Major depressive disorder
|Major depressive disorder|
|Other names||Clinical depression, major depression, unipolar depression, unipolar disorder, recurrent depression|
|Sorrowing Old Man (At Eternity's Gate)|
by Vincent van Gogh (1890)
|Symptoms||Low mood, low self-esteem, loss of interest in normally enjoyable activities, low energy, pain without a clear cause|
|Duration||> 2 weeks|
|Causes||environmental (adverse life experiences, stressful life events), Genetic and psychological factors|
|Risk factors||Family history, major life changes, certain medications, chronic health problems, substance use disorder|
|Differential diagnosis||Bipolar disorder, ADHD, sadness|
|Treatment||Psychotherapy, antidepressant medication, electroconvulsive therapy, exercise|
|Frequency||163 million (2017)|
Major depressive disorder (MDD), also known simply as depression, is a mental disorder characterized by at least two weeks of pervasive low mood, low self-esteem, and loss of interest or pleasure in normally enjoyable activities. Those affected may also occasionally have delusions or hallucinations. Introduced by a group of US clinicians in the mid-1970s, 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) classification, and has become widely used since.
The diagnosis of major depressive disorder is based on the person's reported experiences and a mental status examination. There is no laboratory test for the disorder, but testing may be done to rule out physical conditions that can cause similar symptoms. The most common time of onset is in a person's 20s, with females affected about twice as often as males. The course of the disorder varies widely, from one episode lasting months to a lifelong disorder with recurrent major depressive episodes.
Those with major depressive disorder are typically treated with psychotherapy and antidepressant medication. Medication appears to be effective, but the effect may only be significant in the most severely depressed. 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.
Major depressive disorder is believed to be caused by a combination of genetic, environmental, and psychological factors, with about 40% of the risk being genetic. Risk factors include a family history of the condition, major life changes, certain medications, chronic health problems, and substance use disorders. It can negatively affect a person's personal life, work life, or education as well as sleeping, eating habits, and general health. Major depressive disorder affected approximately 163 million people (2% of the world's population) in 2017. The percentage of people who are affected at one point in their life varies from 7% in Japan to 21% in France. Lifetime rates are higher in the developed world (15%) compared to the developing world (11%). The disorder causes the second-most years lived with disability, after lower back pain.
Symptoms and signs
Major depression significantly affects a person's family and personal relationships, work or school life, sleeping and eating habits, and general health. 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. Depressed people may be preoccupied with—or ruminate over—thoughts and feelings of worthlessness, inappropriate guilt or regret, helplessness or hopelessness. Other symptoms of depression include poor concentration and memory, withdrawal from social situations and activities, 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. Some antidepressants may also cause insomnia due to their stimulating effect. In severe cases, depressed people may have psychotic symptoms. These symptoms include delusions or, less commonly, hallucinations, usually unpleasant. People who have had previous episodes with psychotic symptoms are more likely to have them with future episodes.
A depressed person may report multiple physical symptoms such 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. Appetite often decreases, resulting in weight loss, although increased appetite and weight gain occasionally occur. Family and friends may notice agitation or lethargy. Older depressed people may have cognitive symptoms of recent onset, such as forgetfulness, and a more noticeable slowing of movements.
Depressed children may often display an irritable rather than a depressed mood; most lose interest in school and show a steep decline in academic performance. Diagnosis may be delayed or missed when symptoms are interpreted as "normal moodiness."
The biopsychosocial model proposes that biological, psychological, and social factors all play a role in causing depression. 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, implying an interaction between nature and nurture, or schematic, resulting from views of the world learned in childhood.
Adverse childhood experiences (incorporating childhood abuse, neglect and family dysfunction) markedly increase the risk of major depression, especially if more than one type. Childhood trauma also correlates with severity of depression, poor responsiveness to treatment and length of illness. Some are more susceptible than others to developing mental illness such as depression after trauma, and various genes have been suggested to control susceptibility.
Family and twin studies find that nearly 40% of individual differences in risk for major depressive disorder can be explained by genetic factors. Like most psychiatric disorders, major depressive disorder is likely influenced by many individual genetic changes. In 2018, a genome-wide association study discovered 44 genetic variants linked to risk for major depression; a 2019 study found 102 variants in the genome linked to depression. Research focusing on specific candidate genes has been criticized for its tendency to generate false positive findings. There are also other efforts to examine interactions between life stress and polygenic risk for depression.
Other health problems
Depression can also come secondary to a chronic or terminal medical condition, such as HIV/AIDS or asthma, and may be labeled "secondary depression." It is unknown whether the underlying diseases induce depression through effect on quality of life, or through shared etiologies (such as degeneration of the basal ganglia in Parkinson's disease or immune dysregulation in asthma). Depression may also be iatrogenic (the result of healthcare), such as drug-induced depression. Therapies associated with depression include interferons, beta-blockers, isotretinoin, contraceptives, cardiac agents, anticonvulsants, antimigraine drugs, antipsychotics, and hormonal agents such as gonadotropin-releasing hormone agonist. Substance use in early age is associated with increased risk of developing depression later in life. Depression occurring after giving birth is called postpartum depression and is thought to be the result of hormonal changes associated with pregnancy. Seasonal affective disorder, a type of depression associated with seasonal changes in sunlight, is thought to be triggered by decreased sunlight. Vitamin B2, B6 and B12 deficiency may cause depression in females.
The pathophysiology of depression is not yet 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. 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. 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, and polymorphism of dopamine receptor genes implicate dopamine, another monoamine, in depression. Lastly, increased activity of monoamine oxidase, which degrades monoamines, has been associated with depression. However, the monoamine theory is inconsistent with observations that serotonin depletion does not cause depression in healthy persons, that antidepressants instantly increase levels of monoamines but take weeks to work, and the existence of atypical antidepressants which can be effective despite not targeting this pathway. One proposed explanation for the therapeutic lag, and further support for the deficiency of monoamines, is a desensitization of self-inhibition in raphe nuclei by the increased serotonin mediated by antidepressants. 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 SSRI treatment, and the preference for carbohydrates in people who are depressed. Already limited, the monoamine hypothesis has been further oversimplified when presented to the general public.
Immune system abnormalities have been observed, including increased levels of cytokines involved in generating sickness behavior (which shares overlap with depression). The effectiveness of nonsteroidal anti-inflammatory drugs (NSAIDs) and cytokine inhibitors in treating depression, and normalization of cytokine levels after successful treatment further suggest immune system abnormalities in depression.
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%. These stress-related abnormalities are thought to be the cause of hippocampal volume reductions seen in people who are depressed. Furthermore, a meta-analysis yielded decreased dexamethasone suppression, and increased response to psychological stressors. Further abnormal results have been obscured with the cortisol awakening response, with increased response being associated with depression.
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. Another model, the cortico-striatal model, suggests that abnormalities of the prefrontal cortex in regulating striatal and subcortical structures results in depression. 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.
A diagnostic assessment may be conducted by a suitably trained general practitioner, or by a psychiatrist or psychologist, 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. Specialist mental health services are rare in rural areas, and thus diagnosis and management is left largely to primary-care clinicians. This issue is even more marked in developing countries. 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; these include the Hamilton Rating Scale for Depression, the Beck Depression Inventory or the Suicide Behaviors Questionnaire-Revised.
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.
Before diagnosing major depressive disorder, a doctor generally performs a medical examination and selected investigations to rule out other causes of 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. 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. Vitamin D levels might be evaluated, as low levels of vitamin D have been associated with greater risk for depression. Subjective cognitive complaints appear in older depressed people, but they can also be indicative of the onset of a dementing disorder, such as Alzheimer's disease. Cognitive testing and brain imaging can help distinguish depression from dementia. A CT scan can exclude brain pathology in those with psychotic, rapid-onset or otherwise unusual symptoms. No biological tests confirm major depression. In general, investigations are not repeated for a subsequent episode unless there is a 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 and the World Health Organization's International Statistical Classification of Diseases and Related Health Problems. The latter system is typically used in European countries, while the former is used in the US and many other non-European nations, and the authors of both have worked towards conforming one with the other.
Both DSM-5 and ICD-10 mark out typical (main) depressive symptoms. ICD-10 defines three typical depressive symptoms (depressed mood, anhedonia, and reduced energy), two of which should be present to determine the depressive disorder diagnosis. According to DSM-5, there are two main depressive symptoms: a depressed mood, and loss of interest/pleasure in activities (anhedonia). These symptoms, as well as five out of the nine more specific symptoms listed, must frequently occur for more than two weeks (to the extent in which it impairs functioning) for the diagnosis.
Major depressive disorder is classified as a mood disorder in DSM-5. The diagnosis hinges on the presence of single or recurrent major depressive episodes. 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. The ICD-10 system does not use the term major depressive disorder but lists very similar criteria for the diagnosis of a depressive episode (mild, moderate or severe); the term recurrent may be added if there have been multiple episodes without mania.
Major depressive episode
A major depressive episode is characterized by the presence of a severely depressed mood that persists for at least two weeks. Episodes may be isolated or recurrent and are categorized as mild (few symptoms in excess of minimum criteria), moderate, or severe (marked impact on social or occupational functioning). An episode with psychotic features—commonly referred to as psychotic depression—is automatically rated as severe. 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".
Bereavement is not an exclusion criterion in 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; recurrent brief depression, consisting of briefer depressive episodes; minor depressive disorder, whereby only some symptoms of major depression are present; and adjustment disorder with depressed mood, which denotes low mood resulting from a psychological response to an identifiable event or stressor.
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.
- "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.
- "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.
- "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.
- "Depression with peri-partum onset" refers to the intense, sustained and sometimes disabling depression experienced by women after giving birth or while a woman is pregnant. DSM-IV-TR used the classification "postpartum depression," but this was changed to not exclude cases of depressed woman during pregnancy. Depression with peripartum onset has an incidence rate of 3–6% among new mothers. The DSM-V mandates that to qualify as depression with peripartum onset, onset occurs during pregnancy or within one month of delivery.
- "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.
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). 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. Bipolar disorder, previously known as manic–depressive disorder, is a condition in which depressive phases alternate with periods of mania or hypomania. Although depression is currently categorized as a separate disorder, there is ongoing debate because individuals diagnosed with major depression often experience some hypomanic symptoms, indicating a mood disorder continuum.
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.
Screening and prevention
Preventive efforts may result in decreases in rates of the condition of between 22 and 38%. Since 2016, the United States Preventive Services Task Force (USPSTF) has recommended screening for depression among those over the age 12; though a 2005 Cochrane review found that the routine use of screening questionnaires has little effect on detection or treatment. Screening the general population is not recommended by authorities in the UK or Canada.
Behavioral interventions, such as interpersonal therapy and cognitive-behavioral therapy, are effective at preventing new onset depression. Because such interventions appear to be most effective when delivered to individuals or small groups, it has been suggested that they may be able to reach their large target audience most efficiently through the Internet.
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.
The three most common treatments for depression are psychotherapy, medication, and electroconvulsive therapy. Psychotherapy is the treatment of choice (over medication) for people under 18. 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:
- 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.
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, electroconvulsive therapy (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. There is evidence that collaborative care by a team of health care practitioners produces better results than routine single-practitioner care.
Treatment options are much more limited in developing countries, where access to mental health staff, medication, and psychotherapy is often difficult. Development of mental health services is minimal in many countries; depression is viewed as a phenomenon of the developed world despite evidence to the contrary, and not as an inherently life-threatening condition. There is insufficient evidence to determine the effectiveness of psychological versus medical therapy in children.
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. It is equivalent to the use of medications or psychological therapies in most people. In older people it does appear to decrease depression. Sleep and diet may also play a role in depression, and interventions in these areas may be an effective add-on to conventional methods. In observational studies, smoking cessation has benefits in depression as large as or larger than those of medications.
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. With more complex and chronic forms of depression, a combination of medication and psychotherapy may be used. There is moderate-quality evidence that psychological therapies are a useful addition to standard antidepressant treatment of treatment-resistant depression in the short term. Psychotherapy has been shown to be effective in older people. Successful psychotherapy appears to reduce the recurrence of depression even after it has been stopped or replaced by occasional booster sessions.
