (2): 140–52. doi:10.1016/j.psym.2014.10.007. PMC 4383597. PMID 25591492.
  146. ^ Simkin DR, Black NB (July 2014). "Meditation and mindfulness in clinical practice". Child and Adolescent Psychiatric Clinics of North America. 23 (3): 487–534. doi:10.1016/j.chc.2014.03.002. PMID 24975623.
  147. ^ a b Alexopoulos GS (August 2019). "Mechanisms and treatment of late-life depression". Transl Psychiatry. 9 (1): 188. doi:10.1038/s41398-019-0514-6. PMC 6683149. PMID 31383842.
  148. ^ Dworetzky J (1997). Psychology. Pacific Grove, CA: Brooks/Cole Pub. Co. p. 602. ISBN 978-0-314-20412-7.
  149. ^ Doidge N, Simon B, Lancee WJ, et al. (2002). "Psychoanalytic patients in the U.S., Canada, and Australia: II. A DSM-III-R validation study". Journal of the American Psychoanalytic Association. 50 (2): 615–27. doi:10.1177/00030651020500021101. PMID 12206545. S2CID 25110425.
  150. ^ Barlow & Durand 2005, p. 20.
  151. ^ de Maat S, Dekker J, Schoevers R, et al. (2007). "Short psychodynamic supportive psychotherapy, antidepressants, and their combination in the treatment of major depression: a mega-analysis based on three randomized clinical trials". Depression and Anxiety. 25 (7): 565–74. doi:10.1002/da.20305. PMID 17557313. S2CID 20373635.
  152. ^ Iglesias-González M, Aznar-Lou I, Gil-Girbau M, et al. (November 2017). "Comparing watchful waiting with antidepressants for the management of subclinical depression symptoms to mild-moderate depression in primary care: a systematic review". Family Practice. 34 (6): 639–48. doi:10.1093/fampra/cmx054. PMID 28985309.
  153. ^ "The treatment and management of depression in adults". NICE. October 2009. from the original on 12 November 2014. Retrieved 12 November 2014.
  154. ^ Leucht C, Huhn M, Leucht S (December 2012). Leucht C (ed.). "Amitriptyline versus placebo for major depressive disorder". The Cochrane Database of Systematic Reviews. 12: CD009138. doi:10.1002/14651858.CD009138.pub2. PMID 23235671.
  155. ^ de Vries YA, Roest AM, Bos EH, et al. (January 2019). "Predicting antidepressant response by monitoring early improvement of individual symptoms of depression: individual patient data meta-analysis". The British Journal of Psychiatry. 214 (1): 4–10. doi:10.1192/bjp.2018.122. PMC 7557872. PMID 29952277.
  156. ^ Thase ME (December 2006). "Preventing relapse and recurrence of depression: a brief review of therapeutic options". CNS Spectrums. 11 (12 Suppl 15): 12–21. doi:10.1017/S1092852900015212. PMID 17146414. S2CID 2347144.
  157. ^ a b Royal Pharmaceutical Society of Great Britain 2008, p. 204
  158. ^ Whooley MA, Simon GE (December 2000). "Managing depression in medical outpatients". The New England Journal of Medicine. 343 (26): 1942–50. doi:10.1056/NEJM200012283432607. PMID 11136266.
  159. ^ Zisook S, Rush AJ, Haight BR, Clines DC, Rockett CB (February 2006). "Use of bupropion in combination with serotonin reuptake inhibitors". Biological Psychiatry. 59 (3): 203–10. doi:10.1016/j.biopsych.2005.06.027. PMID 16165100. S2CID 20997303.
  160. ^ Papakostas GI, Thase ME, Fava M, Nelson JC, Shelton RC (December 2007). "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". Biological Psychiatry. 62 (11): 1217–27. doi:10.1016/j.biopsych.2007.03.027. PMID 17588546. S2CID 45621773.
  161. ^ Duff G (31 May 2006). . Medicines and Healthcare products Regulatory Agency (MHRA). Archived from the original on 13 November 2008.
  162. ^ "Antidepressants for children and teenagers: what works for anxiety and depression?". NIHR Evidence (Plain English summary). National Institute for Health and Care Research. 3 November 2022. doi:10.3310/nihrevidence_53342. S2CID 253347210.
  163. ^ a b c Zhou X, Teng T, Zhang Y, Del Giovane C, Furukawa TA, Weisz JR, et al. (July 2020). "Comparative efficacy and acceptability of antidepressants, psychotherapies, and their combination for acute treatment of children and adolescents with depressive disorder: a systematic review and network meta-analysis". The Lancet. Psychiatry. 7 (7): 581–601. doi:10.1016/S2215-0366(20)30137-1. PMC 7303954. PMID 32563306.
  164. ^ a b Hetrick SE, McKenzie JE, Bailey AP, Sharma V, Moller CI, Badcock PB, et al. (Cochrane Common Mental Disorders Group) (May 2021). "New generation antidepressants for depression in children and adolescents: a network meta-analysis". The Cochrane Database of Systematic Reviews. 2021 (5): CD013674. doi:10.1002/14651858.CD013674.pub2. PMC 8143444. PMID 34029378.
  165. ^ Solmi M, Fornaro M, Ostinelli EG, Zangani C, Croatto G, Monaco F, et al. (June 2020). "Safety of 80 antidepressants, antipsychotics, anti-attention-deficit/hyperactivity medications and mood stabilizers in children and adolescents with psychiatric disorders: a large scale systematic meta-review of 78 adverse effects". World Psychiatry. 19 (2): 214–232. doi:10.1002/wps.20765. PMC 7215080. PMID 32394557.
  166. ^ Boaden K, Tomlinson A, Cortese S, Cipriani A (2 September 2020). "Antidepressants in Children and Adolescents: Meta-Review of Efficacy, Tolerability and Suicidality in Acute Treatment". Frontiers in Psychiatry. 11: 717. doi:10.3389/fpsyt.2020.00717. PMC 7493620. PMID 32982805.
  167. ^ Correll CU, Cortese S, Croatto G, Monaco F, Krinitski D, Arrondo G, et al. (June 2021). "Efficacy and acceptability of pharmacological, psychosocial, and brain stimulation interventions in children and adolescents with mental disorders: an umbrella review". World Psychiatry. 20 (2): 244–275. doi:10.1002/wps.20881. PMC 8129843. PMID 34002501.
  168. ^ . NICE Clinical Guidelines. NHS National Institute for Health and Clinical Excellence (28). 2005. Archived from the original on 12 November 2014. Retrieved 12 November 2014.
  169. ^ "Prozac may be the best treatment for young people with depression – but more research is needed". NIHR Evidence (Plain English summary). National Institute for Health and Care Research. 12 October 2020. doi:10.3310/alert_41917. S2CID 242952585.
  170. ^ Boaden K, Tomlinson A, Cortese S, Cipriani A (2 September 2020). "Antidepressants in Children and Adolescents: Meta-Review of Efficacy, Tolerability and Suicidality in Acute Treatment". Frontiers in Psychiatry. 11: 717. doi:10.3389/fpsyt.2020.00717. PMC 7493620. PMID 32982805.
  171. ^ Cipriani A, Zhou X, Del Giovane C, Hetrick SE, Qin B, Whittington C, et al. (August 2016). "Comparative efficacy and tolerability of antidepressants for major depressive disorder in children and adolescents: a network meta-analysis". Lancet. 388 (10047): 881–890. doi:10.1016/S0140-6736(16)30385-3. hdl:11380/1279478. PMID 27289172. S2CID 19728203.
  172. ^ Cheung AH, Zuckerbrot RA, Jensen PS, Laraque D, Stein RE (March 2018). "Guidelines for Adolescent Depression in Primary Care (GLAD-PC): Part II. Treatment and Ongoing Management". Pediatrics. 141 (3): e20174082. doi:10.1542/peds.2017-4082. PMID 29483201.
  173. ^ Nelson JC, Devanand DP (April 2011). "A systematic review and meta-analysis of placebo-controlled antidepressant studies in people with depression and dementia". Journal of the American Geriatrics Society. 59 (4): 577–85. doi:10.1111/j.1532-5415.2011.03355.x. PMID 21453380. S2CID 2592434.
  174. ^ Palmer BF, Gates JR, Lader M (November 2003). "Causes and management of hyponatremia". The Annals of Pharmacotherapy. 37 (11): 1694–702. doi:10.1345/aph.1D105. PMID 14565794. S2CID 37965495.
  175. ^ Guaiana G, Barbui C, Hotopf M (July 2007). "Amitriptyline for depression". The Cochrane Database of Systematic Reviews. 18 (3): CD004186. doi:10.1002/14651858.CD004186.pub2. PMID 17636748.
  176. ^ Anderson IM (April 2000). "Selective serotonin reuptake inhibitors versus tricyclic antidepressants: a meta-analysis of efficacy and tolerability". Journal of Affective Disorders. 58 (1): 19–36. doi:10.1016/S0165-0327(99)00092-0. PMID 10760555.
  177. ^ Krishnan KR (2007). "Revisiting monoamine oxidase inhibitors". The Journal of Clinical Psychiatry. 68 (Suppl 8): 35–41. PMID 17640156.
  178. ^ Bonnet U (2003). "Moclobemide: therapeutic use and clinical studies". CNS Drug Reviews. 9 (1): 97–140. doi:10.1111/j.1527-3458.2003.tb00245.x. PMC 6741704. PMID 12595913.
  179. ^ Braun C, Bschor T, Franklin J, Baethge C (2016). "Suicides and Suicide Attempts during Long-Term Treatment with Antidepressants: A Meta-Analysis of 29 Placebo-Controlled Studies Including 6,934 Patients with Major Depressive Disorder". Psychotherapy and Psychosomatics. 85 (3): 171–79. doi:10.1159/000442293. PMID 27043848. S2CID 40682753.
  180. ^ Hammad TA (16 August 2004). "Review and evaluation of clinical data. Relationship between psychiatric drugs and pediatric suicidality" (PDF). FDA. pp. 42, 115. (PDF) from the original on 25 June 2008. Retrieved 29 May 2008.
  181. ^ Hetrick SE, McKenzie JE, Cox GR, Simmons MB, Merry SN (November 2012). "Newer generation antidepressants for depressive disorders in children and adolescents". The Cochrane Database of Systematic Reviews. 11 (9): CD004851. doi:10.1002/14651858.CD004851.pub3. hdl:11343/59246. PMC 8786271. PMID 23152227.
  182. ^ Gunnell D, Saperia J, Ashby D (February 2005). "Selective serotonin reuptake inhibitors (SSRIs) and suicide in adults: meta-analysis of drug company data from placebo controlled, randomised controlled trials submitted to the MHRA's safety review". BMJ. 330 (7488): 385. doi:10.1136/bmj.330.7488.385. PMC 549105. PMID 15718537.
  183. ^ Fergusson D, Doucette S, Glass KC, et al. (February 2005). "Association between suicide attempts and selective serotonin reuptake inhibitors: systematic review of randomised controlled trials". BMJ. 330 (7488): 396. doi:10.1136/bmj.330.7488.396. PMC 549110. PMID 15718539.
  184. ^ Stone M, Laughren T, Jones ML, et al. (August 2009). "Risk of suicidality in clinical trials of antidepressants in adults: analysis of proprietary data submitted to US Food and Drug Administration". BMJ. 339: b2880. doi:10.1136/bmj.b2880. PMC 2725270. PMID 19671933.
  185. ^ "FDA Proposes New Warnings About Suicidal Thinking, Behavior in Young Adults Who Take Antidepressant Medications". FDA. 2 May 2007. from the original on 23 February 2008. Retrieved 29 May 2008.
  186. ^ Medics and Foods Department. (PDF) (Report). 261 (in Japanese). Ministry of Health, Labour and Welfare (Japan). Archived from the original (PDF) on 29 April 2011. Retrieved 19 May 2010.
  187. ^ Ogawa Y, Takeshima N, Hayasaka Y, et al. (June 2019). "Antidepressants plus benzodiazepines for adults with major depression". The Cochrane Database of Systematic Reviews. 6 (6): CD001026. doi:10.1002/14651858.CD001026.pub2. PMC 6546439. PMID 31158298.
  188. ^ Corriger A, Pickering G (2019). "Ketamine and depression: a narrative review". Drug Des Devel Ther. 13: 3051–3067. doi:10.2147/DDDT.S221437. PMC 6717708. PMID 31695324.
  189. ^ Krystal JH, Abdallah CG, Sanacora G, Charney DS, Duman RS (March 2019). "Ketamine: A Paradigm Shift for Depression Research and Treatment". Neuron. 101 (5): 774–778. doi:10.1016/j.neuron.2019.02.005. PMC 6560624. PMID 30844397.
  190. ^ McIntyre RS, Rosenblat JD, Nemeroff CB, et al. (May 2021). "Synthesizing the Evidence for Ketamine and Esketamine in Treatment-Resistant Depression: An International Expert Opinion on the Available Evidence and Implementation". Am J Psychiatry. 178 (5): 383–399. doi:10.1176/appi.ajp.2020.20081251. PMC 9635017. PMID 33726522. S2CID 232262694.
  191. ^ Bahr R, Lopez A, Rey JA (June 2019). "Intranasal Esketamine (SpravatoTM) for Use in Treatment-Resistant Depression In Conjunction With an Oral Antidepressant". P T. 44 (6): 340–375. PMC 6534172. PMID 31160868.
  192. ^ Appleton KM, Voyias PD, Sallis HM, et al. (November 2021). "Omega-3 fatty acids for depression in adults". Cochrane Database Syst Rev. 2021 (11): CD004692. doi:10.1002/14651858.CD004692.pub5. PMC 8612309. PMID 34817851.
  193. ^ Cipriani A, Hawton K, Stockton S, Geddes JR (June 2013). "Lithium in the prevention of suicide in mood disorders: updated systematic review and meta-analysis". BMJ. 346 (jun27 4): f3646. doi:10.1136/bmj.f3646. PMID 23814104.
  194. ^ Nolen-Hoeksema, Susan. (2014) "Treatment of Mood Disorders". In (6th ed.) Abnormal Psychology p. 196. New York: McGraw-Hill. ISBN 978-0-07-803538-8.
  195. ^ Gelenberg AJ, Freeman MP, Markowitz JC. "Practice Guideline for the Treatment of Patients with Major Depressive Disorder" (PDF) (3rd ed.). American Psychiatric Association (APA). Retrieved 3 November 2014.
  196. ^ Corp SA, Gitlin MJ, Altshuler LL (September 2014). "A review of the use of stimulants and stimulant alternatives in treating bipolar depression and major depressive disorder". The Journal of Clinical Psychiatry. 75 (9): 1010–18. doi:10.4088/JCP.13r08851. PMID 25295426.
  197. ^ Malhi GS, Byrow Y, Bassett D, et al. (March 2016). "Stimulants for depression: On the up and up?". The Australian and New Zealand Journal of Psychiatry. 50 (3): 203–07. doi:10.1177/0004867416634208. PMID 26906078. S2CID 45341424.
  198. ^ Taylor MJ, Carney S, Geddes J, Goodwin G (2003). "Folate for depressive disorders". The Cochrane Database of Systematic Reviews. 2003 (2): CD003390. doi:10.1002/14651858.CD003390. PMC 6991158. PMID 12804463.
  199. ^ Walther A, Breidenstein J, Miller R (January 2019). "Association of Testosterone Treatment With Alleviation of Depressive Symptoms in Men: A Systematic Review and Meta-analysis". JAMA Psychiatry. 76 (1): 31–40. doi:10.1001/jamapsychiatry.2018.2734. PMC 6583468. PMID 30427999.
  200. ^ Rudorfer, MV, Henry, ME, Sackeim, HA (2003). "Electroconvulsive therapy". In A Tasman, J Kay, JA Lieberman (eds) Psychiatry, Second Edition. Chichester: John Wiley & Sons Ltd, 1865–1901.
  201. ^ Beloucif S (April 2013). "Informed consent for special procedures: electroconvulsive therapy and psychosurgery". Current Opinion in Anesthesiology. 26 (2): 182–85. doi:10.1097/ACO.0b013e32835e7380. PMID 23385317. S2CID 36643014.
