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Major depressive disorder

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Major depressive disorder
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Major depressive disorder, also known as major depression, unipolar depression, clinical depression, or simply depression, is a mental disorder characterized by a pervasive low mood, loss of interest in a person's usual activities and diminished ability to experience pleasure. The diagnosis is made if a person has suffered one or more major depressive episodes. The onset is usually in early- to mid-adulthood. Diagnosis is based on the patient's self-reported experiences and observed behavior. There is no laboratory test for major depression, although physicians often test for physical conditions that may cause similar symptoms before arriving at a diagnosis. The course varies widely: it can be a once-in-a-lifetime event or have multiple recurrences; it can appear either gradually or suddenly; and can either last for a few months or be a life-long disorder.

The term "depression" is commonly used in the vernacular to describe a temporary depressed mood, when a person may feel sad or "down." Ideas about what causes and constitutes depression have evolved over the centuries. Today, many mental health professionals regard "major depression" as a serious and often disabling condition that can significantly affect a person's work, family and school life, sleeping and eating habits, general health and ability to enjoy life.[1] Depression is a major risk factor for suicide; in addition, people with depression suffer from higher mortality from other causes.[2] Clinical depression may be isolated or be a secondary result of a primary condition such as bipolar disorder or chronic pain. When specific treatment is indicated, it usually consists of psychotherapy and antidepressants.

Signs and symptoms

A major depressive episode can manifest with a variety of symptoms, but almost all who experience such an episode display a marked change in mood, a deep feeling of sadness, and a noticeable loss of interest or pleasure in favorite activities. The psychological or mood change symptoms may include persistent sad, anxious or "empty" moods, and feelings of worthlessness, inappropriate guilt, helplessness, hopelessness, or pessimism, a sense of restlessness or irritability, and difficulty thinking, concentrating, remembering, or making decisions. Physical symptoms associated with depression include increased or decreased appetite or weight; insomnia, early morning awakening, or oversleeping; decreased energy, fatigue, feeling "slowed down" or sluggish; psychomotor agitation or psychomotor retardation; and persistent physical symptoms that do not respond to treatment, such as headaches, digestive problems, and chronic pain.

Other symptoms include withdrawal from social situations, family gatherings and activities with friends; and thoughts of death or suicide or attempts at suicide. Not all people will suffer from every symptom. The severity of symptoms will vary widely among individuals. According to one diagnostic standard, symptoms, with the exception of suicidal thoughts or attempts, must persist for at least two weeks before being considered a potential sign of depression.[3][1]

Diagnosis of an episode in children is more difficult than in adults. Depression in children is often undiagnosed, and thus untreated, because the symptoms in children are often dismissed as normal childhood moodiness. Children are more likely than adults to show different symptoms depending on the situation.[4] While some children still function reasonably well, most who are suffering from depression will exhibit a noticeable change in their social activities and life, a loss of interest in school and poor academic performance, and possibly drastic changes in appearance. They may also begin abusing drugs or alcohol, particularly past the age of 12. Although much more rarely than adults, children with major depression may attempt suicide or have suicidal thoughts even before the age of 12.[4]

Comorbidity

Depression and anxiety frequently co-occur; the National Comorbidity Survey (US) reports that 58 percent of those with major depression also suffer from lifetime anxiety. Even mild anxiety symptoms can have a major impact on the course of a depressive illness, and the commingling of any anxiety symptoms with the primary depression is important to consider. A pilot study by Ellen Frank et al., at the University of Pittsburgh, found that depressed or bipolar patients with lifetime panic symptoms experienced significant delays in their remission.[5] These patients also had higher levels of residual impairment. On a similar note, Robert Sapolsky of Stanford University argues that the relationship between stress, anxiety, and depression could be measured and demonstrated biologically.[6]

About one-third of individuals diagnosed with attention-deficit hyperactivity disorder (ADHD) may develop comorbid depression.[7] Dysthymia, a form of chronic, low-level depression, is particularly common in adults with undiagnosed ADHD who have encountered years of frustrating ADHD-related problems with education, employment, and interpersonal relationships.[8]

Diagnosis

Before a diagnosis of major depressive disorder is made, a physician may perform a medical examination to rule out a physical cause for the suspected depression. Although there are no biological tests which confirm major depression, tests are carried out to exclude medical illnesses. These include blood tests measuring TSH to exclude hypo- or hyperthyroidism, basic electrolytes and serum calcium to rule out a metabolic disturbance, full blood count including ESR to rule out a systemic infection or chronic disease, and serology to exclude syphilis or HIV infection. Two commonly ordered investigations are EEG to exclude epilepsy, and a CT scan of the head to exclude brain lesions. Early dementia may present with depressive symptoms in older patients.

If no such cause is found, a psychological evaluation should be done by the physician or by referral to a psychiatrist or psychologist.[1] The evaluation will include a complete history of symptoms, a discussion of alcohol and drug use, and a determination of whether the patient has had or is having suicidal thoughts or thinking about death. The evaluation will also include a family medical history to see if other family members suffer from any form of depression or similar mood disorder.[1]

Investigations are not generally repeated for a recurrent episode unless there is a specific medical indication. These may include measuring serum sodium if the person presents with polyuria and is on a selective serotonin reuptake inhibitor (SSRI). Assessment and treatment are usually done on an outpatient basis; admission to an inpatient facility is considered if there is a risk to self or others.

