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Major depressive disorder

From Wikipedia, the free encyclopedia

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] disturbed sleep pattern (insomnia or hypersomnia)
ComplicationsSelf-harm, suicide[2]
Usual onsetAge 20s[3][4]
Duration> 2 weeks[1]
CausesEnvironmental (e.g. adverse life experiences), genetic predisposition, psychological factors such as stress[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, transcranial magnetic stimulation, exercise[1][7]
MedicationAntidepressants
Frequency163 million (2017)[8]

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.

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]

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Transcription

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,[18] 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,[19] as well as day-night rhythm disturbances, such as diurnal mood variation.[20] Some antidepressants may also cause insomnia due to their stimulating effect.[21] In severe cases, depressed people may have psychotic symptoms. These symptoms include delusions or, less commonly, hallucinations, usually unpleasant.[22] People who have had previous episodes with psychotic symptoms are more likely to have them with future episodes.[23]

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.[24] Appetite often decreases, resulting in weight loss, although increased appetite and weight gain occasionally occur.[25] Family and friends may notice agitation or lethargy.[19] Older depressed people may have cognitive symptoms of recent onset, such as forgetfulness,[26] and a more noticeable slowing of movements.[27]

Depressed children may often display an irritable rather than a depressed mood;[19] most lose interest in school and show a steep decline in academic performance.[28] Diagnosis may be delayed or missed when symptoms are interpreted as "normal moodiness."[25] Elderly people may not present with classical depressive symptoms.[29] 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.[29]

Digital media addictions

In April 2013, the Journal of Adolescent Health published a systematic review of 33 studies of adolescent girls that found a positive association between screen time and depression.[30] In June 2014, Children and Youth Services Review published a systematic review of 43 studies published between January 2003 through April 2013 researching social media use and adolescent mental well-being that found that while depression was reported to be among the harmful effects of social media, the majority of the studies reported mixed effects or no effect on adolescent well-being in the aggregate,[31] while BMC Psychiatry published a meta-analysis of 8 studies comprising 1,641 subjects found a significant and positive association between internet addiction and depression.[32] In July 2015, Preventive Medicine published a systematic review of 91 studies found that associations between high levels of screen time and depressive symptoms among school-aged children and adolescents were inconsistent.[33] In September 2015, Perspectives on Psychological Science published a meta-analysis of 101 studies that concluded that the impact of video games on depressive symptoms in children and adolescents was minimal, but along with attention deficit symptoms, that issues of citation bias were common in the research.[34]

In June 2016, Adolescent Research Review published a systematic review of 12 studies of subjects aged 11 to 21 years that concluded that while internet technology may provide adolescents opportunities to seek emotional and social support, the research reviewed did not establish that internet technology lowers rates of adolescent depression.[35] In October 2016, the International Journal of Behavioral Nutrition and Physical Activity published a systematic review of 32 studies that found strong consistent evidence for a relationship between depressive symptoms and leisure screen time.[36] In September 2016, the British Journal of Sports Medicine published a meta-analysis of 12 cross-sectional studies and 4 longitudinal studies published before May 2015 and comprising 127,714 child and adolescent subjects that suggested that screen time in children and adolescents has a non-linear dose–response association with depression risk.[37] In November 2016, JMIR Mental Health published a systematic review of 70 studies published between January 2005 and June 2016 that concluded that the research reviewed established mixed findings on the relationship between SNS use and depression, where SNS interactions of positive quality, social support on SNS, and social connectedness on SNS were associated with lower levels of depression, SNS interactions of negative quality, social comparisons, and SNS addictive were associated with higher levels of depression, and frequency of SNS use and number of SNS friends was inconclusive.[38]

In December 2017, Adolescent Research Review published a systematic review of 11 studies comprising 12,646 child and adolescent subjects that found a small but statistically significant correlation between social media use and depressive symptoms.[39] In January 2018, the Journal of Affective Disorders published a systematic review and meta-analysis of 23 studies comprising 13,929 adolescent and young adult subjects found that problematic Facebook use was positively correlated with depression.[40] In April 2018, the International Journal of Environmental Research and Public Health published a systematic review of 24 studies researching associations between internet gaming disorder (IGD) and various psychopathologies that found an 89% correlation between IGD and depression.[41] In July 2018, JMIR Mental Health published a systematic review of 11 studies investigating social media use and depression among lesbian, gay, and bisexual (LGB) users that found that while qualitative research found that social media use could lead to greater social support and less loneliness for LGB users, LGB users were more likely to report being cyberbullied than heterosexual users, that cyberbullying of LGB users was associated with depression among victims, and constant monitoring of accounts by LGB users was also found to be a stressor associated with depression.[42]

In December 2018, Frontiers in Psychiatry published a systematic review of 9 studies published after 2014 investigating associations between problematic SNS use and comorbid psychiatric disorders that found a positive association between problematic SNS use and depression.[43] In March 2019, the International Journal of Adolescence and Youth published a systematic review of 13 studies comprising 21,231 adolescent subjects aged 13 to 18 years that found that social media screen time, both active and passive social media use, the amount of personal information uploaded, and social media addictive behaviors all correlated with depression.[44] In April 2019, the Journal of Affective Disorders published a meta-analysis assessing associations between SNS use and higher levels of depression that found that greater SNS screen time and frequency of checking SNS accounts had small but statistically significant associations with higher levels of depression, that greater general social comparisons on SNS had a small to moderate association, and greater upward social comparisons on SNS had a moderate association.[45] In November 2019, BMC Public Health published a systematic review and meta-analysis of 12 cross-sectional studies and 7 longitudinal studies that found that screen time-based sedentary behavior is associated with depression risk.[46]

In January 2020, Translational Psychiatry published a meta-analysis of 12 prospective studies comprising 128,553 subjects that found that while sedentary behavior and depression risk had a significant positive association, television viewing and other mentally passive sedentary behaviors were positively associated with depression risk but computer use and other mentally active sedentary behaviors were not.[47] In February 2020, Psychiatry Research published a systematic review and meta-analysis of 14 studies that found positive associations between problematic smartphone use and depression and positive associations between higher levels of problematic smartphone use and elevated risk of depression.[48] Also in February 2020, Frontiers in Psychology published a systematic review of 10 studies of adolescent or young adult subjects in China that concluded that the research reviewed mostly established an association between social networks use disorder and depression among Chinese adolescents and young adults.[49] In March 2020, the Review of General Psychology published a meta-analysis that found a small association between social networking service (SNS) use and self-reported depression.[50] In April 2020, BMC Public Health published a systematic review of 70 cross-sectional and longitudinal studies investigating moderating factors for associations for screen-based sedentary behaviors and depression symptoms among youth that found that the most consistent factor was for screen type since television viewing was not as strongly associated with depression symptoms as other screen types.[51]

In August 2020, the Journal of Medical Internet Research published an umbrella review of 7 systematic reviews on research investigating associations between depression and use of mobile technologies and social media by adolescents that concluded while mobile technology and social media may promote social support, excess social comparison and personal involvement (i.e. increased exposure in general, exposure to specific content that promote depressive symptoms, and degree of personal information posted on social media) could be associated with symptoms of depression.[52] In October 2020, the Journal of Affective Disorders published a meta-analysis of 12 studies with subjects aged 11 to 18 years that found a small but statistically significant positive correlation between social media use and depressive symptoms among adolescents,[53] while the Journal of Behavioral Addictions published a systematic review and meta-analysis of 40 studies with 33,650 post-secondary student subjects that found that a weak-to-moderate positive association between mobile phone addiction and depression.[54] In November 2020, Child and Adolescent Mental Health published a systematic review of research published between January 2005 and March 2019 on associations between SNS use and depression and anxiety symptoms in subjects between ages of 5 to 18 years that found that increased SNS screen time or frequency of SNS use and problematic and addictive SNS use were significantly associated with higher levels of depression symptoms.[55]

In January 2021, Frontiers in Psychiatry published a systematic review of 44 studies investigating social media use and development of psychiatric disorders in childhood and adolescence that concluded that passive social media use (e.g. browsing other user photos or scrolling through comments or news feeds) and depression are bidirectionally associated and that problematic social media use and depressive symptoms are mediated by social comparisons.[56] In February 2021, Research on Child and Adolescent Psychopathology published a meta-analysis of 62 studies comprising 451,229 subjects that found SNS screen time and SNS use intensity to have weak but statistically significant associations with depression symptoms, while problematic SNS use was found to have a moderate association with depression symptoms.[57] In March 2021, Youth & Society published a systematic review where 9 studies found an association between SNS use and adolescent subjective well-being including mood, but that the results over whether the association was positive or negative were mixed.[58] In April 2021, the Journal of Affective Disorders published a systematic review and meta-analysis of 92 studies comprising 15,148 subjects across 25 countries investigating associations between depression and internet gaming disorder found that one-third of the IGD subjects had been diagnosed with depression and major severe depressive symptoms were found in IGD subjects globally without a formal diagnosis. In comparison to the general population.[59]

In May 2021, Current Psychology published a meta-analysis of 55 studies comprising 80,533 subjects that found a small but positive and statistically significant association between SNS use and self-reported depression symptoms.[60] In June 2021, Clinical Psychology Review published a systematic review of 35 longitudinal studies published before August 2020 that found that an association between screen time and subsequent depressive symptoms among young people was small and varied by device type and use.[61] In July 2021, Translational Medicine Communications published a systematic review of 9 studies published between October 2010 and December 2018 with Instagram user subjects between the ages of 19 and 35 years that found an association between Instagram use and depression symptoms.[62] In January 2022, The European Journal of Psychology Applied to Legal Context published a meta-analysis of 13 cross-sectional studies comprising 7,348 subjects that found a statistically significant correlation between cybervictimization and depression with a moderate-to-large effect size.[63] In February 2022, the International Journal of Social Psychiatry published a meta-analysis of 131 studies comprising 244,676 subjects found a moderate mean correlation between problematic social media use and depression.[64]