  202. ^ a b c FDA. FDA Executive Summary 24 September 2015 at the Wayback Machine. Prepared for the 27–28 January 2011 meeting of the Neurological Devices Panel Meeting to Discuss the Classification of Electroconvulsive Therapy Devices (ECT). Quote, p38: "Three major practice guidelines have been published on ECT. These guidelines include: APA Task Force on ECT (2001); Third report of the Royal College of Psychiatrists' Special Committee on ECT (2004); National Institute for Health and Clinical Excellence (NICE 2003; NICE 2009). There is significant agreement between the three sets of recommendations."
  203. ^ Dierckx B, Heijnen WT, van den Broek WW, Birkenhäger TK (March 2012). "Efficacy of electroconvulsive therapy in bipolar versus unipolar major depression: a meta-analysis". Bipolar Disorders. 14 (2): 146–50. doi:10.1111/j.1399-5618.2012.00997.x. PMID 22420590. S2CID 44280002.
  204. ^ Jelovac A, Kolshus E, McLoughlin DM (November 2013). "Relapse following successful electroconvulsive therapy for major depression: a meta-analysis". Neuropsychopharmacology. 38 (12): 2467–74. doi:10.1038/npp.2013.149. PMC 3799066. PMID 23774532.
  205. ^ Surgeon General (1999). Mental Health: A Report of the Surgeon General 12 January 2007 at the Wayback Machine, chapter 4.
  206. ^ Committee on Electroconvulsive Therapy (2001). The practice of electroconvulsive therapy: recommendations for treatment, training, and privileging (2nd ed.). Washington, DC: American Psychiatric Publishing. American Psychiatric Association. ISBN 978-0-89042-206-9.
  207. ^ Pompili M, Dominici G, Giordano G, et al. (December 2014). "Electroconvulsive treatment during pregnancy: a systematic review". Expert Review of Neurotherapeutics. 14 (12): 1377–90. doi:10.1586/14737175.2014.972373. PMID 25346216. S2CID 31209001.
  208. ^ "5 Outdated Beliefs About ECT". Psych Central.com. 17 May 2016. from the original on 8 August 2013.
  209. ^ Abbott CC, Gallegos P, Rediske N, Lemke NT, Quinn DK (March 2014). "A review of longitudinal electroconvulsive therapy: neuroimaging investigations". Journal of Geriatric Psychiatry and Neurology. 27 (1): 33–46. doi:10.1177/0891988713516542. PMC 6624835. PMID 24381234.
  210. ^ . Archived from the original on 4 October 2015.
  211. ^ Melkerson MN (16 December 2008). "Special Premarket 510(k) Notification for NeuroStar® TMS Therapy System for Major Depressive Disorder" (PDF). Food and Drug Administration. (PDF) from the original on 31 March 2010. Retrieved 16 July 2010.
  212. ^ Lefaucheur JP, André-Obadia N, Antal A, et al. (November 2014). "Evidence-based guidelines on the therapeutic use of repetitive transcranial magnetic stimulation (rTMS)" (PDF). Clinical Neurophysiology. 125 (11): 2150–206. doi:10.1016/j.clinph.2014.05.021. PMID 25034472. S2CID 206798663. (PDF) from the original on 23 July 2022.
  213. ^ Gelenberg AJ, Freeman MP, Markowitz JC, Rosenbaum JF, Thase ME, Trivedi MH, Van Rhoads RS, eds. (2010). "Practice Guidelines for the Treatment of Patients with Major Depressive Disorder" (PDF) (3rd ed.). American Psychiatric Association.
  214. ^ Kennedy SH, Lam RW, Parikh SV, Patten SB, Ravindran AV (2009). (PDF). Journal of Affective Disorders. Elsevier BV. 117 (Suppl 1): S1–S64. doi:10.1016/j.jad.2009.06.043. ISSN 0165-0327. PMID 19682750. Archived from the original (PDF) on 23 August 2015.
  215. ^ Rush AJ, Marangell LB, Sackeim HA, et al. (September 2005). "Vagus nerve stimulation for treatment-resistant depression: a randomized, controlled acute phase trial". Biological Psychiatry. 58 (5): 347–54. doi:10.1016/j.biopsych.2005.05.025. PMID 16139580. S2CID 22066326.
  216. ^ Fregni F, El-Hagrassy MM, Pacheco-Barrios K, et al. (April 2021). "Evidence-Based Guidelines and Secondary Meta-Analysis for the Use of Transcranial Direct Current Stimulation in Neurological and Psychiatric Disorders". Int J Neuropsychopharmacol. 24 (4): 256–313. doi:10.1093/ijnp/pyaa051. PMC 8059493. PMID 32710772.
  217. ^ Moffa AH, Martin D, Alonzo A, et al. (April 2020). "Efficacy and acceptability of transcranial direct current stimulation (tDCS) for major depressive disorder: An individual patient data meta-analysis". Progress in Neuro-Psychopharmacology & Biological Psychiatry. 99: 109836. doi:10.1016/j.pnpbp.2019.109836. PMID 31837388. S2CID 209373871.
  218. ^ Ioannou M, Wartenberg C, Greenbrook JT, et al. (January 2021). "Sleep deprivation as treatment for depression: Systematic review and meta-analysis". Acta Psychiatr Scand. 143 (1): 22–35. doi:10.1111/acps.13253. PMC 7839702. PMID 33145770.
  219. ^ Giedke H, Schwärzler F (October 2002). "Therapeutic use of sleep deprivation in depression". Sleep Medicine Reviews. 6 (5): 361–77. doi:10.1053/smrv.2002.0235. PMID 12531127.
  220. ^ Joyce J, Herbison GP (April 2015). "Reiki for depression and anxiety". The Cochrane Database of Systematic Reviews (4): CD006833. doi:10.1002/14651858.cd006833.pub2. PMID 25835541.
  221. ^ Meekums B, Karkou V, Nelson EA (February 2015). "Dance movement therapy for depression" (PDF). The Cochrane Database of Systematic Reviews. 2016 (2): CD009895. doi:10.1002/14651858.cd009895.pub2. PMC 8928931. PMID 25695871.
  222. ^ Black N, Stockings E, Campbell G, et al. (December 2019). "Cannabinoids for the treatment of mental disorders and symptoms of mental disorders: a systematic review and meta-analysis". The Lancet. Psychiatry. 6 (12): 995–1010. doi:10.1016/S2215-0366(19)30401-8. PMC 6949116. PMID 31672337.
  223. ^ Fava GA, Park SK, Sonino N (November 2006). "Treatment of recurrent depression". Expert Review of Neurotherapeutics. 6 (11): 1735–40. doi:10.1586/14737175.6.11.1735. PMID 17144786. S2CID 22808803.
  224. ^ Limosin F, Mekaoui L, Hautecouverture S (November 2007). "[Prophylactic treatment for recurrent major depression]". Presse Médicale. 36 (11 Pt 2): 1627–33. doi:10.1016/j.lpm.2007.03.032. PMID 17555914.
  225. ^ Eaton WW, Shao H, Nestadt G, et al. (May 2008). "Population-based study of first onset and chronicity in major depressive disorder". Archives of General Psychiatry. 65 (5): 513–20. doi:10.1001/archpsyc.65.5.513. PMC 2761826. PMID 18458203.
  226. ^ Holma KM, Holma IA, Melartin TK, Rytsälä HJ, Isometsä ET (February 2008). "Long-term outcome of major depressive disorder in psychiatric patients is variable". The Journal of Clinical Psychiatry. 69 (2): 196–205. doi:10.4088/JCP.v69n0205. PMID 18251627.
  227. ^ Kanai T, Takeuchi H, Furukawa TA, et al. (July 2003). "Time to recurrence after recovery from major depressive episodes and its predictors". Psychological Medicine. 33 (5): 839–45. doi:10.1017/S0033291703007827. PMID 12877398. S2CID 10490348.
  228. ^ "Depression, Major: Prognosis". MDGuidelines. The Guardian Life Insurance Company of America. from the original on 20 April 2010. Retrieved 16 July 2010.
  229. ^ a b Culpepper L, Muskin PR, Stahl SM (September 2015). "Major Depressive Disorder: Understanding the Significance of Residual Symptoms and Balancing Efficacy with Tolerability". The American Journal of Medicine. 128 (9 Suppl): S1–S15. doi:10.1016/j.amjmed.2015.07.001. PMID 26337210.
  230. ^ Geddes JR, Carney SM, Davies C, et al. (February 2003). "Relapse prevention with antidepressant drug treatment in depressive disorders: a systematic review". Lancet. 361 (9358): 653–61. doi:10.1016/S0140-6736(03)12599-8. PMID 12606176. S2CID 20198748.
  231. ^ Posternak MA, Miller I (October 2001). "Untreated short-term course of major depression: a meta-analysis of outcomes from studies using wait-list control groups". Journal of Affective Disorders. 66 (2–3): 139–46. doi:10.1016/S0165-0327(00)00304-9. PMID 11578666.
  232. ^ Posternak MA, Solomon DA, Leon AC, et al. (May 2006). "The naturalistic course of unipolar major depression in the absence of somatic therapy". The Journal of Nervous and Mental Disease. 194 (5): 324–29. doi:10.1097/01.nmd.0000217820.33841.53. PMID 16699380. S2CID 22891687.
  233. ^ Whiteford HA, Harris MG, McKeon G, et al. (10 August 2012). "Estimating remission from untreated major depression: a systematic review and meta-analysis". Psychological Medicine. Cambridge University Press (CUP). 43 (8): 1569–1585. doi:10.1017/s0033291712001717. ISSN 0033-2917. PMID 22883473. S2CID 11068930.
  234. ^ Cassano P, Fava M (October 2002). "Depression and public health: an overview". Journal of Psychosomatic Research. 53 (4): 849–57. doi:10.1016/S0022-3999(02)00304-5. PMID 12377293.
  235. ^ Barlow & Durand 2005, pp. 248–49.
  236. ^ Bachmann S (6 July 2018). "Epidemiology of Suicide and the Psychiatric Perspective". International Journal of Environmental Research and Public Health. 15 (7): 1425. doi:10.3390/ijerph15071425. PMC 6068947. PMID 29986446. Half of all completed suicides are related to depressive and other mood disorders
  237. ^ Strakowski S, Nelson E (2015). Major Depressive Disorder. Oxford University Press. p. PT27. ISBN 978-0-19-026432-1.
  238. ^ Blair-West GW, Mellsop GW (June 2001). "Major depression: does a gender-based down-rating of suicide risk challenge its diagnostic validity?". The Australian and New Zealand Journal of Psychiatry. 35 (3): 322–28. doi:10.1046/j.1440-1614.2001.00895.x. PMID 11437805. S2CID 36975913.
  239. ^ Oquendo MA, Bongiovi-Garcia ME, Galfalvy H, et al. (January 2007). "Sex differences in clinical predictors of suicidal acts after major depression: a prospective study". The American Journal of Psychiatry. 164 (1): 134–41. doi:10.1176/ajp.2007.164.1.134. PMC 3785095. PMID 17202555.
  240. ^ Rush AJ (2007). "The varied clinical presentations of major depressive disorder". The Journal of Clinical Psychiatry. 68 (Supplement 8): 4–10. PMID 17640152.
  241. ^ Swardfager W, Herrmann N, Marzolini S, et al. (September 2011). "Major depressive disorder predicts completion, adherence, and outcomes in cardiac rehabilitation: a prospective cohort study of 195 patients with coronary artery disease". The Journal of Clinical Psychiatry. 72 (9): 1181–88. doi:10.4088/jcp.09m05810blu. PMID 21208573.
  242. ^ Schulman J, Shapiro BA (2008). . Psychiatric Times. 25 (9). Archived from the original on 6 March 2020. Retrieved 10 June 2009.
  243. ^ "WHO Disease and injury country estimates". World Health Organization. 2009. from the original on 11 November 2009. Retrieved 11 November 2009.
  244. ^ a b c . U.S. National Institute of Mental Health (NIMH). January 2022. Archived from the original on 9 August 2022. Retrieved 14 August 2022.   This article incorporates text from this source, which is in the public domain.
  245. ^ a b Kuehner C (September 2003). "Gender differences in unipolar depression: an update of epidemiological findings and possible explanations". Acta Psychiatrica Scandinavica. 108 (3): 163–74. doi:10.1034/j.1600-0447.2003.00204.x. PMID 12890270. S2CID 19538251.
  246. ^ Institute for Health Metrics and Evaluation (2020), Global Burden of Disease 2019 Cause and Risk Summary: Major depressive disorder — Level 4 cause, Seattle, USA: University of Washington, Table 3, retrieved 9 July 2022
  247. ^ Eaton WW, Anthony JC, Gallo J, et al. (November 1997). "Natural history of Diagnostic Interview Schedule/DSM-IV major depression. The Baltimore Epidemiologic Catchment Area follow-up". Archives of General Psychiatry. 54 (11): 993–99. doi:10.1001/archpsyc.1997.01830230023003. PMID 9366655.
  248. ^ Rickards H (March 2005). "Depression in neurological disorders: Parkinson's disease, multiple sclerosis, and stroke". Journal of Neurology, Neurosurgery, and Psychiatry. 76 (Suppl 1): i48–52. doi:10.1136/jnnp.2004.060426. PMC 1765679. PMID 15718222.
  249. ^ Alboni P, Favaron E, Paparella N, Sciammarella M, Pedaci M (April 2008). "Is there an association between depression and cardiovascular mortality or sudden death?". Journal of Cardiovascular Medicine. 9 (4): 356–62. doi:10.2459/JCM.0b013e3282785240. PMID 18334889. S2CID 11051637.
  250. ^ Strik JJ, Honig A, Maes M (May 2001). "Depression and myocardial infarction: relationship between heart and mind". Progress in Neuro-Psychopharmacology & Biological Psychiatry. 25 (4): 879–92. doi:10.1016/S0278-5846(01)00150-6. PMID 11383983. S2CID 45722423.
  251. ^ Gelder, M, Mayou, R and Geddes, J (2005). Psychiatry. 3rd ed. New York: Oxford. p. 105.
  252. ^ Soysal P, Veronese N, Thompson, et al. (July 2017). "Relationship between depression and frailty in older adults: A systematic review and meta-analysis". Ageing Res Rev. 36: 78–87. doi:10.1016/j.arr.2017.03.005. PMID 28366616. S2CID 205668529.
  253. ^ Mathers CD, Loncar D (November 2006). "Projections of global mortality and burden of disease from 2002 to 2030". PLOS Medicine. 3 (11): e442. doi:10.1371/journal.pmed.0030442. PMC 1664601. PMID 17132052.
  254. ^ Andrews G (July 2008). "Reducing the burden of depression". Canadian Journal of Psychiatry. 53 (7): 420–27. doi:10.1177/070674370805300703. PMID 18674396.
  255. ^ Kessler RC, Nelson CB, McGonagle KA, et al. (June 1996). "Comorbidity of DSM-III-R major depressive disorder in the general population: results from the US National Comorbidity Survey". The British Journal of Psychiatry. Supplement. 168 (30): 17–30. doi:10.1192/S0007125000298371. PMID 8864145. S2CID 19525295.
  256. ^ Hirschfeld RM (December 2001). "The Comorbidity of Major Depression and Anxiety Disorders: Recognition and Management in Primary Care". Primary Care Companion to the Journal of Clinical Psychiatry. 3 (6): 244–54. doi:10.4088/PCC.v03n0609. PMC 181193. PMID 15014592.
  257. ^ Grant BF (1995). "Comorbidity between DSM-IV drug use disorders and major depression: results of a national survey of adults". Journal of Substance Abuse. 7 (4): 481–97. doi:10.1016/0899-3289(95)90017-9. PMID 8838629.
  258. ^ Boden JM, Fergusson DM (May 2011). "Alcohol and depression". Addiction. 106 (5): 906–14. doi:10.1111/j.1360-0443.2010.03351.x. hdl:10523/10319. PMID 21382111.
  259. ^ Hallowell EM, Ratey JJ (2005). Delivered from distraction: Getting the most out of life with Attention Deficit Disorder. New York: Ballantine Books. pp. 253–55. ISBN 978-0-345-44231-4.