Rating scales

There are several criteria lists and diagnostic tools that can also aid in the diagnosis of depression. Most are based on the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), a book published by the American Psychiatric Association that defines the criteria used to diagnose various mental disorders, including depression. Many are used in research or as screening tools. No screening tool should be used to confirm diagnosis in the absence of review by a medical practitioner or psychologist.

The Beck Depression Inventory, originally designed by psychiatrist Aaron T. Beck in 1961, is a 21-question patient-completed survey that covers items related to the basic symptoms of depression, such as hopelessness and irritability, cognitions such as guilt or feelings of being punished, as well as physical symptoms such as fatigue, weight loss, and lack of interest in sex.[9] The Beck Inventory is one of the most widely used diagnostic tools for self-diagnosis of depression, although its main purpose is not the diagnosis of depression, but determining the severity and presence of symptoms.[10]

There are also two Patient Health Questionnaires available that are also self-administered questionnaires. The PHQ-2 has only two questions that asks about the frequency of depressed mood and a loss of interest in doing things, with a positive to either question indicating the need for further testing.[11] The PHQ-9 is a slightly more detailed nine question survey covering some of the major symptoms of depression and the frequency a person has experienced them. It is based directly on the diagnostic criteria listed in the DSM-IV and often used as a follow up to a positive PHQ-2 test.[12]

Other scales commonly used include the Geriatric Depression Scale, in older populations, the widely-used Hamilton Depression Rating Scale designed by psychiatrist Max Hamilton in 1960,[13] and the Montgomery-Åsberg Depression Rating Scale (MADRS).

DSM IV-TR 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, the current version being DSM-IV-TR, and the World Health Organization's International Statistical Classification of Diseases and Related Health Problems, currently the ICD-10. The latter system is typically used in European countries, while the DSM criteria are used in the USA and many other non-European nations, and are frequently referenced in research studies.

The DSM IV-TR diagnosis hinges on the presence of a major depressive episode, which may be either single or recurrent. Further qualifiers are used to classify both the episode itself and the course of the disorder. The ICD-10 system does not use the term major depressive disorder, but the diagnosis of depressive episode is very similar. Minor depression is a less-used term for a subclinical depression that does not meet criteria for major depression but in which at least two symptoms are present for two weeks. It is not mentioned in DSM IV-TR.

Major depressive episode

Main article: major depressive episode

A major depressive episode has been defined as a severely depressed mood that persists for at least two weeks. Episodes may be isolated or recurrent and categorized as mild, major or severe. If the patient has already had an episode of mania or markedly elevated mood, a diagnosis of bipolar disorder is made instead. Depression without periods of elation or mania is sometimes referred to as unipolar depression because the mood remains at one emotional state or "pole". The diagnosis usually excludes cases in which the symptoms are a normal result of bereavement (though it is possible for normal bereavement to turn into a depressive episode).

Diagnosticians recognize several possible subtypes:

  • Melancholic depression – melancholia is characterized by a loss of pleasure (anhedonia) 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 – atypical depression is characterized by mood reactivity (paradoxical anhedonia) and positivity, significant weight gain or increased appetite ("comfort eating"),[14] excessive sleep or somnolence (hypersomnia), leaden paralysis, or significant social impairment as a consequence of hypersensitivity to perceived interpersonal rejection. Contrary to its name, atypical depression is the most common form of depression.[15]
  • Psychotic depression – Some people with a major depressive episode, particularly of melancholic nature, may experience psychotic features. They may be presented with hallucinations or delusions that are either mood-congruent (content coincident with depressive themes) or non-mood-congruent (content not coincident with depressive themes). It is clinically more common to encounter a delusional system as an adjunct to depression than to encounter hallucinations, whether visual or auditory.
  • Postpartum depression refers to the intense, sustained and sometimes disabling depression experienced by women after giving birth. Postpartum depression, which has incidence rate of 10-15%, typically sets in within three months of labor, and can last for as long as three months.[16]

Differential diagnoses

  • Dysthymia is a chronic, mild depression in which a person suffers from a depressive mood almost daily over a span of at least two years without episodes of major depression. The symptoms are not as severe as those for major depression, although people with dysthymia are vulnerable to co-occurring episodes of major depression (sometimes referred to as "double depression").[17]
  • Bipolar disorder is an episodic condition characterized by alternating states of mania, hypomania and depression. In the United States, bipolar disorder has also been called "manic depression", but this term is no longer favored by the medical community.
  • Adjustment disorder with depressed mood overlaps with what was previously known as Reactive depression.
  • Recurrent brief depression (RBD) is distinguished from clinical depression primarily by differences in duration. Patients with RBD have depressive episodes about once per month, with individual episodes lasting less than two weeks and typically less than 2–3 days. Diagnosis of RBD requires that the episodes occur over the span of at least one year and, in female patients, independently of the menstrual cycle. People with clinical depression can develop RBD, and vice versa, with both illnesses having similar risks.[18]

Epidemiology

Major depressive disorder affects about 8–17 percent of the population on at least one occasion in their lives, before the age of 40. In some countries, such as Australia, one in four women and one in six men will suffer from depression. In Canada, major depression affects approximately 1.35 million people[citation needed], and in the United States approximately 14 million adults per year.[19] An estimated 121 million people worldwide currently suffer from depression.[20]