The most-studied form of psychotherapy for depression is CBT, which teaches clients to challenge self-defeating, but enduring ways of thinking (cognitions) and change counter-productive behaviors. CBT can perform as well as than antidepressants in people with major depression. CBT has the most research evidence for the treatment of depression in children and adolescents, and CBT and interpersonal psychotherapy (IPT) are preferred therapies for adolescent depression. In people under 18, according to 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. Several variables predict success for cognitive behavioral therapy in adolescents: higher levels of rational thoughts, less hopelessness, fewer negative thoughts, and fewer cognitive distortions. CBT is particularly beneficial in preventing relapse. Cognitive behavioral therapy and occupational programs (including modification of work activities and assistance) have been shown to be effective in reducing sick days taken by workers with depression. Several variants of cognitive behavior therapy have been used in those with depression, the most notable being rational emotive behavior therapy, and mindfulness-based cognitive therapy. Mindfulness-based stress reduction programs may reduce depression symptoms. Mindfulness programs also appear to be a promising intervention in youth.
Psychoanalysis is a school of thought, founded by Sigmund Freud, which emphasizes the resolution of unconscious mental conflicts. Psychoanalytic techniques are used by some practitioners to treat clients presenting with major depression. 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. 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.
Conflicting results have arisen from studies that look at the effectiveness of antidepressants in people with acute, mild to moderate depression. A review commissioned by the National Institute for Health and Care Excellence (UK) concluded that there is strong evidence that selective serotonin reuptake inhibitors (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. 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.
In 2014 the U.S. Food and Drug Administration published a systematic review of all antidepressant maintenance trials submitted to the agency between 1985 and 2012. The authors concluded that maintenance treatment reduced the risk of relapse by 52% compared to placebo, and that this effect was primarily due to recurrent depression in the placebo group rather than a drug withdrawal effect.
To find the most effective antidepressant medication with minimal side-effects, the dosages can be adjusted, and if necessary, combinations of different classes of antidepressants can be tried. Response rates to the first antidepressant administered range from 50 to 75%, and it can take at least six to eight weeks from the start of medication to improvement. Antidepressant medication treatment is usually continued for 16 to 20 weeks after remission, to minimize the chance of recurrence, and even up to one year of continuation is recommended. People with chronic depression may need to take medication indefinitely to avoid relapse.
SSRIs are the primary medications prescribed, owing to their relatively mild side-effects, and because they are less toxic in overdose than other antidepressants. People who do not respond to one SSRI can be switched to another antidepressant, and this results in improvement in almost 50% of cases. Another option is to switch to the atypical antidepressant bupropion. Venlafaxine, an antidepressant with a different mechanism of action, may be modestly more effective than SSRIs. However, venlafaxine is not recommended in the UK as a first-line treatment because of evidence suggesting its risks may outweigh benefits, and it is specifically discouraged in children and adolescents.
For children, some research has supported the use of the SSRI antidepressant fluoxetine. The benefit however appears to be slight in children, while other antidepressants have not been shown to be effective. Medications are not recommended in children with mild disease. There is also insufficient evidence to determine effectiveness in those with depression complicated by dementia. Any antidepressant can cause low blood sodium levels; nevertheless, it has been reported more often with SSRIs. It is not uncommon for SSRIs to cause or worsen insomnia; the sedating atypical antidepressant mirtazapine can be used in such cases.
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. 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.
It is unclear whether antidepressants affect a person's risk of suicide. For children, adolescents, and probably young adults between 18 and 24 years old, there is a higher risk of both suicidal ideations and suicidal behavior in those treated with SSRIs. For adults, it is unclear whether SSRIs affect the risk of suicidality. One review found no connection; another an increased risk; and a third no risk in those 25–65 years old and a decreased risk in those more than 65. 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. Similar precautionary notice revisions were implemented by the Japanese Ministry of Health.
A 2019 Cochrane review on the combined use of antidepressants plus benzodiazepines demonstrated improved effectiveness when compared to antidepressants alone; however, these effects were not maintained in the acute or continuous phase. The benefits of adding a benzodiazepine should be balanced against possible harms and other alternative treatment strategies when antidepressant mono-therapy is considered inadequate.
There is some evidence that omega-3 fatty acids fish oil supplements containing high levels of eicosapentaenoic acid (EPA) to docosahexaenoic acid (DHA) are effective in the treatment of, but not the prevention of major depression. However, a Cochrane review determined there was insufficient high quality evidence to suggest omega-3 fatty acids were effective in depression. There is limited evidence that vitamin D supplementation is of value in alleviating the symptoms of depression in individuals who are vitamin D-deficient. There is some preliminary evidence that COX-2 inhibitors, such as celecoxib, have a beneficial effect on major depression. 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. There is a narrow range of effective and safe dosages of lithium thus close monitoring may be needed. Low-dose thyroid hormone may be added to existing antidepressants to treat persistent depression symptoms in people who have tried multiple courses of medication. Limited evidence suggests stimulants, such as amphetamine and modafinil, may be effective in the short term, or as adjuvant therapy. Also, it is suggested that folate supplements may have a role in depression management. There is tentative evidence for benefit from testosterone in males.
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.: 1880 ECT is used with informed consent as a last line of intervention for major depressive disorder. A round of ECT is effective for about 50% of people with treatment-resistant major depressive disorder, whether it is unipolar or bipolar. Follow-up treatment is still poorly studied, but about half of people who respond relapse within twelve months. Aside from effects in the brain, the general physical risks of ECT are similar to those of brief general anesthesia.: 259 Immediately following treatment, the most common adverse effects are confusion and memory loss. ECT is considered one of the least harmful treatment options available for severely depressed pregnant women.
A usual course of ECT involves multiple administrations, typically given two or three times per week, until the person is no longer suffering symptoms. ECT is administered under anesthesia with a muscle relaxant. Electroconvulsive therapy can differ in its application in three ways: electrode placement, frequency of treatments, and the electrical waveform of the stimulus. These three forms of application have significant differences in both adverse side effects and symptom remission. After treatment, drug therapy is usually continued, and some people receive maintenance ECT.
Transcranial magnetic stimulation
Transcranial magnetic stimulation (TMS) or deep transcranial magnetic stimulation is a noninvasive method used to stimulate small regions of the brain. TMS was approved by the FDA for treatment-resistant major depressive disorder (trMDD) in 2008 and as of 2014 evidence supports that it is probably effective. The American Psychiatric Association the Canadian Network for Mood and Anxiety Disorders, and the Royal Australia and New Zealand College of Psychiatrists have endorsed TMS for trMDD.
Transcranial direct current stimulation
Transcranial direct current stimulation (tDCS) is another noninvasive method used to stimulate small regions of the brain with the help of a weak electric current. Increasing evidence has been gathered for its efficiency as a depression treatment. A meta-analysis was published in 2020 summarising results across nine studies (572 participants) concluded that active tDCS was significantly superior to sham for response (30.9% vs. 18.9%, respectively), remission (19.9% vs. 11.7%) and depression improvement. According to a 2016 meta analysis, 34% of people treated with tDCS showed at least 50% symptom reduction compared to 19% sham-treated across 6 randomised controlled trials.
Bright light therapy reduces depression symptom severity, with benefit for both seasonal affective disorder and for nonseasonal depression, and an effect similar to those for conventional antidepressants. For nonseasonal depression, adding light therapy to the standard antidepressant treatment was not effective. For nonseasonal depression, where light was used mostly in combination with antidepressants or wake therapy, a moderate effect was found, with response better than control treatment in high-quality studies, in studies that applied morning light treatment, and with people who respond to total or partial sleep deprivation. Both analyses noted poor quality, short duration, and small size of most of the reviewed studies.
There is a small amount of evidence that skipping a night's sleep may improve depressive symptoms, 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.
Studies have shown that 80% of those suffering from their first major depressive episode will have at least one more depression during their life, with a lifetime average of 4 episodes. Other general population studies indicate that around half those who have an episode recover (whether treated or not) and remain well, while the other half will have at least one more, and around 15% of those experience chronic recurrence. Studies recruiting from selective inpatient sources suggest lower recovery and higher chronicity, while studies of mostly outpatients show that nearly all recover, with a median episode duration of 11 months. Around 90% of those with severe or psychotic depression, most of whom also meet criteria for other mental disorders, experience recurrence. Cases when outcome is poor are associated with inappropriate treatment, severe initial symptoms including psychosis, early age of onset, previous episodes, incomplete recovery after one year of treatment, pre-existing severe mental or medical disorder, and family dysfunction.
A high proportion of people who experience full symptomatic remission still have at least one not fully resolved symptom after treatment. Recurrence or chronicity is more likely if symptoms have not fully resolved with treatment. Current guidelines recommend continuing antidepressants for four to six months after remission to prevent relapse. Evidence from many randomized controlled trials indicate continuing antidepressant medications after recovery can reduce the chance of relapse by 70% (41% on placebo vs. 18% on antidepressant). The preventive effect probably lasts for at least the first 36 months of use.
Major depressive episodes often resolve over time whether or not they are treated. Outpatients on a waiting list show a 10–15% reduction in symptoms within a few months, with approximately 20% no longer meeting the full criteria for a depressive disorder. The median duration of an episode has been estimated to be 23 weeks, with the highest rate of recovery in the first three months. According to a 2013 review, 23% of untreated adults suffering from mild to moderate depression will remit within 3 months, 32% within 6 months and 53% within 12 months.
Ability to work
Depression may affect people's ability to work. The combination of usual clinical care and support with return to work (like working less hours or changing tasks) probably reduces sick leave by 15%, and leads to fewer depressive symptoms and improved work capacity, reducing sick leave by an annual average of 25 days per year. Helping depressed people return to work without a connection to clinical care has not been shown to have an effect on sick leave days. Additional psychological interventions (such as online cognitive behavioral therapy) leads to fewer sick days compared to standard management only. Streamlining care or adding specific providers for depression care may help to reduce sick leave.
Life expectancy and the risk of suicide
Depressed individuals have a shorter life expectancy than those without depression, in part because people who are depressed are at risk of dying of suicide. Up to 60% 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. About 2–8% of adults with major depression die by suicide, and about 50% of people who die by suicide had depression or another mood disorder. The lifetime risk of suicide associated with a diagnosis of major depression in the US is estimated at 3.4%, which averages two highly disparate figures of almost 7% for men and 1% for women (although suicide attempts are more frequent in women). The estimate is substantially lower than a previously accepted figure of 15%, which had been derived from older studies of people who were hospitalized.
Depressed people have a higher rate of dying from other causes. 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. Cardiologists may not recognize underlying depression that complicates a cardiovascular problem under their care.
Major depressive disorder affected approximately 163 million people in 2017 (2% of the global population). The percentage of people who are affected at one point in their life varies from 7% in Japan to 21% in France. In most countries the number of people who have depression during their lives falls within an 8–18% range. In North America, the probability of having a major depressive episode within a year-long period is 3–5% for males and 8–10% for females. Major depression is about twice as common in women as in men, although it is unclear why this is so, and whether factors unaccounted for are contributing to this. The relative increase in occurrence is related to pubertal development rather than chronological age, reaches adult ratios between the ages of 15 and 18, and appears associated with psychosocial more than hormonal factors. As of 2017, depression is the third most common worldwide cause of disability among both sexes, following low back pain and headache.
People are most likely to develop their first depressive episode between the ages of 30 and 40, and there is a second, smaller peak of incidence between ages 50 and 60. The risk of major depression is increased with neurological conditions such as stroke, Parkinson's disease, or multiple sclerosis, and during the first year after childbirth. 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. Studies conflict on the prevalence of depression in the elderly, but most data suggest there is a reduction in this age group. 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.
Major depression is currently the leading cause of disease burden in North America and other high-income countries, and the fourth-leading cause worldwide. In the year 2030, it is predicted to be the second-leading cause of disease burden worldwide after HIV, according to the WHO. Delay or failure in seeking treatment after relapse and the failure of health professionals to provide treatment are two barriers to reducing disability.
Major depression frequently co-occurs with other psychiatric problems. The 1990–92 National Comorbidity Survey (US) reports that half of those with major depression also have lifetime anxiety and its associated disorders, such as generalized anxiety disorder. Anxiety symptoms can have a major impact on the course of a depressive illness, with delayed recovery, increased risk of relapse, greater disability and increased suicidal behavior. Depressed people have increased rates of alcohol and substance use, particularly dependence, and around a third of individuals diagnosed with attention deficit hyperactivity disorder (ADHD) develop comorbid depression. Post-traumatic stress disorder and depression often co-occur. Depression may also coexist with ADHD, complicating the diagnosis and treatment of both. Depression is also frequently comorbid with alcohol use disorder and personality disorders. 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.