  260. ^ Brunsvold GL, Oepen G (2008). "Comorbid Depression in ADHD: Children and Adolescents". Psychiatric Times. 25 (10). from the original on 24 May 2009.
  261. ^ Melartin TK, Rytsälä HJ, Leskelä US, Lestelä-Mielonen PS, Sokero TP, Isometsä ET (February 2002). "Current comorbidity of psychiatric disorders among DSM-IV major depressive disorder patients in psychiatric care in the Vantaa Depression Study". The Journal of Clinical Psychiatry. 63 (2): 126–34. doi:10.4088/jcp.v63n0207. PMID 11874213.
  262. ^ Hoge E, Bickham D, Cantor J (November 2017). "Digital Media, Anxiety, and Depression in Children". Pediatrics. 140 (Suppl 2): S76–S80. doi:10.1542/peds.2016-1758G. PMID 29093037.
  263. ^ Elhai JD, Dvorak RD, Levine JC, Hall BJ (January 2017). "Problematic smartphone use: A conceptual overview and systematic review of relations with anxiety and depression psychopathology". Journal of Affective Disorders. 207: 251–259. doi:10.1016/j.jad.2016.08.030. PMID 27736736. S2CID 205642153.
  264. ^ Bair MJ, Robinson RL, Katon W, Kroenke K (November 2003). "Depression and pain comorbidity: a literature review". Archives of Internal Medicine. 163 (20): 2433–45. doi:10.1001/archinte.163.20.2433. PMID 14609780.
  265. ^ Yohannes AM, Baldwin RC (2008). . Psychiatric Times. 25 (14). Archived from the original on 14 June 2020. Retrieved 10 June 2009.
February 20, 2023
major, depressive, disorder, other, types, depression, mood, disorder, confused, with, depression, mood, also, known, clinical, depression, mental, disorder, characterized, least, weeks, pervasive, mood, self, esteem, loss, interest, pleasure, normally, enjoya. For other types of depression see Mood disorder Not to be confused with Depression mood Major depressive disorder MDD also known as clinical depression is a mental disorder 9 characterized by at least two weeks of pervasive low mood low self esteem and loss of interest or pleasure in normally enjoyable activities Introduced by a group of US clinicians in the mid 1970s 10 the term was adopted by the American Psychiatric Association for this symptom cluster under mood disorders in the 1980 version of the Diagnostic and Statistical Manual of Mental Disorders DSM III and has become widely used since Major depressive disorderOther namesClinical depression major depression unipolar depression unipolar disorder recurrent depressionSorrowing Old Man At Eternity s Gate by Vincent van Gogh 1890 SpecialtyPsychiatry clinical psychologySymptomsLow mood low self esteem loss of interest in normally enjoyable activities low energy pain without a clear cause 1 ComplicationsSelf harm suicide 2 Usual onset20s 3 4 Duration gt 2 weeks 1 CausesEnvironmental adverse life experiences stressful life events genetic and psychological factors 5 Risk factorsFamily history major life changes certain medications chronic health problems substance use disorder 1 5 Differential diagnosisBipolar disorder ADHD sadness 6 TreatmentPsychotherapy antidepressant medication electroconvulsive therapy exercise 1 7 MedicationAntidepressantsFrequency163 million 2017 8 The diagnosis of major depressive disorder is based on the person s reported experiences behavior reported by relatives or friends and a mental status examination 11 There is no laboratory test for the disorder but testing may be done to rule out physical conditions that can cause similar symptoms 11 The most common time of onset is in a person s 20s 3 4 with females affected about twice as often as males 4 The course of the disorder varies widely from one episode lasting months to a lifelong disorder with recurrent major depressive episodes Those with major depressive disorder are typically treated with psychotherapy and antidepressant medication 1 Medication appears to be effective but the effect may be significant only in the most severely depressed 12 13 Hospitalization which may be involuntary may be necessary in cases with associated self neglect or a significant risk of harm to self or others Electroconvulsive therapy ECT may be considered if other measures are not effective 1 Major depressive disorder is believed to be caused by a combination of genetic environmental and psychological factors 1 with about 40 of the risk being genetic 5 Risk factors include a family history of the condition major life changes certain medications chronic health problems and substance use disorders 1 5 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 1 5 Major depressive disorder affected approximately 163 million people 2 of the world s population in 2017 8 The percentage of people who are affected at one point in their life varies from 7 in Japan to 21 in France 4 Lifetime rates are higher in the developed world 15 compared to the developing world 11 4 The disorder causes the second most years lived with disability after lower back pain 14 Contents 1 Symptoms and signs 2 Cause 2 1 Genetics 2 2 Other health problems 3 Pathophysiology 4 Diagnosis 4 1 Clinical assessment 4 2 DSM and ICD criteria 4 2 1 Major depressive episode 4 2 2 Subtypes 4 3 Differential diagnoses 5 Screening and prevention 6 Management 6 1 Lifestyle 6 2 Talking therapies 6 3 Antidepressants 6 4 Other medications and supplements 6 5 Electroconvulsive therapy 6 6 Other 7 Prognosis 7 1 Ability to work 7 2 Life expectancy and the risk of suicide 8 Epidemiology 8 1 Comorbidity 9 History 10 Society and culture 10 1 Terminology 10 2 Stigma 11 References 11 1 Cited worksSymptoms and signs An 1892 lithograph of a woman diagnosed with melancholia Major depression significantly affects a person s family and personal relationships work or school life sleeping and eating habits and general health 15 A person having a major depressive episode usually exhibits a low mood which pervades all aspects of life and an inability to experience pleasure in previously enjoyable activities 16 Depressed people may be preoccupied with or ruminate over thoughts and feelings of worthlessness inappropriate guilt or regret helplessness or hopelessness 17 Other symptoms of depression include poor concentration and memory withdrawal from social situations and activities reduced sex drive irritability and thoughts of death or suicide Insomnia is common in the typical pattern a person wakes very early and cannot get back to sleep Hypersomnia or oversleeping can also happen 18 Some antidepressants may also cause insomnia due to their stimulating effect 19 In severe cases depressed people may have psychotic symptoms These symptoms include delusions or less commonly hallucinations usually unpleasant 20 People who have had previous episodes with psychotic symptoms are more likely to have them with future episodes 21 A depressed person may report multiple physical symptoms such as fatigue headaches or digestive problems physical complaints are the most common presenting problem in developing countries according to the World Health Organization s criteria for depression 22 Appetite often decreases resulting in weight loss although increased appetite and weight gain occasionally occur 23 Family and friends may notice agitation or lethargy 18 Older depressed people may have cognitive symptoms of recent onset such as forgetfulness 24 and a more noticeable slowing of movements 25 Depressed children may often display an irritable rather than a depressed mood 18 most lose interest in school and show a steep decline in academic performance 26 Diagnosis may be delayed or missed when symptoms are interpreted as normal moodiness 23 Elderly people may not present with classical depressive symptoms 27 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 27 CauseFurther information Biology of depression and Epigenetics of depression A cup analogy demonstrating the diathesis stress model that under the same amount of stressors person 2 is more vulnerable than person 1 because of their predisposition 28 The biopsychosocial model proposes that biological psychological and social factors all play a role in causing depression 5 29 The diathesis stress model specifies that depression results when a preexisting vulnerability or diathesis is activated by stressful life events The preexisting vulnerability can be either genetic 30 31 implying an interaction between nature and nurture or schematic resulting from views of the world learned in childhood 32 American psychiatrist Aaron Beck suggested that a triad of automatic and spontaneous negative thoughts about the self the world or environment and the future may lead to other depressive signs and symptoms 33 34 Adverse childhood experiences incorporating childhood abuse neglect and family dysfunction markedly increase the risk of major depression especially if more than one type 5 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 35 Genetics Family and twin studies find that nearly 40 of individual differences in risk for major depressive disorder can be explained by genetic factors 36 Like most psychiatric disorders major depressive disorder is likely influenced by many individual genetic changes In 2018 a genome wide association study discovered 44 genetic variants linked to risk for major depression 37 a 2019 study found 102 variants in the genome linked to depression 38 Research focusing on specific candidate genes has been criticized for its tendency to generate false positive findings 39 There are also other efforts to examine interactions between life stress and polygenic risk for depression 40 Other health problems Depression can also arise after a chronic or terminal medical condition such as HIV AIDS or asthma and may be labeled secondary depression 41 42 It is unknown whether the underlying diseases induce depression through effect on quality of life or through shared etiologies such as degeneration of the basal ganglia in Parkinson s disease or immune dysregulation in asthma 43 Depression may also be iatrogenic the result of healthcare such as drug induced depression Therapies associated with depression include interferons beta blockers isotretinoin contraceptives 44 cardiac agents anticonvulsants antimigraine drugs antipsychotics and hormonal agents such as gonadotropin releasing hormone agonist 45 Substance use in early age is associated with increased risk of developing depression later in life 46 Depression occurring after giving birth is called postpartum depression and is thought to be the result of hormonal changes associated with pregnancy 47 Seasonal affective disorder a type of depression associated with seasonal changes in sunlight is thought to be triggered by decreased sunlight 48 Vitamin B2 B6 and B12 deficiency may cause depression in females 49 PathophysiologyFurther information Biology of depression and Epigenetics of depression The pathophysiology of depression is not completely understood but current theories center around monoaminergic systems the circadian rhythm immunological dysfunction HPA axis dysfunction 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 of monoamine neurotransmitters is the primary cause of depression Evidence for the monoamine theory comes from multiple areas First acute depletion of tryptophan a necessary precursor of serotonin and 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 50 Second the correlation between depression risk and polymorphisms in the 5 HTTLPR gene which codes for serotonin receptors suggests a link Third decreased size of the locus coeruleus decreased activity of tyrosine hydroxylase increased density of alpha 2 adrenergic receptor and evidence from rat models suggest decreased adrenergic neurotransmission in depression 51 Furthermore decreased levels of homovanillic acid altered response to dextroamphetamine responses of depressive symptoms to dopamine receptor agonists decreased dopamine receptor D1 binding in the striatum 52 and polymorphism of dopamine receptor genes implicate dopamine another monoamine in depression 53 54 Lastly increased activity of monoamine oxidase which degrades monoamines has been associated with depression 55 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 56 One proposed explanation for the therapeutic lag and further support for the deficiency of monoamines is a desensitization of self inhibition in raphe nuclei by the increased serotonin mediated by antidepressants 57 However disinhibition of the dorsal raphe has been proposed to occur as a result of decreased serotonergic 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 jugular 5 HIAA in people who are depressed that normalized with selective serotonin reuptake inhibitor SSRI treatment and the preference for carbohydrates in people who are depressed 58 Already limited the monoamine hypothesis has been further oversimplified when presented to the general public 59 A 2022 review found no consistent evidence supporting the serotonin hypothesis linking serotonin levels and depression 60 Immune system abnormalities have been observed including increased levels of cytokines involved in generating sickness behavior which shares overlap with depression 61 62 63 The effectiveness of nonsteroidal anti inflammatory drugs NSAIDs and cytokine inhibitors in treating depression 64 and normalization of cytokine levels after successful treatment further suggest immune system abnormalities in depression 65 HPA axis abnormalities have been suggested in depression given the association of CRHR1 with depression and the increased frequency of dexamethasone test non suppression in people who are depressed However this abnormality is not adequate as a diagnosis tool because its sensitivity is only 44 66 These stress related abnormalities are thought to be the cause of hippocampal volume reductions seen in people who are depressed 67 Furthermore a meta analysis yielded decreased dexamethasone suppression and increased response to psychological stressors 68 Further abnormal results have been obscured with the cortisol awakening response with increased response being associated with depression 69 Theories unifying neuroimaging findings 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 70 Another model the cortico striatal model suggests that abnormalities of the prefrontal cortex in regulating striatal and subcortical structures result in depression 71 Another model proposes hyperactivity of salience structures in identifying negative stimuli and hypoactivity of cortical regulatory structures resulting in a negative emotional bias and depression consistent with emotional bias studies 72 DiagnosisClinical assessment Further information Rating scales for depression Caricature of a man with depression A diagnostic assessment may be conducted by a suitably trained general practitioner or by a psychiatrist or psychologist 15 who records the person s current circumstances biographical history current symptoms family history and alcohol and drug use The assessment also includes a mental state examination which is an assessment of the person s current mood and thought content in particular the presence of themes of hopelessness or pessimism self harm or suicide and an absence of positive thoughts or plans 15 Specialist mental health services are rare in rural areas and thus diagnosis and management is left largely to primary care clinicians 73 This issue is even more marked in developing countries 74 Rating scales are 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 75 these include the Hamilton Rating Scale for Depression 76 the Beck Depression Inventory 77 or the Suicide Behaviors Questionnaire Revised 78 Primary care physicians have more difficulty with underrecognition and undertreatment of depression compared to psychiatrists These cases may be missed because for some people with depression physical symptoms often 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 79 A doctor generally performs a medical examination and selected investigations to rule out other causes of depressive symptoms These include blood tests measuring TSH and thyroxine to exclude hypothyroidism basic electrolytes and serum calcium to rule out a metabolic disturbance and a full blood count including ESR to rule out a systemic infection or chronic disease 80 Adverse affective reactions to medications or alcohol misuse may be ruled out as well Testosterone levels may be evaluated to diagnose hypogonadism a cause of depression in men 81 Vitamin D levels might be evaluated as low levels of vitamin D have been associated with greater risk for depression 82 Subjective cognitive complaints appear in older depressed people but they can also be indicative of the onset of a dementing disorder such as Alzheimer s disease 83 84 Cognitive testing and brain imaging can help distinguish depression from dementia 85 A CT scan can exclude brain pathology in those with psychotic rapid onset or otherwise unusual symptoms 86 No biological tests confirm major depression 87 In general investigations are not repeated for a subsequent episode unless there is a medical indication DSM and ICD criteria The most widely used criteria for diagnosing depressive conditions are found in the American Psychiatric Association s Diagnostic and Statistical Manual of Mental Disorders DSM and the World Health Organization s