|Major depressive disorder|
|Other names||Clinical depression, major depression, unipolar depression, unipolar disorder, recurrent depression|
|Vincent van Gogh's 1890 painting|
Sorrowing old man ('At Eternity's Gate')
|Symptoms||Low mood, low self-esteem, loss of interest in normally enjoyable activities, low energy, pain without a clear cause|
|Duration||> 2 weeks|
|Causes||Genetic, environmental, and psychological factors|
|Risk factors||Family history, major life changes, certain medications, chronic health problems, substance abuse|
|Differential diagnosis||Bipolar disorder, ADHD, sadness|
|Treatment||Counseling, antidepressant medication, electroconvulsive therapy, exercise|
|Frequency||216 million (2015)|
Major depressive disorder (MDD), also known simply as depression, is a mental disorder characterized by at least two weeks of low mood that is present across most situations. It is often accompanied by low self-esteem, loss of interest in normally enjoyable activities, low energy, and pain without a clear cause. People may also occasionally have false beliefs or see or hear things that others cannot. Some people have periods of depression separated by years in which they are normal, while others nearly always have symptoms present. Major depressive disorder can negatively affect a person's personal life, work life, or education, as well as sleeping, eating habits, and general health. Between 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 cause is believed to be a combination of genetic, environmental, and psychological factors. Risk factors include a family history of the condition, major life changes, certain medications, chronic health problems, and substance abuse. About 40% of the risk appears to be related to genetics. 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 major depression. Testing, however, may be done to rule out physical conditions that can cause similar symptoms. Major depression is more severe and lasts longer than sadness, which is a normal part of life. The United States Preventive Services Task Force (USPSTF) recommends screening for depression among those over the age 12, while a prior Cochrane review found that the routine use of screening questionnaires has little effect on detection or treatment.
Typically, people are treated with counseling and antidepressant medication. Medication appears to be effective, but the effect may only be significant in the most severely depressed. It is unclear whether medications affect the risk of suicide. Types of counseling used include cognitive behavioral therapy (CBT) and interpersonal therapy. If other measures are not effective, electroconvulsive therapy (ECT) may be considered. Hospitalization may be necessary in cases with a risk of harm to self and may occasionally occur against a person's wishes.
Major depressive disorder affected approximately 216 million people (3% of the world's population) in 2015. 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%). It causes the second-most years lived with disability, after lower back pain. The most common time of onset is in a person's 20s and 30s. Females are affected about twice as often as males. The American Psychiatric Association added "major depressive disorder" to the Diagnostic and Statistical Manual of Mental Disorders (DSM-III) in 1980. It was 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. Those currently or previously affected may be stigmatized.
Signs and symptoms
An 1892 lithograph of a woman diagnosed with depression
Major depression significantly affects a person's family and personal relationships, work or school life, sleeping and eating habits, and general health. Its impact on functioning and well-being has been compared to that of other chronic medical conditions, such as diabetes.
A person having a major depressive episode usually exhibits a very low mood, which pervades all aspects of life, and an inability to experience pleasure in activities that were formerly enjoyed. Depressed people may be preoccupied with, or ruminate over, thoughts and feelings of worthlessness, inappropriate guilt or regret, helplessness, hopelessness, and self-hatred. In severe cases, depressed people may have symptoms of psychosis. These symptoms include delusions or, less commonly, hallucinations, usually unpleasant. Other symptoms of depression include poor concentration and memory (especially in those with melancholic or psychotic features), withdrawal from social situations and activities, reduced sex drive, irritability, and thoughts of death or suicide. Insomnia is common among the depressed. 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.
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, with resulting weight loss, although increased appetite and weight gain occasionally occur. Family and friends may notice that the person's behavior is either agitated or lethargic. Older depressed people may have cognitive symptoms of recent onset, such as forgetfulness, and a more noticeable slowing of movements. Depression often coexists with physical disorders common among the elderly, such as stroke, other cardiovascular diseases, Parkinson's disease, and chronic obstructive pulmonary disease.
Depressed children may often display an irritable mood rather than a depressed one, and show varying symptoms depending on age and situation. Most lose interest in school and show a decline in academic performance. They may be described as clingy, demanding, dependent, or insecure. Diagnosis may be delayed or missed when symptoms are interpreted as "normal moodiness."
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 suicide attempts. There are increased rates of alcohol and drug abuse and particularly dependence, and around a third of individuals diagnosed with ADHD develop comorbid depression. Post-traumatic stress disorder and depression often co-occur. Depression may also coexist with attention deficit hyperactivity disorder (ADHD), complicating the diagnosis and treatment of both. Depression is also frequently comorbid with alcohol abuse and personality disorders. Depression can also be exacerbated during particular months (usually winter) for those with seasonal affective disorder.