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 be suffering from depression, depending on the setting—a lower prevalence in general practice, and higher in specialty clinics. Depression is often underrecognized, and therefore undertreated, in patients presenting with pain. Depression often coexists with physical disorders common among the elderly, such as stroke, other cardiovascular diseases, Parkinson's disease, and chronic obstructive pulmonary disease.
The Ancient Greek physician Hippocrates described a syndrome of melancholia as a distinct disease with particular mental and physical symptoms; he characterized all "fears and despondencies, if they last a long time" as being symptomatic of the ailment. 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.
The term depression itself was derived from the Latin verb deprimere, "to press down". From the 14th century, "to depress" meant to subjugate or to bring down in spirits. It was used in 1665 in English 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. 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. Since Aristotle, melancholia had been associated with men of learning and intellectual brilliance, a hazard of contemplation and creativity. The newer concept abandoned these associations and through the 19th century, became more associated with women.
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. 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. The person's decline of self-perception is revealed in his belief of his own blame, inferiority, and unworthiness. He also emphasized early life experiences as a predisposing factor. Adolf 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. 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.
In the mid-20th century, researchers theorized that depression was caused by a chemical imbalance in neurotransmitters in the brain, a theory based on observations made in the 1950s of the effects of reserpine and isoniazid in altering monoamine neurotransmitter levels and affecting depressive symptoms. The chemical imbalance theory has never been proven.
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), and was incorporated into the DSM-III in 1980. The American Psychiatric Association added "major depressive disorder" to the Diagnostic and Statistical Manual of Mental Disorders (DSM-III), 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. 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. 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. There has been some criticism of the expansion of coverage of the diagnosis, related to the development and promotion of antidepressants and the biological model since the late 1950s.
Society and culture
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." There are cultural differences in the extent to which serious depression is considered an illness requiring personal professional treatment, or is an indicator of something else, such as the need to address social or moral problems, the result of biological imbalances, or a reflection of individual differences in the understanding of distress that may reinforce feelings of powerlessness, and emotional struggle.
The diagnosis is less common in some countries, such as China. It has been argued that the Chinese traditionally deny or somatize emotional depression (although since the early 1980s, the Chinese denial of depression may have modified). Alternatively, it may be that Western cultures reframe and elevate some expressions of human distress to disorder status. Australian professor Gordon Parker and others have argued that the Western concept of depression "medicalizes" sadness or misery. Similarly, Hungarian-American psychiatrist Thomas Szasz and others argue that depression is a metaphorical illness that is inappropriately regarded as an actual disease. There has also been concern that the DSM, as well as the field of descriptive psychiatry that employs it, tends to reify abstract phenomena such as depression, which may in fact be social constructs. American archetypal psychologist James Hillman writes that depression can be healthy for the soul, insofar as "it brings refuge, limitation, focus, gravity, weight, and humble powerlessness." Hillman argues that therapeutic attempts to eliminate depression echo the Christian theme of resurrection, but have the unfortunate effect of demonizing a soulful state of being.
Historical figures were often reluctant to discuss or seek treatment for depression due to social 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, American-British writer Henry James, and American president Abraham Lincoln. Some well-known contemporary people with possible depression include Canadian songwriter Leonard Cohen and American playwright and novelist Tennessee Williams. Some pioneering psychologists, such as Americans William James and John B. Watson, 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. British literature gives many examples of reflections on depression. 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." English writer Samuel Johnson used the term "the black dog" in the 1780s to describe his own depression, and it was subsequently popularized by depression sufferer former British Prime Minister Sir Winston Churchill.
Social stigma of major depression is widespread, and contact with mental health services reduces this only slightly. Public opinions on treatment differ markedly to those of health professionals; alternative treatments are held to be more helpful than pharmacological ones, which are viewed poorly. In the UK, 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; a MORI study conducted afterwards showed a small positive change in public attitudes to depression and treatment.
Depression is especially common among those over 65 years of age and increases in frequency beyond this age. In addition, the risk of depression increases in relation to the frailty of the individual. Depression is one of the most important factors which negatively impact quality of life in adults, as well as the elderly. Both symptoms and treatment among the elderly differ from those of the rest of the population.
As with many other diseases, it is common among the elderly not to present with classical depressive symptoms. Diagnosis and treatment is further complicated in that the elderly are often simultaneously treated with a number of other drugs, and often have other concurrent diseases. Treatment differs in that studies of SSRIs have shown lesser and often inadequate effects among the elderly, while other drugs, such as duloxetine (a serotonin-norepinephrine reuptake inhibitor), with more clear effects have adverse effects, such as dizziness, dryness of the mouth, diarrhea and constipation, which can be especially difficult to handle among the elderly.
Problem solving therapy was, as of 2015, the only psychological therapy with proven effect, and can be likened to a simpler form of cognitive behavioral therapy. However, elderly with depression are seldom offered any psychological treatment, and the evidence proving other treatments effective is incomplete. ECT has been used in the elderly, and register-studies suggest it is effective, although less so as compared to the rest of the population. The risks involved with treatment of depression among the elderly as opposed to benefits are not entirely clear.
MRI scans of people with depression have revealed a number of differences in brain structure compared to those who are not depressed. Meta-analyses of neuroimaging studies in major depression reported that, compared to controls, people who are depressed had increased volume of the lateral ventricles and adrenal gland and smaller volumes of the basal ganglia, thalamus, hippocampus, and frontal lobe (including the orbitofrontal cortex and gyrus rectus). Hyperintensities have been associated with people with a late age of onset, and have led to the development of the theory of vascular depression.
Trials are looking at the effects of botulinum toxins on depression. The idea is that the drug is used to make the person look less frowning and that this stops the negative facial feedback from the face. In 2015 results showed, however, that the partly positive effects that had been observed until then could have been due to placebo effects.
In 2018–2019, the US Food and Drug Administration (FDA) granted Breakthrough therapy designation to Compass Pathways and, separately, Usona Institute. Compass is a for-profit company studying psilocybin for treatment-resistant depression; Usona is a non-profit organization studying psilocybin for major depressive disorder more broadly.
Models of depression in animals for the purpose of study include iatrogenic depression models (such as drug-induced), forced swim tests, tail suspension test, and learned helplessness models. Criteria frequently used to assess depression in animals include expression of despair, neurovegetative changes, and anhedonia, as many other criteria for depression are untestable in animals, such as guilt and suicidality.
- "Depression". NIMH. May 2016. Archived from the original on 5 August 2016. Retrieved 31 July 2016.
- Richards CS, O'Hara MW (2014). The Oxford Handbook of Depression and Comorbidity. Oxford University Press. p. 254. ISBN 978-0-19-979704-2.
- American Psychiatric Association 2013, p. 165.
- 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.
- American Psychiatric Association 2013, p. 166.
- American Psychiatric Association 2013, pp. 167–168.
- 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. 9 (9): CD004366. doi:10.1002/14651858.CD004366.pub6. PMID 24026850.
- 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.
- Drs; Sartorius, Norman; Henderson, A.S.; Strotzka, H.; Lipowski, Z.; Yu-cun, Shen; You-xin, Xu; Strömgren, E.; Glatzel, J.; Kühne, G.-E.; Misès, R.; Soldatos, C.R.; Pull, C.B.; Giel, R.; Jegede, R.; Malt, U.; Nadzharov, R.A.; Smulevitch, A.B.; Hagberg, B.; Perris, C.; Scharfetter, C.; Clare, A.; Cooper, J.E.; Corbett, J.A.; Griffith Edwards, J.; Gelder, M.; Goldberg, D.; Gossop, M.; Graham, P.; Kendell, R.E.; Marks, I.; Russell, G.; Rutter, M.; Shepherd, M.; West, D.J.; Wing, J.; Wing, L.; Neki, J.S.; Benson, F.; Cantwell, D.; Guze, S.; Helzer, J.; Holzman, P.; Kleinman, A.; Kupfer, D.J.; Mezzich, J.; Spitzer, R.; Lokar, J. "The ICD-10 Classification of Mental and Behavioural Disorders Clinical descriptions and diagnostic guidelines" (PDF). www.who.int World Health Organization. Microsoft Word. bluebook.doc. Retrieved 23 June 2021 – via Microsoft Bing.
- 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.
- Patton LL (2015). The ADA Practical Guide to Patients with Medical Conditions (2 ed.). John Wiley & Sons. p. 339. ISBN 978-1-118-92928-5.
- Fournier JC, DeRubeis RJ, Hollon SD, Dimidjian S, Amsterdam JD, Shelton RC, Fawcett J (January 2010). "Antidepressant drug effects and depression severity: a patient-level meta-analysis". JAMA. 303 (1): 47–53. doi:10.1001/jama.2009.1943. PMC 3712503. PMID 20051569.
- Kirsch I, Deacon BJ, Huedo-Medina TB, Scoboria A, Moore TJ, Johnson BT (February 2008). "Initial severity and antidepressant benefits: a meta-analysis of data submitted to the Food and Drug Administration". PLOS Medicine. 5 (2): e45. doi:10.1371/journal.pmed.0050045. PMC 2253608. PMID 18303940.
- Global Burden of Disease Study 2013 Collaborators (August 2015). "Global, regional, and national incidence, prevalence, and years lived with disability for 301 acute and chronic diseases and injuries in 188 countries, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013". Lancet. 386 (9995): 743–800. doi:10.1016/S0140-6736(15)60692-4. PMC 4561509. PMID 26063472.
- Depression (PDF). National Institute of Mental Health (NIMH). Retrieved 13 October 2021.
- American Psychiatric Association 2013, p. 160.
- American_Psychiatric_Association 2013, p. 161.
- American Psychiatric Association 2013, p. 163.
- "Insomnia: Assessment and Management in Primary Care". American Family Physician. 59 (11): 3029–3038. 1999. Archived from the original on 26 July 2011. Retrieved 12 November 2014.
- American Psychiatric Association 2000a, p. 412
- Nelson JC, Bickford D, Delucchi K, Fiedorowicz JG, Coryell WH (2018). "Risk of Psychosis in Recurrent Episodes of Psychotic and Nonpsychotic Major Depressive Disorder: A Systematic Review and Meta-Analysis". Am J Psychiatry. 175 (9): 897–904. doi:10.1176/appi.ajp.2018.17101138. PMID 29792050. S2CID 43951278.
- Fisher JC, Powers WE, Tuerk DB, Edgerton MT (March 1975). "Development of a plastic surgical teaching service in a women's correctional institution". American Journal of Surgery. 129 (3): 269–72. doi:10.1136/bmj.322.7284.482. PMC 1119689. PMID 11222428.
- American Psychiatric Association 2000a, p. 349
- Delgado PL, Schillerstrom J (2009). "Cognitive Difficulties Associated With Depression: What Are the Implications for Treatment?". Psychiatric Times. 26 (3). Archived from the original on 22 July 2009.
- Faculty of Psychiatry of Old Age, NSW Branch, RANZCP, Kitching D, Raphael B (2001). Consensus Guidelines for Assessment and Management of Depression in the Elderly (PDF). North Sydney, New South Wales: NSW Health Department. p. 2. ISBN 978-0-7347-3341-2. Archived (PDF) from the original on 1 April 2015.
- American Psychiatric Association 2013, p. 164.
- Hankin BL, Abela JR (2005). Development of Psychopathology: A Vulnerability-Stress Perspective. SAGE Publications. pp. 32–34. ISBN 9781412904902.
- Department of Health and Human Services (1999). "The fundamentals of mental health and mental illness" (PDF). Mental Health: A Report of the Surgeon General. Archived (PDF) from the original on 17 December 2008. Retrieved 11 November 2008.
- Caspi A, Sugden K, Moffitt TE, Taylor A, Craig IW, Harrington H, McClay J, Mill J, Martin J, Braithwaite A, Poulton R (July 2003). "Influence of life stress on depression: moderation by a polymorphism in the 5-HTT gene". Science. 301 (5631): 386–89. Bibcode:2003Sci...301..386C. doi:10.1126/science.1083968. PMID 12869766. S2CID 146500484.
- Haeffel GJ, Getchell M, Koposov RA, Yrigollen CM, Deyoung CG, Klinteberg BA, Oreland L, Ruchkin VV, Grigorenko EL (January 2008). "Association between polymorphisms in the dopamine transporter gene and depression: evidence for a gene-environment interaction in a sample of juvenile detainees" (PDF). Psychological Science. 19 (1): 62–69. doi:10.1111/j.1467-9280.2008.02047.x. PMID 18181793. S2CID 15520723. Archived (PDF) from the original on 17 December 2008.