International 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 88 and the authors of both have worked towards conforming one with the other 89 Both DSM and ICD mark out typical main depressive symptoms 90 The most recent edition of the DSM is the Fifth Edition Text Revision DSM 5 TR 91 and the most recent edition of the ICD is the Eleventh Edition ICD 11 92 Under mood disorders ICD 11 classifies major depressive disorder as either single episode depressive disorder where there is no history of depressive episodes or of mania or recurrent depressive disorder where there is a history of prior episodes with no history of mania 93 ICD 11 symptoms present nearly every day for at least two weeks are a depressed mood or anhedonia 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 93 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 93 These two disorders are classified as Depressive disorders in the category of Mood disorders 93 According to DSM 5 there are two main depressive symptoms a depressed mood and loss of interest pleasure in activities anhedonia 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 94 failed verification Major depressive disorder is classified as a mood disorder in the DSM 5 95 The diagnosis hinges on the presence of single or recurrent major depressive episodes 96 Further qualifiers are used to classify both the episode itself and the course of the disorder The category Unspecified Depressive Disorder is diagnosed if the depressive episode s manifestation does not meet the criteria for a major depressive episode 95 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 23 Episodes may be isolated or recurrent and are categorized as mild few symptoms in excess of minimum criteria moderate or severe marked impact on social or occupational functioning An episode with psychotic features commonly referred to as psychotic depression is automatically rated as severe 95 If the person has had an episode of mania or markedly elevated mood a diagnosis of bipolar disorder is made instead Depression without mania is sometimes referred to as unipolar because the mood remains at one emotional state or pole 97 Bereavement is 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 including dysthymia which involves a chronic but milder mood disturbance 98 recurrent brief depression consisting of briefer depressive episodes 99 100 minor depressive disorder whereby only some symptoms of major depression are present 101 and adjustment disorder with depressed mood which denotes low mood resulting from a psychological response to an identifiable event or stressor 102 Subtypes The DSM 5 recognizes six further subtypes of MDD called specifiers in addition to noting the length severity and presence of psychotic features Melancholic depression is characterized by a loss of pleasure in most or all activities a failure of reactivity to pleasurable stimuli a quality of depressed mood more pronounced than that of grief or loss a worsening of symptoms in the morning hours early morning waking psychomotor retardation excessive weight loss not to be confused with anorexia nervosa or excessive guilt 103 Atypical depression is characterized by mood reactivity paradoxical anhedonia and positivity significant weight gain or increased appetite comfort eating excessive sleep or sleepiness hypersomnia a sensation of heaviness in limbs known as leaden paralysis and significant long term social impairment as a consequence of hypersensitivity to perceived interpersonal rejection 104 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 in schizophrenia or in manic episodes or may be caused by neuroleptic malignant syndrome 105 Depression with anxious distress was added into the DSM 5 as a means to emphasize the common co occurrence between depression or mania and 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 95 Depression with peri partum onset 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 V mandates that to qualify as depression with peripartum onset onset occurs during pregnancy or within one month of delivery 106 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 107 Differential diagnoses Main article Differential diagnoses of depression To confirm major depressive disorder as the most likely diagnosis other potential diagnoses must be considered including dysthymia adjustment disorder with depressed mood or bipolar disorder Dysthymia is a chronic milder mood disturbance in which a person reports a low mood almost daily over a span of at least two years The symptoms are not as severe as those for major depression although people with dysthymia are vulnerable to secondary episodes of major depression sometimes referred to as double depression 98 Adjustment disorder with depressed mood is a mood disturbance appearing as a psychological response to an identifiable event or stressor in which the resulting emotional or behavioral symptoms are significant but do not meet the criteria for a major depressive episode 102 Other disorders need to be ruled out before diagnosing major depressive disorder They include depressions due to physical illness medications and substance use disorders Depression due to physical illness is diagnosed as a mood disorder due to a general medical condition This condition is determined based on history laboratory findings or physical examination When the depression is caused by a medication non medical use of a psychoactive substance or exposure to a toxin it is then diagnosed as a specific mood disorder previously called substance induced mood disorder 108 Screening and preventionPreventive efforts may result in decreases in rates of the condition of between 22 and 38 109 Since 2016 the United States Preventive Services Task Force USPSTF has recommended screening for depression among those over the age 12 110 111 though a 2005 Cochrane review found that the routine use of screening questionnaires has little effect on detection or treatment 112 Screening the general population is not recommended by authorities in the UK or Canada 113 Behavioral interventions such as interpersonal therapy and cognitive behavioral therapy are effective at preventing new onset depression 109 114 115 Because such interventions appear to be most effective when delivered to individuals or small groups it has been suggested that they may be able to reach their large target audience most efficiently through the Internet 116 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 114 117 ManagementMain 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 118 American Psychiatric Association treatment 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 or light therapy Antidepressant medication 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 119 There is evidence that collaborative care by a team of health care practitioners produces better results than routine single practitioner care 120 Psychotherapy is the treatment of choice over medication for people under 18 121 and cognitive behavioral therapy CBT third wave CBT and interpersonal therapy may help prevent depression 122 The UK National Institute for Health and Care Excellence NICE 2004 guidelines indicate that antidepressants should not be used for the initial treatment of mild depression because the risk benefit ratio is poor The guidelines recommend that antidepressants treatment in combination with psychosocial interventions should be considered for 121 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 that antidepressant treatment should be continued for at least six months to reduce the risk of relapse and that SSRIs are better tolerated than tricyclic antidepressants 121 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 123 There is insufficient evidence to determine the effectiveness of psychological versus medical therapy in children 124 Lifestyle Further information Neurobiological effects of physical exercise Major depressive disorder Physical exercise is one recommended way to manage mild depression Physical exercise has 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 125 It is equivalent to the use of medications or psychological therapies in most people 7 In older people it does appear to decrease depression 126 Sleep and diet may also play a role in depression and interventions in these areas may be an effective add on to conventional methods 127 In observational studies smoking cessation has benefits in depression as large as or larger than those of medications 128 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 clinical social workers counselors and psychiatric nurses A 2012 review found psychotherapy to be better than no treatment but not other treatments 129 With more complex and chronic forms of depression a combination of medication and psychotherapy may be used 130 131 There is moderate quality evidence that psychological therapies are a useful addition to standard antidepressant treatment of treatment resistant depression in the short term 132 Psychotherapy has been shown to be effective in older people 133 134 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 135 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 136 In people under 18 according to the National Institute for Health and Clinical Excellence medication should be offered only in conjunction with a psychological therapy such as CBT interpersonal therapy or family therapy 137 Several variables predict success for cognitive behavioral therapy in adolescents higher levels of rational thoughts less hopelessness fewer negative thoughts and fewer cognitive distortions 138 CBT is particularly beneficial in preventing relapse 139 140 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 141 Several variants of cognitive behavior therapy have been used in those with depression the most notable being rational emotive behavior therapy 142 and mindfulness based cognitive therapy 143 Mindfulness based stress reduction programs may reduce depression symptoms 144 145 Mindfulness programs also appear to be a promising intervention in youth 146 Problem solving therapy cognitive behavioral therapy and interpersonal therapy are effective interventions in the elderly 147 Psychoanalysis is a school of thought founded by Sigmund Freud which emphasizes the resolution of unconscious mental conflicts 148 Psychoanalytic techniques are used by some practitioners to treat clients presenting with major depression 149 A more widely practiced therapy called psychodynamic 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 150 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 151 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 152 A review commissioned by the National Institute for Health and Care Excellence UK concluded that there is strong evidence that SSRIs such as escitalopram paroxetine and sertraline have greater efficacy than placebo on 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 153 Similarly a Cochrane systematic review of clinical trials of the generic tricyclic antidepressant amitriptyline concluded that there is strong evidence that its efficacy is superior to placebo 154 Antidepressants work less well for the elderly than for younger individuals with depression 147 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 119 155 Antidepressant medication treatment is usually continued for 16 to 20 weeks after remission to minimize the chance of recurrence 119 and even up to one year of continuation is recommended 156 People with chronic depression may need to take medication indefinitely to avoid relapse 15 SSRIs are the primary medications prescribed owing to their relatively mild side effects and because they are less toxic in overdose than other antidepressants 157 People who do not respond to one SSRI can be switched to another antidepressant and this results in improvement in almost 50 of cases 158 Another option is to switch to the atypical antidepressant bupropion 159 Venlafaxine an antidepressant with a different mechanism of action may be modestly more effective than SSRIs 160 However venlafaxine is not recommended in the UK as a first line treatment because of evidence suggesting its risks may outweigh benefits 161 and it is specifically discouraged in children and adolescents as it increases the risk of suicidal thoughts or attempts 162 163 164 165 166 167 168 For children and adolescents with moderate to severe depressive disorder fluoxetine seems to be the best treatment either with or without cognitive behavioural therapy but more research is needed to be certain 169 163 170 164 Sertraline escitalopram duloxetine might also help in reducing symptoms Some antidepressants have not been shown to be effective 171 163 Medications are not recommended in children with mild disease 172 There is also insufficient evidence to determine effectiveness in those with depression complicated by dementia 173 Any antidepressant can cause low blood sodium levels 174 nevertheless it has been reported more often with SSRIs 157 It is not uncommon for SSRIs to cause or worsen insomnia the sedating atypical antidepressant mirtazapine can be used in such cases 175 176 Irreversible monoamine oxidase inhibitors an older class of antidepressants have been plagued by potentially life threatening dietary and drug interactions They are still used only rarely although newer and better tolerated agents of this class have been developed 177 The safety profile is different with reversible monoamine oxidase inhibitors such as moclobemide where the risk of serious dietary interactions is negligible and dietary restrictions are less strict 178 It is unclear whether antidepressants affect a person s risk of suicide 179 For children adolescents and probably young adults between 18 and 24 years old there is a higher risk of both suicidal ideations and suicidal behavior in those treated with SSRIs 180 181 For adults it is unclear whether SSRIs affect the risk of suicidality One review found no connection 182 another an increased risk 183 and a third no risk in those 25 65 years old and a decreased risk in those more than 65 184 A black box warning was 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 185 Similar precautionary notice revisions were implemented by the Japanese Ministry of Health 186 Other medications and supplements The combined use of antidepressants plus benzodiazepines demonstrates 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 187 Ketamine may 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 188 189 A nasal spray form of esketamine was 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 190 191 There is insufficient high quality evidence to suggest omega 3 fatty acids are effective in depression 192 There is limited evidence that vitamin D supplementation is of value in alleviating the symptoms of depression in individuals who are vitamin D deficient 82 Lithium appears effective at lowering the risk of suicide in those with bipolar disorder and unipolar depression to nearly the same levels as the general population 193 There is a narrow range of effective and safe dosages of lithium thus close monitoring may be needed 194 Low dose thyroid hormone may be added to existing antidepressants to treat persistent depression symptoms in people who have tried multiple courses of medication 195 Limited evidence suggests stimulants such as amphetamine and modafinil may be effective in the short term or as adjuvant therapy 196 197 Also it is suggested that folate supplements may have a role in depression management 198 There is tentative evidence for benefit from testosterone in males 199 Electroconvulsive therapy Electroconvulsive therapy ECT is a standard psychiatric treatment in which seizures are electrically induced in a person with depression to provide relief from psychiatric illnesses 200 1880 ECT is used with informed consent 201 as a last line of intervention for major depressive disorder 202 A round of ECT is effective for about 50 of people with treatment resistant major depressive disorder whether it is unipolar or bipolar 203 Follow up treatment is still poorly studied but about half of people who respond relapse within twelve months 204 Aside from effects in the brain the general physical risks of ECT are similar to those of brief general anesthesia 205 259 Immediately following treatment the most common adverse effects are confusion and memory loss 202 206 ECT is considered one of the least harmful treatment options available for severely depressed pregnant women 207 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 under anesthesia with a muscle relaxant 208 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 202 ECT appears to work in the short term via an anticonvulsant effect mostly in the frontal lobes and longer term via neurotrophic effects primarily in the medial temporal lobe 209 Other Transcranial magnetic stimulation TMS or deep transcranial magnetic stimulation is a noninvasive method used to stimulate small regions of the brain 210 TMS was approved by the FDA for treatment resistant major depressive disorder trMDD in 2008 211 and as of 2014 evidence supports that it is probably effective 212 The