People who have had one episode of depression may be more than normally likely to have more episodes in the future, so the first time a young person becomes depressed is important as both a personal and public health concern.[21]

About twice as many females as males report or receive treatment for clinical depression, though this imbalance has recently shrunk, and the difference seems to disappear completely for those over the age of 50–55. Clinical depression is currently the leading cause of disability in North America, and is expected to become the second leading cause of disability worldwide (after heart disease) by the year 2020, according to the World Health Organization.[22]

The diagnostic criteria for depression may be too broad, resulting in diagnosis of major depression in people who are not truly suffering from the disorder, but who have shown normal responses to negative events.[23]

Causes

Current theories regarding the risk factors and causes of clinical depression can be broadly classified into three categories: psychological, physiological, and environmental:

Psychological

Low self-esteem and self-defeating or distorted thinking are connected with depression. The question of whether this is the result of depression or a cause of it is a matter of debate. In either case, it is known that depressed persons who are able to make corrections in their thinking patterns can show improved mood and self-esteem.[24] Psychological factors related to depression include the complex development of one's personality and how one has learned to cope with external environmental factors, such as stress.[25]

Existential psychologists argue that "depression is the inability to construct a future."[26] In order to construct a future, people must become acutely aware of both their mortality and their freedom, and they must exercise the latter within the explicit framework of the former. This awareness and responsibility produce "normal anxiety,"[27] whereas the lack of these things leads to "neurotic anxiety,"[27] "self-alienation,"[28] "inauthentic" living,[29] and depression. Humanistic psychologists agree with many facets of existentialism, but argue that depression results from a specific incongruity between society on the one hand, and the individual's innate drive to self-actualize on the other.[30]

Physiological

Genetic predisposition

The tendency to develop depression may be inherited. According to the National Institute of Mental Health[31] there is some evidence that depression may run in families. Most experts believe that both biological and psychological factors play a role. The heritability of depression may have originated in our evolutionary past; depression might have increased genetic fitness in ancestral populations. For example, psychic pain may have evolved in an analogous way to physical pain so that organisms avoid behaviour which hinders reproduction.[32][33][34] This insight may be helpful in counselling therapy.[35][36] Proponents of the psychic pain theory tend to view clinical depression as a dysfunctional extreme of low mood or mild depression.

Brain chemicals called neurotransmitters allow electrical signals to move from the axon of one nerve cell to the soma of another. A shortage of neurotransmitters impairs brain communication.

Neurological

Many modern antidepressant drugs change synaptic levels of certain neurotransmitters, especially serotonin and norepinephrine. However, the precise relationships among serotonin, SSRIs, and depression are largely unknown and, typically, are greatly oversimplified when presented to the public.[37]

There may be a link between depression and neurogenesis of the hippocampus,[38] a center for both mood and memory. Loss of neurons in the hippocampus is found in some depressed individuals and correlates with impaired memory and dysthymic mood. Drugs may increase serotonin levels in the brain, stimulating neurogenesis and thereby increasing the total mass of the hippocampus. This increase in mass may help to restore mood and memory.[citation needed]

Depression may also be caused in part by an overactive hypothalamic-pituitary-adrenal axis (HPA axis) that resembles the neuro-endocrine response to stress. These HPA axis abnormalities participate in the development of depressive symptoms, and antidepressants serve to regulate HPA axis function.[39]

Many individuals with clinical depression exhibit markedly higher levels of monoamine oxidase A (MAO-A) in the brain compared to people without depression.[40] MAO-A is an enzyme which reacts with and decreases the concentration of monoamines such as serotonin, norepinephrine and dopamine.

Medical conditions

Certain illnesses, including cardiovascular disease,[41] hepatitis, mononucleosis, hypothyroidism, fructose malabsorption,[42] sleep apnea, and organic brain damage caused by degenerative conditions such as Parkinson's disease, multiple sclerosis or by traumatic blunt force injury may contribute to depression, as may certain prescription drugs such as hormonal contraception methods and steroids. Depression also occurs in patients with chronic pain, such as chronic back pain, much more frequently than in the general population. Fibromyalgia sufferers also experience depression and anxiety.

Environmental

Early experiences

Events such as the death of a parent, issues with biological development, school related problems, abandonment or rejection, neglect, chronic illness, and physical, psychological, or sexual abuse can increase the likelihood of depression later in life. Post-traumatic stress disorder (PTSD) and depression often co-occur, and both can result from childhood trauma.[43]

Life experiences

Stressful or traumatic life experiences or circumstances, including rape, assault, or the death of a relative or friend, may trigger a depressive episode. A depressive episode may also be triggered by other major changes such as unemployment, divorce, or a loss of religious faith.[44] Ongoing issues, such as financial difficulties or poverty, ongoing major health problems (e.g., eating disorders), addictions (e.g., gambling addiction or drug addiction), sexual difficulties, or work-related stress can also contribute to depression.

Treatment

The three most often used conventional treatments are medication, psychotherapy, and electroconvulsive therapy.