- Slavich GM (2004). "Deconstructing depression: A diathesis-stress perspective (Opinion)". APS Observer. Archived from the original on 11 May 2011. Retrieved 11 November 2008.
- Saveanu RV, Nemeroff CB (March 2012). "Etiology of depression: genetic and environmental factors". The Psychiatric Clinics of North America. 35 (1): 51–71. doi:10.1016/j.psc.2011.12.001. PMID 22370490.
- Sullivan PF, Neale MC, Kendler KS (October 2000). "Genetic epidemiology of major depression: review and meta-analysis". The American Journal of Psychiatry. 157 (10): 1552–62. doi:10.1176/appi.ajp.157.10.1552. PMID 11007705.
- Wray, NR (May 2018). "Genome-wide association analyses identify 44 risk variants and refine the genetic architecture of major depression". Nature Genetics. 50 (5): 668–681. doi:10.1038/s41588-018-0090-3. hdl:11370/3a0e2468-99e7-40c3-80f4-9d25adfae485. PMC 5934326. PMID 29700475.
- Howard DM, Adams MJ, Clarke TK, Hafferty JD, Gibson J, Shirali M, et al. (March 2019). "Genome-wide meta-analysis of depression identifies 102 independent variants and highlights the importance of the prefrontal brain regions". Nature Neuroscience. 22 (3): 343–352. doi:10.1038/s41593-018-0326-7. PMC 6522363. PMID 30718901.[needs update]
- Duncan LE, Keller MC (October 2011). "A critical review of the first 10 years of candidate gene-by-environment interaction research in psychiatry". The American Journal of Psychiatry. 168 (10): 1041–9. doi:10.1176/appi.ajp.2011.11020191. PMC 3222234. PMID 21890791.
- Peyrot WJ, Van der Auwera S, Milaneschi Y, Dolan CV, Madden PA, Sullivan PF, Strohmaier J, Ripke S, Rietschel M, Nivard MG, Mullins N, Montgomery GW, Henders AK, Heat AC, Fisher HL, Dunn EC, Byrne EM, et al. (July 2018). "Does Childhood Trauma Moderate Polygenic Risk for Depression? A Meta-analysis of 5765 Subjects From the Psychiatric Genomics Consortium". Biological Psychiatry. 84 (2): 138–147. doi:10.1016/j.biopsych.2017.09.009. PMC 5862738. PMID 29129318.
- Simon GE (November 2001). "Treating depression in patients with chronic disease: recognition and treatment are crucial; depression worsens the course of a chronic illness". The Western Journal of Medicine. 175 (5): 292–93. doi:10.1136/ewjm.175.5.292. PMC 1071593. PMID 11694462.
- Clayton PJ, Lewis CE (March 1981). "The significance of secondary depression". Journal of Affective Disorders. 3 (1): 25–35. doi:10.1016/0165-0327(81)90016-1. PMID 6455456.
- Kewalramani A, Bollinger ME, Postolache TT (1 January 2008). "Asthma and Mood Disorders". International Journal of Child Health and Human Development. 1 (2): 115–23. PMC 2631932. PMID 19180246.
- Rogers D, Pies R (December 2008). "General medical with depression drugs associated". Psychiatry. 5 (12): 28–41. PMC 2729620. PMID 19724774.
- Botts S, Ryan M. Drug-Induced Diseases Section IV: Drug-Induced Psychiatric Diseases Chapter 18: Depression. pp. 1–23. Archived from the original on 23 December 2010.
- Brook DW, Brook JS, Zhang C, Cohen P, Whiteman M (November 2002). "Drug use and the risk of major depressive disorder, alcohol dependence, and substance use disorders". Archives of General Psychiatry. 59 (11): 1039–44. doi:10.1001/archpsyc.59.11.1039. PMID 12418937.
- Meltzer-Brody S (9 January 2017). "New insights into perinatal depression: pathogenesis and treatment during pregnancy and postpartum". Dialogues in Clinical Neuroscience. 13 (1): 89–100. PMC 3181972. PMID 21485749.
- Melrose S (1 January 2015). "Seasonal Affective Disorder: An Overview of Assessment and Treatment Approaches". Depression Research and Treatment. 2015: 178564. doi:10.1155/2015/178564. PMC 4673349. PMID 26688752.
- Wu, Yanjun; Zhang, Liming; Li, Suyun; Zhang, Dongfeng (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). doi:10.1093/nutrit/nuab014. ISSN 0029-6643. PMID 33912967.
- 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.
- Delgado PL, Moreno FA (2000). "Role of norepinephrine in depression". The Journal of Clinical Psychiatry. 61 Suppl 1: 5–12. PMID 10703757.
- Savitz JB, Drevets WC (April 2013). "Neuroreceptor imaging in depression". Neurobiology of Disease. 52: 49–65. doi:10.1016/j.nbd.2012.06.001. PMID 22691454.
- Hasler G (October 2010). "Pathophysiology of depression: do we have any solid evidence of interest to clinicians?". World Psychiatry. 9 (3): 155–61. doi:10.1002/j.2051-5545.2010.tb00298.x. PMC 2950973. PMID 20975857.
- Dunlop BW, Nemeroff CB (March 2007). "The role of dopamine in the pathophysiology of depression". Archives of General Psychiatry. 64 (3): 327–37. doi:10.1001/archpsyc.64.3.327. PMID 17339521.
- Meyer JH, Ginovart N, Boovariwala A, Sagrati S, Hussey D, Garcia A, Young T, Praschak-Rieder N, Wilson AA, Houle S (November 2006). "Elevated monoamine oxidase a levels in the brain: an explanation for the monoamine imbalance of major depression". Archives of General Psychiatry. 63 (11): 1209–16. doi:10.1001/archpsyc.63.11.1209. PMID 17088501.
- Davis KL, Charney D, Coyle JT, Nemeroff C, eds. (2002). Neuropsychopharmacology: the fifth generation of progress: an official publication of the American College of Neuropsychopharmacology (5th ed.). Philadelphia: Lippincott Williams & Wilkins. pp. 1139–63. ISBN 978-0-7817-2837-9.
- Adell A (April 2015). "Revisiting the role of raphe and serotonin in neuropsychiatric disorders". The Journal of General Physiology. 145 (4): 257–59. doi:10.1085/jgp.201511389. PMC 4380212. PMID 25825168.
- Andrews PW, Bharwani A, Lee KR, Fox M, Thomson JA (April 2015). "Is serotonin an upper or a downer? The evolution of the serotonergic system and its role in depression and the antidepressant response". Neuroscience and Biobehavioral Reviews. 51: 164–88. doi:10.1016/j.neubiorev.2015.01.018. PMID 25625874. S2CID 23980182.
- Lacasse JR, Leo J (December 2005). "Serotonin and depression: a disconnect between the advertisements and the scientific literature". PLOS Medicine. 2 (12): e392. doi:10.1371/journal.pmed.0020392. PMC 1277931. PMID 16268734.
- Krishnadas R, Cavanagh J (May 2012). "Depression: an inflammatory illness?". Journal of Neurology, Neurosurgery, and Psychiatry. 83 (5): 495–502. doi:10.1136/jnnp-2011-301779. PMID 22423117.
- Patel A (September 2013). "Review: the role of inflammation in depression". Psychiatria Danubina. 25 Suppl 2: S216–23. PMID 23995180.
- Dowlati Y, Herrmann N, Swardfager W, Liu H, Sham L, Reim EK, 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.
- 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.
- Raedler TJ (November 2011). "Inflammatory mechanisms in major depressive disorder". Current Opinion in Psychiatry. 24 (6): 519–25. doi:10.1097/YCO.0b013e32834b9db6. PMID 21897249. S2CID 24215407.
- Arana GW, Baldessarini RJ, Ornsteen M (December 1985). "The dexamethasone suppression test for diagnosis and prognosis in psychiatry. Commentary and review". Archives of General Psychiatry. 42 (12): 1193–204. doi:10.1001/archpsyc.1985.01790350067012. PMID 3000317.
- Arana GW, Baldessarini RJ, Ornsteen M (1985). "The dexamethasone suppression test for diagnosis and prognosis in psychiatry. Commentary and review". Archives of General Psychiatry. 42 (12): 1193–1204. doi:10.1001/archpsyc.1985.01790350067012. PMID 3000317.
- Varghese FP, Brown ES (August 2001). "The Hypothalamic-Pituitary-Adrenal Axis in Major Depressive Disorder: A Brief Primer for Primary Care Physicians". Primary Care Companion to the Journal of Clinical Psychiatry. 3 (4): 151–55. doi:10.4088/pcc.v03n0401. PMC 181180. PMID 15014598.
- Lopez-Duran NL, Kovacs M, George CJ (2009). "Hypothalamic-pituitary-adrenal axis dysregulation in depressed children and adolescents: a meta-analysis". Psychoneuroendocrinology. 34 (9): 1272–1283. doi:10.1016/j.psyneuen.2009.03.016. PMC 2796553. PMID 19406581.
- Dedovic K, Ngiam J (2015). "The cortisol awakening response and major depression: examining the evidence". Neuropsychiatric Disease and Treatment. 11: 1181–1189. doi:10.2147/NDT.S62289. PMC 4437603. PMID 25999722.
- Mayberg HS (1997). "Limbic-cortical dysregulation: a proposed model of depression". The Journal of Neuropsychiatry and Clinical Neurosciences. 9 (3): 471–81. doi:10.1176/jnp.9.3.471. PMID 9276848.
- Graham J, Salimi-Khorshidi G, Hagan C, Walsh N, Goodyer I, Lennox B, Suckling J (2013). "Meta-analytic evidence for neuroimaging models of depression: state or trait?". Journal of Affective Disorders. 151 (2): 423–431. doi:10.1016/j.jad.2013.07.002. PMID 23890584.
- Hamilton JP, Etkin A, Furman DJ, Lemus MG, Johnson RF, Gotlib IH (July 2012). "Functional neuroimaging of major depressive disorder: a meta-analysis and new integration of base line activation and neural response data". The American Journal of Psychiatry. 169 (7): 693–703. doi:10.1176/appi.ajp.2012.11071105. PMID 22535198.
- Kaufmann IM (1993). "Rural psychiatric services. A collaborative model". Canadian Family Physician. 39: 1957–1961. PMC 2379905. PMID 8219844.
- "Call for action over Third World depression". BBC News (Health). British Broadcasting Corporation (BBC). 1 November 1999. Archived from the original on 13 May 2008. Retrieved 11 October 2008.
- Sharp LK, Lipsky MS (September 2002). "Screening for depression across the lifespan: a review of measures for use in primary care settings". American Family Physician. 66 (6): 1001–08. PMID 12358212.
- Zimmerman M, Chelminski I, Posternak M (September 2004). "A review of studies of the Hamilton depression rating scale in healthy controls: implications for the definition of remission in treatment studies of depression". The Journal of Nervous and Mental Disease. 192 (9): 595–601. doi:10.1097/01.nmd.0000138226.22761.39. PMID 15348975. S2CID 24291799.
- McPherson A, Martin CR (February 2010). "A narrative review of the Beck Depression Inventory (BDI) and implications for its use in an alcohol-dependent population". Journal of Psychiatric and Mental Health Nursing. 17 (1): 19–30. doi:10.1111/j.1365-2850.2009.01469.x. PMID 20100303.
- Osman A, Bagge CL, Gutierrez PM, Konick LC, Kopper BA, Barrios FX (December 2001). "The Suicidal Behaviors Questionnaire-Revised (SBQ-R): validation with clinical and nonclinical samples". Assessment. 8 (4): 443–54. doi:10.1177/107319110100800409. PMID 11785588. S2CID 11477277.
- Cepoiu M, McCusker J, Cole MG, Sewitch M, Belzile E, Ciampi A (January 2008). "Recognition of depression by non-psychiatric physicians—a systematic literature review and meta-analysis". Journal of General Internal Medicine. 23 (1): 25–36. doi:10.1007/s11606-007-0428-5. PMC 2173927. PMID 17968628.
- Dale J, Sorour E, Milner G (2008). "Do psychiatrists perform appropriate physical investigations for their patients? A review of current practices in a general psychiatric inpatient and outpatient setting". Journal of Mental Health. 17 (3): 293–98. doi:10.1080/09638230701498325. S2CID 72755878.