American Psychiatric Association 213 the Canadian Network for Mood and Anxiety Disorders 214 and the Royal Australia and New Zealand College of Psychiatrists have endorsed TMS for trMDD 215 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 216 217 There is a small amount of evidence that sleep deprivation may improve depressive symptoms in some individuals 218 with the effects usually showing up within a day This effect is usually temporary Besides sleepiness this method can cause a side effect of mania or hypomania 219 There is insufficient evidence for Reiki 220 and dance movement therapy in depression 221 Cannabis is specifically not recommended as a treatment 222 PrognosisStudies have shown that 80 of those with a first major depressive episode will have at least one more during their life 223 with a lifetime average of four episodes 224 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 225 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 226 227 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 and family dysfunction 228 A high proportion of people who experience full symptomatic remission still have at least one not fully resolved symptom after treatment 229 Recurrence or chronicity is more likely if symptoms have not fully resolved with treatment 229 Current guidelines recommend continuing antidepressants for four to six months after remission to prevent relapse Evidence from many randomized controlled trials indicates continuing antidepressant medications after recovery can reduce the chance of relapse by 70 41 on placebo vs 18 on antidepressant The preventive effect probably lasts for at least the first 36 months of use 230 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 231 The median duration of an episode has been estimated to be 23 weeks with the highest rate of recovery in the first three months 232 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 233 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 141 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 141 Life expectancy and the risk of suicide Depressed individuals have a shorter life expectancy than those without depression in part because people who are depressed are at risk of dying of suicide 234 About 50 of people who die of suicide have a mood disorder such as major depression and the risk is especially high if a person has a marked sense of hopelessness or has both depression and borderline personality disorder 235 236 About 2 8 of adults with major depression die by suicide 2 237 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 238 even though suicide attempts are more frequent in women 239 Depressed people have a higher rate of dying from other causes 240 There is a 1 5 to 2 fold increased risk of cardiovascular disease independent of other known risk factors and is itself linked directly or indirectly to risk factors such as smoking and obesity People with major depression are less likely to follow medical recommendations for treating and preventing cardiovascular disorders further increasing their risk of medical complications 241 Cardiologists may not recognize underlying depression that complicates a cardiovascular problem under their care 242 EpidemiologyMain article Epidemiology of depression Disability adjusted life year for unipolar depressive disorders per 100 000 inhabitants in 2004 243 no data lt 700 700 775 775 850 850 925 925 1000 1000 1075 1075 1150 1150 1225 1225 1300 1300 1375 1375 1450 gt 1450 Major depressive disorder affected approximately 163 million people in 2017 2 of the global population 8 The percentage of people who are affected at one point in their life varies from 7 in Japan to 21 in France 4 In most countries the number of people who have depression during their lives falls within an 8 18 range 4 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 17 244 Among adolescents between the ages of 12 and 17 17 of the U S population 4 1 million individuals had a major depressive episode in 2020 females 25 2 males 9 2 244 Among individuals reporting two or more races the US prevalence is highest 244 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 245 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 245 In 2019 major depressive disorder was identified using either the DSM IV TR or ICD 10 in the Global Burden of Disease Study as the fifth most common cause of years lived with disability and the 18th most common for disability adjusted life years 246 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 60 247 The risk of major depression is increased with neurological conditions such as stroke Parkinson s disease or multiple sclerosis and during the first year after childbirth 248 It is also more common after cardiovascular illnesses and is related more to those with a poor cardiac disease outcome than to a better one 249 250 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 251 Depression is common among those over 65 years of age and increases in frequency beyond this age 27 The risk of depression increases in relation to the frailty of the individual 252 Depression is one of the most important factors which negatively impact quality of life in adults as well as the elderly 27 Both symptoms and treatment among the elderly differ from those of the rest of the population 27 Major depression was the leading cause of disease burden in 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 after HIV according to the WHO 253 Delay or failure in seeking treatment after relapse and the failure of health professionals to provide treatment are two barriers to reducing disability 254 Comorbidity Major depression frequently co occurs with other psychiatric problems The 1990 92 National Comorbidity Survey US reported that half of those with major depression also have lifetime anxiety and its associated disorders such as generalized anxiety disorder 255 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 256 Depressed people have increased rates of alcohol and substance use particularly dependence 257 258 and around a third of individuals diagnosed with attention deficit hyperactivity disorder ADHD develop comorbid depression 259 Post traumatic stress disorder and depression often co occur 15 Depression may also coexist with ADHD complicating the diagnosis and treatment of both 260 Depression is also frequently comorbid with alcohol use disorder and personality disorders 261 Depression can also be exacerbated during particular months usually winter in those with seasonal affective disorder While overuse of digital media has been associated with depressive symptoms using digital media may also improve mood in some situations 262 263 Depression and pain often 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 264 Depression often coexists with physical disorders common among the elderly such as stroke other cardiovascular diseases Parkinson s disease and chronic obstructive pulmonary disease 265 HistoryMain article History of depression The Ancient Greek physician Hippocrates described a syndrome of melancholia melagxolia melankholia 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 266 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 267 Diagnoses of depression go back at least as far as Hippocrates The term depression itself was derived from the Latin verb deprimere meaning to press down 268 From the 14th century to depress meant to subjugate or to bring down in spirits It was used in 1665 in English author Richard Baker s Chronicle to refer to someone having a great depression of spirit and by English author Samuel Johnson in a similar sense in 1753 269 The term also came into use in physiology and economics An early usage referring to a psychiatric symptom was by French psychiatrist Louis Delasiauve in 1856 and by the 1860s it was appearing in medical dictionaries to refer to a physiological and metaphorical lowering of emotional function 270 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 267 Although melancholia remained the dominant diagnostic term depression gained increasing currency in medical treatises and was a synonym by the end of the century German psychiatrist Emil Kraepelin may have been the first to use it as the overarching term referring to different kinds of melancholia as depressive states 271 Freud likened the state of melancholia to mourning in his 1917 paper Mourning and Melancholia He theorized that objective loss such as the loss of a valued relationship through death or a romantic break up results in subjective loss as well the depressed individual has identified with the object of affection through an unconscious narcissistic process called the libidinal cathexis of the ego Such loss results in severe melancholic symptoms more profound than mourning not only is the outside world viewed negatively but the ego itself is compromised 272 The person s decline of self perception is revealed in his belief of his own blame inferiority and unworthiness 273 He also emphasized early life experiences as a predisposing factor 267 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 274 The first version of the DSM DSM I 1952 contained depressive reaction and the DSM II 1968 depressive neurosis defined as an excessive reaction to internal conflict or an identifiable event and also included a depressive type of manic depressive psychosis within Major affective disorders 275 The term unipolar along with the related term bipolar was coined by the neurologist and psychiatrist Karl Kleist and subsequently used by his disciples Edda Neele and Karl Leonhard 276 The term Major depressive disorder was introduced by a group of US clinicians in the mid 1970s as part of proposals for diagnostic criteria based on patterns of symptoms called the Research Diagnostic Criteria building on earlier Feighner Criteria 10 and was incorporated into the DSM III in 1980 277 The American Psychiatric Association added major depressive disorder to the Diagnostic and Statistical Manual of Mental Disorders DSM III 278 as a split of the previous depressive neurosis in the DSM II which also encompassed the conditions now known as dysthymia and adjustment disorder with depressed mood 278 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 90 277 The ancient idea of melancholia still survives in the notion of a melancholic subtype The new definitions of depression were widely accepted albeit with some conflicting findings and views There have been some continued empirically based arguments for a return to the diagnosis of melancholia 279 280 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 281 Society and cultureFurther information Depression and culture Terminology The 16th American president Abraham Lincoln had melancholy a condition that now may be referred to as clinical depression 282 The term depression is used in a number of different ways It is often used to mean this syndrome but may refer to other mood disorders or 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 283 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 284 285 Stigma Historical figures were often reluctant to discuss or seek treatment for depression due to social stigma about the condition or due to ignorance of diagnosis or treatments Nevertheless analysis or interpretation of letters journals artwork writings or statements of family and friends of some historical personalities has led to the presumption that they may have had some form of depression People who may have had depression include English author Mary Shelley 286 American British writer Henry James 287 and American president Abraham Lincoln 288 Some well known contemporary people with possible depression include Canadian songwriter Leonard Cohen 289 and American playwright and novelist Tennessee Williams 290 Some pioneering psychologists such as Americans William James 291 292 and John B Watson 293 dealt with their own depression There has been a continuing discussion of whether neurological disorders and mood disorders may be linked to creativity a discussion that goes back to Aristotelian times 294 295 British literature gives many examples of reflections on depression 296 English philosopher John Stuart Mill experienced a several months long period of what he called a dull state of nerves when one is unsusceptible to enjoyment or pleasurable excitement one of those moods when what is pleasure at other times becomes insipid or indifferent He quoted English poet Samuel Taylor Coleridge s Dejection as a perfect description of his case A grief without a pang void dark and drear A drowsy stifled unimpassioned grief Which finds no natural outlet or relief In word or sigh or tear 297 298 English writer Samuel Johnson used the term the black dog in the 1780s to describe his own depression 299 and it was subsequently popularized by British Prime Minister Sir Winston Churchill who also had the disorder 299 Johann Wolfgang von Goethe in his Faust Part I published in 1808 has Mephistopheles assume the form of a black dog specifically a poodle 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 300 In the UK the Royal College of Psychiatrists and the Royal College of General Practitioners conducted a joint Five year Defeat Depression campaign to educate and reduce stigma from 1992 to 1996 301 a MORI study conducted afterwards showed a small positive change in public attitudes to depression and treatment 302 References a b c d e f g h i Depression U S National Institute of Mental Health NIMH May 2016 Archived from the original on 5 August 2016 Retrieved 31 July 2016 a b Richards CS O Hara MW 2014 The Oxford Handbook of Depression and Comorbidity Oxford University Press p 254 ISBN 978 0 19 979704 2 a b American Psychiatric Association 2013 p 165 a b c d e f g Kessler RC Bromet EJ 2013 The epidemiology of depression across cultures Annual Review of Public Health 34 119 38 doi 10 1146 annurev publhealth 031912 114409 PMC 4100461 PMID 23514317 a b c d e f g American Psychiatric Association 2013 p 166 American Psychiatric Association 2013 pp 167 168 a b Cooney GM Dwan K Greig CA Lawlor DA Rimer J Waugh FR McMurdo M Mead GE September 2013 Mead GE ed Exercise for depression The Cochrane Database of Systematic Reviews 2013 9 CD004366 doi 10 1002 14651858 CD004366 pub6 PMC 9721454 PMID 24026850 a b c GBD 2017 Disease and Injury Incidence and Prevalence Collaborators 10 November 2018 Global regional and national incidence prevalence and years lived with disability for 354 diseases and injuries for 195 countries and territories 1990 2017 a systematic analysis for the Global Burden of Disease Study 2017 Lancet 392 10159 1789 1858 doi 10 1016 S0140 6736 18 32279 7 PMC 6227754 PMID 30496104 Sartorius N Henderson AS Strotzka H et al The ICD 10 Classification of Mental and Behavioural Disorders Clinical descriptions and diagnostic guidelines PDF World Health Organization Archived PDF from the original on 5 February 2022 Retrieved 23 June 2021 a b Spitzer RL Endicott J Robins E 1975 The development of diagnostic criteria in psychiatry PDF Archived PDF from the original on 14 December 2005 Retrieved 8 November 2008 a b Patton LL 2015 The ADA Practical Guide to Patients with Medical Conditions 2nd ed John Wiley amp Sons p 339 ISBN 978 1 118 92928 5 Fournier JC DeRubeis RJ Hollon SD Dimidjian S Amsterdam JD Shelton RC Fawcett J January 2010 Antidepressant drug effects and depression severity a patient level meta analysis JAMA 303 1 47 53 doi 10 1001 jama 2009 1943 PMC 3712503 PMID 20051569 Kirsch I Deacon BJ Huedo Medina TB Scoboria A Moore TJ Johnson BT February 2008 Initial severity and antidepressant benefits a meta analysis of data submitted to the Food and Drug Administration PLOS Medicine 5 2 e45 doi 10 1371 journal pmed 0050045 PMC 2253608 PMID 18303940 Global Burden of Disease Study 2013 Collaborators August 2015 Global regional and national incidence prevalence and years lived with disability for 301 acute and chronic diseases and injuries in 188 countries 1990 2013 a systematic analysis for the Global Burden of Disease Study 2013 Lancet 386 9995 743 800 doi 10 1016 S0140 6736 15 60692 4 PMC 4561509 PMID 26063472 a b c d e Depression PDF National Institute of Mental Health NIMH Archived PDF from the original on 28 August 2021 Retrieved 13 October 2021 American Psychiatric Association 2013 p 160 American Psychiatric Association 2013 p 161 a b c American Psychiatric Association 2013 p 163 Insomnia Assessment and Management in Primary Care American Family Physician 59 11 3029 3038 1999 Archived from the original on 26 July 2011 Retrieved 12 November 2014 American Psychiatric Association 2000a p 412 Nelson JC Bickford D Delucchi K Fiedorowicz JG Coryell WH 2018 Risk of Psychosis in Recurrent Episodes of Psychotic and Nonpsychotic Major Depressive Disorder A Systematic Review and Meta Analysis Am J Psychiatry 175 9 897 904 doi 10 1176 appi ajp 2018 17101138 PMID 29792050 S2CID 43951278 Fisher JC Powers WE Tuerk DB Edgerton MT March 1975 Development of a plastic surgical teaching service in a women s correctional institution American Journal of Surgery 129 3 269 72 doi 10 1136 bmj 322 7284 482 PMC 1119689 PMID 11222428 a b c American