Depression and pain often co-occur. One or more pain symptoms are present in 65% of depressed patients, and anywhere from 5 to 85% of patients with pain will be suffering from depression, depending on the setting; there is a lower prevalence in general practice, and higher in specialty clinics. The diagnosis of depression is often delayed or missed, and the outcome can worsen if the depression is noticed but completely misunderstood.
Depression is also associated with 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, which further increases their risk of medical complications. In addition, cardiologists may not recognize underlying depression that complicates a cardiovascular problem under their care.
A cup analogy demonstrating the diathesis–stress model
that under the same amount of stressors, person 2 is more vulnerable than person 1, because of their predisposition.
The cause of major depressive disorder is unknown. 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.
Childhood abuse, either physical, sexual or psychological, are all risk factors for depression, among other psychiatric issues that co-occur such as anxiety and drug abuse. Childhood trauma also correlates with severity of depression, lack of response to treatment and length of illness. However, some are more susceptible 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 to be influenced by many individual genetic changes. In 2018, a genome-wide association study discovered 44 variants in the genome linked to risk for major depression. This was followed by a 2019 study that found 102 variants in the genome linked to depression. These results have enabled scientists to calculate polygenic risk scores, which combine the estimated effects across the genome into a single score in order to estimate a person’s genetic liability for depression. Although these scores explain a small proportion (less than 2%) of individual differences in the risk for major depressive disorder.
The 5-HTTLPR, or serotonin transporter promoter gene's short allele has been associated with increased risk of depression. However, since the 1990s, results have been inconsistent, with three recent reviews finding an effect and two finding none. Other genes that have been linked to a gene-environment interaction include CRHR1, FKBP5 and BDNF, the first two of which are related to the stress reaction of the HPA axis, and the latter of which is involved in neurogenesis. There is no conclusive effects of candidate gene on depression, either alone or in combination with life stress. 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 may 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, of 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. Drug abuse in early age is also associated with increased risk of developing depression later in life. Depression that occurs as a result of pregnancy 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 the result of decreased sunlight.
The pathophysiology of depression is not yet understood, but the current theories center around monoaminergic systems, the circadian rhythm, immunological dysfunction, HPA axis dysfunction and structural or functional abnormalities of emotional circuits.
The monoamine theory, derived from the efficacy of monoaminergic drugs in treating depression, was the dominant theory until recently. The theory postulates that insufficient activity of monoamine neurotransmitters is the primary cause of depression. Evidence for the monoamine theory comes from multiple areas. Firstly, acute depletion of tryptophan, a necessary precursor of serotonin, a monoamine, can cause depression in those in remission or relatives of depressed patients; this suggests that decreased serotonergic neurotransmission is important in depression. Secondly, 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, this theory is inconsistent with the fact that serotonin depletion does not cause depression in healthy persons, the fact 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 depressed patients that normalized with SSRI treatment, and the preference for carbohydrates in depressed patients. 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 depressed patients. However, this abnormality is not adequate as a diagnosis tool, because its sensitivity is only 44%. These stress-related abnormalities have been hypothesized to be the cause of hippocampal volume reductions seen in depressed patients. 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 "Corito-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, and family history. The broad clinical aim is to formulate the relevant biological, psychological, and social factors that may be impacting on the individual's mood. The assessor may also discuss the person's current ways of regulating mood (healthy or otherwise) such as 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. The mental health examination may include the use of a rating scale such as the Hamilton Rating Scale for Depression, the Beck Depression Inventory or the Suicide Behaviors Questionnaire-Revised. The score on a rating scale alone is insufficient to diagnose depression to the satisfaction of the DSM or ICD, but it provides 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.
Primary-care physicians and other non-psychiatrist physicians have more difficulty with underrecognition and undertreatment of depression compared to psychiatric physicians, in part because of the physical symptoms that often accompany depression, in addition to many potential patient, provider, and system barriers. A review found that non-psychiatrist physicians miss about two-thirds of cases, though this has improved somewhat in more recent studies.
Before diagnosing a major depressive disorder, in general a doctor 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 are often 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. In general, investigations are not repeated for a subsequent episode unless there is a medical indication.
No biological tests confirm major depression. Biomarkers of depression have been sought to provide an objective method of diagnosis. There are several potential biomarkers, including brain-derived neurotrophic factor and various functional MRI (fMRI) techniques. One study developed a decision tree model of interpreting a series of fMRI scans taken during various activities. In their subjects, the authors of that study were able to achieve a sensitivity of 80% and a specificity of 87%, corresponding to a negative predictive value of 98% and a positive predictive value of 32% (positive and negative likelihood ratios were 6.15, 0.23, respectively). However, much more research is needed before these tests can be used clinically.