- Orengo CA, Fullerton G, Tan R (October 2004). "Male depression: a review of gender concerns and testosterone therapy". Geriatrics. 59 (10): 24–30. PMID 15508552.
- Parker GB, Brotchie H, Graham RK (January 2017). "Vitamin D and depression". Journal of Affective Disorders. 208: 56–61. doi:10.1016/j.jad.2016.08.082. PMID 27750060.
- Reid LM, Maclullich AM (2006). "Subjective memory complaints and cognitive impairment in older people". Dementia and Geriatric Cognitive Disorders. 22 (5–6): 471–85. doi:10.1159/000096295. PMID 17047326. S2CID 9328852.
- Katz IR (1998). "Diagnosis and treatment of depression in patients with Alzheimer's disease and other dementias". The Journal of Clinical Psychiatry. 59 Suppl 9: 38–44. PMID 9720486.
- Wright SL, Persad C (December 2007). "Distinguishing between depression and dementia in older persons: neuropsychological and neuropathological correlates". Journal of Geriatric Psychiatry and Neurology. 20 (4): 189–98. doi:10.1177/0891988707308801. PMID 18004006. S2CID 33714179.
- Sadock 2002, p. 108
- Sadock 2002, p. 260
- "Mental and behavioural disorders: Mood [affective] disorders". World Health Organization. 2010. Archived from the original on 2 November 2014. Retrieved 8 November 2008.
- Sadock 2002, p. 288
- American Psychiatric Association 2013, p. xii.
- Gruenberg AM, Goldstein RD, Pincus HA (2005). "Classification of Depression: Research and Diagnostic Criteria: DSM-IV and ICD-10" (PDF). Biology of Depression. Biology of Depression: From Novel Insights to Therapeutic Strategies (eds J. Licinio and M-L Wong). Wiley-VCH Verlag GmbH. pp. 1–12. doi:10.1002/9783527619672.ch1. ISBN 978-3-527-61967-2. Retrieved 30 October 2008.
- "The ICD-10 Classification of Mental and Behavioural Disorders: Clinical descriptions and diagnostic guidelines" (PDF). World Health Organization. 2010. Archived (PDF) from the original on 23 March 2014. Retrieved 12 November 2014.
- The ICD-10 classification of mental and behavioral disorders. Clinical description and diagnostic guideline. Geneva: World Health Organization, 1992
- "Diagnostic Criteria for Major Depressive Disorder and Depressive Episodes" (PDF). City of Palo Alto Project Safety Net.
- Parker, George F. (1 June 2014). "DSM-5 and Psychotic and Mood Disorders". Journal of the American Academy of Psychiatry and the Law Online. 42 (2): 182–190. ISSN 1093-6793. PMID 24986345.
- American Psychiatric Association 2013, p. 162
- Parker 1996, p. 173
- Sadock 2002, p. 552
- American Psychiatric Association 2013, p. 183.
- Carta MG, Altamura AC, Hardoy MC, Pinna F, Medda S, Dell'Osso L, Carpiniello B, Angst J (June 2003). "Is recurrent brief depression an expression of mood spectrum disorders in young people? Results of a large community sample". European Archives of Psychiatry and Clinical Neuroscience. 253 (3): 149–53. doi:10.1007/s00406-003-0418-5. hdl:2434/521599. PMID 12904979. S2CID 26860606.
- Rapaport MH, Judd LL, Schettler PJ, Yonkers KA, Thase ME, Kupfer DJ, Frank E, Plewes JM, Tollefson GD, Rush AJ (April 2002). "A descriptive analysis of minor depression". The American Journal of Psychiatry. 159 (4): 637–43. doi:10.1176/appi.ajp.159.4.637. PMID 11925303.
- American Psychiatric Association 2013, p. 168.
- American Psychiatric Association 2013, p. 185.
- American Psychiatric Association 2013, pp. 185–186.
- American Psychiatric Association 2013, pp. 119–120.
- American Psychiatric Association 2013, p. 186-187.
- American Psychiatric Association 2013, p. 187.
- Akiskal HS, Benazzi F (May 2006). "The DSM-IV and ICD-10 categories of recurrent [major] depressive and bipolar II disorders: evidence that they lie on a dimensional spectrum". Journal of Affective Disorders. 92 (1): 45–54. doi:10.1016/j.jad.2005.12.035. PMID 16488021.
- American_Psychiatric_Association 2013, p. 167.
- Cuijpers P, van Straten A, Smit F, Mihalopoulos C, Beekman A (October 2008). "Preventing the onset of depressive disorders: a meta-analytic review of psychological interventions". The American Journal of Psychiatry. 165 (10): 1272–80. doi:10.1176/appi.ajp.2008.07091422. hdl:1871/16952. PMID 18765483.
- Siu AL, Bibbins-Domingo K, Grossman DC, Baumann LC, Davidson KW, Ebell M, García FA, Gillman M, Herzstein J, Kemper AR, Krist AH, Kurth AE, Owens DK, Phillips WR, Phipps MG, Pignone MP (January 2016). "Screening for Depression in Adults: US Preventive Services Task Force Recommendation Statement". JAMA. 315 (4): 380–87. doi:10.1001/jama.2015.18392. PMID 26813211.
- Siu AL (March 2016). "Screening for Depression in Children and Adolescents: U.S. Preventive Services Task Force Recommendation Statement". Annals of Internal Medicine. 164 (5): 360–66. doi:10.7326/M15-2957. PMID 26858097.
- Gilbody S, House AO, Sheldon TA (October 2005). "Screening and case finding instruments for depression". The Cochrane Database of Systematic Reviews (4): CD002792. doi:10.1002/14651858.CD002792.pub2. PMC 6769050. PMID 16235301.
- Ferenchick EK, Ramanuj P, Pincus HA (2019). "Depression in primary care: part 1—screening and diagnosis". British Medical Journal. 365: l794. doi:10.1136/bmj.l794. PMID 30962184. S2CID 104296515.
- 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.
- Cuijpers, P (20 September 2012). Prevention and early treatment of mental ill-health (PDF). PSYCHOLOGY FOR HEALTH: Contributions to Policy Making, Brussels. Archived from the original (PDF) on 12 May 2013. Retrieved 16 June 2013.
- Griffiths KM, Farrer L, Christensen H (2010). "The efficacy of internet interventions for depression and anxiety disorders: a review of randomised controlled trials" (PDF). Medical Journal of Australia. 192 (11): 4–11. doi:10.5694/j.1326-5377.2010.tb03685.x. PMID 20528707. S2CID 1948009. Archived (PDF) from the original on 12 November 2014. Retrieved 12 November 2014.
- Cuijpers P, 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.
- "Depression". National Institute for Health and Care Excellence. December 2004. Archived from the original on 15 November 2008. Retrieved 20 March 2013.
- "Practice guideline for the treatment of patients with major depressive disorder (revision). American Psychiatric Association". The American Journal of Psychiatry. 157 (4 Suppl): 1–45. April 2000. PMID 10767867.; Third edition doi:10.1176/appi.books.9780890423363.48690
- Archer J, Bower P, Gilbody S, Lovell K, Richards D, Gask L, Dickens C, Coventry P (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.
- 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.
- Cox GR, Callahan P, Churchill R, Hunot V, Merry SN, Parker AG, Hetrick SE (November 2014). "Psychological therapies versus antidepressant medication, alone and in combination for depression in children and adolescents". The Cochrane Database of Systematic Reviews. 2014 (11): CD008324. doi:10.1002/14651858.CD008324.pub3. PMC 8556660. PMID 25433518.
- Josefsson T, Lindwall M, Archer T (April 2014). "Physical exercise intervention in depressive disorders: meta-analysis and systematic review". Scandinavian Journal of Medicine & Science in Sports. 24 (2): 259–72. doi:10.1111/sms.12050. PMID 23362828. S2CID 29351791.
- Bridle C, Spanjers K, Patel S, Atherton NM, Lamb SE (September 2012). "Effect of exercise on depression severity in older people: systematic review and meta-analysis of randomised controlled trials". The British Journal of Psychiatry. 201 (3): 180–85. doi:10.1192/bjp.bp.111.095174. PMID 22945926.
- Lopresti AL, Hood SD, Drummond PD (May 2013). "A review of lifestyle factors that contribute to important pathways associated with major depression: diet, sleep and exercise" (PDF). Journal of Affective Disorders. 148 (1): 12–27. doi:10.1016/j.jad.2013.01.014. PMID 23415826. Archived (PDF) from the original on 9 January 2017.
- Taylor G, McNeill A, Girling A, Farley A, Lindson-Hawley N, Aveyard P (February 2014). "Change in mental health after smoking cessation: systematic review and meta-analysis". BMJ. 348 (feb13 1): g1151. doi:10.1136/bmj.g1151. PMC 3923980. PMID 24524926.
- Khan A, Faucett J, Lichtenberg P, Kirsch I, Brown WA (30 July 2012). "A systematic review of comparative efficacy of treatments and controls for depression". PLOS ONE. 7 (7): e41778. Bibcode:2012PLoSO...741778K. doi:10.1371/journal.pone.0041778. PMC 3408478. PMID 22860015.
- Thase ME (1999). "When are psychotherapy and pharmacotherapy combinations the treatment of choice for major depressive disorder?". The Psychiatric Quarterly. 70 (4): 333–46. doi:10.1023/A:1022042316895. PMID 10587988. S2CID 45091134.
- Cordes J (2013). "Depression". Encyclopedia of Sciences and Religions. pp. 610–16. doi:10.1007/978-1-4020-8265-8_301. ISBN 978-1-4020-8264-1.
- Ijaz S, Davies P, Williams CJ, Kessler D, Lewis G, Wiles N (May 2018). "Psychological therapies for treatment-resistant depression in adults". The Cochrane Database of Systematic Reviews. 5 (8): CD010558. doi:10.1002/14651858.CD010558.pub2. PMC 6494651. PMID 29761488.
- Wilson KC, Mottram PG, Vassilas CA (January 2008). "Psychotherapeutic treatments for older depressed people". The Cochrane Database of Systematic Reviews. 23 (1): CD004853. doi:10.1002/14651858.CD004853.pub2. PMID 18254062.
- Cuijpers P, van Straten A, Smit F (December 2006). "Psychological treatment of late-life depression: a meta-analysis of randomized controlled trials". International Journal of Geriatric Psychiatry. 21 (12): 1139–49. doi:10.1002/gps.1620. hdl:1871/16894. PMID 16955421. S2CID 14778731.
- Gartlehner G, Wagner G, Matyas N, et al. (June 2017). "Pharmacological and non-pharmacological treatments for major depressive disorder: review of systematic reviews". BMJ Open. 7 (6): e014912. doi:10.1136/bmjopen-2016-014912. PMC 5623437. PMID 28615268.
- Childhood Depression. abct.org. Last updated: 30 July 2010
- NICE (2005). NICE guidelines: Depression in children and adolescents. London: NICE. p. 5. ISBN 978-1-84629-074-9. Archived from the original on 24 September 2008. Retrieved 16 August 2008.
- Becker SJ (2008). "Cognitive-Behavioral Therapy for Adolescent Depression: Processes of Cognitive Change". Psychiatric Times. 25 (14).
- Almeida AM, Lotufo Neto F (October 2003). "[Cognitive-behavioral therapy in prevention of depression relapses and recurrences: a review]". Revista Brasileira de Psiquiatria. 25 (4): 239–44. doi:10.1590/S1516-44462003000400011. PMID 15328551.
- Paykel ES (February 2007). "Cognitive therapy in relapse prevention in depression". The International Journal of Neuropsychopharmacology. 10 (1): 131–36. doi:10.1017/S1461145706006912. PMID 16787553.
- Nieuwenhuijsen K, Verbeek JH, Neumeyer-Gromen A, Verhoeven AC, Bültmann U, Faber B (October 2020). "Interventions to improve return to work in depressed people". Cochrane Database Syst Rev. 10 (12): CD006237. doi:10.1002/14651858.CD006237.pub4. PMC 8094165. PMID 33052607.
- Beck 1987, p. 10
- Coelho HF, Canter PH, Ernst E (December 2007). "Mindfulness-based cognitive therapy: evaluating current evidence and informing future research". Journal of Consulting and Clinical Psychology. 75 (6): 1000–05. doi:10.1037/0022-006X.75.6.1000. PMID 18085916.