Medication

Main article: Antidepressant

A patient's doctor may change the antidepressant taken, adjust the dosages of medications, or try different combinations of antidepressants before finding the most effective option; response rates to the first agent administered may be as low as 50 percent.[45] It may take anywhere from three to eight weeks after the start of medication before its therapeutic effects can be fully discovered. Patients are generally advised not to stop taking an antidepressant suddenly and to continue its use for at least four months to prevent the chance of recurrence. For patients who have chronic depression, medication may be continued for the remainder of their lives.[1]

A wide range of antidepressant drugs can be prescribed to treat depression. These drugs have historically been divided into four major groups: selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs), monoamine oxidase inhibitors (MAOIs), and other antidepressants.

Selective serotonin reuptake inhibitors, such as sertraline (Zoloft), escitalopram (Lexapro), fluoxetine (Prozac), paroxetine (Paxil) and citalopram (Celexa) are the primary medications considered for patients, due to their relatively mild side effects and broad effect on the symptoms of depression and anxiety. Those who do not respond to the first SSRI tried, can be switched to another SSRI antidepressant. Such a switch results in improvement in almost 50% of cases.[46] Another popular option is to switch the patient to the atypical antidepressant bupropion (Wellbutrin) or to add bupropion to the existing therapy[47] with the latter strategy possibly more effective.[48][49] Venlafaxine (Effexor) may be moderately more effective than SSRIs;[50] however, it is not recommended as a first line treatment because of the high rate of the side effects.[51] Tricyclic antidepressants are less well tolerated than SSRIs and are usually reserved for the treatment of inpatients, for whom the tricyclic antidepressant amitriptyline, in particular, appears to be more effective.[52][53] Their adverse side effect profile and toxicity in overdose limit their use.[citation needed] The causing or worsening of insomnia is not uncommon with SSRIs; a sedating antidepressant mirtazapine (Zispin, Remeron) can be used in such cases.[54][55][56] Monoamine oxidase inhibitors have historically been plagued by questionable efficacy and life-threatening adverse effects. They are still used only rarely, although newer agents of this class, with a better side effect profile, have been developed.[57]

A meta-analysis combined 35 clinical trials submitted to the FDA before licensing of four newer antidepressants. The authors found that although the antidepressants were statistically superior to placebo they often did not exceed the NICE criteria for a 'clinically significant' effect. In particular they found that the effect size was very small for moderate depression but increased with severity reaching 'clinical significance' for very severe depression.[58] This result is consistent with the earlier clinical studies in which only patients with severe depression benefited from the treatment with a tricyclic antidepressant, imipramine, or from psychotherapy more than from the placebo treatment.[59][60][61]

Psychotherapy

See also: Psychotherapy

There are a number of different psychotherapies for depression, which may be provided to individuals or groups. Psychotherapy can be delivered by a variety of mental health professionals, including psychotherapists, psychiatrists, psychologists, clinical social workers, and psychiatric nurses. The most studied form of psychotherapy for depression is Cognitive behavioral therapy. Several clinical trials have shown that CBT is as effective as antidepressant medications, even among more severely depressed clients. CBT is thought to work by teaching clients to learn a set of cognitive and behavioral skills, which they can employ on their own. This type of therapy attempts to teach people to learn healthier behaviors. Earlier research suggested that psychotherapy, specifically cognitive-behavioral therapy, was not as effective as medication in the treatment of depression; however, recent research suggests that CBT can perform as well as anti-depressant medication in the treatment of moderate to severe depression treated on an outpatient basis.[62] With more complex and chronic forms of depression the most effective treatment is often considered to be a combination of medication and psychotherapy.[63]

Two randomized, controlled trials of mindfulness-based cognitive therapy (MBCT), which includes elements of meditation, have been reviewed. MBCT was significantly more effective than "usual care" for the prevention of recurrent depression in patients who had had three or more depressive episodes. According to the review, the "usual care" did not include antidepressant treatment or any psychotherapy, and the improvement observed may have reflected the non-specific or placebo effects.[64]

Interpersonal psychotherapy focuses on the social and interpersonal triggers that may cause depression. There is evidence that it is an effective treatment for depression. Here, the therapy takes a structured course with a set number of weekly sessions (often 12) as in the case of CBT, however the focus is on relationships with others. Therapy can be used to help a person develop or improve interpersonal skills in order to allow him or her to communicate more effectively and reduce stress.[65]

Psychoanalysis, a school of thought founded by Sigmund Freud that emphasizes the resolution of unconscious mental conflicts,[66] is used by its practitioners to treat clients presenting with major depression.[67] A more widely practiced, eclectic technique, called psychodynamic psychotherapy, is loosely based on psychoanalysis and has an additional social and interpersonal focus.[68] In a meta-analysis of three controlled trials, psychodynamic psychotherapy was found to be as effective as medication for mild to moderate depression.[69]

Electroconvulsive therapy

Electroconvulsive therapy (ECT), also known as electroshock, is a treatment in which seizures are electrically induced in anesthetized patients for therapeutic effect. Today, ECT is a last resort, and is most often used as a treatment for severe major depression which has not responded to other treatment. An estimated 1 million people worldwide receive ECT every year[70] usually in a course of 6-12 treatments administered 2 or 3 times a week. In a study, ECT was shown clinically to be the most effective treatment for severe depression, and to result in improved quality of life in both short- and long-term.[71] After treatment, drug therapy can be continued, and some patients receive continuation/maintenance ECT. Short-term memory loss, disorientation, and headache are very common side effects. Detailed neuropsychological testing in clinical studies has not been able to prove permanent effects on memory.