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 which uses the name depressive episode for a single episode and recurrent depressive disorder for repeated episodes. 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 patient 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".
DSM-IV-TR excludes cases where the symptoms are a result of bereavement, although it is possible for normal bereavement to evolve into a depressive episode if the mood persists and the characteristic features of a major depressive episode develop. The criteria were criticized because they do not take into account any other aspects of the personal and social context in which depression can occur. In addition, some studies have found little empirical support for the DSM-IV cut-off criteria, indicating they are a diagnostic convention imposed on a continuum of depressive symptoms of varying severity and duration. Bereavement is no longer an exclusion criterion in DSM-5, and it is now 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. Three new depressive disorders were added to the DSM-5: disruptive mood dysregulation disorder, classified by significant childhood irritability and tantrums, premenstrual dysphoric disorder (PMDD), causing periods of anxiety, depression, or irritability in the week or two before a woman's menstruation, and persistent depressive disorder.
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 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-V 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 in order to not exclude cases of depressed woman during pregnancy. Depression with peripartum onset has an incidence rate of 10–15% among new mothers. The DSM-V mandates that, in order to qualify as depression with peripartum onset, onset occur during pregnancy or within one month of delivery. It has been said that postpartum depression can last as long as three months.
- "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.
In 2016, the United States Preventive Services Task Force (USPSTF) recommended screening in the adult populations with evidence that it increases the detection of people with depression and with proper treatment improves outcomes. They recommend screening in those between the age of 12 to 18 as well.
A Cochrane review from 2005 found screening programs do not significantly improve detection rates, treatment, or outcome.
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, also 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. Further differential diagnoses involve chronic fatigue syndrome.
Other disorders need to be ruled out before diagnosing major depressive disorder. They include depressions due to physical illness, medications, and substance abuse. 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, drug of abuse, or exposure to a toxin, it is then diagnosed as a specific mood disorder (previously called substance-induced mood disorder in the DSM-IV-TR).
Preventative efforts may result in decreases in rates of the condition of between 22 and 38%. Eating large amounts of fish may also reduce the risk.
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.
However, an earlier meta-analysis found preventive programs with a competence-enhancing component to be superior to behavior-oriented programs overall, and found behavioral programs to be particularly unhelpful for older people, for whom social support programs were uniquely beneficial. In addition, the programs that best prevented depression comprised more than eight sessions, each lasting between 60 and 90 minutes, were provided by a combination of lay and professional workers, had a high-quality research design, reported attrition rates, and had a well-defined intervention.
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 patient 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 patients 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. A 2014 Cochrane review found insufficient evidence to determine the effectiveness of psychological versus medical therapy in children.
Physical exercise is recommended for management of mild depression, and has a moderate effect on symptoms. Exercise has also been found to be effective for (unipolar) major depression. It is equivalent to the use of medications or psychological therapies in most people. In older people it does appear to decrease depression. Exercise may be recommended to people who are willing, motivated, and physically healthy enough to participate in an exercise program as treatment.
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.
In observational studies, smoking cessation has benefits in depression as large as or larger than those of medications.
Besides exercise, sleep and diet may play a role in depression, and interventions in these areas may be an effective add-on to conventional methods.
Psychotherapy can be delivered to individuals, groups, or families by mental health professionals. A 2015 review found that cognitive behavioral therapy appears to be similar to antidepressant medication in terms of effect. 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. A 2014 Cochrane review found that work-directed interventions combined with clinical interventions helped to reduce sick days taken by people with depression. 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 terminated or replaced by occasional booster sessions.
Cognitive behavioral therapy
Cognitive behavioral therapy (CBT) currently 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. Cognitive behavioral therapy has also been shown to reduce the number of sick days taken by people with depression, when used in conjunction with primary care.
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. Research beginning in the mid-1990s suggested that CBT could perform as well as or better than antidepressants in patients with moderate to severe depression. CBT may be effective in depressed adolescents, although its effects on severe episodes are not definitively known. 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.
(Zoloft) is used primarily to treat major depression in adults.
Conflicting results have arisen from studies that look at the effectiveness of antidepressants in people with acute, mild to moderate depression. Stronger evidence supports the usefulness of antidepressants in the treatment of depression that is chronic (dysthymia) or severe.
While small benefits were found, researchers Irving Kirsch and Thomas Moore state they may be due to issues with the trials rather than a true effect of the medication. In a later publication, Kirsch concluded that the overall effect of new-generation antidepressant medication is below recommended criteria for clinical significance. Similar results were obtained in a meta-analysis by Fornier.