In March 2022, Computers in Human Behavior published a systematic review and meta-analysis of 531 cross-sectional or longitudinal studies with subjects aged 10 to 24 years that found a small bidirectional association between online media use and depressive symptoms and that the effect size did not differ between general internet use, smartphone use, social media use, or online gaming, but also found that studies that measured online media use with media addiction scales rather than by screen time found significantly greater associations.[65] Also in March 2022, JAMA Psychiatry published a systematic review and meta-analysis of 87 studies with 159,425 subjects 12 years of age or younger that found a small but statistically significant correlation between screen time and depression in children,[66] while Adolescent Psychiatry published a systematic review of research published from June 2010 through June 2020 studying associations between social media use and depression among adolescent subjects aged 13 to 18 years that established that 82.6% of studies reviewed reported positive associations between social media use and depression.[67] In April 2022, the International Journal of Environmental Research and Public Health published a meta-analysis of 21 cross-sectional studies and 5 longitudinal studies comprising 55,340 adolescent subjects that found social media screen time had a linear dose–response association with depression risk among adolescents and that depression risk increased by 13% for each additional hour of social media screen time.[68]

Also in April 2022, researchers in the Department of Communication at Stanford University performed a meta-analysis of 226 studies comprising 275,728 subjects that found a small but positive association between social media use and depression,[69] while JMIR Mental Health published a systematic review and meta-analysis of 18 studies comprising 9,269 adolescent and young adult subjects that found a moderate but statistically significant associations between problematic social media use and depression.[70] In August 2022, the International Journal of Environmental Research and Public Health published a systematic review and meta-analysis of 16 studies comprising 8,077 subjects that established a significant association between binge-watching and depression and a stronger association between binge-watching and depression was found during the COVID-19 pandemic than pre-pandemic.[71] In November 2022, Cyberpsychology, Behavior, and Social Networking published a systematic review of 1,747 articles on problematic social media use that found a strong bidirectional relationship between social media use and depression.[72] In December 2022, Frontiers in Psychiatry published a meta-analysis of 18 cohort studies comprising 241,398 subjects that found that screen time is a predictor of depressive symptoms.[73] In March 2023, the Journal of Public Health published a meta-analysis of 27 studies published after 2014 comprising 120,895 subjects that found a moderate and robust association between problematic smartphone use and depression.[74]

In April 2023, Trauma, Violence, & Abuse published a systematic review and meta-analysis of 17 studies comprising 79,202 adolescent subjects between the ages of 10 and 19 years that found that depression was three times more common among cyberbullying victims than control groups.[75] In July 2023, Current Psychology published a meta-analysis of 38 studies comprising 14,935 subjects in Turkey that found a small but positive association between problematic social media use and depression.[76] In September 2023, Clinical Psychological Science published a preregistered review and meta-analysis of 34 articles published between 2018 and 2020 studying associations between adolescent depression and social media use to identify the proportion of samples taken from the Global North and Global South, and found that more than 70% examined Global North populations and that associations in the Global North were positive and significant while associations in the Global South were null and non-significant.[77] In September 2023, BJPsych Open published a systematic review of 140 studies published from 2000 through 2020 found that social media use for more than 3 hours per day and passive browsing was associated with increased depression.[78] In February 2024, The Egyptian Journal of Neurology, Psychiatry and Neurosurgery published a systematic review of 15 studies researching associations between problematic social media use and depression in subjects from the Middle East and North Africa (including 4 studies with subjects exclusively between the ages of 12 and 19 years) that established that most studies found a significant association.[79]

Cause

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[80]

The etiology of depression is not yet fully understood.[81][82][83][84] The biopsychosocial model proposes that biological, psychological, and social factors all play a role in causing depression.[5][85] 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,[86][87] implying an interaction between nature and nurture, or schematic, resulting from views of the world learned in childhood.[88] 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.[89][90]

Genetics

Genes play a major role in the development of depression.[91] Family and twin studies find that nearly 40% of individual differences in risk for major depressive disorder can be explained by genetic factors.[92] Like most psychiatric disorders, major depressive disorder is likely influenced by many individual genetic changes.[93] In 2018, a genome-wide association study discovered 44 genetic variants linked to risk for major depression;[94] a 2019 study found 102 variants in the genome linked to depression.[95] However, it appears that major depression is less heritable compared to bipolar disorder and schizophrenia.[96][97] Research focusing on specific candidate genes has been criticized for its tendency to generate false positive findings.[98] There are also other efforts to examine interactions between life stress and polygenic risk for depression.[99]

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."[100][101] 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).[102] Depression may also be iatrogenic (the result of healthcare), such as drug-induced depression. Therapies associated with depression include interferons, beta-blockers, isotretinoin, contraceptives,[103] cardiac agents, anticonvulsants, antimigraine drugs, antipsychotics, and hormonal agents such as gonadotropin-releasing hormone agonist (GnRH agonist).[104] Celiac disease is another possible contributing factor.[105]

Substance use in early age is associated with increased risk of developing depression later in life.[106] Depression occurring after giving birth is called postpartum depression and is thought to be the result of hormonal changes associated with pregnancy.[107] Seasonal affective disorder, a type of depression associated with seasonal changes in sunlight, is thought to be triggered by decreased sunlight.[108] Vitamin B2, B6 and B12 deficiency may cause depression in females.[109]

Environmental

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.[110] Couples in unhappy marriages have a higher risk of developing clinical depression.[111]

There appears to be a link between air pollution and depression and suicide. There may be an association between long-term PM2.5 exposure and depression, and a possible association between short-term PM10 exposure and suicide.[112]

Pathophysiology

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.[113] 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.[114] 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,[115] and polymorphism of dopamine receptor genes implicate dopamine, another monoamine, in depression.[116][117] Lastly, increased activity of monoamine oxidase, which degrades monoamines, has been associated with depression.[118] 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.[119]

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.[120] 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.[121] Already limited, the monoamine hypothesis has been further oversimplified when presented to the general public.[122] A 2022 review found no consistent evidence supporting the serotonin hypothesis, linking serotonin levels and depression.[123]

Immune system abnormalities have been observed, including increased levels of cytokines involved in generating sickness behavior (which shares overlap with depression).[124][125][126] The effectiveness of nonsteroidal anti-inflammatory drugs (NSAIDs) and cytokine inhibitors in treating depression,[127] and normalization of cytokine levels after successful treatment further suggest immune system abnormalities in depression.[128]

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%.[129] These stress-related abnormalities are thought to be the cause of hippocampal volume reductions seen in people who are depressed.[130] Furthermore, a meta-analysis yielded decreased dexamethasone suppression, and increased response to psychological stressors.[131] Further abnormal results have been obscured with the cortisol awakening response, with increased response being associated with depression.[132]

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.[133] Another model, the cortico-striatal model, suggests that abnormalities of the prefrontal cortex in regulating striatal and subcortical structures result in depression.[134] 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.[135]

Diagnosis

Clinical assessment

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.[136] This issue is even more marked in developing countries.[137] 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;[138] these include the Hamilton Rating Scale for Depression,[139] the Beck Depression Inventory[140] or the Suicide Behaviors Questionnaire-Revised.[141]

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.[142]

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.[143] 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.[144] Vitamin D levels might be evaluated, as low levels of vitamin D have been associated with greater risk for depression.[145] 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.[146][147] Cognitive testing and brain imaging can help distinguish depression from dementia.[148] A CT scan can exclude brain pathology in those with psychotic, rapid-onset or otherwise unusual symptoms.[149] No biological tests confirm major depression.[150] 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,[151] and the authors of both have worked towards conforming one with the other.[152] Both DSM and ICD mark out typical (main) depressive symptoms.[153] The most recent edition of the DSM is the Fifth Edition, Text Revision (DSM-5-TR),[154] and the most recent edition of the ICD is the Eleventh Edition (ICD-11).[155]

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).[156] 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."[156] 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).[156] These two disorders are classified as "Depressive disorders", in the category of "Mood disorders".[156]

According to DSM-5, at least one of the symptoms is either depressed mood or loss of interest or pleasure. Depressed mood occurs nearly every day as subjective feelings like sadness, emptiness, and hopelessness or observations made by others (e.g. appears tearful). Loss of interest or pleasure occurs in all, or almost all activities of the day, nearly every day. These symptoms, as well as five out of the nine more specific symptoms listed, must frequently occur for more than two weeks (to the extent in which it impairs functioning) for the diagnosis [157].[158][failed verification] Major depressive disorder is classified as a mood disorder in the DSM-5.[159] The diagnosis hinges on the presence of single or recurrent major depressive episodes.[160] 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.[159]

Major depressive episode

A major depressive episode is characterized by the presence of a severely depressed mood that persists for at least two weeks.[25] 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.[159] 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".[161]

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;[162] recurrent brief depression, consisting of briefer depressive episodes;[163][164] minor depressive disorder, whereby only some symptoms of major depression are present;[165] and adjustment disorder with depressed mood, which denotes low mood resulting from a psychological response to an identifiable event or stressor.[166]

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.[167]
  • "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.[168]
  • "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.[169]
  • "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.[159]
  • "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-5 mandates that to qualify as depression with peripartum onset, onset occurs during pregnancy or within one month of delivery.[170]
  • "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.[171]

Differential diagnoses

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).[162] 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.[166]

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).[172]

Screening and prevention

Preventive efforts may result in decreases in rates of the condition of between 22 and 38%.[173] Since 2016, the United States Preventive Services Task Force (USPSTF) has recommended screening for depression among those over the age 12;[174][175] though a 2005 Cochrane review found that the routine use of screening questionnaires has little effect on detection or treatment.[176] Screening the general population is not recommended by authorities in the UK or Canada.[177]

Behavioral interventions, such as interpersonal therapy and cognitive-behavioral therapy, are effective at preventing new onset depression.[173][178][179] 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.[180]