ECT produces a very fast response in the client; however, this response has been shown not always to last unless maintenance electroshock or maintenance medication is used. Whereas antidepressants usually take around a month to take effect, the results of ECT have been shown to be much faster. For this reason, it is the treatment of choice in emergencies (e.g., in catatonic depression in which the patient has ceased oral intake of fluid or nutrients). The American Psychiatric Association and the National Institute for Health and Clinical Excellence have concluded that the procedure does not cause brain damage.[72][73] Like all forms of psychiatric treatment, ECT can be given without a patient's consent,[citation needed] but this is subject to legal conditions dependent on the jurisdiction. In Oregon, patient consent is necessary by statute.[74]

Other conventional methods of treatment

  • St John's wort extract is used extensively in Europe to treat mild and moderate depression. It is a prescription antidepressant in several European countries but is classified as herbal supplement and sold over the counter in the U.S. The opinions on its efficacy for major depression differ. The systematic meta-analysis of 37 trials conducted by Cochrane Collaboration indicated statistically significant weak-to-moderate effect as compared to placebo. The same meta-analysis found that St John's wort efficacy for major depression is not different from prescription antidepressants.[75] NCCAM and other NIH-affiliated organizations hold that St John's wort has minimal or no effects beyond placebo in the treatment of major depression, based primarily on one study with negative outcome conducted by NCCAM.[76][77]
  • S-Adenosyl methionine (SAM-e) is available as a prescription antidepressant in Europe and an over-the-counter dietary supplement in the United States. A fairly strong evidence, based on 16 clinical trials, suggests it to be more effective than placebo and as effective as standard antidepressant medication for the treatment of major depression.[78][79]
  • Repetitive transcranial magnetic stimulation (rTMS) use in treatment-resistant depression is supported by multiple controlled studies, and it has been approved for this indication in Europe, Canada and Australia, but not in the U.S.[80] A 2008 meta-analysis based on 32 trials found a robust effect of this method on depression, and it appeared similarly effective for both uncomplicated depression and depression resistant to medication.[81] However, in a side-by-side randomized trial rTMS was inferior to electroconvulsive therapy.[82]
  • Vagus nerve stimulation (VNS) is an approved therapy for treatment-resistant depression and is used as an adjunctive to existing antidepressant treatment. The support for this method comes primarily from open-label trials, which indicate that a several month period may be necessary for the therapy to become effective.[80] The only large double-blind trial conducted lasted only 10 weeks and yielded inconclusive results. VNS failed to show superiority over a sham treatment on the primary efficacy outcome but the result were more favorable for the secondary outcome.[83]

Alternative treatment methods

  • A meta-analysis of bright light therapy commissioned by the American Psychiatric Association found it to be more effective than placebo—usually, dim light—for both seasonal affective disorder and for nonseasonal depression, with effect sizes similar to those for conventional antidepressants. For non-seasonal depression, adding light therapy to the standard antidepressant treatment was not effective.[84] A meta-analysis of light therapy for non-seasonal depression conducted by Cochrane Collaboration, studied a different set of trials, where light was used mostly as an addition to medication or sleep deprivation. A moderate statistically significant effect of light therapy was found; however, it disappeared if a different statistical technique was used.[85] Both analyses noted poor quality of most studies and their small size, and urged caution in the interpretation of their results. The short 1-2 weeks duration of most trials makes it unclear whether the effect of light therapy could be sustained in the longer term.
  • A 2004 Cochrane Review concluded that there was insufficient evidence to judge the efficacy of acupuncture in the management of depression. Although acupuncture showed no difference in the improvement of depression compared with conventional medication, the methodological quality of the evidence base was found to be poor.[86]
  • Exercise, when used in conjunction with medication with non-suicidal patients can have beneficial effects in preventing the return of depression. Patients that completed 30 minutes of brisk exercise at least three times a week were found to have a significantly lower incidence of relapse.[87]
  • Tryptophan and 5-hydroxytryptophan may be more effective than placebo in alleviating depression according to the Cochrane Collaboration meta-analysis. However, only two out of 108 trials were of sufficient quality to be included in this analysis.[88]
  • Omega-3 fatty acids have been studied in clinical trials for major depression primarily as an adjunctive to antidepressant therapy. A meta-analysis of eight such trials indicated a statistically significant superiority of combinations with omega-3 fatty acids over single antidepressants; however, the authors warned that, due to multiple problems with these trials, a reliable conclusion is difficult to achieve.[89]
  • Dehydroepiandrosterone (DHEA), available as a supplement in the U.S., has been shown to be more effective than placebo for major depression in two small double-blind trials: in one—as an adjunctive to antidepressant treatment[90], in another—as monotherapy.[91]
  • Zinc supplementation was found in a single small study to augment the effect of antidepressants.[93]
  • Cranial electrotherapy stimulation (CES, electrosleep) devices currently on the market have been granted marketing authorization by the FDA based on the legacy waver, that is because a sufficiently similar device had been marketed before 1976, when the new regulations requiring controlled testing were introduced.[94] The FDA considers them to be the class III devices—"devices for which insufficient information exists to ... provide reasonable assurance of safety and effectiveness"[95] The effects of CES on depression were inconclusive or negative in multiple double-blind studies of psychiatric patients.[96][97][98][99][97][100] In one of them, four out of six clinically depressed patients dropped out of the study because of the massive worsening of depressive symptoms, with two of them becoming actively suicidal.[100] One of the authors of the latter study cautioned that CES “should not be used as a treatment of choice” for the patients with the primary diagnosis of depression, “and should be used with caution if this diagnosis is suspected.”[101] Nevertheless, the CES practitioners continue to employ it as a treatment of choice for depression.[102][103]