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 50–75%, and it can take at least six to eight weeks from the start of medication to remission. 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.
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 patients younger than 24 years old. Similar precautionary notice revisions were implemented by the Japanese Ministry of Health.
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 patients 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 patient 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 patients receive maintenance ECT.
ECT appears to work in the short term via an anticonvulsant effect mostly in the frontal lobes, and longer term via neurotrophic effects primarily in the medial temporal lobe.
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.
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 insufficient evidence for Reiki and dance movement therapy in depression.
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.
Studies have shown that 80% of those suffering from their first major depressive episode will suffer from at least one more 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.
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.
People experiencing repeated episodes of depression require ongoing treatment in order to prevent more severe, long-term depression. In some cases, people must take medications for the rest of their lives.
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.
Depressed individuals have a shorter life expectancy than those without depression, in part because depressed patients are at risk of dying of suicide. However, they also have a higher rate of dying from other causes, being more susceptible to medical conditions such as heart disease. 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. 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 hospitalized patients.
Depression is often associated with unemployment and poverty. 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.
Disability-adjusted life year
for unipolar depressive disorders per 100,000 inhabitants in 2004.
Major depressive disorder affects approximately 216 million people in 2015 (3% 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. Depression is a major cause of disability worldwide.
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.
Diagnoses of depression go back at least as far as Hippocrates
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.
A historical caricature of a man with an approaching depression
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.
Sigmund 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 patient'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 "unipolar" (along with the related term "bipolar") was coined by the neurologist and psychiatrist Karl Kleist, and subsequently used by his disciples Edda Neele and Karl Leonhard.
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. 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.
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.
MRI scans of patients 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, depressed patients 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 patients with a late age of onset, and have led to the development of the theory of vascular depression.
In 2018, following several smaller studies investigating psilocybin-assisted psychotherapy in the treatment of depression, the Food and Drug Administration (FDA) approved a Phase 2 study on psilocybin in the treatment of treatment-resistant depression and granted Breakthrough Therapy Designation.
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.
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.
- ^ a b c d e f g h i j k l m n "Depression". NIMH. May 2016. Archived from the original on 5 August 2016. Retrieved 31 July 2016.
- ^ a b Richards CS, O'Hara MW (2014). The Oxford Handbook of Depression and Comorbidity. Oxford University Press. p. 254. ISBN 978-0-19-979704-2.
- ^ a b c d e f g h i j k l m American Psychiatric Association (2013), Diagnostic and Statistical Manual of Mental Disorders (5th ed.), Arlington: American Psychiatric Publishing, pp. 160–68, ISBN 978-0-89042-555-8, archived from the original on 31 July 2016, retrieved 22 July 2016
- ^ a b c d e f g Kessler RC, Bromet EJ (2013). "The epidemiology of depression across cultures". Annual Review of Public Health. 34: 119–38. doi:10.1146/annurev-publhealth-031912-114409. PMC 4100461. PMID 23514317.
- ^ a b c 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.
- ^ a b c GBD 2015 Disease and Injury Incidence and Prevalence Collaborators (October 2016). "Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015". Lancet. 388 (10053): 1545–602. doi:10.1016/S0140-6736(16)31678-6. PMC 5055577. PMID 27733282.
- ^ 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
- ^ a b 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.
- ^ a b 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.
- ^ a b 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.
- ^ a b 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. PMID 16235301.
- ^ a b c 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.
- ^ a b 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.
- ^ 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.
- ^ Driessen E, Hollon SD (September 2010). "Cognitive behavioral therapy for mood disorders: efficacy, moderators and mediators". The Psychiatric Clinics of North America. 33 (3): 537–55. doi:10.1016/j.psc.2010.04.005. PMC 2933381. PMID 20599132.
- ^ American Psychiatric Association (2006). American Psychiatric Association Practice Guidelines for the Treatment of Psychiatric Disorders: Compendium 2006. American Psychiatric Pub. p. 780. ISBN 978-0-89042-385-1.
- ^ Global Burden of Disease Study 2013 Collaborators (August 2015). "Global, regional, and national incidence, prevalence, and years lived with disability for 301 acute and chronic diseases and injuries in 188 countries, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013". Lancet. 386 (9995): 743–800. doi:10.1016/S0140-6736(15)60692-4. PMC 4561509. PMID 26063472.
- ^ a b 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.
- ^ Strakowski SM, Nelson E (2015). "Introduction". Major Depressive Disorder. Oxford University Press. p. Chapter 1. ISBN 978-0-19-020618-5.
- ^ a b c d e Depression (PDF). National Institute of Mental Health (NIMH). Archived from the original (PDF) on 27 July 2011. Retrieved 7 September 2008.