Psychiatric Association 2000a p 349 Delgado PL Schillerstrom J 2009 Cognitive Difficulties Associated With Depression What Are the Implications for Treatment Psychiatric Times 26 3 Archived from the original on 22 July 2009 Faculty of Psychiatry of Old Age NSW Branch RANZCP Kitching D Raphael B 2001 Consensus Guidelines for Assessment and Management of Depression in the Elderly PDF North Sydney New South Wales NSW Health Department p 2 ISBN 978 0 7347 3341 2 Archived PDF from the original on 1 April 2015 American Psychiatric Association 2013 p 164 a b c d e Swedish Agency for Health Technology Assessment and Assessment of Social Services SBU 27 January 2015 Depression treatment for the elderly sbu se Archived from the original on 18 June 2016 Retrieved 16 June 2016 Hankin BL Abela JR 2005 Development of Psychopathology A Vulnerability Stress Perspective SAGE Publications pp 32 34 ISBN 9781412904902 Department of Health and Human Services 1999 The fundamentals of mental health and mental illness PDF Mental Health A Report of the Surgeon General Archived PDF from the original on 17 December 2008 Retrieved 11 November 2008 Caspi A Sugden K Moffitt TE Taylor A Craig IW Harrington H McClay J Mill J Martin J Braithwaite A Poulton R July 2003 Influence of life stress on depression moderation by a polymorphism in the 5 HTT gene Science 301 5631 386 89 Bibcode 2003Sci 301 386C doi 10 1126 science 1083968 PMID 12869766 S2CID 146500484 Haeffel GJ Getchell M Koposov RA Yrigollen CM Deyoung CG Klinteberg BA Oreland L Ruchkin VV Grigorenko EL January 2008 Association between polymorphisms in the dopamine transporter gene and depression evidence for a gene environment interaction in a sample of juvenile detainees PDF Psychological Science 19 1 62 69 doi 10 1111 j 1467 9280 2008 02047 x PMID 18181793 S2CID 15520723 Archived PDF from the original on 17 December 2008 Slavich GM 2004 Deconstructing depression A diathesis stress perspective Opinion APS Observer Archived from the original on 11 May 2011 Retrieved 11 November 2008 Beck AT Rush AJ Shaw BF Emery G 1979 Cognitive therapy of depression New York The Guilford Press pp 11 12 ISBN 0 89862 000 7 Retrieved 26 February 2022 Nieto I Robles E Vasquez C 1 November 2020 Self reported cognitive biases in depression A meta analysis Clinical Psychology Review ScienceDirect 82 101934 doi 10 1016 j cpr 2020 101934 PMID 33137610 S2CID 226243519 Retrieved 26 February 2022 Saveanu RV Nemeroff CB March 2012 Etiology of depression genetic and environmental factors The Psychiatric Clinics of North America 35 1 51 71 doi 10 1016 j psc 2011 12 001 PMID 22370490 Sullivan PF Neale MC Kendler KS October 2000 Genetic epidemiology of major depression review and meta analysis The American Journal of Psychiatry 157 10 1552 62 doi 10 1176 appi ajp 157 10 1552 PMID 11007705 Wray NR May 2018 Genome wide association analyses identify 44 risk variants and refine the genetic architecture of major depression Nature Genetics 50 5 668 681 doi 10 1038 s41588 018 0090 3 hdl 11370 3a0e2468 99e7 40c3 80f4 9d25adfae485 PMC 5934326 PMID 29700475 Howard DM Adams MJ Clarke TK Hafferty JD Gibson J Shirali M et al March 2019 Genome wide meta analysis of depression identifies 102 independent variants and highlights the importance of the prefrontal brain regions Nature Neuroscience 22 3 343 352 doi 10 1038 s41593 018 0326 7 PMC 6522363 PMID 30718901 Duncan LE Keller MC October 2011 A critical review of the first 10 years of candidate gene by environment interaction research in psychiatry The American Journal of Psychiatry 168 10 1041 9 doi 10 1176 appi ajp 2011 11020191 PMC 3222234 PMID 21890791 Peyrot WJ Van der Auwera S Milaneschi Y Dolan CV Madden PA Sullivan PF Strohmaier J Ripke S Rietschel M Nivard MG Mullins N Montgomery GW Henders AK Heat AC Fisher HL Dunn EC Byrne EM et al July 2018 Does Childhood Trauma Moderate Polygenic Risk for Depression A Meta analysis of 5765 Subjects From the Psychiatric Genomics Consortium Biological Psychiatry 84 2 138 147 doi 10 1016 j biopsych 2017 09 009 PMC 5862738 PMID 29129318 Simon GE November 2001 Treating depression in patients with chronic disease recognition and treatment are crucial depression worsens the course of a chronic illness The Western Journal of Medicine 175 5 292 93 doi 10 1136 ewjm 175 5 292 PMC 1071593 PMID 11694462 Clayton PJ Lewis CE March 1981 The significance of secondary depression Journal of Affective Disorders 3 1 25 35 doi 10 1016 0165 0327 81 90016 1 PMID 6455456 Kewalramani A Bollinger ME Postolache TT 1 January 2008 Asthma and Mood Disorders International Journal of Child Health and Human Development 1 2 115 23 PMC 2631932 PMID 19180246 Rogers D Pies R December 2008 General medical with depression drugs associated Psychiatry 5 12 28 41 PMC 2729620 PMID 19724774 Botts S Ryan M Drug Induced Diseases Section IV Drug Induced Psychiatric Diseases Chapter 18 Depression pp 1 23 Archived from the original on 23 December 2010 Brook DW Brook JS Zhang C Cohen P Whiteman M November 2002 Drug use and the risk of major depressive disorder alcohol dependence and substance use disorders Archives of General Psychiatry 59 11 1039 44 doi 10 1001 archpsyc 59 11 1039 PMID 12418937 Meltzer Brody S 9 January 2017 New insights into perinatal depression pathogenesis and treatment during pregnancy and postpartum Dialogues in Clinical Neuroscience 13 1 89 100 doi 10 31887 DCNS 2011 13 1 smbrody PMC 3181972 PMID 21485749 Melrose S 1 January 2015 Seasonal Affective Disorder An Overview of Assessment and Treatment Approaches Depression Research and Treatment 2015 178564 doi 10 1155 2015 178564 PMC 4673349 PMID 26688752 Wu Y Zhang L Li S Zhang D 29 April 2021 Associations of dietary vitamin B1 vitamin B2 vitamin B6 and vitamin B12 with the risk of depression a systematic review and meta analysis Nutrition Reviews Oxford University Press OUP 80 3 351 366 doi 10 1093 nutrit nuab014 ISSN 0029 6643 PMID 33912967 Ruhe HG Mason NS Schene AH April 2007 Mood is indirectly related to serotonin norepinephrine and dopamine levels in humans a meta analysis of monoamine depletion studies Molecular Psychiatry 12 4 331 59 doi 10 1038 sj mp 4001949 PMID 17389902 Delgado PL Moreno FA 2000 Role of norepinephrine in depression The Journal of Clinical Psychiatry 61 Suppl 1 5 12 PMID 10703757 Savitz JB Drevets WC April 2013 Neuroreceptor imaging in depression Neurobiology of Disease 52 49 65 doi 10 1016 j nbd 2012 06 001 PMID 22691454 Hasler G October 2010 Pathophysiology of depression do we have any solid evidence of interest to clinicians World Psychiatry 9 3 155 61 doi 10 1002 j 2051 5545 2010 tb00298 x PMC 2950973 PMID 20975857 Dunlop BW Nemeroff CB March 2007 The role of dopamine in the pathophysiology of depression Archives of General Psychiatry 64 3 327 37 doi 10 1001 archpsyc 64 3 327 PMID 17339521 Meyer JH Ginovart N Boovariwala A et al November 2006 Elevated monoamine oxidase a levels in the brain an explanation for the monoamine imbalance of major depression Archives of General Psychiatry 63 11 1209 16 doi 10 1001 archpsyc 63 11 1209 PMID 17088501 Davis KL Charney D Coyle JT Nemeroff C eds 2002 Neuropsychopharmacology the fifth generation of progress an official publication of the American College of Neuropsychopharmacology 5th ed Philadelphia Lippincott Williams amp Wilkins pp 1139 63 ISBN 978 0 7817 2837 9 Adell A April 2015 Revisiting the role of raphe and serotonin in neuropsychiatric disorders The Journal of General Physiology 145 4 257 59 doi 10 1085 jgp 201511389 PMC 4380212 PMID 25825168 Andrews PW Bharwani A Lee KR Fox M Thomson JA April 2015 Is serotonin an upper or a downer The evolution of the serotonergic system and its role in depression and the antidepressant response Neuroscience and Biobehavioral Reviews 51 164 88 doi 10 1016 j neubiorev 2015 01 018 PMID 25625874 S2CID 23980182 Lacasse JR Leo J December 2005 Serotonin and depression a disconnect between the advertisements and the scientific literature PLOS Medicine 2 12 e392 doi 10 1371 journal pmed 0020392 PMC 1277931 PMID 16268734 Moncrieff J Cooper RE Stockman T et al July 2022 The serotonin theory of depression a systematic umbrella review of the evidence Mol Psychiatry doi 10 1038 s41380 022 01661 0 PMID 35854107 S2CID 250646781 Lay source Medicalxpress Krishnadas R Cavanagh J May 2012 Depression an inflammatory illness Journal of Neurology Neurosurgery and Psychiatry 83 5 495 502 doi 10 1136 jnnp 2011 301779 PMID 22423117 Patel A September 2013 Review the role of inflammation in depression Psychiatria Danubina 25 Suppl 2 S216 23 PMID 23995180 Dowlati Y Herrmann N Swardfager W Liu H Sham L Reim EK Lanctot KL March 2010 A meta analysis of cytokines in major depression Biological Psychiatry 67 5 446 57 doi 10 1016 j biopsych 2009 09 033 PMID 20015486 S2CID 230209 Kohler O Benros ME Nordentoft M Farkouh ME Iyengar RL Mors O Krogh J December 2014 Effect of anti inflammatory treatment on depression depressive symptoms and adverse effects a systematic review and meta analysis of randomized clinical trials PDF JAMA Psychiatry 71 12 1381 91 doi 10 1001 jamapsychiatry 2014 1611 PMID 25322082 Archived PDF from the original on 20 July 2018 Raedler TJ November 2011 Inflammatory mechanisms in major depressive disorder Current Opinion in Psychiatry 24 6 519 25 doi 10 1097 YCO 0b013e32834b9db6 PMID 21897249 S2CID 24215407 Arana GW Baldessarini RJ Ornsteen M December 1985 The dexamethasone suppression test for diagnosis and prognosis in psychiatry Commentary and review Archives of General Psychiatry 42 12 1193 204 doi 10 1001 archpsyc 1985 01790350067012 PMID 3000317 Varghese FP Brown ES August 2001 The Hypothalamic Pituitary Adrenal Axis in Major Depressive Disorder A Brief Primer for Primary Care Physicians Primary Care Companion to the Journal of Clinical Psychiatry 3 4 151 55 doi 10 4088 pcc v03n0401 PMC 181180 PMID 15014598 Lopez Duran NL Kovacs M George CJ 2009 Hypothalamic pituitary adrenal axis dysregulation in depressed children and adolescents a meta analysis Psychoneuroendocrinology 34 9 1272 1283 doi 10 1016 j psyneuen 2009 03 016 PMC 2796553 PMID 19406581 Dedovic K Ngiam J 2015 The cortisol awakening response and major depression examining the evidence Neuropsychiatric Disease and Treatment 11 1181 1189 doi 10 2147 NDT S62289 PMC 4437603 PMID 25999722 Mayberg HS 1997 Limbic cortical dysregulation a proposed model of depression The Journal of Neuropsychiatry and Clinical Neurosciences 9 3 471 81 doi 10 1176 jnp 9 3 471 PMID 9276848 Graham J Salimi Khorshidi G Hagan C Walsh N Goodyer I Lennox B Suckling J 2013 Meta analytic evidence for neuroimaging models of depression state or trait Journal of Affective Disorders 151 2 423 431 doi 10 1016 j jad 2013 07 002 PMID 23890584 Hamilton JP Etkin A Furman DJ Lemus MG Johnson RF Gotlib IH July 2012 Functional neuroimaging of major depressive disorder a meta analysis and new integration of base line activation and neural response data The American Journal of Psychiatry 169 7 693 703 doi 10 1176 appi ajp 2012 11071105 PMID 22535198 Kaufmann IM 1993 Rural psychiatric services A collaborative model Canadian Family Physician 39 1957 1961 PMC 2379905 PMID 8219844 Call for action over Third World depression BBC News Health British Broadcasting Corporation BBC 1 November 1999 Archived from the original on 13 May 2008 Retrieved 11 October 2008 Sharp LK Lipsky MS September 2002 Screening for depression across the lifespan a review of measures for use in primary care settings American Family Physician 66 6 1001 08 PMID 12358212 Zimmerman M Chelminski I Posternak M September 2004 A review of studies of the Hamilton depression rating scale in healthy controls implications for the definition of remission in treatment studies of depression The Journal of Nervous and Mental Disease 192 9 595 601 doi 10 1097 01 nmd 0000138226 22761 39 PMID 15348975 S2CID 24291799 McPherson A Martin CR February 2010 A narrative review of the Beck Depression Inventory BDI and implications for its use in an alcohol dependent population Journal of Psychiatric and Mental Health Nursing 17 1 19 30 doi 10 1111 j 1365 2850 2009 01469 x PMID 20100303 Osman A Bagge CL Gutierrez PM Konick LC Kopper BA Barrios FX December 2001 The Suicidal Behaviors Questionnaire Revised SBQ R validation with clinical and nonclinical samples Assessment 8 4 443 54 doi 10 1177 107319110100800409 PMID 11785588 S2CID 11477277 Cepoiu M McCusker J Cole MG Sewitch M Belzile E Ciampi A January 2008 Recognition of depression by non psychiatric physicians a systematic literature review and meta analysis Journal of General Internal Medicine 23 1 25 36 doi 10 1007 s11606 007 0428 5 PMC 2173927 PMID 17968628 Dale J Sorour E Milner G 2008 Do psychiatrists perform appropriate physical investigations for their patients A review of current practices in a general psychiatric inpatient and outpatient setting Journal of Mental Health 17 3 293 98 doi 10 1080 09638230701498325 S2CID 72755878 Orengo CA Fullerton G Tan R October 2004 Male depression a review of gender concerns and testosterone therapy Geriatrics 59 10 24 30 PMID 15508552 a b Parker GB Brotchie H Graham RK January 2017 Vitamin D and depression Journal of Affective Disorders 208 56 61 doi 10 1016 j jad 2016 08 082 PMID 27750060 Reid LM Maclullich AM 2006 Subjective memory complaints and cognitive impairment in older people Dementia and Geriatric Cognitive Disorders 22 5 6 471 85 doi 10 1159 000096295 PMID 17047326 S2CID 9328852 Katz IR 1998 Diagnosis and treatment of depression in patients with Alzheimer s disease and other dementias The Journal of Clinical Psychiatry 59 Suppl 9 38 44 PMID 9720486 Wright SL Persad C December 2007 Distinguishing between depression and dementia in older persons neuropsychological and neuropathological correlates Journal of Geriatric Psychiatry and Neurology 20 4 189 98 doi 10 1177 0891988707308801 PMID 18004006 S2CID 33714179 Sadock 2002 p 108 Sadock 2002 p 260 Sadock 2002 p 288 American Psychiatric Association 2013 p xii a b Gruenberg AM Goldstein RD Pincus HA 2005 Classification of Depression Research and Diagnostic Criteria DSM IV and ICD 10 PDF In Licinio J Wong ML eds Biology of Depression Biology of Depression From Novel Insights to Therapeutic Strategies Wiley VCH Verlag GmbH pp 1 12 doi 10 1002 9783527619672 ch1 ISBN 978 3 527 61967 2 Archived PDF from the original on 3 May 2005 Retrieved 30 October 2008 Diagnostic and Statistical Manual of Mental Disorders DSM 5 TR American Psychiatric Association Retrieved 9 July 2022 The Diagnostic and Statistical Manual of Mental Disorders Fifth Edition Text Revision DSM 5 TR features the most current text updates based on scientific literature with contributions from more than 200 subject matter experts International Statistical Classification of Diseases and Related Health Problems ICD World Health Organization Retrieved 9 July 2022 the latest version of the ICD ICD 11 was adopted by the 72nd World Health Assembly in 2019 and came into effect on 1st January 2022 a b c d ICD 11 6A70 Single episode depressive disorder and 6A71 Recurrent depressive disorder Diagnostic Criteria for Major Depressive Disorder and Depressive Episodes PDF City of Palo Alto Project Safety Net Archived from the original PDF on 3 August 2020 Retrieved 21 February 2019 a b c d Parker GF 1 June 2014 DSM 5 and Psychotic and Mood Disorders Journal of the American Academy of Psychiatry and the Law Online 42 2 182 190 ISSN 1093 6793 PMID 24986345 American Psychiatric Association 2013 p 162 Parker 1996 p 173 a b Sadock 2002 p 552 American Psychiatric Association 2013 p 183 Carta MG Altamura AC Hardoy MC Pinna F Medda S Dell Osso L Carpiniello B Angst J June 2003 Is recurrent brief depression an expression of mood spectrum disorders in young people Results of a large community sample European Archives of Psychiatry and Clinical Neuroscience 253 3 149 53 doi 10 1007 s00406 003 0418 5 hdl 2434 521599 PMID 12904979 S2CID 26860606 Rapaport MH Judd LL Schettler PJ Yonkers KA Thase ME Kupfer DJ Frank E Plewes JM Tollefson GD Rush AJ April 2002 A descriptive analysis of minor depression The American Journal of Psychiatry 159 4 637 43 doi 10 1176 appi ajp 159 4 637 PMID 11925303 a b American Psychiatric Association 2013 p 168 American Psychiatric Association 2013 p 185 American Psychiatric Association 2013 pp 185 186 American Psychiatric Association 2013 pp 119 120 American Psychiatric Association 2013 pp 186 187 American Psychiatric Association 2013 p 187 American Psychiatric Association 2013 p 167 a b Cuijpers P van Straten A Smit F Mihalopoulos C Beekman A October 2008 Preventing the onset of depressive disorders a meta analytic review of psychological interventions The American Journal of Psychiatry 165 10 1272 80 doi 10 1176 appi ajp 2008 07091422 hdl 1871 16952 PMID 18765483 Siu AL Bibbins Domingo K Grossman DC et al January 2016 Screening for Depression in Adults US Preventive Services Task Force Recommendation Statement JAMA 315 4 380 87 doi 10 1001 jama 2015 18392 PMID 26813211 Siu AL March 2016 Screening for Depression in Children and Adolescents U S Preventive Services Task Force Recommendation Statement Annals of Internal Medicine 164 5 360 66 doi 10 7326 