Prognosis

Recurrence is more likely if treatment has not resulted in full remission of symptoms.4 Current guidelines for antidepressant use recommend 4 to 6 months of continuing treatment after symptom resolution to prevent relapse. Combined evidence from many randomized controlled trials indicates that continuing antidepressant medications after recovery can reduce the odds 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. Thus, in a significant minority of patients depression recurs despite the prolonged treatment with antidepressants.[104] The reason for recurrence in these cases is as poorly understood and could be a "true pharmacologic failure or a worsening of the disease, a relapse that overrides medication." Because of the difficulties of carrying out controlled clinical trials of longer duration, the approval of most antidepressants for the prevention of recurrence is based on up to a year-long trials.[105]

History

In prehistory, humans probably "saw mental illness as possession by supernatural forces." Supporting this theory, "human skulls have been found with large holes in them." This may have resulted from an attempt to "let evil spirits out."[106][unreliable source?] The Greek scholar Empedocles (490-430 BC) proposed that humans experienced disease when their four humours were imbalanced. The four humours were Fire (Blood); Earth (Phlegm); water (Yellow bile); and Air (Black bile). Empedocles' theories were further developed by Hippocrates (460-377 BC), who argued that "mental disorder must be explained on the basis of natural causes" such as the "sudden flow of bile to the brain". Hippocrates believed that the appropriate treatment for a mental disorder depended on which humor had caused the problem.[107][unreliable source?]

Plato (427-347 BC) argued that there were two types of mental illness: "divinely inspired" mental illness that gave the person prophetic powers, and a second type that was caused by a physical disease.[108][unreliable source?] Aristotle (384-322 BC), who studied under Plato, abandoned the divinely-caused mental illness theory, and proposed instead that all mental illness was caused by physical problems. The Roman physician Asclepiades claimed that emotional disturbances were “passions of sensations”. Arateus (ca AD 30-90) suggested that it is hard to pinpoint where a mental illness comes from. His contemporary Galen (AD 30-90) rehashed the Greek theories, proposing that there are "animal spirits" which cause melancholy. The modern idea of depression appears similar to the much older concept of melancholia. The name melancholia derives from "black bile", one of the four humours postulated by Galen. In the Old Testament, the description of King Saul includes symptoms that resemble some elements in the modern diagnosis of depression; eventually the King commits suicide.

In the 14th century, the treatment of people with mental illness varied. While some people with mental illnesses were treated at hospitals such as Bethlehem hospital (better known by its nickname, “Bedlam”), others were persecuted as witches. [109] For people deemed to be witches, the treatment was exorcism, often in the form of physical punishments that aimed to drive out the devil and save the person’s soul. The witch-hunting attitude was not held in all quarters. [110]A Franciscan monk named Bartholemew Anglicus described depression in his book De Proprietatibis Rerum, and he suggested that music would help their condition. In the 16th century, Paracelsus rejected the witch-hunt and demonology approach to mental illness. [111] His near-contemporary, Weyer (b. 1515) argued that the mental illnesses attributed that were often claimed to be demon possession of witches came from natural causes. [112]

In the 16th century, the physician Johann Weyer (1515-1588) argued against the witchcraft and demon-possession theories, and proposed that mental illnesses had natural causes. The Catholic church banned Weyer’s book, De Praestigiis Daemonum, and Weyer was accused of being a sorcerer. [113] Juan Luis Vives (1492-1540) founded hospitals for the mentally ill. Robert Burton wrote Anatomy of Melancholy in 1621, which suggested that depression could be combated with “ exercise, music, drugs and diet”, along with talking about the problem. [114]In the 1670s, several “madhouses” were established in London. [115]

With the turn of the 17th century, science gained increasing prestige, and emotions and anatomy were studied more closely. The philosopher Spinoza (1632-1677) argued that the mind and body are closely connected. Literary figures such as William Shakespeare (1564-1616) and Miguel de Cervantes (1547-1616) described mental illness in an insightful way in their works. Phillipe Pinel in France argued that insanity was caused by factors in the environment or in a person's background. Franz Joseph Gall proposed the theory of phrenology, which claimed that locations of the brain are connected to body parts.[116][unreliable source?]

In the 19th century, Johann Christian Heinroth revived the notion that mental illness was caused by moral sins of the patient. But by the mid-19th century, scholars began to believe that mental illness was caused by physical, organic conditions. The German psychiatrist Wilhelm Griesinger (1817-1868) argued that mental illnesses were caused by the brain. Emil Kraepelin (1855-1926) argued that metabolic factors caused mental illness. Freud argued that each patient's unique life history and experiences caused their mental problems. Freud's psychoanalysis was one of the main theories of mental illness until the 1970s.