- ^ Hays RD, Wells KB, Sherbourne CD, Rogers W, Spritzer K (January 1995). "Functioning and well-being outcomes of patients with depression compared with chronic general medical illnesses". Archives of General Psychiatry. 52 (1): 11–19. doi:10.1001/archpsyc.1995.03950130011002. PMID 7811158.
- ^ a b c d e f American Psychiatric Association 2000a, p. 349
- ^ American Psychiatric Association 2000a, p. 412
- ^ a b 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.
- ^ Judd LL, Schettler PJ, Coryell W, Akiskal HS, Fiedorowicz JG (November 2013). "Overt irritability/anger in unipolar major depressive episodes: past and current characteristics and implications for long-term course". JAMA Psychiatry. 70 (11): 1171–80. doi:10.1001/jamapsychiatry.2013.1957. PMID 24026579.
- ^ a b c d American Psychiatric Association 2000a, p. 350
- ^ "Insomnia: Assessment and Management in Primary Care". American Family Physician. 59 (11): 3029–38. 1999. Archived from the original on 26 July 2011. Retrieved 12 November 2014.
- ^ 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.
- ^ 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 from the original (PDF) on 1 April 2015.
- ^ Yohannes AM, Baldwin RC (2008). "Medical Comorbidities in Late-Life Depression". Psychiatric Times. 25 (14).
- ^ American Psychiatric Association 2000a, p. 354
- ^ 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. 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. 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. 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.
- ^ 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.
- ^ 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).
- ^ Hankin, Benjamin L.; Abela, John R. Z. (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 from the original (PDF) on 17 December 2008. Retrieved 11 November 2008.
- ^ a b 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.
- ^ 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. Archived from the original (PDF) 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. 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. PMID 30718901.
- ^ Kendler KS, Kuhn JW, Vittum J, Prescott CA, Riley B (May 2005). "The interaction of stressful life events and a serotonin transporter polymorphism in the prediction of episodes of major depression: a replication". Archives of General Psychiatry. 62 (5): 529–35. doi:10.1001/archpsyc.62.5.529. PMID 15867106.
- ^ Risch N, Herrell R, Lehner T, Liang KY, Eaves L, Hoh J, Griem A, Kovacs M, Ott J, Merikangas KR (June 2009). "Interaction between the serotonin transporter gene (5-HTTLPR), stressful life events, and risk of depression: a meta-analysis". JAMA. 301 (23): 2462–71. doi:10.1001/jama.2009.878. PMC 2938776. PMID 19531786.
- ^ Munafò MR, Durrant C, Lewis G, Flint J (February 2009). "Gene X environment interactions at the serotonin transporter locus". Biological Psychiatry. 65 (3): 211–19. doi:10.1016/j.biopsych.2008.06.009. PMID 18691701.
- ^ Karg K, Burmeister M, Shedden K, Sen S (May 2011). "The serotonin transporter promoter variant (5-HTTLPR), stress, and depression meta-analysis revisited: evidence of genetic moderation". Archives of General Psychiatry. 68 (5): 444–54. doi:10.1001/archgenpsychiatry.2010.189. PMC 3740203. PMID 21199959.
- ^ Culverhouse RC, Saccone NL, Horton AC, Ma Y, Anstey KJ, Banaschewski T, et al. (January 2018). "Collaborative meta-analysis finds no evidence of a strong interaction between stress and 5-HTTLPR genotype contributing to the development of depression". Molecular Psychiatry. 23 (1): 133–142. doi:10.1038/mp.2017.44. PMC 5628077. PMID 28373689.
- ^ 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: 1–6. doi:10.1155/2015/178564. PMC 4673349. PMID 26688752.
- ^ 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 MD 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.
- ^ 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.
- ^ 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". 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.
- ^ 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 (December 1985). "The dexamethasone suppression test for diagnosis and prognosis in psychiatry. Commentary and review". Archives of General Psychiatry. 42 (12): 1193–204. doi:10.1001/archpsyc.1985.01790350067012. PMID 3000317.
- ^ Varghese FP, Brown ES (August 2001). "The Hypothalamic-Pituitary-Adrenal Axis in Major Depressive Disorder: A Brief Primer for Primary Care Physicians". Primary Care Companion to the Journal of Clinical Psychiatry. 3 (4): 151–55. doi:10.4088/pcc.v03n0401. PMC 181180. PMID 15014598.
- ^ Lopez-Duran NL, Kovacs M, George CJ (October 2009). "Hypothalamic-pituitary-adrenal axis dysregulation in depressed children and adolescents: a meta-analysis". Psychoneuroendocrinology. 34 (9): 1272–83. doi:10.1016/j.psyneuen.2009.03.016. PMC 2796553. PMID 19406581.