- Khoury B, Lecomte T, Fortin G, Masse M, Therien P, Bouchard V, Chapleau MA, Paquin K, Hofmann SG (August 2013). "Mindfulness-based therapy: a comprehensive meta-analysis". Clinical Psychology Review. 33 (6): 763–71. doi:10.1016/j.cpr.2013.05.005. PMID 23796855.
- Jain FA, Walsh RN, Eisendrath SJ, Christensen S, Rael Cahn B (2014). "Critical analysis of the efficacy of meditation therapies for acute and subacute phase treatment of depressive disorders: a systematic review". Psychosomatics. 56 (2): 140–52. doi:10.1016/j.psym.2014.10.007. PMC 4383597. PMID 25591492.
- Simkin DR, Black NB (July 2014). "Meditation and mindfulness in clinical practice". Child and Adolescent Psychiatric Clinics of North America. 23 (3): 487–534. doi:10.1016/j.chc.2014.03.002. PMID 24975623.
- Dworetzky J (1997). Psychology. Pacific Grove, CA: Brooks/Cole Pub. Co. p. 602. ISBN 978-0-314-20412-7.
- Doidge N, Simon B, Lancee WJ, First M, Brunshaw J, Brauer L, Grant DC, Stevens A, Oldham JM, Mosher P (2002). "Psychoanalytic patients in the U.S., Canada, and Australia: II. A DSM-III-R validation study". Journal of the American Psychoanalytic Association. 50 (2): 615–27. doi:10.1177/00030651020500021101. PMID 12206545. S2CID 25110425.
- Barlow 2005, p. 20
- de Maat S, Dekker J, Schoevers R, van Aalst G, Gijsbers-van Wijk C, Hendriksen M, Kool S, Peen J, Van R, de Jonghe F (2007). "Short psychodynamic supportive psychotherapy, antidepressants, and their combination in the treatment of major depression: a mega-analysis based on three randomized clinical trials". Depression and Anxiety. 25 (7): 565–74. doi:10.1002/da.20305. PMID 17557313. S2CID 20373635.
- Iglesias-González M, Aznar-Lou I, Gil-Girbau M, Moreno-Peral P, Peñarrubia-María MT, Rubio-Valera M, Serrano-Blanco A (November 2017). "Comparing watchful waiting with antidepressants for the management of subclinical depression symptoms to mild-moderate depression in primary care: a systematic review". Family Practice. 34 (6): 639–48. doi:10.1093/fampra/cmx054. PMID 28985309.
- "The treatment and management of depression in adults". NICE. October 2009. Archived from the original on 12 November 2014. Retrieved 12 November 2014.
- Leucht C, Huhn M, Leucht S (December 2012). Leucht C (ed.). "Amitriptyline versus placebo for major depressive disorder". The Cochrane Database of Systematic Reviews. 12: CD009138. doi:10.1002/14651858.CD009138.pub2. PMID 23235671.
- de Vries YA, Roest AM, Bos EH, Burgerhof JG, van Loo HM, de Jonge P (January 2019). "Predicting antidepressant response by monitoring early improvement of individual symptoms of depression: individual patient data meta-analysis". The British Journal of Psychiatry. 214 (1): 4–10. doi:10.1192/bjp.2018.122. PMC 7557872. PMID 29952277.
- Thase ME (December 2006). "Preventing relapse and recurrence of depression: a brief review of therapeutic options". CNS Spectrums. 11 (12 Suppl 15): 12–21. doi:10.1017/S1092852900015212. PMID 17146414. S2CID 2347144.
- Royal Pharmaceutical Society of Great Britain 2008, p. 204
- Whooley MA, Simon GE (December 2000). "Managing depression in medical outpatients". The New England Journal of Medicine. 343 (26): 1942–50. doi:10.1056/NEJM200012283432607. PMID 11136266.
- Zisook S, Rush AJ, Haight BR, Clines DC, Rockett CB (February 2006). "Use of bupropion in combination with serotonin reuptake inhibitors". Biological Psychiatry. 59 (3): 203–10. doi:10.1016/j.biopsych.2005.06.027. PMID 16165100. S2CID 20997303.
- Papakostas GI, Thase ME, Fava M, Nelson JC, Shelton RC (December 2007). "Are antidepressant drugs that combine serotonergic and noradrenergic mechanisms of action more effective than the selective serotonin reuptake inhibitors in treating major depressive disorder? A meta-analysis of studies of newer agents". Biological Psychiatry. 62 (11): 1217–27. doi:10.1016/j.biopsych.2007.03.027. PMID 17588546. S2CID 45621773.
- Gordon Duff (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.
- "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.
- Mayers AG, Baldwin DS (December 2005). "Antidepressants and their effect on sleep". Human Psychopharmacology. 20 (8): 533–59. doi:10.1002/hup.726. PMID 16229049. S2CID 17912673.
- Cipriani A, Zhou X, Del Giovane C, Hetrick SE, Qin B, Whittington C, Coghill D, Zhang Y, Hazell P, Leucht S, Cuijpers P, Pu J, Cohen D, Ravindran AV, Liu Y, Michael KD, Yang L, Liu L, Xie P (August 2016). "Comparative efficacy and tolerability of antidepressants for major depressive disorder in children and adolescents: a network meta-analysis". Lancet. 388 (10047): 881–90. doi:10.1016/S0140-6736(16)30385-3. PMID 27289172. S2CID 19728203.
- Tsapakis EM, Soldani F, Tondo L, Baldessarini RJ (July 2008). "Efficacy of antidepressants in juvenile depression: meta-analysis". The British Journal of Psychiatry. 193 (1): 10–17. doi:10.1192/bjp.bp.106.031088. PMID 18700212.
- Cheung AH, Zuckerbrot RA, Jensen PS, Laraque D, Stein RE (February 2018). "Guidelines for Adolescent Depression in Primary Care (GLAD-PC): Part II. Treatment and Ongoing Management". Pediatrics. 141 (3): e20174082. doi:10.1542/peds.2017-4082. PMID 29483201.
- Nelson JC, Devanand DP (April 2011). "A systematic review and meta-analysis of placebo-controlled antidepressant studies in people with depression and dementia". Journal of the American Geriatrics Society. 59 (4): 577–85. doi:10.1111/j.1532-5415.2011.03355.x. PMID 21453380. S2CID 2592434.
- Palmer BF, Gates JR, Lader M (November 2003). "Causes and management of hyponatremia". The Annals of Pharmacotherapy. 37 (11): 1694–702. doi:10.1345/aph.1D105. PMID 14565794. S2CID 37965495.
- Guaiana G, Barbui C, Hotopf M (July 2007). "Amitriptyline for depression". The Cochrane Database of Systematic Reviews. 18 (3): CD004186. doi:10.1002/14651858.CD004186.pub2. PMID 17636748.
- Anderson IM (April 2000). "Selective serotonin reuptake inhibitors versus tricyclic antidepressants: a meta-analysis of efficacy and tolerability". Journal of Affective Disorders. 58 (1): 19–36. doi:10.1016/S0165-0327(99)00092-0. PMID 10760555.
- Krishnan KR (2007). "Revisiting monoamine oxidase inhibitors". The Journal of Clinical Psychiatry. 68 Suppl 8: 35–41. PMID 17640156.
- Bonnet U (2003). "Moclobemide: therapeutic use and clinical studies". CNS Drug Reviews. 9 (1): 97–140. doi:10.1111/j.1527-3458.2003.tb00245.x. PMC 6741704. PMID 12595913.
- Braun C, Bschor T, Franklin J, Baethge C (2016). "Suicides and Suicide Attempts during Long-Term Treatment with Antidepressants: A Meta-Analysis of 29 Placebo-Controlled Studies Including 6,934 Patients with Major Depressive Disorder". Psychotherapy and Psychosomatics. 85 (3): 171–79. doi:10.1159/000442293. PMID 27043848. S2CID 40682753.
- Hammad TA (16 August 2004). "Review and evaluation of clinical data. Relationship between psychiatric drugs and pediatric suicidality" (PDF). FDA. pp. 42, 115. Archived (PDF) from the original on 25 June 2008. Retrieved 29 May 2008.
- Hetrick SE, McKenzie JE, Cox GR, Simmons MB, Merry SN (November 2012). "Newer generation antidepressants for depressive disorders in children and adolescents". The Cochrane Database of Systematic Reviews. 11 (9): CD004851. doi:10.1002/14651858.CD004851.pub3. hdl:11343/59246. PMID 23152227.
- Gunnell D, Saperia J, Ashby D (February 2005). "Selective serotonin reuptake inhibitors (SSRIs) and suicide in adults: meta-analysis of drug company data from placebo controlled, randomised controlled trials submitted to the MHRA's safety review". BMJ. 330 (7488): 385. doi:10.1136/bmj.330.7488.385. PMC 549105. PMID 15718537.
- Fergusson D, Doucette S, Glass KC, Shapiro S, Healy D, Hebert P, Hutton B (February 2005). "Association between suicide attempts and selective serotonin reuptake inhibitors: systematic review of randomised controlled trials". BMJ. 330 (7488): 396. doi:10.1136/bmj.330.7488.396. PMC 549110. PMID 15718539.
- Stone M, Laughren T, Jones ML, Levenson M, Holland PC, Hughes A, Hammad TA, Temple R, Rochester G (August 2009). "Risk of suicidality in clinical trials of antidepressants in adults: analysis of proprietary data submitted to US Food and Drug Administration". BMJ. 339: b2880. doi:10.1136/bmj.b2880. PMC 2725270. PMID 19671933.
- "FDA Proposes New Warnings About Suicidal Thinking, Behavior in Young Adults Who Take Antidepressant Medications". FDA. 2 May 2007. Archived from the original on 23 February 2008. Retrieved 29 May 2008.
- Medics and Foods Department. Pharmaceuticals and Medical Devices Safety Information (PDF) (Report). 261 (in Japanese). Ministry of Health, Labour and Welfare (Japan). Archived from the original (PDF) on 29 April 2011. Retrieved 19 May 2010.
- Ogawa Y, Takeshima N, Hayasaka Y, Tajika A, Watanabe N, Streiner D, Furukawa TA (June 2019). "Antidepressants plus benzodiazepines for adults with major depression". The Cochrane Database of Systematic Reviews. 6: CD001026. doi:10.1002/14651858.CD001026.pub2. PMC 6546439. PMID 31158298.
- Hallahan B, Ryan T, Hibbeln JR, Murray IT, Glynn S, Ramsden CE, SanGiovanni JP, Davis JM (September 2016). "Efficacy of omega-3 highly unsaturated fatty acids in the treatment of depression". The British Journal of Psychiatry. 209 (3): 192–201. doi:10.1192/bjp.bp.114.160242. PMID 27103682.
- Appleton KM, Sallis HM, Perry R, Ness AR, Churchill R (November 2015). "Omega-3 fatty acids for depression in adults". The Cochrane Database of Systematic Reviews (11): CD004692. doi:10.1002/14651858.cd004692.pub4. PMC 5321518. PMID 26537796.
- Müller N, Myint AM, Schwarz MJ (February 2011). "Inflammatory biomarkers and depression". Neurotoxicity Research. 19 (2): 308–18. doi:10.1007/s12640-010-9210-2. PMID 20658274. S2CID 3225744.
- Cipriani A, Hawton K, Stockton S, Geddes JR (June 2013). "Lithium in the prevention of suicide in mood disorders: updated systematic review and meta-analysis". BMJ. 346 (jun27 4): f3646. doi:10.1136/bmj.f3646. PMID 23814104.
- Nolen-Hoeksema, Susan. (2014) "Treatment of Mood Disorders". In (6th ed.) Abnormal Psychology p. 196. New York: McGraw-Hill. ISBN 978-0-07-803538-8.
- Gelenberg AJ, Freeman MP, Markowitz JC. "Practice Guideline for the Treatment of Patients with Major Depressive Disorder" (PDF) (3rd ed.). American Psychiatric Association (APA). Retrieved 3 November 2014.
- Corp SA, Gitlin MJ, Altshuler LL (September 2014). "A review of the use of stimulants and stimulant alternatives in treating bipolar depression and major depressive disorder". The Journal of Clinical Psychiatry. 75 (9): 1010–18. doi:10.4088/JCP.13r08851. PMID 25295426.