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.[178][181]

Management

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.[182] 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.[183] There is evidence that collaborative care by a team of health care practitioners produces better results than routine single-practitioner care.[184]

Psychotherapy is the treatment of choice (over medication) for people under 18,[185] and cognitive behavioral therapy (CBT), third wave CBT and interpersonal therapy may help prevent depression.[186] 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:[185]

  • 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.[185]

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.[187] There is insufficient evidence to determine the effectiveness of psychological versus medical therapy in children.[188]

Lifestyle

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.[189] It is equivalent to the use of medications or psychological therapies in most people.[7] In older people it does appear to decrease depression.[190] Sleep and diet may also play a role in depression, and interventions in these areas may be an effective add-on to conventional methods.[191] In observational studies, smoking cessation has benefits in depression as large as or larger than those of medications.[192]

Talking therapies

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.[193] With more complex and chronic forms of depression, a combination of medication and psychotherapy may be used.[194][195] There is moderate-quality evidence that psychological therapies are a useful addition to standard antidepressant treatment of treatment-resistant depression in the short term.[196] Psychotherapy has been shown to be effective in older people.[197][198] 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.[199] 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.[200] 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.[201] Several variables predict success for cognitive behavioral therapy in adolescents: higher levels of rational thoughts, less hopelessness, fewer negative thoughts, and fewer cognitive distortions.[202] CBT is particularly beneficial in preventing relapse.[203][204] 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.[205] Several variants of cognitive behavior therapy have been used in those with depression, the most notable being rational emotive behavior therapy,[206] and mindfulness-based cognitive therapy.[207] Mindfulness-based stress reduction programs may reduce depression symptoms.[208][209] Mindfulness programs also appear to be a promising intervention in youth.[210] Problem solving therapy, cognitive behavioral therapy, and interpersonal therapy are effective interventions in the elderly.[211]

Psychoanalysis is a school of thought, founded by Sigmund Freud, which emphasizes the resolution of unconscious mental conflicts.[212] Psychoanalytic techniques are used by some practitioners to treat clients presenting with major depression.[213] 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.[214] 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.[215]

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.[216] 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.[217] 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.[218] Antidepressants work less well for the elderly than for younger individuals with depression.[211]

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.[183][219] Antidepressant medication treatment is usually continued for 16 to 20 weeks after remission, to minimize the chance of recurrence,[183] and even up to one year of continuation is recommended.[220] 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.[221] People who do not respond to one SSRI can be switched to another antidepressant, and this results in improvement in almost 50% of cases.[222] Another option is to augment the atypical antidepressant bupropion to the SSRI as an adjunctive treatment.[223] Venlafaxine, an antidepressant with a different mechanism of action, may be modestly more effective than SSRIs.[224] However, venlafaxine is not recommended in the UK as a first-line treatment because of evidence suggesting its risks may outweigh benefits,[225] and it is specifically discouraged in children and adolescents as it increases the risk of suicidal thoughts or attempts.[226][227][228][229][230][231][232]

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.[233][227][234][228] Sertraline, escitalopram, duloxetine might also help in reducing symptoms. Some antidepressants have not been shown to be effective.[235][227] Medications are not recommended in children with mild disease.[236]

There is also insufficient evidence to determine effectiveness in those with depression complicated by dementia.[237] Any antidepressant can cause low blood sodium levels;[238] nevertheless, it has been reported more often with SSRIs.[221] It is not uncommon for SSRIs to cause or worsen insomnia; the sedating atypical antidepressant mirtazapine can be used in such cases.[239][240]

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.[241] 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.[242]

It is unclear whether antidepressants affect a person's risk of suicide.[243] 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.[244][245] For adults, it is unclear whether SSRIs affect the risk of suicidality. One review found no connection;[246] another an increased risk;[247] and a third no risk in those 25–65 years old and a decreased risk in those more than 65.[248] 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.[249] Similar precautionary notice revisions were implemented by the Japanese Ministry of Health.[250]

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.[251]

For treatment-resistant depression, adding on the atypical antipsychotic brexpiprazole for short-term or acute management may be considered.[252] Brexpiprazole may be effective for some people, however, the evidence as of 2023 supporting its use is weak and this medication has potential adverse effects including weight gain and akathisia.[252] Brexpiprazole has not been sufficiently studied in older people or children and the use and effectiveness of this adjunctive therapy for longer term management is not clear.[252]

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.[253][254] 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.[255][256]

There is insufficient high quality evidence to suggest omega-3 fatty acids are effective in depression.[257] There is limited evidence that vitamin D supplementation is of value in alleviating the symptoms of depression in individuals who are vitamin D-deficient.[145] 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.[258] There is a narrow range of effective and safe dosages of lithium thus close monitoring may be needed.[259] Low-dose thyroid hormone may be added to existing antidepressants to treat persistent depression symptoms in people who have tried multiple courses of medication.[260] Limited evidence suggests stimulants, such as amphetamine and modafinil, may be effective in the short term, or as adjuvant therapy.[261][262] Also, it is suggested that folate supplements may have a role in depression management.[263] There is tentative evidence for benefit from testosterone in males.[264]

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.[265]: 1880  ECT is used with informed consent[266] as a last line of intervention for major depressive disorder.[267] A round of ECT is effective for about 50% of people with treatment-resistant major depressive disorder, whether it is unipolar or bipolar.[268] Follow-up treatment is still poorly studied, but about half of people who respond relapse within twelve months.[269] Aside from effects in the brain, the general physical risks of ECT are similar to those of brief general anesthesia.[270]: 259  Immediately following treatment, the most common adverse effects are confusion and memory loss.[267][271] ECT is considered one of the least harmful treatment options available for severely depressed pregnant women.[272]

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.[273] 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.[267]

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.[274]

Other

Transcranial magnetic stimulation (TMS) or deep transcranial magnetic stimulation is a noninvasive method used to stimulate small regions of the brain.[275] TMS was approved by the FDA for treatment-resistant major depressive disorder (trMDD) in 2008[276] and as of 2014 evidence supports that it is probably effective.[277] The American Psychiatric Association,[278] the Canadian Network for Mood and Anxiety Disorders,[279] and the Royal Australia and New Zealand College of Psychiatrists have endorsed TMS for trMDD.[280] 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.[281][282]

There is a small amount of evidence that sleep deprivation may improve depressive symptoms in some individuals,[283] 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.[284] There is insufficient evidence for Reiki[285] and dance movement therapy in depression.[286] Cannabis is specifically not recommended as a treatment.[287]

Prognosis

Studies have shown that 80% of those with a first major depressive episode will have at least one more during their life,[288] with a lifetime average of four episodes.[289] 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.[290] 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.[291][292] 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.[293]

A high proportion of people who experience full symptomatic remission still have at least one not fully resolved symptom after treatment.[294] Recurrence or chronicity is more likely if symptoms have not fully resolved with treatment.[294] 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.[295]

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.[296] The median duration of an episode has been estimated to be 23 weeks, with the highest rate of recovery in the first three months.[297] 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.[298]

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.[205] 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.[205]

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.[299] 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.[300][301] About 2–8% of adults with major depression die by suicide.[2][302] 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,[303] even though suicide attempts are more frequent in women.[304]

Depressed people have a higher rate of dying from other causes.[305] 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.[306] Cardiologists may not recognize underlying depression that complicates a cardiovascular problem under their care.[307]

Epidemiology

Disability-adjusted life year for unipolar depressive disorders per 100,000 inhabitants in 2004:[308]
  no data
  <700
  700–775
  775–850
  850–925
  925–1,000
  1,000–1,075
  1,075–1,150
  1,150–1,225
  1,225–1,300
  1,300–1,375
  1,375–1,450
  >1,450

Major depressive disorder affected approximately 163 million people in 2017 (2% of the global population).[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%).[309] 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%).[309] Among individuals reporting two or more races, the US prevalence is highest.[309]

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.[310] 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.[310] 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.[311]

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.[312] 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.[313] 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.[314][315] 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.[316] Depression is common among those over 65 years of age and increases in frequency beyond this age.[29] The risk of depression increases in relation to the frailty of the individual.[317] Depression is one of the most important factors which negatively impact quality of life in adults, as well as the elderly.[29] Both symptoms and treatment among the elderly differ from those of the rest of the population.[29]

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.[318] Delay or failure in seeking treatment after relapse and the failure of health professionals to provide treatment are two barriers to reducing disability.[319]

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.[320] 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.[321] Depressed people have increased rates of alcohol and substance use, particularly dependence,[322][323] and around a third of individuals diagnosed with attention deficit hyperactivity disorder (ADHD) develop comorbid depression.[324] Post-traumatic stress disorder and depression often co-occur.[15] Depression may also coexist with ADHD, complicating the diagnosis and treatment of both.[325] Depression is also frequently comorbid with alcohol use disorder and personality disorders.[326] 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.[327][328]

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.[329] Depression often coexists with physical disorders common among the elderly, such as stroke, other cardiovascular diseases, Parkinson's disease, and chronic obstructive pulmonary disease.[330]

History

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.[331] 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.[332]

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".[333] 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.[334] 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.[335] Since Aristotle, melancholia had been associated with men of learning and intellectual brilliance, a hazard of contemplation and creativity. However, by the 19th century, this association has largely shifted and melancholia became more commonly linked with women.[332]

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.[336] 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.[337] The person's decline of self-perception is revealed in his belief of his own blame, inferiority, and unworthiness.[338] He also emphasized early life experiences as a predisposing factor.[332] 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.[339] 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.[340]

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.[341]

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.[342] The American Psychiatric Association added "major depressive disorder" to the Diagnostic and Statistical Manual of Mental Disorders (DSM-III),[343] 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.[343] 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.[153][342] 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.[344][345] 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.[346]

Society and culture

Terminology

The 16th American president, Abraham Lincoln, had "melancholy", a condition that now may be referred to as clinical depression.[347]

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."[348] 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.[349][350]

Cultural Dimension

Cultural differences contribute to different prevalence of symptoms. “Do the Chinese somatize depression? A cross-cultural study” by Parker et al. discusses the cultural differences in prevalent symptoms of depression between individualistic and collectivistic cultures. The authors reveal that individuals with depression in collectivistic cultures tend to present more somatic symptoms and less affective symptoms compared to those in individualistic cultures. The finding suggests that individualistic cultures ‘warranting’ or validating one’s expression of emotions explains this cultural difference since collectivistic cultures see this as a taboo against the social cooperation it deems one of the most significant values.[351]

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,[352] American-British writer Henry James,[353] and American president Abraham Lincoln.[354] Some well-known contemporary people with possible depression include Canadian songwriter Leonard Cohen[355] and American playwright and novelist Tennessee Williams.[356] Some pioneering psychologists, such as Americans William James[357][358] and John B. Watson,[359] 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.[360][361] British literature gives many examples of reflections on depression.[362] 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."[363][364] English writer Samuel Johnson used the term "the black dog" in the 1780s to describe his own depression,[365] and it was subsequently popularized by British Prime Minister Sir Winston Churchill, who also had the disorder.[365] Johann Wolfgang von Goethe in his Faust, Part I, published in 1808, has Mephistopheles assume the form of a black dog, specifically a poodle.