- ^ Dedovic K, Ngiam J (14 May 2015). "The cortisol awakening response and major depression: examining the evidence". Neuropsychiatric Disease and Treatment. 11: 1181–89. doi:10.2147/NDT.S62289. PMC 4437603. PMID 25999722.
- ^ Mayberg HS (1 August 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 (November 2013). "Meta-analytic evidence for neuroimaging models of depression: state or trait?". Journal of Affective Disorders. 151 (2): 423–31. 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 (September 1993). "Rural psychiatric services. A collaborative model". Canadian Family Physician. 39: 1957–61. 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.
- ^ 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.
- ^ 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.
- ^ a b 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.
- ^ 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.
- ^ 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.
- ^ 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.
- ^ Sadock 2002, p. 108
- ^ Sadock 2002, p. 260
- ^ Hahn T, Marquand AF, Ehlis AC, Dresler T, Kittel-Schneider S, Jarczok TA, Lesch KP, Jakob PM, Mourao-Miranda J, Brammer MJ, Fallgatter AJ (April 2011). "Integrating neurobiological markers of depression" (PDF). Archives of General Psychiatry. 68 (4): 361–68. doi:10.1001/archgenpsychiatry.2010.178. PMID 21135315.
- ^ a b "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 2000a, p. xxix
- ^ a b 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.CS1 maint: multiple names: authors list (link)
- ^ "The ICD-10 Classification of Mental and Behavioural Disorders: Clinical descriptions and diagnostic guidelines" (PDF). World Health Organization. 2010. Archived from the original (PDF) 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.
- ^ a b c d e 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.
- ^ Parker 1996, p. 173
- ^ American Psychiatric Association 2000a, p. 352
- ^ Wakefield JC, Schmitz MF, First MB, Horwitz AV (April 2007). "Extending the bereavement exclusion for major depression to other losses: evidence from the National Comorbidity Survey". Archives of General Psychiatry. 64 (4): 433–40. doi:10.1001/archpsyc.64.4.433. PMID 17404120.
- ^ Kendler KS, Gardner CO (February 1998). "Boundaries of major depression: an evaluation of DSM-IV criteria". The American Journal of Psychiatry. 155 (2): 172–77. doi:10.1176/ajp.155.2.172 (inactive 20 October 2018). PMID 9464194.
- ^ a b Sadock 2002, p. 552
- ^ American Psychiatric Association 2000a, p. 778
- ^ 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. PMID 12904979.
- ^ Rapaport MH, Judd LL, Schettler PJ, Yonkers KA, Thase ME, Kupfer DJ, Frank E, Plewes JM, Tollefson GD, Rush AJ (April 2002). "A descriptive analysis of minor depression". The American Journal of Psychiatry. 159 (4): 637–43. doi:10.1176/appi.ajp.159.4.637. PMID 11925303.
- ^ a b American Psychiatric Association 2000a, p. 355
- ^ "NIMH » Disruptive Mood Dysregulation Disorder". www.nimh.nih.gov. Retrieved 21 February 2019.
- ^ "Premenstrual dysphoric disorder (PMDD)". womenshealth.gov. 12 July 2017. Retrieved 21 February 2019.
- ^ American Psychiatric Association 2000a, pp. 419–20
- ^ American Psychiatric Association 2000a, pp. 421–22
- ^ American Psychiatric Association 2000a, pp. 417–18
- ^ DSM-5 Task Force (2013). Diagnostic and statistical manual of mental disorders : DSM-5. American Psychiatric Association. ISBN 9780890425541. OCLC 1026055291.
- ^ Nonacs, Ruta M (4 December 2007). "Postpartum depression". eMedicine. Archived from the original on 13 October 2008. Retrieved 30 October 2008.
- ^ American Psychiatric Association 2000a, p. 425
- ^ 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.
- ^ Hawk C, Jason LA, Torres-Harding S (1 January 2006). "Differential diagnosis of chronic fatigue syndrome and major depressive disorder". International Journal of Behavioral Medicine. 13 (3): 244–51. CiteSeerX 10.1.1.574.3376. doi:10.1207/s15327558ijbm1303_8. PMID 17078775.
- ^ a b Cuijpers P, van Straten A, Smit F, Mihalopoulos C, Beekman A (October 2008). "Preventing the onset of depressive disorders: a meta-analytic review of psychological interventions". The American Journal of Psychiatry. 165 (10): 1272–80. doi:10.1176/appi.ajp.2008.07091422. hdl:1871/16952. PMID 18765483.