In the mid 20th century, many considered clinical depression to be a chemical imbalance in transmitters 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.[117] Subsequently, many other causes for clinical depression have been proposed.[118]

Psychiatrist David Healy wrote about the growth of the diagnosis, along with perspectives on the development and promotion of antidepressants and the biological model since the late 1950s.[119] After the 1970s, scholars proposed a range of "genetic, biochemical and neuropathological causes of mental disorder."[120][unreliable source?]

Sociocultural aspects

See also: List of people with depression

Samuel Johnson first coined the term "the black dog" when describing his own battles with depression [121]. The phrase was subsequently popularised by another famous sufferer, the former British Prime Minister Sir Winston Churchill. Journeys with the Black Dog is an anthology of essays of sufferers writing on their experiences. The critically acclaimed 1980 film Ordinary People depicts a young man's torrid course of a severe depressive episode,[122] while the 1956 Alfred Hitchcock film The Wrong Man has the protagonist's wife Rose suffering.[123]

References

  1. ^ a b c d e Mayo Clinic Staff (2006-03-06). "Depression" (PDF). National Institute of Mental Health (NIMH). Retrieved 2007-10-20.
  2. ^ Rush AJ (2007). "The varied clinical presentations of major depressive disorder". The Journal of clinical psychiatry. 68 Suppl 8: 4–10. PMID 17640152.
  3. ^ "Let's Talk Facts About Depression" (PDF). American Psychiatric Association. 2006-11. Retrieved 2007-10-21. {{cite web}}: Check date values in: |date= (help)
  4. ^ a b "Depression in Children". MedicineNet.com and the Cleveland Clinic. 2005-01-31. Retrieved 2007-10-21.
  5. ^ Arch Gen Psychiatry - Abstract: Conceptualization and rationale for consensus definitions of terms in major depressive disorder. Remission, recovery, relapse, and recurrence, September 1991, Frank et al. 48 (9): 851
  6. ^ Sapolsky, Robert M., Ph.D. (2004). Why Zebras Don't Get Ulcers. Henry Holt and Company, LLC. pp. 291–298. ISBN 0-8050-7369-8.{{cite book}}: CS1 maint: multiple names: authors list (link)
  7. ^ Hallowell, Edward M.; John J. Ratey (2005). Delivered from Distraction : Getting the Most out of Life with Attention Deficit Disorder. New York: Ballantine Books, p. 253–5. ISBN 0-345-44231-8.
  8. ^ see Hallowell and Ratey, 2005
  9. ^ Beck, A. T. (1972). Depression: Causes and Treatment. Philadelphia: University of Pennsylvania Press. ISBN 0-8122-1032-8.
  10. ^ "Beck Depression Inventory - 2nd Edition". Nova Southeastern University Center for Center for Psychological Studies. Retrieved 2007-10-22.
  11. ^ Spitzer RL, Kroenke K, Williams JB. Validation and utility of a self-report version of PRIME-MD: the PHQ primary care study. Primary Care Evaluation of Mental Disorders. Patient Health Questionnaire. JAMA. 1999;282:1737-44. PMID 10568646
  12. ^ The MacArthur Initiative on Depression Primary Care - Resources for Clinicians: Patient Health Questionnaire
  13. ^ Hamilton, M (1960) A rating scale for depression. Journal of Neurology, Neurosurgery and Psychiatry. 23: 56-62 PMID 14399272 (HRSD-21)
  14. ^ DepNet | Other types of depression
  15. ^ Atypical Depression Actually Very Typical
  16. ^ eMedicine - Postpartum Depression : Article by Ruta M Nonacs
  17. ^ Double depression
  18. ^ General Practice Notebook - Recurrent brief depression
  19. ^ Kessler RC, McGonagle KA, Zhao S, et al. Lifetime and 12-month prevalence of DSM-III-R psychiatric disorders in the United States: results from the National Comorbidity Survey. Arch Gen Psychiatry 1994;51:8-19.
  20. ^ WHO | Depression
  21. ^ Bos et al. (2005). Cognitive, physiological, and personality correlates of recurrence of depression. Journal of Affective Disorders 87 (2005) 221-229.
  22. ^ Murray, C.J.L. (1997). "Alternative projections of mortality and disability by cause 1990-2020: Global Burden of Disease Study". Lancet. 349: 1498?1504. doi:10.1016/S0140-6736(96)07492-2. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  23. ^ Vedantam, Shankar (2007-04-03). "Criteria for Depression Are Too Broad, Researchers Say". Washington Post. Retrieved 2007-09-10. {{cite news}}: Italic or bold markup not allowed in: |publisher= (help)
  24. ^ "NAMI". {{cite web}}: Text "Cognitive-Behavioral Therapy" ignored (help)
  25. ^ Personality styles may predict susceptibility to depression
  26. ^ http://www.psychiatrictimes.com/display/article/10168/51281
  27. ^ a b May, Rollo (1996). The Meaning Of Anxiety. New York, NY, USA: W. W. Norton and Company. ISBN 0-393-31456-1.
  28. ^ Fromm, Erich (1941). Escape from Freedom. New York, NY, USA: Holt, Rinehart, & Winston.
  29. ^ Heidegger, Martin (1927). Being and Time. Halle, Germany: Niemeyer.