In 1998, the Norwegian PM Kjell Magne Bondevik publicly announced he will take a break in order to recover from a depressive episode.

Social stigma of major depression is widespread, and contact with mental health services reduces this only slightly. Public opinions on treatment differ markedly to those of health professionals; alternative treatments are held to be more helpful than pharmacological ones, which are viewed poorly.[366] 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;[367] a MORI study conducted afterwards showed a small positive change in public attitudes to depression and treatment.[368]

While serving his first term as Prime Minister of Norway, Kjell Magne Bondevik attracted international attention in August 1998 when he announced that he was suffering from a depressive episode, becoming the highest ranking world leader to admit to suffering from a mental illness while in office. Upon this revelation, Anne Enger became acting Prime Minister for three weeks, from 30 August to 23 September, while he recovered from the depressive episode. Bondevik then returned to office. Bondevik received thousands of supportive letters, and said that the experience had been positive overall, both for himself and because it made mental illness more publicly acceptable.[369][370]

References

  1. ^ 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.
  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. Archived from the original (PDF) 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). Archived (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). Archived (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. ^ Everaert J, Vrijsen JN, Martin-Willett R, van de Kraats L, Joormann J (2022). "A meta-analytic review of the relationship between explicit memory bias and depression: Depression features an explicit memory bias that persists beyond a depressive episode". Psychological Bulletin. 148 (5–6): 435–463. doi:10.1037/bul0000367. ISSN 1939-1455. S2CID 253306482.
  19. ^ a b c American Psychiatric Association 2013, p. 163.
  20. ^ Murray G (September 2007). "Diurnal mood variation in depression: a signal of disturbed circadian function?". Journal of Affective Disorders. 102 (1–3): 47–53. doi:10.1016/j.jad.2006.12.001. PMID 17239958.
  21. ^ "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.
  22. ^ American Psychiatric Association 2000a, p. 412
  23. ^ Nelson JC, Bickford D, Delucchi K, Fiedorowicz JG, Coryell WH (September 2018). "Risk of Psychosis in Recurrent Episodes of Psychotic and Nonpsychotic Major Depressive Disorder: A Systematic Review and Meta-Analysis". The American Journal of Psychiatry. 175 (9): 897–904. doi:10.1176/appi.ajp.2018.17101138. PMID 29792050. S2CID 43951278.
  24. ^ 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.
  25. ^ a b c American Psychiatric Association 2000a, p. 349
  26. ^ 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.
  27. ^ 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.
  28. ^ American Psychiatric Association 2013, p. 164.
  29. ^ a b c d e "Depression treatment for the elderly". Swedish Agency for Health Technology Assessment and Assessment of Social Services (SBU). 27 January 2015. Archived from the original on 18 June 2016. Retrieved 16 June 2016.
  30. ^ Costigan SA, Barnett L, Plotnikoff RC, Lubans DR (2013). "The Health Indicators Associated With Screen-Based Sedentary Behavior Among Adolescent Girls: A Systematic Review". Journal of Adolescent Health. Elsevier. 52 (4): 382–392. doi:10.1016/j.jadohealth.2012.07.018. PMID 23299000.
  31. ^ Best P, Manktelow R, Taylor B (2014). "Online communication, social media and adolescent wellbeing: A systematic narrative review". Children and Youth Services Review. Elsevier. 41: 27–36. doi:10.1016/j.childyouth.2014.03.001.
  32. ^ Ho RC, Zhang MW, Tsang TY, Toh AH, Pan F, Lu Y, Cheng C, Yip PS, Lam LT, Lai C, Watanabe H, Mak K (2014). "The association between internet addiction and psychiatric co-morbidity: a meta-analysis". BMC Psychiatry. BioMed Central. 14: 183. doi:10.1186/1471-244X-14-183. PMC 4082374. PMID 24947851.
  33. ^ Suchert V, Hanewinkel R, Isensee B (2015). "Sedentary behavior and indicators of mental health in school-aged children and adolescents: A systematic review". Preventive Medicine. Elsevier. 76: 48–57. doi:10.1016/j.ypmed.2015.03.026. PMID 25895839.
  34. ^ Ferguson CJ (2015). "Do Angry Birds Make for Angry Children? A Meta-Analysis of Video Game Influences on Children's and Adolescents' Aggression, Mental Health, Prosocial Behavior, and Academic Performance". Perspectives on Psychological Science. Sage Publishing. 10 (5): 646–666. doi:10.1177/1745691615592234. PMID 26386002.
  35. ^ Wu Y, Outley C, Matarrita-Cascante D, Murphrey TP (2016). "A Systematic Review of Recent Research on Adolescent Social Connectedness and Mental Health with Internet Technology Use". Adolescent Research Review. Springer. 1 (2): 153–162. doi:10.1007/s40894-015-0013-9.
  36. ^ Hoare E, Milton K, Foster C, Allender S (2016). "The associations between sedentary behaviour and mental health among adolescents: a systematic review". International Journal of Behavioral Nutrition and Physical Activity. BioMed Central. 13: 108. doi:10.1186/s12966-016-0432-4. PMID 27717387.
  37. ^ Liu M, Wu L, Yao S (2016). "Dose–response association of screen time-based sedentary behaviour in children and adolescents and depression: a meta-analysis of observational studies". British Journal of Sports Medicine. BMJ. 50 (20): 1252–1258. doi:10.1136/bjsports-2015-095084. PMC 4977203. PMID 26552416.
  38. ^ Seabrook EM, Kern ML, Rickard NS (2016). "Social Networking Sites, Depression, and Anxiety: A Systematic Review". JMIR Mental Health. JMIR Publications. 3 (4): e50. doi:10.2196/mental.5842. PMC 5143470. PMID 27881357.
  39. ^ McCrae N, Gettings S, Purssell E (2017). "Social Media and Depressive Symptoms in Childhood and Adolescence: A Systematic Review". Adolescent Research Review. Springer. 2 (4): 315–330. doi:10.1007/s40894-017-0053-4.
  40. ^ Marino C, Gini G, Vieno A, Spada MM (2018). "The associations between problematic Facebook use, psychological distress and well-being among adolescents and young adults: A systematic review and meta-analysis". Journal of Affective Disorders. Elsevier. 226: 274–281. doi:10.1016/j.jad.2017.10.007. PMID 29024900.
  41. ^ González-Bueso V, Santamaría JJ, Fernández D, Merino L, Montero E, Ribas J (2018). "Association between Internet Gaming Disorder or Pathological Video-Game Use and Comorbid Psychopathology: A Comprehensive Review". International Journal of Environmental Research and Public Health. MDPI. 15 (4): 668. doi:10.3390/ijerph15040668. PMC 5923710. PMID 29614059.
  42. ^ Escobar-Viera CG, Whitfield DL, Wessel CB, Shensa A, Sidani JE, Brown AL, Chandler CJ, Hoffman BL, Marshal MP, Primack BA (2018). "For Better or for Worse? A Systematic Review of the Evidence on Social Media Use and Depression Among Lesbian, Gay, and Bisexual Minorities". JMIR Mental Health. JMIR Publications. 5 (3): e10496. doi:10.2196/10496. PMC 6079300. PMID 30037786.
  43. ^ Hussain Z, Griffiths MD (2018). "Problematic Social Networking Site Use and Comorbid Psychiatric Disorders: A Systematic Review of Recent Large-Scale Studies". Frontiers in Psychiatry. Frontiers Media. 9: 686. doi:10.3389/fpsyt.2018.00686. PMC 6302102. PMID 30618866.
  44. ^ Keles B, McCrae N, Grealish A (2019). "A systematic review: the influence of social media on depression, anxiety and psychological distress in adolescents". International Journal of Adolescence and Youth. Taylor & Francis. 25 (1): 79–93. doi:10.1080/02673843.2019.1590851.
  45. ^ Yoon S, Kleinman M, Mertz J, Brannick M (2019). "Is social network site usage related to depression? A meta-analysis of Facebook–depression relations". Journal of Affective Disorders. Elsevier. 248: 65–72. doi:10.1016/j.jad.2019.01.026. PMID 30711871.
  46. ^ Wang X, Li Y, Fan H (2019). "The associations between screen time-based sedentary behavior and depression: a systematic review and meta-analysis". BMC Public Health. BioMed Central. 19 (1): 1524. doi:10.1186/s12889-019-7904-9. PMC 6857327. PMID 31727052.
  47. ^ Huang Y, Li L, Gan Y, Wang C, Jiang H, Cao S, Lu Z (2020). "Sedentary behaviors and risk of depression: a meta-analysis of prospective studies". Translational Psychiatry. Nature Portfolio. 10 (1): 26. doi:10.1038/s41398-020-0715-z. PMC 7026102. PMID 32066686.
  48. ^ Jiaxin Y, Xi F, Xiaoli L, Yamin L (2020). "Association of problematic smartphone use with poor sleep quality, depression, and anxiety: A systematic review and meta-analysis". Psychiatry Research. Elsevier. 284: 112686. doi:10.1016/j.psychres.2019.112686. PMID 31757638. S2CID 207974088.
  49. ^ Hussain Z, Wegmann E, Yang H, Montag C (2020). "Social Networks Use Disorder and Associations With Depression and Anxiety Symptoms: A Systematic Review of Recent Research in China". Frontiers in Psychology. Frontiers Media. 11: 211. doi:10.3389/fpsyg.2020.00211. PMC 7046800. PMID 32153455.
  50. ^ Appel M, Marker C, Gnambs T (2020). "Are Social Media Ruining Our Lives? A Review of Meta-Analytic Evidence". Review of General Psychology. American Psychological Association. 24 (1): 60–74. doi:10.1177/1089268019880891.
  51. ^ Zink J, Belcher BR, Imm K, Leventhal AM (2020). "The relationship between screen-based sedentary behaviors and symptoms of depression and anxiety in youth: a systematic review of moderating variables". BMC Public Health. BioMed Central. 20 (1): 472. doi:10.1186/s12889-020-08572-1. PMC 7147040. PMID 32272906.
  52. ^ Arias-de la Torre J, Puigdomenech E, García X, Valderas JM, Eiroa-Orosa FJ, Fernández-Villa T, Molina AJ, Martín V, Serrano-Blanco A, Alonso J, Espallargues M (2020). "Relationship Between Depression and the Use of Mobile Technologies and Social Media Among Adolescents: Umbrella Review". Journal of Medical Internet Research. JMIR Publications. 22 (8): e16388. doi:10.2196/16388. PMC 7481866. PMID 32663157.
  53. ^ Ivie EJ, Pettitt A, Moses LJ, Allen NB (2020). "A meta-analysis of the association between adolescent social media use and depressive symptoms". Journal of Affective Disorders. Elsevier. 275: 165–174. doi:10.1016/j.jad.2020.06.014. PMID 32734903.
  54. ^ Li Y, Li G, Liu L, Wu H (2020). "Correlations between mobile phone addiction and anxiety, depression, impulsivity, and poor sleep quality among college students: A systematic review and meta-analysis". Journal of Behavioral Addictions. Akadémiai Kiadó. 9 (3): 551–571. doi:10.1556/2006.2020.00057. PMC 8943681. PMID 32903205.
  55. ^ Piteo EM, Ward K (2020). "Review: Social networking sites and associations with depressive and anxiety symptoms in children and adolescents – a systematic review". Child and Adolescent Mental Health. Wiley-Blackwell. 25 (4): 201–216. doi:10.1111/camh.12373. PMID 33118256.
  56. ^ Cataldo I, Lepri B, Neoh MJ, Esposito G (2021). "Social Media Usage and Development of Psychiatric Disorders in Childhood and Adolescence: A Review". Frontiers in Psychiatry. Frontiers Media. 11. doi:10.3389/fpsyt.2020.508595. PMC 7838524. PMID 33519535.
  57. ^ Cunningham S, Hudson CC, Harkness K (2021). "Social Media and Depression Symptoms: a Meta-Analysis". Research on Child and Adolescent Psychopathology. Springer. 49 (2): 241–253. doi:10.1007/s10802-020-00715-7. PMID 33404948.
  58. ^ Webster D, Dunne L, Hunter R (2021). "Association Between Social Networks and Subjective Well-Being in Adolescents: A Systematic Review". Youth & Society. Sage Publishing. 53 (2): 175–210. doi:10.1177/0044118X20919589.
  59. ^ Ostinelli EG, Zangani C, Giordano B, Maestri D, Gambini O, D'Agostino A, Furukawa TA, Purgato M (2021). "Depressive symptoms and depression in individuals with internet gaming disorder: A systematic review and meta-analysis". Journal of Affective Disorders. Elsevier. 284: 136–142. doi:10.1016/j.jad.2021.02.014. hdl:2434/848082. PMID 33592432.
  60. ^ Vahedi Z, Zannella L (2021). "The association between self-reported depressive symptoms and the use of social networking sites (SNS): A meta-analysis". Current Psychology. Springer. 40 (5): 2174–2189. doi:10.1007/s12144-019-0150-6.