- Malhi GS, Byrow Y, Bassett D, Boyce P, Hopwood M, Lyndon W, Mulder R, Porter R, Singh A, Murray G (March 2016). "Stimulants for depression: On the up and up?". The Australian and New Zealand Journal of Psychiatry. 50 (3): 203–07. doi:10.1177/0004867416634208. PMID 26906078. S2CID 45341424.
- Taylor MJ, Carney S, Geddes J, Goodwin G (2003). "Folate for depressive disorders". The Cochrane Database of Systematic Reviews (2): CD003390. doi:10.1002/14651858.CD003390. PMC 6991158. PMID 12804463.
- Walther A, Breidenstein J, Miller R (January 2019). "Association of Testosterone Treatment With Alleviation of Depressive Symptoms in Men: A Systematic Review and Meta-analysis". JAMA Psychiatry. 76 (1): 31–40. doi:10.1001/jamapsychiatry.2018.2734. PMC 6583468. PMID 30427999.
- Rudorfer, MV, Henry, ME, Sackeim, HA (2003). "Electroconvulsive therapy". In A Tasman, J Kay, JA Lieberman (eds) Psychiatry, Second Edition. Chichester: John Wiley & Sons Ltd, 1865–1901.
- Beloucif S (April 2013). "Informed consent for special procedures: electroconvulsive therapy and psychosurgery". Current Opinion in Anesthesiology. 26 (2): 182–85. doi:10.1097/ACO.0b013e32835e7380. PMID 23385317. S2CID 36643014.
- FDA. FDA Executive Summary Archived 24 September 2015 at the Wayback Machine. Prepared for the 27–28 January 2011 meeting of the Neurological Devices Panel Meeting to Discuss the Classification of Electroconvulsive Therapy Devices (ECT). Quote, p38: "Three major practice guidelines have been published on ECT. These guidelines include: APA Task Force on ECT (2001); Third report of the Royal College of Psychiatrists' Special Committee on ECT (2004); National Institute for Health and Clinical Excellence (NICE 2003; NICE 2009). There is significant agreement between the three sets of recommendations."
- Dierckx B, Heijnen WT, van den Broek WW, 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.
- Jelovac A, Kolshus E, McLoughlin DM (November 2013). "Relapse following successful electroconvulsive therapy for major depression: a meta-analysis". Neuropsychopharmacology. 38 (12): 2467–74. doi:10.1038/npp.2013.149. PMC 3799066. PMID 23774532.
- Surgeon General (1999). Mental Health: A Report of the Surgeon General Archived 12 January 2007 at the Wayback Machine, chapter 4.
- Committee on Electroconvulsive Therapy (2001). The practice of electroconvulsive therapy: recommendations for treatment, training, and privileging (2nd ed.). Washington, DC: American Psychiatric Publishing. American Psychiatric Association. ISBN 978-0-89042-206-9.
- Pompili M, Dominici G, Giordano G, Longo L, Serafini G, Lester D, Amore M, Girardi P (December 2014). "Electroconvulsive treatment during pregnancy: a systematic review". Expert Review of Neurotherapeutics. 14 (12): 1377–90. doi:10.1586/14737175.2014.972373. PMID 25346216. S2CID 31209001.
- "5 Outdated Beliefs About ECT". Psych Central.com. 17 May 2016. Archived from the original on 8 August 2013.
- Abbott CC, Gallegos P, Rediske N, Lemke NT, Quinn DK (March 2014). "A review of longitudinal electroconvulsive therapy: neuroimaging investigations". Journal of Geriatric Psychiatry and Neurology. 27 (1): 33–46. doi:10.1177/0891988713516542. PMC 6624835. PMID 24381234.
- "NiCE. January 2014 Transcranial magnetic stimulation for treating and preventing migraine". Archived from the original on 4 October 2015.
- "Melkerson, MN (2008-12-16). "Special Premarket 510(k) Notification for NeuroStar® TMS Therapy System for Major Depressive Disorder" (pdf). Food and Drug Administration. Retrieved 2010-07-16" (PDF). Archived (PDF) from the original on 31 March 2010.
- Lefaucheur JP, André-Obadia N, Antal A, Ayache SS, Baeken C, Benninger DH, Cantello RM, Cincotta M, de Carvalho M, De Ridder D, Devanne H, Di Lazzaro V, Filipović SR, Hummel FC, Jääskeläinen SK, Kimiskidis VK, Koch G, Langguth B, Nyffeler T, Oliviero A, Padberg F, Poulet E, Rossi S, Rossini PM, Rothwell JC, Schönfeldt-Lecuona C, Siebner HR, Slotema CW, Stagg CJ, Valls-Sole J, Ziemann U, Paulus W, Garcia-Larrea L (November 2014). "Evidence-based guidelines on the therapeutic use of repetitive transcranial magnetic stimulation (rTMS)". Clinical Neurophysiology. 125 (11): 2150–206. doi:10.1016/j.clinph.2014.05.021. PMID 25034472. S2CID 206798663.
- "American Psychiatric Association (2010). (eds: Gelenberg, AJ, Freeman, MP, Markowitz, JC, Rosenbaum, JF, Thase, ME, Trivedi, MH, Van Rhoads, RS). Practice Guidelines for the Treatment of Patients with Major Depressive Disorder, 3rd Edition" (PDF).
- "Journal of Affective Disorders" (PDF). 2009. pp. S1–S64. Archived from the original (PDF) on 23 August 2015.
- Rush AJ, Marangell LB, Sackeim HA, George MS, Brannan SK, Davis SM, Howland R, Kling MA, Rittberg BR, Burke WJ, Rapaport MH, Zajecka J, Nierenberg AA, Husain MM, Ginsberg D, Cooke RG (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.
- 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.
- Brunoni AR, Moffa AH, Fregni F, et al. (June 2016). "Transcranial direct current stimulation for acute major depressive episodes: meta-analysis of individual patient data". The British Journal of Psychiatry. 208 (6): 522–31. doi:10.1192/bjp.bp.115.164715. PMC 4887722. PMID 27056623.
- Golden RN, Gaynes BN, Ekstrom RD, Hamer RM, Jacobsen FM, Suppes T, Wisner KL, Nemeroff CB (April 2005). "The efficacy of light therapy in the treatment of mood disorders: a review and meta-analysis of the evidence". The American Journal of Psychiatry. 162 (4): 656–62. doi:10.1176/appi.ajp.162.4.656. PMID 15800134.
- Tuunainen A, Kripke DF, Endo T (2004). Tuunainen A (ed.). "Light therapy for non-seasonal depression". The Cochrane Database of Systematic Reviews (2): CD004050. doi:10.1002/14651858.CD004050.pub2. PMC 6669243. PMID 15106233.
- 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.
- Joyce J, Herbison GP (April 2015). "Reiki for depression and anxiety". The Cochrane Database of Systematic Reviews (4): CD006833. doi:10.1002/14651858.cd006833.pub2. PMID 25835541.
- Meekums B, Karkou V, Nelson EA (February 2015). "Dance movement therapy for depression" (PDF). The Cochrane Database of Systematic Reviews (2): CD009895. doi:10.1002/14651858.cd009895.pub2. PMID 25695871.
- Black N, Stockings E, Campbell G, et al. (December 2019). "Cannabinoids for the treatment of mental disorders and symptoms of mental disorders: a systematic review and meta-analysis". The Lancet. Psychiatry. 6 (12): 995–1010. doi:10.1016/S2215-0366(19)30401-8. PMC 6949116. PMID 31672337.
- Fava GA, Park SK, Sonino N (November 2006). "Treatment of recurrent depression". Expert Review of Neurotherapeutics. 6 (11): 1735–40. doi:10.1586/14737220.127.116.115. PMID 17144786. S2CID 22808803.
- 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.
- Eaton WW, Shao H, Nestadt G, Lee HB, Lee BH, Bienvenu OJ, Zandi P (May 2008). "Population-based study of first onset and chronicity in major depressive disorder". Archives of General Psychiatry. 65 (5): 513–20. doi:10.1001/archpsyc.65.5.513. PMC 2761826. PMID 18458203.
- Holma KM, Holma IA, Melartin TK, 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.
- Kanai T, Takeuchi H, Furukawa TA, Yoshimura R, Imaizumi T, Kitamura T, Takahashi K (July 2003). "Time to recurrence after recovery from major depressive episodes and its predictors". Psychological Medicine. 33 (5): 839–45. doi:10.1017/S0033291703007827. PMID 12877398. S2CID 10490348.
- "Depression, Major: Prognosis". MDGuidelines. The Guardian Life Insurance Company of America. Archived from the original on 20 April 2010. Retrieved 16 July 2010.
- Culpepper L, Muskin PR, Stahl SM (September 2015). "Major Depressive Disorder: Understanding the Significance of Residual Symptoms and Balancing Efficacy with Tolerability". The American Journal of Medicine. 128 (9 Suppl): S1–S15. doi:10.1016/j.amjmed.2015.07.001. PMID 26337210.
- Geddes JR, Carney SM, Davies C, Furukawa TA, Kupfer DJ, Frank E, Goodwin GM (February 2003). "Relapse prevention with antidepressant drug treatment in depressive disorders: a systematic review". Lancet. 361 (9358): 653–61. doi:10.1016/S0140-6736(03)12599-8. PMID 12606176. S2CID 20198748.
- Posternak MA, Miller I (October 2001). "Untreated short-term course of major depression: a meta-analysis of outcomes from studies using wait-list control groups". Journal of Affective Disorders. 66 (2–3): 139–46. doi:10.1016/S0165-0327(00)00304-9. PMID 11578666.
- Posternak MA, Solomon DA, Leon AC, Mueller TI, Shea MT, Endicott J, Keller MB (May 2006). "The naturalistic course of unipolar major depression in the absence of somatic therapy". The Journal of Nervous and Mental Disease. 194 (5): 324–29. doi:10.1097/01.nmd.0000217820.33841.53. PMID 16699380. S2CID 22891687.
- Whiteford, H. A.; Harris, M. G.; McKeon, G.; Baxter, A.; Pennell, C.; Barendregt, J. J.; Wang, J. (10 August 2012). "Estimating remission from untreated major depression: a systematic review and meta-analysis". Psychological Medicine. Cambridge University Press (CUP). 43 (8): 1569–1585. doi:10.1017/s0033291712001717. ISSN 0033-2917. PMID 22883473. S2CID 11068930.
- Cassano P, Fava M (October 2002). "Depression and public health: an overview". Journal of Psychosomatic Research. 53 (4): 849–57. doi:10.1016/S0022-3999(02)00304-5. PMID 12377293.
- Barlow DH, Durand VM (2005). Abnormal psychology: An integrative approach (5th ed.). Belmont, CA: Thomson Wadsworth. pp. 248–49. ISBN 978-0-534-63356-1.
- Strakowski S, Nelson E (2015). Major Depressive Disorder. Oxford University Press. p. PT27. ISBN 978-0-19-026432-1.
- 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
- Blair-West GW, Mellsop GW (June 2001). "Major depression: does a gender-based down-rating of suicide risk challenge its diagnostic validity?". The Australian and New Zealand Journal of Psychiatry. 35 (3): 322–28. doi:10.1046/j.1440-1614.2001.00895.x. PMID 11437805. S2CID 36975913.
- Oquendo MA, Bongiovi-Garcia ME, Galfalvy H, Goldberg PH, Grunebaum MF, Burke AK, Mann JJ (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.
- Bostwick JM, Pankratz VS (December 2000). "Affective disorders and suicide risk: a reexamination". The American Journal of Psychiatry. 157 (12): 1925–32. doi:10.1176/appi.ajp.157.12.1925. PMID 11097952.
- Rush AJ (2007). "The varied clinical presentations of major depressive disorder". The Journal of Clinical Psychiatry. 68 Suppl 8 (Supplement 8): 4–10. PMID 17640152.
- Swardfager W, Herrmann N, Marzolini S, Saleem M, Farber SB, Kiss A, Oh PI, Lanctôt KL (September 2011). "Major depressive disorder predicts completion, adherence, and outcomes in cardiac rehabilitation: a prospective cohort study of 195 patients with coronary artery disease". The Journal of Clinical Psychiatry. 72 (9): 1181–88. doi:10.4088/jcp.09m05810blu. PMID 21208573.
- Schulman J, Shapiro BA (2008). "Depression and Cardiovascular Disease: What Is the Correlation?". Psychiatric Times. 25 (9).
- "WHO Disease and injury country estimates". World Health Organization. 2009. Archived from the original on 11 November 2009. Retrieved 11 November 2009.