- ^ Li F, Liu X, Zhang D (March 2016). "Fish consumption and risk of depression: a meta-analysis". Journal of Epidemiology and Community Health. 70 (3): 299–304. doi:10.1136/jech-2015-206278. PMID 26359502.
- ^ a b Muñoz RF, Beardslee WR, Leykin Y (May–June 2012). "Major depression can be prevented". The American Psychologist. 67 (4): 285–95. doi:10.1037/a0027666. PMC 4533896. PMID 22583342.
- ^ 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.
- ^ 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. Archived from the original (PDF) on 12 November 2014. Retrieved 12 November 2014.
- ^ Jané-Llopis E, Hosman C, Jenkins R, Anderson P (2003). "Predictors of efficacy in depression prevention programmes" (PDF). British Journal of Psychiatry. Archived from the original (PDF) on 26 March 2009. Retrieved 2 April 2009.
- ^ 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.
- ^ a b c "Practice guideline for the treatment of patients with major depressive disorder (revision). American Psychiatric Association". The American Journal of Psychiatry. 157 (4 Suppl): 1–45. April 2000. PMID 10767867.; Third edition doi:10.1176/appi.books.9780890423363.48690
- ^ Archer J, Bower P, Gilbody S, 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.
- ^ 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. 11 (11): CD008324. doi:10.1002/14651858.CD008324.pub3. PMID 25433518.
- ^ "Management of depression in primary and secondary care" (PDF). National Clinical Practice Guideline Number 23. National Institute for Health and Clinical Excellence. 2007. Archived from the original (PDF) on 17 December 2008. Retrieved 4 November 2008.
- ^ a b 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.
- ^ 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.
- ^ 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.
- ^ 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.
- ^ Lopresti, Hood, Drummond (1 January 2006). "3) 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 from the original (PDF) on 9 January 2017.
- ^ Amick HR, Gartlehner G, Gaynes BN, Forneris C, Asher GN, Morgan LC, Coker-Schwimmer E, Boland E, Lux LJ, Gaylord S, Bann C, Pierl CB, Lohr KN (December 2015). "Comparative benefits and harms of second generation antidepressants and cognitive behavioral therapies in initial treatment of major depressive disorder: systematic review and meta-analysis". BMJ. 351: h6019. doi:10.1136/bmj.h6019. PMC 4673103. PMID 26645251.
- ^ 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.
- ^ 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.
- ^ a b c Nieuwenhuijsen K, Faber B, Verbeek JH, Neumeyer-Gromen A, Hees HL, Verhoeven AC, van der Feltz-Cornelis CM, Bültmann U (December 2014). "Interventions to improve return to work in depressed people". The Cochrane Database of Systematic Reviews. 12 (12): CD006237. doi:10.1002/14651858.CD006237.pub3. PMID 25470301.
- ^ 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: CD010558. doi:10.1002/14651858.CD010558.pub2. 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.
- ^ 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.
- ^ Dobson KS (June 1989). "A meta-analysis of the efficacy of cognitive therapy for depression". Journal of Consulting and Clinical Psychology. 57 (3): 414–19. doi:10.1037/0022-006X.57.3.414. PMID 2738214.
- ^ Roth A, Fonagy P (2005) . What Works for Whom? Second Edition: A Critical Review of Psychotherapy Research. Guilford Press. p. 78. ISBN 978-1-59385-272-6.
- ^ Weersing VR, Walker PN (August 2008). "Review: cognitive behavioural therapy for adolescents with depression". Evidence-Based Mental Health. 11 (3): 76. doi:10.1136/ebmh.11.3.76. PMID 18669678.
- ^ Harrington R, Whittaker J, Shoebridge P, Campbell F (May 1998). "Systematic review of efficacy of cognitive behaviour therapies in childhood and adolescent depressive disorder". BMJ. 316 (7144): 1559–63. doi:10.1136/bmj.316.7144.1559. PMC 28555. PMID 9596592.
- ^ 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.
- ^ 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.
- ^ 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.
- ^ 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.
- ^ Kirsch I, Moore TJ, Scoboria A, Nicholls SS (2002). "The emperor's new drugs: An analysis of antidepressant medication data submitted to the U.S. Food and Drug Administration". Prevention & Treatment. 5. doi:10.1037/1522-3718.104.22.1683a.
- ^ "The treatment and management of depression in adults". NICE. October 2009. Archived from the original (PDF) 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.
- ^ Thase ME (December 2006). "Preventing relapse and recurrence of depression: a brief review of therapeutic options". CNS Spectrums. 11 (12 Suppl 15): 12–21. PMID 17146414.