  61. ^ Tang S, Werner-Seidler A, Torok M, Mackinnon AJ, Christensen H (2021). "The relationship between screen time and mental health in young people: A systematic review of longitudinal studies". Clinical Psychology Review. Elsevier. 86: 102021. doi:10.1016/j.cpr.2021.102021. PMID 33798997.
  62. ^ Adeyanju GC, Solfa RP, Tran TL, Wohlfarth S, Büttner J, Osobajo OA, Otitoju A (2021). "Behavioural symptoms of mental health disorder such as depression among young people using Instagram: a systematic review". Translational Medicine Communications. Springer. 6: 15. doi:10.1186/s41231-021-00092-3.
  63. ^ Molero MM, Martos Á, Barragán AB, Pérez-Fuentes MC, Gázquez JJ (2022). "Anxiety and Depression from Cybervictimization in Adolescents: A Metaanalysis and Meta-regression Study". The European Journal of Psychology Applied to Legal Context. Madrid Regional Association of Psychology. 14 (1): 42–50. doi:10.5093/ejpalc2022a5.
  64. ^ Huang C (2022). "A meta-analysis of the problematic social media use and mental health". International Journal of Social Psychiatry. Sage Publishing. 68 (1): 12–33. doi:10.1177/0020764020978434. PMID 33295241.
  65. ^ Shin M, Juventin M, Chu JT, Manor Y, Kemps E (2022). "Online media consumption and depression in young people: A systematic review and meta-analysis". Computers in Human Behavior. Elsevier. 128: 107129. doi:10.1016/j.chb.2021.107129.
  66. ^ Eirich R, McArthur BA, Anhorn C, McGuinness C, Christakis DA, Madigan S (2022). "Association of Screen Time With Internalizing and Externalizing Behavior Problems in Children 12 Years or Younger: A Systematic Review and Meta-analysis". JAMA Psychiatry. American Medical Association. 79 (5): 393–405. doi:10.1001/jamapsychiatry.2022.0155. PMC 8928099. PMID 35293954.
  67. ^ Damodar S, Lokemoen C, Gurusamy V, Takhi M, Bishev D, Parrill A, Deviney M, Person U, Korie I, Branch R (2022). "Trending: A Systematic Review of Social Media Use's Influence on Adolescent Anxiety and Depression". Adolescent Psychiatry. Bentham Science Publishers. 12 (1): 11–22. doi:10.2174/2210676612666220225122720.
  68. ^ Liu M, Kamper-DeMarco KE, Zhang J, Xiao J, Dong D, Xue P (2022). "Time Spent on Social Media and Risk of Depression in Adolescents: A Dose–Response Meta-Analysis". International Journal of Environmental Research and Public Health. MDPI. 19 (9): 5164. doi:10.3390/ijerph19095164. PMC 9103874. PMID 35564559.
  69. ^ Hancock J, Liu SX, Luo M, Mieczkowski H (2022). "Psychological Well-Being and Social Media Use: A Meta-Analysis of Associations between Social Media Use and Depression, Anxiety, Loneliness, Eudaimonic, Hedonic and Social Well-Being". doi:10.2139/ssrn.4053961. SSRN 4053961.
  70. ^ Shannon H, Bush K, Villeneuve P, Hellemans K, Guimond S (2022). "Problematic Social Media Use in Adolescents and Young Adults: Systematic Review and Meta-analysis". JMIR Mental Health. JMIR Publications. 9 (4): e33450. doi:10.2196/33450. PMC 9052033. PMID 35436240.
  71. ^ Alimoradi Z, Jafari E, Potenza MN, Lin C, Wu C, Pakpour AH (2022). "Binge-Watching and Mental Health Problems: A Systematic Review and Meta-Analysis". International Journal of Environmental Research and Public Health. MDPI. 19 (15): 9707. doi:10.3390/ijerph19159707. PMC 9368441. PMID 35955069.
  72. ^ Lopes LS, Valentini JP, Monteiro TH, de Freitas Costacurta MC, Soares LO, Telfar-Barnard L, Nunes PV (2022). "Problematic Social Media Use and Its Relationship with Depression or Anxiety: A Systematic Review". Cyberpsychology, Behavior, and Social Networking. Mary Ann Liebert. 25 (11): 691–702. doi:10.1089/cyber.2021.0300. PMID 36219756.
  73. ^ Li L, Zhang Q, Zhu L, Zeng G, Huang H, Zhuge J, Kuang X, Yang S, Yang D, Chen Z, Gan Y, Lu Z, Wu C (2022). "Screen time and depression risk: A meta-analysis of cohort studies". Frontiers in Psychiatry. Frontiers Media. 13: 1058572. doi:10.3389/fpsyt.2022.1058572. PMC 9815119. PMID 36620668.
  74. ^ Augner C, Vlasak T, Aichhorn W, Barth A (2023). "The association between problematic smartphone use and symptoms of anxiety and depression—a meta-analysis". Journal of Public Health. Oxford University Press. 45 (1): 193–201. doi:10.1093/pubmed/fdab350. PMID 34585243.
  75. ^ Tran HG, Thai TT, Dang NT, Vo DK, Duong MH (2023). "Cyber-Victimization and Its Effect on Depression in Adolescents: A Systematic Review and Meta-Analysis". Trauma, Violence, & Abuse. Sage Publishing. 24 (2): 1124–1139. doi:10.1177/15248380211050597. PMID 34689637.
  76. ^ Yigiter MS, Demir S, Dogan N (2023). "The Relationship Between Problematic Social Media Use and Depression: A Meta-Analysis Study". Current Psychology. Springer. doi:10.1007/s12144-023-04972-9.
  77. ^ Ghai S, Fassi L, Awadh F, Orben A (2023). "Lack of Sample Diversity in Research on Adolescent Depression and Social Media Use: A Scoping Review and Meta-Analysis". Clinical Psychological Science. Sage Publishing. 11 (5): 759–772. doi:10.1177/21677026221114859. PMC 10491482. PMID 37694229.
  78. ^ Hilty DM, Stubbe D, McKean AJ, Hoffman PE, Zalpuri I, Myint MT, Joshi SV, Pakyurek M, Li ST (2023). "A scoping review of social media in child, adolescents and young adults: research findings in depression, anxiety and other clinical challenges". BJPsych Open. Cambridge University Press. 9 (5): e152. doi:10.1192/bjo.2023.523. PMC 10594088. PMID 37563766.
  79. ^ Abbouyi S, Bouazza S, El Kinany S, El Rhazi K, Zarrouq B (2024). "Depression and anxiety and its association with problematic social media use in the MENA region: a systematic review". The Egyptian Journal of Neurology, Psychiatry and Neurosurgery. Springer. 60: 15. doi:10.1186/s41983-024-00793-0.
  80. ^ Hankin BL, Abela JR (2005). Development of Psychopathology: A Vulnerability-Stress Perspective. SAGE Publications. pp. 32–34. ISBN 978-1-4129-0490-2.
  81. ^ Otte C, Gold SM, Penninx BW, Pariante CM, Etkin A, Fava M, et al. (September 2016). "Major depressive disorder" (PDF). Nature Reviews. Disease Primers. Springer Nature (published 15 September 2016). 2 (1): 16065. doi:10.1038/nrdp.2016.65. PMID 27629598. S2CID 4047310. Despite advances in our understanding of the neuro-biology of MDD, no established mechanism can explain all aspects of the disease.
  82. ^ Boland RJ, Verduin ML (14 March 2022). Kaplan & Sadock's concise textbook of clinical psychiatry (5th ed.). Philadelphia: Wolters Kluwer. ISBN 978-1-9751-6748-6. OCLC 1264172789. Although there is no single unifying theory, several theories have emerged over the last century that attempt to account for the various clinical, psychological, and biologic findings in depression.
  83. ^ Sontheimer H (20 May 2021). Diseases of the nervous system (2nd ed.). Elsevier. p. 286. ISBN 978-0-12-821396-4. OCLC 1260160457. A number of risk factors for depression are known or suspected, but only in rare cases is the link to disease strong.
  84. ^ Mann JJ, McGrath PJ, Roose SP, eds. (June 2013). Clinical handbook for the management of mood disorders. Cambridge: Cambridge University Press. p. 1. doi:10.1017/CBO9781139175869. ISBN 978-1-107-05563-6. OCLC 843944119. Although genes are an important cause of major depression and bipolar disorder, we have not confirmed the identity of the responsible genes.
  85. ^ 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.
  86. ^ Caspi A, Sugden K, Moffitt TE, Taylor A, Craig IW, Harrington H, et al. (July 2003). "Influence of life stress on depression: moderation by a polymorphism in the 5-HTT gene". Science. 301 (5631): 386–389. Bibcode:2003Sci...301..386C. doi:10.1126/science.1083968. PMID 12869766. S2CID 146500484.
  87. ^ Haeffel GJ, Getchell M, Koposov RA, Yrigollen CM, Deyoung CG, Klinteberg BA, et al. (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.
  88. ^ Slavich GM (2004). "Deconstructing depression: A diathesis-stress perspective (Opinion)". APS Observer. Archived from the original on 11 May 2011. Retrieved 11 November 2008.
  89. ^ 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.
  90. ^ Nieto I, Robles E, Vazquez C (December 2020). "Self-reported cognitive biases in depression: A meta-analysis". Clinical Psychology Review. 82: 101934. doi:10.1016/j.cpr.2020.101934. PMID 33137610. S2CID 226243519.
  91. ^ Do MC, Weersing VR (3 April 2017). Wenzel A (ed.). The SAGE encyclopedia of abnormal and clinical psychology. Thousand Oaks, California: SAGE Publishing. p. 1014. doi:10.4135/9781483365817. ISBN 978-1-4833-6582-4. OCLC 982958263. Depression is highly heritable, as youths with a parent with a history of depression are approximately 4 times as likely to develop the disorder as youths who do not have a parent with depression.
  92. ^ Sullivan PF, Neale MC, Kendler KS (October 2000). "Genetic epidemiology of major depression: review and meta-analysis". The American Journal of Psychiatry. 157 (10): 1552–1562. doi:10.1176/appi.ajp.157.10.1552. PMID 11007705.
  93. ^ Belmaker RH, Agam G (January 2008). "Major depressive disorder". The New England Journal of Medicine. 358 (1): 55–68. doi:10.1056/NEJMra073096. PMID 18172175. S2CID 12566638. It is clear from studies of families that major depression is not caused by any single gene but is a disease with complex genetic features.
  94. ^ Wray NR, Ripke S, Mattheisen M, Trzaskowski M, Byrne EM, Abdellaoui A, et al. (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.
  95. ^ 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.
  96. ^ Sullivan PF, Neale MC, Kendler KS (October 2000). "Genetic epidemiology of major depression: review and meta-analysis". The American Journal of Psychiatry. 157 (10): 1552–1562. doi:10.1176/appi.ajp.157.10.1552. PMID 11007705. The heritability of major depression is likely to be in the range of 31%–42%. This is probably the lower bound, and the level of heritability is likely to be substantially higher for reliably diagnosed major depression or for subtypes such as recurrent major depression. In comparison, the heritabilities of schizophrenia and bipolar disorder are estimated to be approximately 70%.
  97. ^ Jorde LB, Carey JC, Bamshad MJ (27 September 2019). Medical genetics (6th ed.). Philadelphia: Elsevier. p. 247. ISBN 978-0-323-59653-4. OCLC 1138027525. Thus it appears that bipolar disorder is more strongly influenced by genetic factors than is major depressive disorder.
  98. ^ 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): 1041–1049. doi:10.1176/appi.ajp.2011.11020191. PMC 3222234. PMID 21890791.
  99. ^ Peyrot WJ, Van der Auwera S, Milaneschi Y, Dolan CV, Madden PA, Sullivan PF, 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.
  100. ^ 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.
  101. ^ 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.
  102. ^ 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.
  103. ^ Rogers D, Pies R (December 2008). "General medical with depression drugs associated". Psychiatry. 5 (12): 28–41. PMC 2729620. PMID 19724774.
  104. ^ 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.
  105. ^ Zingone F, Swift GL, Card TR, Sanders DS, Ludvigsson JF, Bai JC (April 2015). "Psychological morbidity of celiac disease: A review of the literature". United European Gastroenterology Journal. 3 (2): 136–145. doi:10.1177/2050640614560786. ISSN 2050-6406. PMC 4406898. PMID 25922673.
  106. ^ 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.
  107. ^ 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.
  108. ^ 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.
  109. ^ 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.
  110. ^ 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.
  111. ^ Goldfarb MR, Trudel G (6 May 2019). "Marital quality and depression: a review". Marriage & Family Review. Routledge: Taylor & Francis Group. 55 (8): 737–763. doi:10.1080/01494929.2019.1610136. S2CID 165116052. Citing among others: Weissman MM (April 1987). "Advances in psychiatric epidemiology: rates and risks for major depression". Am J Public Health. 77 (4): 445–51. doi:10.2105/ajph.77.4.445. PMC 1646931. PMID 3826462.