- Kessler RC, Berglund P, Demler O, Jin R, Merikangas KR, Walters EE (June 2005). "Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication". Archives of General Psychiatry. 62 (6): 593–602. doi:10.1001/archpsyc.62.6.593. PMID 15939837.
- Murphy JM, Laird NM, Monson RR, Sobol AM, Leighton AH (March 2000). "A 40-year perspective on the prevalence of depression: the Stirling County Study". Archives of General Psychiatry. 57 (3): 209–15. doi:10.1001/archpsyc.57.3.209. PMID 10711905.
- 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.
- James, Spencer L.; Abate, Degu; Abate, Kalkidan Hassen; Abay, Solomon M.; Abbafati, Cristiana; Abbasi, Nooshin; Abbastabar, Hedayat; Abd-Allah, Foad; Abdela, Jemal; Abdelalim, Ahmed; Abdollahpour, Ibrahim; Abdulkader, Rizwan Suliankatchi; Abebe, Zegeye; Abera, Semaw F.; Abil, Olifan Zewdie; Abraha, Haftom Niguse; Abu-Raddad, Laith Jamal; Abu-Rmeileh, Niveen M E.; Accrombessi, Manfred Mario Kokou; Acharya, Dilaram; Acharya, Pawan; Ackerman, Ilana N.; Adamu, Abdu A.; Adebayo, Oladimeji M.; Adekanmbi, Victor; Adetokunboh, Olatunji O.; Adib, Mina G.; Adsuar, Jose C.; Afanvi, Kossivi Agbelenko; et al. (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.
- Eaton WW, Anthony JC, Gallo J, Cai G, Tien A, Romanoski A, Lyketsos C, Chen LS (November 1997). "Natural history of Diagnostic Interview Schedule/DSM-IV major depression. The Baltimore Epidemiologic Catchment Area follow-up". Archives of General Psychiatry. 54 (11): 993–99. doi:10.1001/archpsyc.1997.01830230023003. PMID 9366655.
- Rickards H (March 2005). "Depression in neurological disorders: Parkinson's disease, multiple sclerosis, and stroke". Journal of Neurology, Neurosurgery, and Psychiatry. 76 Suppl 1: i48–52. doi:10.1136/jnnp.2004.060426. PMC 1765679. PMID 15718222.
- Alboni P, Favaron E, Paparella N, Sciammarella M, Pedaci M (April 2008). "Is there an association between depression and cardiovascular mortality or sudden death?". Journal of Cardiovascular Medicine. 9 (4): 356–62. doi:10.2459/JCM.0b013e3282785240. PMID 18334889. S2CID 11051637.
- Strik JJ, Honig A, Maes M (May 2001). "Depression and myocardial infarction: relationship between heart and mind". Progress in Neuro-Psychopharmacology & Biological Psychiatry. 25 (4): 879–92. doi:10.1016/S0278-5846(01)00150-6. PMID 11383983. S2CID 45722423.
- Jorm AF (January 2000). "Does old age reduce the risk of anxiety and depression? A review of epidemiological studies across the adult life span". Psychological Medicine. 30 (1): 11–22. doi:10.1017/S0033291799001452. PMID 10722172. S2CID 20822498.
- Gelder, M, Mayou, R and Geddes, J (2005). Psychiatry. 3rd ed. New York: Oxford. p. 105.
- Mathers CD, Loncar D (November 2006). "Projections of global mortality and burden of disease from 2002 to 2030". PLOS Medicine. 3 (11): e442. doi:10.1371/journal.pmed.0030442. PMC 1664601. PMID 17132052.
- Andrews G (July 2008). "Reducing the burden of depression". Canadian Journal of Psychiatry. 53 (7): 420–27. doi:10.1177/070674370805300703. PMID 18674396.
- Kessler RC, Nelson CB, McGonagle KA, Liu J, Swartz M, Blazer DG (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.
- Hirschfeld RM (December 2001). "The Comorbidity of Major Depression and Anxiety Disorders: Recognition and Management in Primary Care". Primary Care Companion to the Journal of Clinical Psychiatry. 3 (6): 244–54. doi:10.4088/PCC.v03n0609. PMC 181193. PMID 15014592.
- Grant BF (1995). "Comorbidity between DSM-IV drug use disorders and major depression: results of a national survey of adults". Journal of Substance Abuse. 7 (4): 481–97. doi:10.1016/0899-3289(95)90017-9. PMID 8838629.
- Boden JM, Fergusson DM (May 2011). "Alcohol and depression". Addiction. 106 (5): 906–14. doi:10.1111/j.1360-0443.2010.03351.x. hdl:10523/10319. PMID 21382111.
- Hallowell EM, Ratey JJ (2005). Delivered from distraction: Getting the most out of life with Attention Deficit Disorder. New York: Ballantine Books. pp. 253–55. ISBN 978-0-345-44231-4.
- Brunsvold GL, Oepen G (2008). "Comorbid Depression in ADHD: Children and Adolescents". Psychiatric Times. 25 (10). Archived from the original on 24 May 2009.
- Melartin TK, 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.
- Hoge E, Bickham D, Cantor J (November 2017). "Digital Media, Anxiety, and Depression in Children". Pediatrics. 140 (Suppl 2): S76–S80. doi:10.1542/peds.2016-1758G. PMID 29093037.
- Elhai JD, Dvorak RD, Levine JC, Hall BJ (January 2017). "Problematic smartphone use: A conceptual overview and systematic review of relations with anxiety and depression psychopathology". Journal of Affective Disorders. 207: 251–259. doi:10.1016/j.jad.2016.08.030. PMID 27736736.
- Bair MJ, Robinson RL, Katon W, Kroenke K (November 2003). "Depression and pain comorbidity: a literature review". Archives of Internal Medicine. 163 (20): 2433–45. doi:10.1001/archinte.163.20.2433. PMID 14609780.
- Yohannes AM, Baldwin RC (2008). "Medical Comorbidities in Late-Life Depression". Psychiatric Times. 25 (14).
- Hippocrates, Aphorisms, Section 6.23
- 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.
- depress. (n.d.). Online Etymology Dictionary. Retrieved 30 June 2008, from Dictionary.com Archived 3 December 2008 at the Wayback Machine
- 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.
- 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.
- Davison, K (2006). "Historical aspects of mood disorders". Psychiatry. 5 (4): 115–18. doi:10.1383/psyt.2006.5.4.115.
- 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.
- 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.
- Lewis, AJ (1934). "Melancholia: A historical review". Journal of Mental Science. 80 (328): 1–42. doi:10.1192/bjp.80.328.1.
- 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 October 2021).CS1 maint: DOI inactive as of October 2021 (link)
- Schildkraut JJ (November 1965). "The catecholamine hypothesis of affective disorders: a review of supporting evidence". The American Journal of Psychiatry. 122 (5): 509–22. doi:10.1176/ajp.122.5.509. PMID 5319766.
- Paris J (March 2014). "The mistreatment of major depressive disorder". Canadian Journal of Psychiatry (Review). 59 (3): 148–51. doi:10.1177/070674371405900306. PMC 4079242. PMID 24881163.
- 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.
- 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.
- 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.
- 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.
- 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.
- Healy D (1999). The Antidepressant Era. Cambridge, MA: Harvard University Press. p. 42. ISBN 978-0-674-03958-2.
- Wolf, Joshua "Lincoln's Great Depression" Archived 9 October 2011 at the Wayback Machine, The Atlantic, October 2005, Retrieved 10 October 2009
- 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.
- 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.
- 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.
- Parker G, Gladstone G, Chee KT (June 2001). "Depression in the planet's largest ethnic group: the Chinese". The American Journal of Psychiatry. 158 (6): 857–64. doi:10.1176/appi.ajp.158.6.857. PMID 11384889.
- Parker G (August 2007). "Is depression overdiagnosed? Yes". BMJ. 335 (7615): 328. doi:10.1136/bmj.39268.475799.AD. PMC 1949440. PMID 17703040.
- Pilgrim D, Bentall R (1999). "The medicalisation of misery: A critical realist analysis of the concept of depression". Journal of Mental Health. 8 (3): 261–74. doi:10.1080/09638239917580.
- Steibel W (Producer) (1998). "Is depression a disease?". Debatesdebates. Archived from the original on 28 December 2008. Retrieved 16 November 2008.
- Blazer DG (2005). The age of melancholy: "Major depression" and its social origins. New York: Routledge. ISBN 978-0-415-95188-3.
- Hillman J (1989). Moore T (ed.). A blue fire: Selected writings by James Hillman. New York: Harper & Row. pp. 152–53. ISBN 978-0-06-016132-3.
- Seymour M (2002). Mary Shelley. Grove Press. pp. 560–61. ISBN 978-0-8021-3948-1.
- "Biography of Henry James". pbs.org. Archived from the original on 8 October 2008. Retrieved 19 August 2008.
- Burlingame M (1997). The Inner World of Abraham Lincoln. Urbana: University of Illinois Press. pp. xvii, 92–113. ISBN 978-0-252-06667-2.
- Pita E (26 September 2001). "An Intimate Conversation with...Leonard Cohen". Archived from the original on 11 October 2008. Retrieved 3 October 2008.
- 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.
- James H (1920). Letters of William James (Vols. 1 and 2). Montana: Kessinger Publishing Co. pp. 147–48. ISBN 978-0-7661-7566-2.
- Hergenhahn 2005, p. 311
- Cohen D (1979). J. B. Watson: The Founder of Behaviourism. London: Routledge & Kegan Paul. p. 7. ISBN 978-0-7100-0054-5.
- 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.
- 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.
- Heffernan CF (1996). The melancholy muse: Chaucer, Shakespeare and early medicine. Pittsburgh: Duquesne University Press. ISBN 978-0-8207-0262-9.
- 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.
- 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.
- "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.
- 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.
- Paykel ES, Tylee A, Wright A, Priest RG, Rix S, Hart D (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.
- 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.
- Swedish Agency for Health Technology Assessment and Assessment of Social Services (SBU) (27 January 2015). "Depression treatment for the elderly". www.sbu.se. Archived from the original on 18 June 2016. Retrieved 16 June 2016.
- Kempton MJ, Salvador Z, Munafò MR, Geddes JR, Simmons A, Frangou S, Williams SC (2011). "Structural neuroimaging studies in major depressive disorder. Meta-analysis and comparison with bipolar disorder". Archives of General Psychiatry. 68 (7): 675–690. doi:10.1001/archgenpsychiatry.2011.60. PMID 21727252. see also MRI database at www.depressiondatabase.org Archived 29 September 2011 at the Wayback Machine
- Arnone D, McIntosh AM, Ebmeier KP, Munafò MR, Anderson IM (2012). "Magnetic resonance imaging studies in unipolar depression: systematic review and meta-regression analyses". European Neuropsychopharmacology. 22 (1): 1–16. doi:10.1016/j.euroneuro.2011.05.003. PMID 21723712. S2CID 42105719.
- Herrmann LL, Le Masurier M, Ebmeier KP (2008). "White matter hyperintensities in late life depression: a systematic review". Journal of Neurology, Neurosurgery, and Psychiatry. 79 (6): 619–624. doi:10.1136/jnnp.2007.124651. PMID 17717021. S2CID 23759460.
- Kruger TH, Wollmer MA (2015). "Depression—An emerging indication for botulinum toxin treatment". Toxicon. 107 (Pt A): 154–157. doi:10.1016/j.toxicon.2015.09.035. PMID 26415901.
- Milev R (2015). "Response of depression to botulinum toxin treatment: agitation as a predictor". Frontiers in Psychiatry. 6: 55. doi:10.3389/fpsyt.2015.00055. PMC 4403301. PMID 25941497..
- "COMPASS Pathways Receives FDA Breakthrough Therapy Designation for Psilocybin Therapy for Treatment-resistant Depression – COMPASS". Retrieved 11 April 2019.
- "FDA grants Breakthrough Therapy Designation to Usona Institute's psilocybin program for major depressive disorder". www.businesswire.com. 22 November 2019. Retrieved 25 November 2019.
- Krishnan V, Nestler EJ (2011). "Animal Models of Depression: Molecular Perspectives". Molecular and Functional Models in Neuropsychiatry. Current Topics in Behavioral Neurosciences. 7. pp. 121–47. doi:10.1007/7854_2010_108. ISBN 978-3-642-19702-4. PMC 3270071. PMID 21225412.
- 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) . 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.
- Hadzi-Pavlovic D, Parker G (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.