M15 2957 PMID 26858097 Gilbody S House AO Sheldon TA October 2005 Screening and case finding instruments for depression The Cochrane Database of Systematic Reviews 2005 4 CD002792 doi 10 1002 14651858 CD002792 pub2 PMC 6769050 PMID 16235301 Ferenchick EK Ramanuj P Pincus HA 2019 Depression in primary care part 1 screening and diagnosis British Medical Journal 365 l794 doi 10 1136 bmj l794 PMID 30962184 S2CID 104296515 a b Munoz RF Beardslee WR Leykin Y May June 2012 Major depression can be prevented The American Psychologist 67 4 285 95 doi 10 1037 a0027666 PMC 4533896 PMID 22583342 Cuijpers P 20 September 2012 Prevention and early treatment of mental ill health PDF Psychology for Health Contributions to Policy Making Brussels Archived from the original PDF on 12 May 2013 Retrieved 16 June 2013 Griffiths KM Farrer L Christensen H 2010 The efficacy of internet interventions for depression and anxiety disorders a review of randomised controlled trials PDF Medical Journal of Australia 192 11 4 11 doi 10 5694 j 1326 5377 2010 tb03685 x PMID 20528707 S2CID 1948009 Archived PDF from the original on 12 November 2014 Retrieved 12 November 2014 Cuijpers P Munoz RF Clarke GN Lewinsohn PM July 2009 Psychoeducational treatment and prevention of depression the Coping with Depression course thirty years later Clinical Psychology Review 29 5 449 58 doi 10 1016 j cpr 2009 04 005 PMID 19450912 Karrouri R Hammani Z Benjelloun R Otheman Y November 2021 Major depressive disorder Validated treatments and future challenges World J Clin Cases Review 9 31 9350 9367 doi 10 12998 wjcc v9 i31 9350 PMC 8610877 PMID 34877271 a b c Practice guideline for the treatment of patients with major depressive disorder revision American Psychiatric Association The American Journal of Psychiatry 157 4 Suppl 1 45 April 2000 PMID 10767867 Third edition doi 10 1176 appi books 9780890423363 48690 Archer J Bower P Gilbody S et al October 2012 Collaborative care for depression and anxiety problems The Cochrane Database of Systematic Reviews 10 CD006525 doi 10 1002 14651858 CD006525 pub2 hdl 10871 13751 PMID 23076925 a b c Depression National Institute for Health and Care Excellence December 2004 Archived from the original on 15 November 2008 Retrieved 20 March 2013 Hetrick SE Cox GR Witt KG Bir JJ Merry SN August 2016 Cognitive behavioural therapy CBT third wave CBT and interpersonal therapy IPT based interventions for preventing depression in children and adolescents The Cochrane Database of Systematic Reviews 2016 8 CD003380 doi 10 1002 14651858 CD003380 pub4 PMC 8407360 PMID 27501438 Patel V Araya R Bolton P May 2004 Treating depression in the developing world Tropical Medicine amp International Health 9 5 539 41 doi 10 1111 j 1365 3156 2004 01243 x PMID 15117296 S2CID 73073889 Cox GR Callahan P Churchill R et al November 2014 Psychological therapies versus antidepressant medication alone and in combination for depression in children and adolescents The Cochrane Database of Systematic Reviews 2014 11 CD008324 doi 10 1002 14651858 CD008324 pub3 PMC 8556660 PMID 25433518 Josefsson T Lindwall M Archer T April 2014 Physical exercise intervention in depressive disorders meta analysis and systematic review Scandinavian Journal of Medicine amp Science in Sports 24 2 259 72 doi 10 1111 sms 12050 PMID 23362828 S2CID 29351791 Bridle C Spanjers K Patel S Atherton NM Lamb SE September 2012 Effect of exercise on depression severity in older people systematic review and meta analysis of randomised controlled trials The British Journal of Psychiatry 201 3 180 85 doi 10 1192 bjp bp 111 095174 PMID 22945926 Lopresti AL Hood SD Drummond PD May 2013 A review of lifestyle factors that contribute to important pathways associated with major depression diet sleep and exercise PDF Journal of Affective Disorders 148 1 12 27 doi 10 1016 j jad 2013 01 014 PMID 23415826 Archived PDF from the original on 9 January 2017 Taylor G McNeill A Girling A et al February 2014 Change in mental health after smoking cessation systematic review and meta analysis BMJ 348 feb13 1 g1151 doi 10 1136 bmj g1151 PMC 3923980 PMID 24524926 Khan A Faucett J Lichtenberg P Kirsch I Brown WA 30 July 2012 A systematic review of comparative efficacy of treatments and controls for depression PLOS ONE 7 7 e41778 Bibcode 2012PLoSO 741778K doi 10 1371 journal pone 0041778 PMC 3408478 PMID 22860015 Thase ME 1999 When are psychotherapy and pharmacotherapy combinations the treatment of choice for major depressive disorder The Psychiatric Quarterly 70 4 333 46 doi 10 1023 A 1022042316895 PMID 10587988 S2CID 45091134 Cordes J 2013 Depression Encyclopedia of Sciences and Religions pp 610 16 doi 10 1007 978 1 4020 8265 8 301 ISBN 978 1 4020 8264 1 Ijaz S Davies P Williams CJ et al May 2018 Psychological therapies for treatment resistant depression in adults The Cochrane Database of Systematic Reviews 5 8 CD010558 doi 10 1002 14651858 CD010558 pub2 PMC 6494651 PMID 29761488 Wilson KC Mottram PG Vassilas CA January 2008 Psychotherapeutic treatments for older depressed people The Cochrane Database of Systematic Reviews 23 1 CD004853 doi 10 1002 14651858 CD004853 pub2 PMID 18254062 Cuijpers P van Straten A Smit F December 2006 Psychological treatment of late life depression a meta analysis of randomized controlled trials International Journal of Geriatric Psychiatry 21 12 1139 49 doi 10 1002 gps 1620 hdl 1871 16894 PMID 16955421 S2CID 14778731 Gartlehner G Wagner G Matyas N et al June 2017 Pharmacological and non pharmacological treatments for major depressive disorder review of systematic reviews BMJ Open 7 6 e014912 doi 10 1136 bmjopen 2016 014912 PMC 5623437 PMID 28615268 Childhood Depression abct org Last updated 30 July 2010 NICE guidelines Depression in children and adolescents London NICE 2005 p 5 ISBN 978 1 84629 074 9 Archived from the original on 24 September 2008 Retrieved 16 August 2008 Becker SJ 2008 Cognitive Behavioral Therapy for Adolescent Depression Processes of Cognitive Change Psychiatric Times 25 14 Almeida AM Lotufo Neto F October 2003 Cognitive behavioral therapy in prevention of depression relapses and recurrences a review Revista Brasileira de Psiquiatria 25 4 239 44 doi 10 1590 S1516 44462003000400011 PMID 15328551 Paykel ES February 2007 Cognitive therapy in relapse prevention in depression The International Journal of Neuropsychopharmacology 10 1 131 36 doi 10 1017 S1461145706006912 PMID 16787553 a b c Nieuwenhuijsen K Verbeek JH Neumeyer Gromen A et al October 2020 Interventions to improve return to work in depressed people Cochrane Database Syst Rev 10 12 CD006237 doi 10 1002 14651858 CD006237 pub4 PMC 8094165 PMID 33052607 Beck et al 1987 p 10 Coelho HF Canter PH Ernst E December 2007 Mindfulness based cognitive therapy evaluating current evidence and informing future research Journal of Consulting and Clinical Psychology 75 6 1000 05 doi 10 1037 0022 006X 75 6 1000 PMID 18085916 Khoury B Lecomte T Fortin G et al August 2013 Mindfulness based therapy a comprehensive meta analysis Clinical Psychology Review 33 6 763 71 doi 10 1016 j cpr 2013 05 005 PMID 23796855 Jain FA Walsh RN Eisendrath SJ Christensen S Rael Cahn B 2014 Critical analysis of the efficacy of meditation therapies for acute and subacute phase treatment of depressive disorders a systematic review Psychosomatics 56 2 140 52 doi 10 1016 j psym 2014 10 007 PMC 4383597 PMID 25591492 Simkin DR Black NB July 2014 Meditation and mindfulness in clinical practice Child and Adolescent Psychiatric Clinics of North America 23 3 487 534 doi 10 1016 j chc 2014 03 002 PMID 24975623 a b Alexopoulos GS August 2019 Mechanisms and treatment of late life depression Transl Psychiatry 9 1 188 doi 10 1038 s41398 019 0514 6 PMC 6683149 PMID 31383842 Dworetzky J 1997 Psychology Pacific Grove CA Brooks Cole Pub Co p 602 ISBN 978 0 314 20412 7 Doidge N Simon B Lancee WJ et al 2002 Psychoanalytic patients in the U S Canada and Australia II A DSM III R validation study Journal of the American Psychoanalytic Association 50 2 615 27 doi 10 1177 00030651020500021101 PMID 12206545 S2CID 25110425 Barlow amp Durand 2005 p 20 de Maat S Dekker J Schoevers R et al 2007 Short psychodynamic supportive psychotherapy antidepressants and their combination in the treatment of major depression a mega analysis based on three randomized clinical trials Depression and Anxiety 25 7 565 74 doi 10 1002 da 20305 PMID 17557313 S2CID 20373635 Iglesias Gonzalez M Aznar Lou I Gil Girbau M et al November 2017 Comparing watchful waiting with antidepressants for the management of subclinical depression symptoms to mild moderate depression in primary care a systematic review Family Practice 34 6 639 48 doi 10 1093 fampra cmx054 PMID 28985309 The treatment and management of depression in adults NICE October 2009 Archived from the original on 12 November 2014 Retrieved 12 November 2014 Leucht C Huhn M Leucht S December 2012 Leucht C ed Amitriptyline versus placebo for major depressive disorder The Cochrane Database of Systematic Reviews 12 CD009138 doi 10 1002 14651858 CD009138 pub2 PMID 23235671 de Vries YA Roest AM Bos EH et al January 2019 Predicting antidepressant response by monitoring early improvement of individual symptoms of depression individual patient data meta analysis The British Journal of Psychiatry 214 1 4 10 doi 10 1192 bjp 2018 122 PMC 7557872 PMID 29952277 Thase ME December 2006 Preventing relapse and recurrence of depression a brief review of therapeutic options CNS Spectrums 11 12 Suppl 15 12 21 doi 10 1017 S1092852900015212 PMID 17146414 S2CID 2347144 a b Royal Pharmaceutical Society of Great Britain 2008 p 204 Whooley MA Simon GE December 2000 Managing depression in medical outpatients The New England Journal of Medicine 343 26 1942 50 doi 10 1056 NEJM200012283432607 PMID 11136266 Zisook S Rush AJ Haight BR Clines DC Rockett CB February 2006 Use of bupropion in combination with serotonin reuptake inhibitors Biological Psychiatry 59 3 203 10 doi 10 1016 j biopsych 2005 06 027 PMID 16165100 S2CID 20997303 Papakostas GI Thase ME Fava M Nelson JC Shelton RC December 2007 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 Biological Psychiatry 62 11 1217 27 doi 10 1016 j biopsych 2007 03 027 PMID 17588546 S2CID 45621773 Duff G 31 May 2006 Updated prescribing advice for venlafaxine Efexor Efexor XL Medicines and Healthcare products Regulatory Agency MHRA Archived from the original on 13 November 2008 Antidepressants for children and teenagers what works for anxiety and depression NIHR Evidence Plain English summary National Institute for Health and Care Research 3 November 2022 doi 10 3310 nihrevidence 53342 S2CID 253347210 a b c Zhou X Teng T Zhang Y Del Giovane C Furukawa TA Weisz JR et al July 2020 Comparative efficacy and acceptability of antidepressants psychotherapies and their combination for acute treatment of children and adolescents with depressive disorder a systematic review and network meta analysis The Lancet Psychiatry 7 7 581 601 doi 10 1016 S2215 0366 20 30137 1 PMC 7303954 PMID 32563306 a b Hetrick SE McKenzie JE Bailey AP Sharma V Moller CI Badcock PB et al Cochrane Common Mental Disorders Group May 2021 New generation antidepressants for depression in children and adolescents a network meta analysis The Cochrane Database of Systematic Reviews 2021 5 CD013674 doi 10 1002 14651858 CD013674 pub2 PMC 8143444 PMID 34029378 Solmi M Fornaro M Ostinelli EG Zangani C Croatto G Monaco F et al June 2020 Safety of 80 antidepressants antipsychotics anti attention deficit hyperactivity medications and mood stabilizers in children and adolescents with psychiatric disorders a large scale systematic meta review of 78 adverse effects World Psychiatry 19 2 214 232 doi 10 1002 wps 20765 PMC 7215080 PMID 32394557 Boaden K Tomlinson A Cortese S Cipriani A 2 September 2020 Antidepressants in Children and Adolescents Meta Review of Efficacy Tolerability and Suicidality in Acute Treatment Frontiers in Psychiatry 11 717 doi 10 3389 fpsyt 2020 00717 PMC 7493620 PMID 32982805 Correll CU Cortese S Croatto G Monaco F Krinitski D Arrondo G et al June 2021 Efficacy and acceptability of pharmacological psychosocial and brain stimulation interventions in children and adolescents with mental disorders an umbrella review World Psychiatry 20 2 244 275 doi 10 1002 wps 20881 PMC 8129843 PMID 34002501 Depression in children and young people Identification and management in primary community and secondary care NICE Clinical Guidelines NHS National Institute for Health and Clinical Excellence 28 2005 Archived from the original on 12 November 2014 Retrieved 12 November 2014 Prozac may be the best treatment for young people with depression but more research is needed NIHR Evidence Plain English summary National Institute for Health and Care Research 12 October 2020 doi 10 3310 alert 41917 S2CID 242952585 Boaden K Tomlinson A Cortese S Cipriani A 2 September 2020 Antidepressants in Children and Adolescents Meta Review of Efficacy Tolerability and Suicidality in Acute Treatment Frontiers in Psychiatry 11 717 doi 10 3389 fpsyt 2020 00717 PMC 7493620 PMID 32982805 Cipriani A Zhou X Del Giovane C Hetrick SE Qin B Whittington C et al August 2016 Comparative efficacy and tolerability of antidepressants for major depressive disorder in children and adolescents a network meta analysis Lancet 388 10047 881 890 doi 10 1016 S0140 6736 16 30385 3 hdl 11380 1279478 PMID 27289172 S2CID 19728203 Cheung AH Zuckerbrot RA Jensen PS Laraque D Stein RE March 2018 Guidelines for Adolescent Depression in Primary Care GLAD PC Part II Treatment and Ongoing Management Pediatrics 141 3 e20174082 doi 10 1542 peds 2017 4082 PMID 29483201 Nelson JC Devanand DP April 2011 A systematic review and meta analysis of placebo controlled antidepressant studies in people with depression and dementia Journal of the American Geriatrics Society 59 4 577 85 doi 10 1111 j 1532 5415 2011 03355 x PMID 21453380 S2CID 2592434 Palmer BF Gates JR Lader M November 2003 Causes and management of hyponatremia The Annals of Pharmacotherapy 37 11 1694 702 doi 10 1345 aph 1D105 PMID 14565794 S2CID 37965495 Guaiana G Barbui C Hotopf M July 2007 Amitriptyline for depression The Cochrane Database of Systematic Reviews 18 3 CD004186 doi 10 1002 14651858 CD004186 pub2 PMID 17636748 Anderson IM April 2000 Selective serotonin reuptake inhibitors versus tricyclic antidepressants a meta analysis of efficacy and tolerability Journal of Affective Disorders 58 1 19 36 doi 10 1016 S0165 0327 99 00092 0 PMID 10760555 Krishnan KR 2007 Revisiting monoamine oxidase inhibitors The Journal of Clinical Psychiatry 68 Suppl 8 35 41 PMID 17640156 Bonnet U 2003 Moclobemide therapeutic use and clinical studies CNS Drug Reviews 9 1 97 140 doi 10 1111 j 1527 3458 2003 tb00245 x PMC 6741704 PMID 12595913 Braun C Bschor T Franklin J Baethge C 2016 Suicides and Suicide Attempts during Long Term Treatment with Antidepressants A Meta Analysis of 29 Placebo Controlled Studies Including 6 934 Patients with Major Depressive Disorder Psychotherapy and Psychosomatics 85 3 171 79 doi 10 1159 000442293 PMID 27043848 S2CID 40682753 Hammad TA 16 August 2004 Review and evaluation of clinical data Relationship between psychiatric drugs and pediatric suicidality PDF FDA pp 42 115 Archived PDF from the original on 25 June 2008 Retrieved 29 May 2008 Hetrick SE McKenzie JE Cox GR Simmons MB Merry SN November 2012 Newer generation antidepressants for depressive disorders in children and adolescents The Cochrane Database of Systematic Reviews 11 9 CD004851 doi 10 1002 14651858 CD004851 pub3 hdl 11343 59246 PMC 8786271 PMID 23152227 Gunnell D Saperia J Ashby D February 2005 Selective serotonin reuptake inhibitors SSRIs and suicide in adults meta analysis of drug company data from placebo controlled randomised controlled trials submitted to the MHRA s safety review BMJ 330 7488 385 doi 10 1136 bmj 330 7488 385 PMC 549105 PMID 15718537 Fergusson D Doucette S Glass KC et al February 2005 Association between suicide attempts and selective serotonin reuptake inhibitors systematic review of randomised controlled trials BMJ 330 7488 396 doi 10 1136 bmj 330 7488 396 PMC 549110 PMID 15718539 Stone M Laughren T Jones ML et al August 2009 Risk of suicidality in clinical trials of antidepressants in adults analysis of proprietary data submitted to US Food and Drug Administration BMJ 339 b2880 doi 10 1136 bmj b2880 PMC 2725270 PMID 19671933 FDA Proposes New Warnings About Suicidal Thinking Behavior in Young Adults Who Take Antidepressant Medications FDA 2 May 2007 Archived from the original on 23 February 2008 Retrieved 29 May 2008 Medics and Foods Department Pharmaceuticals and Medical Devices Safety Information PDF Report 261 in Japanese Ministry of Health Labour and Welfare Japan Archived from the original PDF on 29 April 2011 Retrieved 19 May 2010 Ogawa Y Takeshima N Hayasaka Y et al June 2019 Antidepressants plus benzodiazepines for adults with major depression The Cochrane Database of Systematic Reviews 6 6 CD001026 doi 10 1002 14651858 CD001026 pub2 PMC 6546439 PMID 31158298 Corriger A Pickering G 2019 Ketamine and depression a narrative review Drug Des Devel Ther 13 3051 3067 doi 10 2147 DDDT