- ^ a b Royal Pharmaceutical Society of Great Britain 2008, p. 204
- ^ Whooley MA, Simon GE (December 2000). "Managing depression in medical outpatients". The New England Journal of Medicine. 343 (26): 1942–50. doi:10.1056/NEJM200012283432607. PMID 11136266.
- ^ Zisook S, Rush AJ, Haight BR, Clines DC, Rockett CB (February 2006). "Use of bupropion in combination with serotonin reuptake inhibitors". Biological Psychiatry. 59 (3): 203–10. doi:10.1016/j.biopsych.2005.06.027. PMID 16165100.
- ^ 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.
- ^ 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". NHS National Institute for Health and Clinical Excellence. 2005. Archived from the original (PDF) 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.
- ^ a b c 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.
- ^ 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.
- ^ 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.
- ^ 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. PMID 12595913.
- ^ Hammad TA (16 August 2004). "Review and evaluation of clinical data. Relationship between psychiatric drugs and pediatric suicidality" (PDF). FDA. pp. 42, 115. Archived from the original (PDF) 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: CD004851. doi:10.1002/14651858.CD004851.pub3. 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.
- ^ 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.
- ^ 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.
- ^ 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.
- ^ 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.
- ^ 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. PMID 12804463.
- ^ Walther, A; Breidenstein, J; Miller, R (1 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. 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.
- ^ a b c FDA. FDA Executive Summary Archived 24 September 2015 at the Wayback Machine. Prepared for the 27–28 January 2011 meeting of the Neurological Devices Panel Meeting to Discuss the Classification of Electroconvulsive Therapy Devices (ECT). Quote, p38: "Three major practice guidelines have been published on ECT. These guidelines include: APA Task Force on ECT (2001); Third report of the Royal College of Psychiatrists' Special Committee on ECT (2004); National Institute for Health and Clinical Excellence (NICE 2003; NICE 2009). There is significant agreement between the three sets of recommendations."
- ^ Dierckx B, Heijnen WT, van den Broek WW, 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.
- ^ 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.
- ^ "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. 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 from the original (PDF) 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.
- ^ "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.
- ^ 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. PMID 15106233.
- ^ 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". The Cochrane Database of Systematic Reviews (2): CD009895. doi:10.1002/14651858.cd009895.pub2. PMID 25695871.
- ^ 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.
- ^ Fava GA, Park SK, Sonino N (November 2006). "Treatment of recurrent depression". Expert Review of Neurotherapeutics. 6 (11): 1735–40. doi:10.1586/1473722.214.171.1245. PMID 17144786.
- ^ 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.
- ^ a b Culpepper L, Muskin PR, Stahl SM (September 2015). "Major Depressive Disorder: Understanding the Significance of Residual Symptoms and Balancing Efficacy with Tolerability". The American Journal of Medicine. 128 (9 Suppl): S1–S15. doi:10.1016/j.amjmed.2015.07.001. PMID 26337210.
- ^ Geddes JR, Carney SM, Davies C, 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.
- ^ "Major Depression". MedlinePlus. 10 March 2014. Archived from the original on 7 July 2010. Retrieved 16 July 2010.
- ^ "Depression, Major: Prognosis". MDGuidelines. The Guardian Life Insurance Company of America. Archived from the original on 20 April 2010. Retrieved 16 July 2010.
- ^ 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.
- ^ 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.
- ^ a b 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.
- ^ 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.
- ^ 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.
- ^ 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.
- ^ Weich S, Lewis G (July 1998). "Poverty, unemployment, and common mental disorders: population based cohort study". BMJ. 317 (7151): 115–19. doi:10.1136/bmj.317.7151.115. PMC 28602. PMID 9657786.
- ^ 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.
- ^ "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.
- ^ a b Kuehner C (September 2003). "Gender differences in unipolar depression: an update of epidemiological findings and possible explanations". Acta Psychiatrica Scandinavica. 108 (3): 163–74. doi:10.1034/j.1600-0447.2003.00204.x. PMID 12890270.
- ^ "The world health report 2001 – Mental Health: New Understanding, New Hope". WHO website. World Health Organization. 2001. Archived from the original on 16 October 2008. Retrieved 19 October 2008.
- ^ 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.
- ^ 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.
- ^ 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.
- ^ Gelder, M, Mayou, R and Geddes, J (2005). Psychiatry. 3rd ed. New York: Oxford. p. 105.
- ^ Hippocrates, Aphorisms, Section 6.23
- ^ a b c Radden, J (2003). "Is this dame melancholy? Equating today's depression and past melancholia". Philosophy, Psychiatry, & Psychology. 10 (1): 37–52. doi:10.1353/ppp.2003.0081.
- ^ 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.