  112. ^ Braithwaite I, Zhang S, Kirkbride JB, Osborn DP, Hayes JF (December 2019). "Air Pollution (Particulate Matter) Exposure and Associations with Depression, Anxiety, Bipolar, Psychosis and Suicide Risk: A Systematic Review and Meta-Analysis". Environmental Health Perspectives. 127 (12): 126002. doi:10.1289/EHP4595. PMC 6957283. PMID 31850801.
  113. ^ 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.
  114. ^ Delgado PL, Moreno FA (2000). "Role of norepinephrine in depression". The Journal of Clinical Psychiatry. 61 (Suppl 1): 5–12. PMID 10703757.
  115. ^ 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.
  116. ^ 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.
  117. ^ 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. S2CID 26550661.
  118. ^ 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.
  119. ^ 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.
  120. ^ 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.
  121. ^ 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.
  122. ^ 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.
  123. ^ Moncrieff J, Cooper RE, Stockman T, et al. (July 2022). "The serotonin theory of depression: a systematic umbrella review of the evidence". Mol Psychiatry. 28 (8): 3243–3256. doi:10.1038/s41380-022-01661-0. PMC 10618090. PMID 35854107. S2CID 250646781. Lay source Medicalxpress
  124. ^ 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.
  125. ^ Patel A (September 2013). "Review: the role of inflammation in depression". Psychiatria Danubina. 25 (Suppl 2): S216–23. PMID 23995180.
  126. ^ 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.
  127. ^ 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. Archived (PDF) from the original on 20 July 2018.
  128. ^ 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.
  129. ^ 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.
  130. ^ 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.
  131. ^ 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.
  132. ^ 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.
  133. ^ 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.
  134. ^ 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.
  135. ^ 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.
  136. ^ Kaufmann IM (1993). "Rural psychiatric services. A collaborative model". Canadian Family Physician. 39: 1957–1961. PMC 2379905. PMID 8219844.
  137. ^ "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.
  138. ^ 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.
  139. ^ 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.
  140. ^ 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.
  141. ^ 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.
  142. ^ 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.
  143. ^ 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.
  144. ^ 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.
  145. ^ 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.
  146. ^ 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.
  147. ^ 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.
  148. ^ 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.
  149. ^ Sadock 2002, p. 108
  150. ^ Sadock 2002, p. 260
  151. ^ Sadock 2002, p. 288
  152. ^ American Psychiatric Association 2013, p. xii.
  153. ^ 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: 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.
  154. ^ "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.
  155. ^ "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.
  156. ^ a b c d ICD-11, 6A70 Single episode depressive disorder and 6A71 Recurrent depressive disorder
  157. ^ Diagnostic and statistical manual of mental disorders: DSM-5 (5th ed.). Washington: American psychiatric association. 2013. ISBN 978-0-89042-554-1.
  158. ^ "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.
  159. ^ 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.
  160. ^ American Psychiatric Association 2013, p. 162
  161. ^ Parker 1996, p. 173
  162. ^ a b Sadock 2002, p. 552
  163. ^ American Psychiatric Association 2013, p. 183.
  164. ^ 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.
  165. ^ 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.
  166. ^ a b American Psychiatric Association 2013, p. 168.
  167. ^ American Psychiatric Association 2013, p. 185.
  168. ^ American Psychiatric Association 2013, pp. 185–186.
  169. ^ American Psychiatric Association 2013, pp. 119–120.
  170. ^ American Psychiatric Association 2013, pp. 186–187.
  171. ^ American Psychiatric Association 2013, p. 187.
  172. ^ American_Psychiatric_Association 2013, p. 167.
  173. ^ 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.
  174. ^ 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.
  175. ^ 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.
  176. ^ 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.
  177. ^ 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.
  178. ^ 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.
  179. ^ 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.
  180. ^ 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.
  181. ^ 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.
  182. ^ 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.
  183. ^ 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
  184. ^ 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.
  185. ^ 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.
  186. ^ 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.
  187. ^ 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.
  188. ^ 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.
  189. ^ 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.
  190. ^ 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.
  191. ^ 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. S2CID 22218602. Archived (PDF) from the original on 9 January 2017.
  192. ^ 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.
  193. ^ 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.
  194. ^ 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.
  195. ^ 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.
  196. ^ 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.
  197. ^ 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.
  198. ^ 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.
  199. ^ 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.
  200. ^ Childhood Depression. abct.org. Last updated: 30 July 2010
  201. ^ 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.
  202. ^ Becker SJ (2008). "Cognitive-Behavioral Therapy for Adolescent Depression: Processes of Cognitive Change". Psychiatric Times. 25 (14).
  203. ^ 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.
  204. ^ 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.
  205. ^ 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.
  206. ^ Beck et al. 1987, p. 10.
  207. ^ 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.
  208. ^ 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.
  209. ^ 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.
  210. ^ 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.
  211. ^ 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.
  212. ^ Dworetzky J (1997). Psychology. Pacific Grove, CA: Brooks/Cole Pub. Co. p. 602. ISBN 978-0-314-20412-7.
  213. ^ 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.
  214. ^ Barlow & Durand 2005, p. 20.
  215. ^ 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.
  216. ^ 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.
  217. ^ "The treatment and management of depression in adults". NICE. October 2009. Archived from the original on 12 November 2014. Retrieved 12 November 2014.
  218. ^ 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.
  219. ^ 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.
  220. ^ 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.
  221. ^ a b Royal Pharmaceutical Society of Great Britain 2008, p. 204
  222. ^ 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.
  223. ^ 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.
  224. ^ 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.
  225. ^ 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.
  226. ^ "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.
  227. ^ 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.
  228. ^ 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.
  229. ^ 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.
  230. ^ 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.
  231. ^ 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.
  232. ^ "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.
  233. ^ "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.
  234. ^ 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.
  235. ^ 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.
  236. ^ 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.
  237. ^ 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.
  238. ^ 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.
  239. ^ 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.
  240. ^ 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.
  241. ^ Krishnan KR (2007). "Revisiting monoamine oxidase inhibitors". The Journal of Clinical Psychiatry. 68 (Suppl 8): 35–41. PMID 17640156.
  242. ^ 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.
  243. ^ 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.
  244. ^ 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.
  245. ^ 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.
  246. ^ 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.
  247. ^ 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.
  248. ^ 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.
  249. ^ "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.
  250. ^ 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.
  251. ^ 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.
  252. ^ a b c Ralovska S, Koyvhev I, Marinov P, Furukawa TA, Mulsant B, Cipriani A, et al. (Cochrane Common Mental Disorders Group) (July 2023). "Brexpiprazole versus placebo or other antidepressive agents for treating depression". Cochrane Database of Systematic Reviews. 2023 (7): CD013866. doi:10.1002/14651858.CD013866.pub2. PMC 10406422.
  253. ^ 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.
  254. ^ 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.
  255. ^ 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.
  256. ^ 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.
  257. ^ 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.
  258. ^ 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.
  259. ^ 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.
  260. ^ 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.
  261. ^ 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.
  262. ^ 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.
  263. ^ 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.
  264. ^ 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.
  265. ^ 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.
  266. ^ 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.
  267. ^ 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."
  268. ^ 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.
  269. ^ 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.
  270. ^ Surgeon General (1999). Mental Health: A Report of the Surgeon General Archived 12 January 2007 at the Wayback Machine, chapter 4.
  271. ^ Committee on Electroconvulsive Therapy (2001). The practice of electroconvulsive therapy: recommendations for treatment, training, and privileging (2nd ed.). Washington, DC: American Psychiatric Association. ISBN 978-0-89042-206-9.
  272. ^ 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.
  273. ^ "5 Outdated Beliefs About ECT". Psych Central.com. 17 May 2016. Archived from the original on 8 August 2013.