S221437 PMC 6717708 PMID 31695324 Krystal JH Abdallah CG Sanacora G Charney DS Duman RS March 2019 Ketamine A Paradigm Shift for Depression Research and Treatment Neuron 101 5 774 778 doi 10 1016 j neuron 2019 02 005 PMC 6560624 PMID 30844397 McIntyre RS Rosenblat JD Nemeroff CB et al May 2021 Synthesizing the Evidence for Ketamine and Esketamine in Treatment Resistant Depression An International Expert Opinion on the Available Evidence and Implementation Am J Psychiatry 178 5 383 399 doi 10 1176 appi ajp 2020 20081251 PMC 9635017 PMID 33726522 S2CID 232262694 Bahr R Lopez A Rey JA June 2019 Intranasal Esketamine SpravatoTM for Use in Treatment Resistant Depression In Conjunction With an Oral Antidepressant P T 44 6 340 375 PMC 6534172 PMID 31160868 Appleton KM Voyias PD Sallis HM et al November 2021 Omega 3 fatty acids for depression in adults Cochrane Database Syst Rev 2021 11 CD004692 doi 10 1002 14651858 CD004692 pub5 PMC 8612309 PMID 34817851 Cipriani A Hawton K Stockton S Geddes JR June 2013 Lithium in the prevention of suicide in mood disorders updated systematic review and meta analysis BMJ 346 jun27 4 f3646 doi 10 1136 bmj f3646 PMID 23814104 Nolen Hoeksema Susan 2014 Treatment of Mood Disorders In 6th ed Abnormal Psychology p 196 New York McGraw Hill ISBN 978 0 07 803538 8 Gelenberg AJ Freeman MP Markowitz JC Practice Guideline for the Treatment of Patients with Major Depressive Disorder PDF 3rd ed American Psychiatric Association APA Retrieved 3 November 2014 Corp SA Gitlin MJ Altshuler LL September 2014 A review of the use of stimulants and stimulant alternatives in treating bipolar depression and major depressive disorder The Journal of Clinical Psychiatry 75 9 1010 18 doi 10 4088 JCP 13r08851 PMID 25295426 Malhi GS Byrow Y Bassett D et al March 2016 Stimulants for depression On the up and up The Australian and New Zealand Journal of Psychiatry 50 3 203 07 doi 10 1177 0004867416634208 PMID 26906078 S2CID 45341424 Taylor MJ Carney S Geddes J Goodwin G 2003 Folate for depressive disorders The Cochrane Database of Systematic Reviews 2003 2 CD003390 doi 10 1002 14651858 CD003390 PMC 6991158 PMID 12804463 Walther A Breidenstein J Miller R January 2019 Association of Testosterone Treatment With Alleviation of Depressive Symptoms in Men A Systematic Review and Meta analysis JAMA Psychiatry 76 1 31 40 doi 10 1001 jamapsychiatry 2018 2734 PMC 6583468 PMID 30427999 Rudorfer MV Henry ME Sackeim HA 2003 Electroconvulsive therapy In A Tasman J Kay JA Lieberman eds Psychiatry Second Edition Chichester John Wiley amp Sons Ltd 1865 1901 Beloucif S April 2013 Informed consent for special procedures electroconvulsive therapy and psychosurgery Current Opinion in Anesthesiology 26 2 182 85 doi 10 1097 ACO 0b013e32835e7380 PMID 23385317 S2CID 36643014 a b c FDA FDA Executive Summary Archived 24 September 2015 at the Wayback Machine Prepared for the 27 28 January 2011 meeting of the Neurological Devices Panel Meeting to Discuss the Classification of Electroconvulsive Therapy Devices ECT Quote p38 Three major practice guidelines have been published on ECT These guidelines include APA Task Force on ECT 2001 Third report of the Royal College of Psychiatrists Special Committee on ECT 2004 National Institute for Health and Clinical Excellence NICE 2003 NICE 2009 There is significant agreement between the three sets of recommendations Dierckx B Heijnen WT van den Broek WW Birkenhager TK March 2012 Efficacy of electroconvulsive therapy in bipolar versus unipolar major depression a meta analysis Bipolar Disorders 14 2 146 50 doi 10 1111 j 1399 5618 2012 00997 x PMID 22420590 S2CID 44280002 Jelovac A Kolshus E McLoughlin DM November 2013 Relapse following successful electroconvulsive therapy for major depression a meta analysis Neuropsychopharmacology 38 12 2467 74 doi 10 1038 npp 2013 149 PMC 3799066 PMID 23774532 Surgeon General 1999 Mental Health A Report of the Surgeon General Archived 12 January 2007 at the Wayback Machine chapter 4 Committee on Electroconvulsive Therapy 2001 The practice of electroconvulsive therapy recommendations for treatment training and privileging 2nd ed Washington DC American Psychiatric Publishing American Psychiatric Association ISBN 978 0 89042 206 9 Pompili M Dominici G Giordano G et al December 2014 Electroconvulsive treatment during pregnancy a systematic review Expert Review of Neurotherapeutics 14 12 1377 90 doi 10 1586 14737175 2014 972373 PMID 25346216 S2CID 31209001 5 Outdated Beliefs About ECT Psych Central com 17 May 2016 Archived from the original on 8 August 2013 Abbott CC Gallegos P Rediske N Lemke NT Quinn DK March 2014 A review of longitudinal electroconvulsive therapy neuroimaging investigations Journal of Geriatric Psychiatry and Neurology 27 1 33 46 doi 10 1177 0891988713516542 PMC 6624835 PMID 24381234 NiCE January 2014 Transcranial magnetic stimulation for treating and preventing migraine Archived from the original on 4 October 2015 Melkerson MN 16 December 2008 Special Premarket 510 k Notification for NeuroStar TMS Therapy System for Major Depressive Disorder PDF Food and Drug Administration Archived PDF from the original on 31 March 2010 Retrieved 16 July 2010 Lefaucheur JP Andre Obadia N Antal A et al November 2014 Evidence based guidelines on the therapeutic use of repetitive transcranial magnetic stimulation rTMS PDF Clinical Neurophysiology 125 11 2150 206 doi 10 1016 j clinph 2014 05 021 PMID 25034472 S2CID 206798663 Archived PDF from the original on 23 July 2022 Gelenberg AJ Freeman MP Markowitz JC Rosenbaum JF Thase ME Trivedi MH Van Rhoads RS eds 2010 Practice Guidelines for the Treatment of Patients with Major Depressive Disorder PDF 3rd ed American Psychiatric Association Kennedy SH Lam RW Parikh SV Patten SB Ravindran AV 2009 Canadian Network for Mood and Anxiety Treatments CANMAT Clinical guidelines for the management of major depressive disorder in adults PDF Journal of Affective Disorders Elsevier BV 117 Suppl 1 S1 S64 doi 10 1016 j jad 2009 06 043 ISSN 0165 0327 PMID 19682750 Archived from the original PDF on 23 August 2015 Rush AJ Marangell LB Sackeim HA et al September 2005 Vagus nerve stimulation for treatment resistant depression a randomized controlled acute phase trial Biological Psychiatry 58 5 347 54 doi 10 1016 j biopsych 2005 05 025 PMID 16139580 S2CID 22066326 Fregni F El Hagrassy MM Pacheco Barrios K et al April 2021 Evidence Based Guidelines and Secondary Meta Analysis for the Use of Transcranial Direct Current Stimulation in Neurological and Psychiatric Disorders Int J Neuropsychopharmacol 24 4 256 313 doi 10 1093 ijnp pyaa051 PMC 8059493 PMID 32710772 Moffa AH Martin D Alonzo A et al April 2020 Efficacy and acceptability of transcranial direct current stimulation tDCS for major depressive disorder An individual patient data meta analysis Progress in Neuro Psychopharmacology amp Biological Psychiatry 99 109836 doi 10 1016 j pnpbp 2019 109836 PMID 31837388 S2CID 209373871 Ioannou M Wartenberg C Greenbrook JT et al January 2021 Sleep deprivation as treatment for depression Systematic review and meta analysis Acta Psychiatr Scand 143 1 22 35 doi 10 1111 acps 13253 PMC 7839702 PMID 33145770 Giedke H Schwarzler F October 2002 Therapeutic use of sleep deprivation in depression Sleep Medicine Reviews 6 5 361 77 doi 10 1053 smrv 2002 0235 PMID 12531127 Joyce J Herbison GP April 2015 Reiki for depression and anxiety The Cochrane Database of Systematic Reviews 4 CD006833 doi 10 1002 14651858 cd006833 pub2 PMID 25835541 Meekums B Karkou V Nelson EA February 2015 Dance movement therapy for depression PDF The Cochrane Database of Systematic Reviews 2016 2 CD009895 doi 10 1002 14651858 cd009895 pub2 PMC 8928931 PMID 25695871 Black N Stockings E Campbell G et al December 2019 Cannabinoids for the treatment of mental disorders and symptoms of mental disorders a systematic review and meta analysis The Lancet Psychiatry 6 12 995 1010 doi 10 1016 S2215 0366 19 30401 8 PMC 6949116 PMID 31672337 Fava GA Park SK Sonino N November 2006 Treatment of recurrent depression Expert Review of Neurotherapeutics 6 11 1735 40 doi 10 1586 14737175 6 11 1735 PMID 17144786 S2CID 22808803 Limosin F Mekaoui L Hautecouverture S November 2007 Prophylactic treatment for recurrent major depression Presse Medicale 36 11 Pt 2 1627 33 doi 10 1016 j lpm 2007 03 032 PMID 17555914 Eaton WW Shao H Nestadt G et al May 2008 Population based study of first onset and chronicity in major depressive disorder Archives of General Psychiatry 65 5 513 20 doi 10 1001 archpsyc 65 5 513 PMC 2761826 PMID 18458203 Holma KM Holma IA Melartin TK Rytsala HJ Isometsa ET February 2008 Long term outcome of major depressive disorder in psychiatric patients is variable The Journal of Clinical Psychiatry 69 2 196 205 doi 10 4088 JCP v69n0205 PMID 18251627 Kanai T Takeuchi H Furukawa TA et al July 2003 Time to recurrence after recovery from major depressive episodes and its predictors Psychological Medicine 33 5 839 45 doi 10 1017 S0033291703007827 PMID 12877398 S2CID 10490348 Depression Major Prognosis MDGuidelines The Guardian Life Insurance Company of America Archived from the original on 20 April 2010 Retrieved 16 July 2010 a b Culpepper L Muskin PR Stahl SM September 2015 Major Depressive Disorder Understanding the Significance of Residual Symptoms and Balancing Efficacy with Tolerability The American Journal of Medicine 128 9 Suppl S1 S15 doi 10 1016 j amjmed 2015 07 001 PMID 26337210 Geddes JR Carney SM Davies C et al February 2003 Relapse prevention with antidepressant drug treatment in depressive disorders a systematic review Lancet 361 9358 653 61 doi 10 1016 S0140 6736 03 12599 8 PMID 12606176 S2CID 20198748 Posternak MA Miller I October 2001 Untreated short term course of major depression a meta analysis of outcomes from studies using wait list control groups Journal of Affective Disorders 66 2 3 139 46 doi 10 1016 S0165 0327 00 00304 9 PMID 11578666 Posternak MA Solomon DA Leon AC et al May 2006 The naturalistic course of unipolar major depression in the absence of somatic therapy The Journal of Nervous and Mental Disease 194 5 324 29 doi 10 1097 01 nmd 0000217820 33841 53 PMID 16699380 S2CID 22891687 Whiteford HA Harris MG McKeon G et al 10 August 2012 Estimating remission from untreated major depression a systematic review and meta analysis Psychological Medicine Cambridge University Press CUP 43 8 1569 1585 doi 10 1017 s0033291712001717 ISSN 0033 2917 PMID 22883473 S2CID 11068930 Cassano P Fava M October 2002 Depression and public health an overview Journal of Psychosomatic Research 53 4 849 57 doi 10 1016 S0022 3999 02 00304 5 PMID 12377293 Barlow amp Durand 2005 pp 248 49 Bachmann S 6 July 2018 Epidemiology of Suicide and the Psychiatric Perspective International Journal of Environmental Research and Public Health 15 7 1425 doi 10 3390 ijerph15071425 PMC 6068947 PMID 29986446 Half of all completed suicides are related to depressive and other mood disorders Strakowski S Nelson E 2015 Major Depressive Disorder Oxford University Press p PT27 ISBN 978 0 19 026432 1 Blair West GW Mellsop GW June 2001 Major depression does a gender based down rating of suicide risk challenge its diagnostic validity The Australian and New Zealand Journal of Psychiatry 35 3 322 28 doi 10 1046 j 1440 1614 2001 00895 x PMID 11437805 S2CID 36975913 Oquendo MA Bongiovi Garcia ME Galfalvy H et al January 2007 Sex differences in clinical predictors of suicidal acts after major depression a prospective study The American Journal of Psychiatry 164 1 134 41 doi 10 1176 ajp 2007 164 1 134 PMC 3785095 PMID 17202555 Rush AJ 2007 The varied clinical presentations of major depressive disorder The Journal of Clinical Psychiatry 68 Supplement 8 4 10 PMID 17640152 Swardfager W Herrmann N Marzolini S et al September 2011 Major depressive disorder predicts completion adherence and outcomes in cardiac rehabilitation a prospective cohort study of 195 patients with coronary artery disease The Journal of Clinical Psychiatry 72 9 1181 88 doi 10 4088 jcp 09m05810blu PMID 21208573 Schulman J Shapiro BA 2008 Depression and Cardiovascular Disease What Is the Correlation Psychiatric Times 25 9 Archived from the original on 6 March 2020 Retrieved 10 June 2009 WHO Disease and injury country estimates World Health Organization 2009 Archived from the original on 11 November 2009 Retrieved 11 November 2009 a b c Major depression U S National Institute of Mental Health NIMH January 2022 Archived from the original on 9 August 2022 Retrieved 14 August 2022 This article incorporates text from this source which is in the public domain a b Kuehner C September 2003 Gender differences in unipolar depression an update of epidemiological findings and possible explanations Acta Psychiatrica Scandinavica 108 3 163 74 doi 10 1034 j 1600 0447 2003 00204 x PMID 12890270 S2CID 19538251 Institute for Health Metrics and Evaluation 2020 Global Burden of Disease 2019 Cause and Risk Summary Major depressive disorder Level 4 cause Seattle USA University of Washington Table 3 retrieved 9 July 2022 Eaton WW Anthony JC Gallo J et al November 1997 Natural history of Diagnostic Interview Schedule DSM IV major depression The Baltimore Epidemiologic Catchment Area follow up Archives of General Psychiatry 54 11 993 99 doi 10 1001 archpsyc 1997 01830230023003 PMID 9366655 Rickards H March 2005 Depression in neurological disorders Parkinson s disease multiple sclerosis and stroke Journal of Neurology Neurosurgery and Psychiatry 76 Suppl 1 i48 52 doi 10 1136 jnnp 2004 060426 PMC 1765679 PMID 15718222 Alboni P Favaron E Paparella N Sciammarella M Pedaci M April 2008 Is there an association between depression and cardiovascular mortality or sudden death Journal of Cardiovascular Medicine 9 4 356 62 doi 10 2459 JCM 0b013e3282785240 PMID 18334889 S2CID 11051637 Strik JJ Honig A Maes M May 2001 Depression and myocardial infarction relationship between heart and mind Progress in Neuro Psychopharmacology amp Biological Psychiatry 25 4 879 92 doi 10 1016 S0278 5846 01 00150 6 PMID 11383983 S2CID 45722423 Gelder M Mayou R and Geddes J 2005 Psychiatry 3rd ed New York Oxford p 105 Soysal P Veronese N Thompson et al July 2017 Relationship between depression and frailty in older adults A systematic review and meta analysis Ageing Res Rev 36 78 87 doi 10 1016 j arr 2017 03 005 PMID 28366616 S2CID 205668529 Mathers CD Loncar D November 2006 Projections of global mortality and burden of disease from 2002 to 2030 PLOS Medicine 3 11 e442 doi 10 1371 journal pmed 0030442 PMC 1664601 PMID 17132052 Andrews G July 2008 Reducing the burden of depression Canadian Journal of Psychiatry 53 7 420 27 doi 10 1177 070674370805300703 PMID 18674396 Kessler RC Nelson CB McGonagle KA et al June 1996 Comorbidity of DSM III R major depressive disorder in the general population results from the US National Comorbidity Survey The British Journal of Psychiatry Supplement 168 30 17 30 doi 10 1192 S0007125000298371 PMID 8864145 S2CID 19525295 Hirschfeld RM December 2001 The Comorbidity of Major Depression and Anxiety Disorders Recognition and Management in Primary Care Primary Care Companion to the Journal of Clinical Psychiatry 3 6 244 54 doi 10 4088 PCC v03n0609 PMC 181193 PMID 15014592 Grant BF 1995 Comorbidity between DSM IV drug use disorders and major depression results of a national survey of adults Journal of Substance Abuse 7 4 481 97 doi 10 1016 0899 3289 95 90017 9 PMID 8838629 Boden JM Fergusson DM May 2011 Alcohol and depression Addiction 106 5 906 14 doi 10 1111 j 1360 0443 2010 03351 x hdl 10523 10319 PMID 21382111 Hallowell EM Ratey JJ 2005 Delivered from distraction Getting the most out of life with Attention Deficit Disorder New York Ballantine Books pp 253 55 ISBN 978 0 345 44231 4 Brunsvold GL Oepen G 2008 Comorbid Depression in ADHD Children and Adolescents Psychiatric Times 25 10 Archived from the original on 24 May 2009 Melartin TK Rytsala HJ Leskela US Lestela Mielonen PS Sokero TP Isometsa ET February 2002 Current comorbidity of psychiatric disorders among DSM IV major depressive disorder patients in psychiatric care in the Vantaa Depression Study The Journal of Clinical Psychiatry 63 2 126 34 doi 10 4088 jcp v63n0207 PMID 11874213 Hoge E Bickham D Cantor J November 2017 Digital Media Anxiety and Depression in Children Pediatrics 140 Suppl 2 S76 S80 doi 10 1542 peds 2016 1758G PMID 29093037 Elhai JD Dvorak RD Levine JC Hall BJ January 2017 Problematic smartphone use A conceptual overview and systematic review of relations with anxiety and depression psychopathology Journal of Affective Disorders 207 251 259 doi 10 1016 j jad 2016 08 030 PMID 27736736 S2CID 205642153 Bair MJ Robinson RL Katon W Kroenke K November 2003 Depression and pain comorbidity a literature review Archives of Internal Medicine 163 20 2433 45 doi 10 1001 archinte 163 20 2433 PMID 14609780 Yohannes AM Baldwin RC 2008 Medical Comorbidities in Late Life Depression Psychiatric Times 25 14 Archived from the original on 14 June 2020 Retrieved 10 June 2009 span, wikipedia, wiki, book, books, library,

article

, read, download, free, free download, mp3, video, mp4, 3gp, jpg, jpeg, gif, png, picture, music, song, movie, book, game, games.