  274. ^ 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.
  275. ^ "NiCE. January 2014 Transcranial magnetic stimulation for treating and preventing migraine". Archived from the original on 4 October 2015.
  276. ^ 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.
  277. ^ 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. Archived (PDF) from the original on 23 July 2022.
  278. ^ 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.
  279. ^ 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.
  280. ^ 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.
  281. ^ 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.
  282. ^ 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.
  283. ^ 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.
  284. ^ 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.
  285. ^ 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.
  286. ^ 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.
  287. ^ 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.
  288. ^ 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.
  289. ^ 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.
  290. ^ 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.
  291. ^ 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.
  292. ^ 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.
  293. ^ "Depression, Major: Prognosis". MDGuidelines. The Guardian Life Insurance Company of America. Archived from the original on 20 April 2010. Retrieved 16 July 2010.
  294. ^ 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.
  295. ^ 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.
  296. ^ 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.
  297. ^ 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.
  298. ^ 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.
  299. ^ 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.
  300. ^ Barlow & Durand 2005, pp. 248–49.
  301. ^ 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
  302. ^ Strakowski S, Nelson E (2015). Major Depressive Disorder. Oxford University Press. p. PT27. ISBN 978-0-19-026432-1.
  303. ^ 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.
  304. ^ 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.
  305. ^ Rush AJ (2007). "The varied clinical presentations of major depressive disorder". The Journal of Clinical Psychiatry. 68 (Supplement 8): 4–10. PMID 17640152.
  306. ^ 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.
  307. ^ 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.
  308. ^ "WHO Disease and injury country estimates". World Health Organization. 2009. Archived from the original on 11 November 2009. Retrieved 11 November 2009.
  309. ^ 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. Public Domain This article incorporates text from this source, which is in the public domain.
  310. ^ 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.
  311. ^ Institute for Health Metrics and Evaluation (2020), Global Burden of Disease 2019 Cause and Risk Summary: Major depressive disorder — Level 4 cause, Seattle, US: University of Washington, Table 3, retrieved 9 July 2022
  312. ^ 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.
  313. ^ 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.
  314. ^ 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.
  315. ^ 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.
  316. ^ Gelder, M, Mayou, R and Geddes, J (2005). Psychiatry. 3rd ed. New York: Oxford. p. 105.
  317. ^ 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.
  318. ^ 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.
  319. ^ Andrews G (July 2008). "Reducing the burden of depression". Canadian Journal of Psychiatry. 53 (7): 420–27. doi:10.1177/070674370805300703. PMID 18674396.
  320. ^ 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.
  321. ^ 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.
  322. ^ 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.
  323. ^ 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.
  324. ^ 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.
  325. ^ Brunsvold GL, Oepen G (2008). "Comorbid Depression in ADHD: Children and Adolescents". Psychiatric Times. 25 (10). Archived from the original on 24 May 2009.
  326. ^ 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.
  327. ^ 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.
  328. ^ 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.
  329. ^ 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.
  330. ^ 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.
  331. ^ Hippocrates, Aphorisms, Section 6.23
  332. ^ a b c Radden J (2003). "Is this dame melancholy? Equating today's depression and past melancholia". Philosophy, Psychiatry, & Psychology. 10 (1): 37–52. doi:10.1353/ppp.2003.0081. S2CID 143684460.
  333. ^ "Definition of depress | Dictionary.com". www.dictionary.com. Retrieved 14 August 2022.
  334. ^ Wolpert L (1999). "Malignant Sadness: The Anatomy of Depression". The New York Times. Archived from the original on 9 April 2009. Retrieved 30 October 2008.
  335. ^ Berrios GE (September 1988). "Melancholia and depression during the 19th century: a conceptual history". The British Journal of Psychiatry. 153 (3): 298–304. doi:10.1192/bjp.153.3.298. PMID 3074848. S2CID 145445990.
  336. ^ Davison K (2006). "Historical aspects of mood disorders". Psychiatry. 5 (4): 115–18. doi:10.1383/psyt.2006.5.4.115.
  337. ^ Carhart-Harris RL, Mayberg HS, Malizia AL, Nutt D (July 2008). "Mourning and melancholia revisited: correspondences between principles of Freudian metapsychology and empirical findings in neuropsychiatry". Annals of General Psychiatry. 7: 9. doi:10.1186/1744-859X-7-9. PMC 2515304. PMID 18652673.
  338. ^ Freud S (1984). "Mourning and Melancholia". In Richards A (ed.). 11. On Metapsychology: The Theory of Psycholoanalysis. Aylesbury, Bucks: Pelican. pp. 245–69. ISBN 978-0-14-021740-7.
  339. ^ Lewis AJ (1934). "Melancholia: A historical review". Journal of Mental Science. 80 (328): 1–42. doi:10.1192/bjp.80.328.1.
  340. ^ American Psychiatric Association (1968). "Schizophrenia" (PDF). Diagnostic and statistical manual of mental disorders: DSM-II. Washington, DC: American Psychiatric Publishing, Inc. pp. 36–37, 40. doi:10.1176/appi.books.9780890420355.dsm-ii (inactive 31 January 2024).{{cite book}}: CS1 maint: DOI inactive as of January 2024 (link)
  341. ^ Angst J. Terminology, history and definition of bipolar spectrum. In: Maj M, Akiskal HS, López-Ibor JJ, Sartorius N (eds.), Bipolar disorders. Chichester: Wiley & Sons, LTD; 2002. pp. 53–55.
  342. ^ a b Philipp M, Maier W, Delmo CD (1991). "The concept of major depression. I. Descriptive comparison of six competing operational definitions including ICD-10 and DSM-III-R". European Archives of Psychiatry and Clinical Neuroscience. 240 (4–5): 258–65. doi:10.1007/BF02189537. PMID 1829000. S2CID 36768744.
  343. ^ a b Hersen M, Rosqvist J (2008). Handbook of Psychological Assessment, Case Conceptualization, and Treatment, Volume 1: Adults. John Wiley & Sons. p. 32. ISBN 978-0-470-17356-5.
  344. ^ Bolwig TG (2007). "Melancholia: Beyond DSM, Beyond Neurotransmitters. Proceedings of a conference, May 2006, Copenhagen, Denmark". Acta Psychiatrica Scandinavica. Supplementum. 115 (433): 4–183. doi:10.1111/j.1600-0447.2007.00956.x. PMID 17280564. S2CID 221452354.
  345. ^ Fink M, Bolwig TG, Parker G, Shorter E (February 2007). "Melancholia: restoration in psychiatric classification recommended". Acta Psychiatrica Scandinavica. 115 (2): 89–92. doi:10.1111/j.1600-0447.2006.00943.x. PMC 3712974. PMID 17244171.
  346. ^ Healy D (1999). The Antidepressant Era. Cambridge, MA: Harvard University Press. p. 42. ISBN 978-0-674-03958-2.
  347. ^ Wolf, Joshua "Lincoln's Great Depression" Archived 9 October 2011 at the Wayback Machine, The Atlantic, October 2005. Retrieved 10 October 2009
  348. ^ Maloney F (3 November 2005). "The Depression Wars: Would Honest Abe Have Written the Gettysburg Address on Prozac?". Slate. Archived from the original on 25 September 2008. Retrieved 3 October 2008.
  349. ^ Karasz A (April 2005). "Cultural differences in conceptual models of depression". Social Science & Medicine. 60 (7): 1625–35. doi:10.1016/j.socscimed.2004.08.011. PMID 15652693.
  350. ^ Tilbury F, Rapley M (2004). "'There are orphans in Africa still looking for my hands': African women refugees and the sources of emotional distress". Health Sociology Review. 13 (1): 54–64. doi:10.5172/hesr.13.1.54. S2CID 145545714.
  351. ^ Parker J (25 January 2001). "Do the Chinese somatize depression? A cross-cultural study". Social Psychiatry and Psychiatric Epidemiology. 36 (6): 287–293. doi:10.1007/s001270170046. PMID 11583458. S2CID 24932164.
  352. ^ Seymour M (2002). Mary Shelley. Grove Press. pp. 560–61. ISBN 978-0-8021-3948-1.
  353. ^ "Biography of Henry James". PBS. Archived from the original on 8 October 2008. Retrieved 19 August 2008.
  354. ^ Burlingame M (1997). The Inner World of Abraham Lincoln. Urbana: University of Illinois Press. pp. xvii, 92–113. ISBN 978-0-252-06667-2.
  355. ^ Pita E (26 September 2001). "An Intimate Conversation with...Leonard Cohen". Archived from the original on 11 October 2008. Retrieved 3 October 2008.
  356. ^ Jeste ND, Palmer BW, Jeste DV (2004). "Tennessee Williams". The American Journal of Geriatric Psychiatry. 12 (4): 370–75. doi:10.1097/00019442-200407000-00004. PMID 15249274.
  357. ^ James H (1920). Letters of William James (Vols. 1 and 2). Montana: Kessinger Publishing Co. pp. 147–48. ISBN 978-0-7661-7566-2.
  358. ^ Hergenhahn 2005, p. 311
  359. ^ Cohen D (1979). J. B. Watson: The Founder of Behaviourism. London: Routledge & Kegan Paul. p. 7. ISBN 978-0-7100-0054-5.
  360. ^ Andreasen NC (2008). "The relationship between creativity and mood disorders". Dialogues in Clinical Neuroscience. 10 (2): 251–5. doi:10.31887/DCNS.2008.10.2/ncandreasen. PMC 3181877. PMID 18689294.
  361. ^ Simonton DK (2005). "Are genius and madness related? Contemporary answers to an ancient question". Psychiatric Times. 22 (7). Archived from the original on 14 January 2009.
  362. ^ Heffernan CF (1996). The melancholy muse: Chaucer, Shakespeare and early medicine. Pittsburgh: Duquesne University Press. ISBN 978-0-8207-0262-9.
  363. ^ Mill JS (2003). "A crisis in my mental history: One stage onward" (txt). Autobiography. Project Gutenberg EBook. pp. 1826–32. ISBN 978-1-4212-4200-2. Archived from the original on 21 September 2008. Retrieved 9 August 2008.
  364. ^ Sterba R (1947). "The 'Mental Crisis' of John Stuart Mill". Psychoanalytic Quarterly. 16 (2): 271–72. Archived from the original on 12 January 2009. Retrieved 5 November 2008.
  365. ^ a b "Churchill's Black Dog?: The History of the 'Black Dog' as a Metaphor for Depression" (PDF). Black Dog Institute website. Black Dog Institute. 2005. Archived from the original (PDF) on 10 September 2008. Retrieved 18 August 2008.
  366. ^ Jorm AF, Angermeyer M, Katschnig H (2000). "Public knowledge of and attitudes to mental disorders: a limiting factor in the optimal use of treatment services". In Andrews G, Henderson S (eds.). Unmet Need in Psychiatry:Problems, Resources, Responses. Cambridge University Press. p. 409. ISBN 978-0-521-66229-1.
  367. ^ Paykel ES, Tylee A, Wright A, et al. (June 1997). "The Defeat Depression Campaign: psychiatry in the public arena". The American Journal of Psychiatry. 154 (6 Suppl): 59–65. doi:10.1176/ajp.154.6.59. PMID 9167546.
  368. ^ Paykel ES, Hart D, Priest RG (December 1998). "Changes in public attitudes to depression during the Defeat Depression Campaign". The British Journal of Psychiatry. 173 (6): 519–22. doi:10.1192/bjp.173.6.519. PMID 9926082. S2CID 21172113.
  369. ^ Bondevik KM (December 2011). "Fighting stigma with openness. Interview by Ben Jones". Bulletin of the World Health Organization. 89 (12): 862–863. doi:10.2471/BLT.11.041211. PMC 3260893. PMID 22271941. Archived from the original on 31 October 2013. Retrieved 19 July 2013.
  370. ^ BBC Newsnight, 21 January 2008.

Cited works

  • American Psychiatric Association (2000a). Diagnostic and statistical manual of mental disorders (Fourth Edition, Text Revision: DSM-IV-TR ed.). Washington, DC: American Psychiatric Publishing, Inc. ISBN 978-0-89042-025-6.
  • American Psychiatric Association (2013). Diagnostic and statistical manual of mental disorders (Fifth Edition: DSM-5 ed.). Washington, DC: American Psychiatric Publishing, Inc. ISBN 978-0-89042-555-8.
  • Barlow DH, Durand VM (2005). Abnormal psychology: An integrative approach (5th ed.). Belmont, CA: Thomson Wadsworth. ISBN 978-0-534-63356-1.
  • Beck AT, Rush J, Shaw BF, Emery G (1987) [1979]. Cognitive therapy of depression. New York: Guilford Press. ISBN 978-0-89862-919-4.
  • Hergenhahn BR (2005). An Introduction to the History of Psychology (5th ed.). Belmont, CA: Thomson Wadsworth. ISBN 978-0-534-55401-9.
  • Parker G, Hadzi-Pavlovic D, eds. (1996). Melancholia: a disorder of movement and mood: a phenomenological and neurobiological review. Cambridge: Cambridge University Press. ISBN 978-0-521-47275-3.
  • Royal Pharmaceutical Society of Great Britain (2008). British National Formulary (BNF 56). UK: BMJ Group and RPS Publishing. ISBN 978-0-85369-778-7.
  • Sadock VA, Sadock BJ, Kaplan HI (2003). Kaplan & Sadock's synopsis of psychiatry: behavioral sciences/clinical psychiatry. Philadelphia: Lippincott Williams & Wilkins. ISBN 978-0-7817-3183-6.
  • "6A70 Single episode depressive disorder". International Classification of Diseases 11th Revision. World Health Organization. February 2022 [adopted in 2019]. Retrieved 9 July 2022.
  • "6A71 Recurrent depressive disorder". International Classification of Diseases 11th Revision. World Health Organization. February 2022 [adopted in 2019]. Retrieved 9 July 2022.
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