  30. ^ Hergenhahn, B. R. (2005). An Introduction to the History of Psychology (5th ed.). Belmont, CA, USA: Thomson Wadsworth. pp. 546–547. ISBN 0-534-55401-6.
  31. ^ Genetic Link Found for Depression
  32. ^ Thornhill NW, Thornhill R (1991). "An evolutionary analysis of psychological pain following human (Homo sapiens) rape: IV. The effect of the nature of the sexual assault". J Comp Psychol. 105 (3): 243–52. PMID 1935004.
  33. ^ Neese, Randolph M. (2005-01). "Is Depression an Adaptation?" (PDF). Archives of General Psychology. 57 (1). American Medical Association: 14–20. doi:10.1001/archpsyc.57.1.14. {{cite journal}}: Check date values in: |date= (help)
  34. ^ Suarez, S.D. (1991). "Depression as a response to reproductive failure". Journal of Social and Biological Structures. 8: 279–287. doi:10.1016/0140-1750(85)90071-5. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  35. ^ Tony J. Carey (September 2005), "Evolution, depression and counselling", Counselling Psychology Quarterly, Volume 18, Number 3: 215–222 {{citation}}: |volume= has extra text (help)
  36. ^ Tom Geoghegan (Thursday, 28 February 2008), Is depression good for you? {{citation}}: Check date values in: |date= (help)
  37. ^ http://medicine.plosjournals.org/archive/1549-1676/2/12/pdf/10.1371_journal.pmed.0020392-L.pdf
  38. ^ Dr Helen Mayberg, quoted in http://www.sciammind.com/article.cfm?&articleID=0002AD36-CF84-14C7-8DCC83414B7F0000 Scientific American, volume 17, number 4, pp. 26-31
  39. ^ Carmine M. Pariante, Institute of Psychiatry, King’s College London Depression, stress and the adrenal axis. The British Society for Neuroendocrinology, 2003.
  40. ^ Jeffrey H. Meyer, MD, PhD; Nathalie Ginovart, PhD; Anahita Boovariwala, BSc; Sandra Sagrati, BSc; Doug Hussey, BSc; Armando Garcia, BSc; Trevor Young, MD, PhD; Nicole Praschak-Rieder, MD; Alan A. Wilson, PhD; Sylvain Houle, MD, PhD, "Elevated Monoamine Oxidase A Levels in the Brain -- An Explanation for the Monoamine Imbalance of Major Depression," Arch Gen Psychiatry. 2006;63:1209-1216.[1]
  41. ^ Manev, R (2004). "5-Lipoxygenase as a putative link between cardiovascular and psychiatric disorders". Critical Reviews in Neurobiology. 16 (1?2): 181?6. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  42. ^ Ledochowski M, Sperner-Unterweger B, Widner B, Fuchs D (1998). "Fructose malabsorption is associated with early signs of mental depression". Eur. J. Med. Res. 3 (6): 295–8. PMID 9620891.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  43. ^ PTSD and Childhood Trauma
  44. ^ NJC Andreasen (1972), "The role of religion in depression", Journal of Religion and Health, Springer
  45. ^ Depression Guideline Panel. Depression in primary care. Vol. 2. Treatment of major depression. Clinical practice guideline. No. 5. Rockville, MD: Agency for Health Care Policy and Research, 1999.
  46. ^ Sutherland JE, Sutherland SJ, Hoehns JD (2003). "Achieving the best outcome in treatment of depression". J Fam Pract. 52 (3): 201–9. PMID 12620174. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  47. ^ For the most recent review, see: Zisook S, Rush AJ, Haight BR, Clines DC, Rockett CB (2006). "Use of bupropion in combination with serotonin reuptake inhibitors". Biol Psychiatry. 59 (3): 203–10. doi:10.1016/j.biopsych.2005.06.027. PMID 16165100.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  48. ^ Rush AJ, Trivedi MH, Wisniewski SR, Stewart JW, Nierenberg AA, Thase ME, Ritz L, Biggs MM, Warden D, Luther JF, Shores-Wilson K, Niederehe G, Fava M (2006). "Bupropion-SR, sertraline, or venlafaxine-XR after failure of SSRIs for depression". N. Engl. J. Med. 354 (12): 1231–42. doi:10.1056/NEJMoa052963. PMID 16554525.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  49. ^ Trivedi MH, Fava M, Wisniewski SR, Thase ME, Quitkin F, Warden D, Ritz L, Nierenberg AA, Lebowitz BD, Biggs MM, Luther JF, Shores-Wilson K, Rush AJ (2006). "Medication augmentation after the failure of SSRIs for depression". N. Engl. J. Med. 354 (12): 1243–52. doi:10.1056/NEJMoa052964. PMID 16554526.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  50. ^ Papakostas GI, Thase ME, Fava M, Nelson JC, Shelton RC (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". Biol. Psychiatry. 62 (11): 1217–27. doi:10.1016/j.biopsych.2007.03.027. PMID 17588546. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  51. ^ "NeLM - MHRA issues updated prescribing advice for venlafaxine (Efexor/Efexor XL)" (htm). Retrieved 2008-06-07.
  52. ^ Anderson IM (1998). "SSRIS versus tricyclic antidepressants in depressed inpatients: a meta-analysis of efficacy and tolerability". Depress Anxiety. 7 Suppl 1: 11–7. doi:10.1002/(SICI)1520-6394(1998)7:1 <11::AID-DA4>3.0.CO;2-I. PMID 9597346. {{cite journal}}: Check |doi= value (help); Unknown parameter |doilabel= ignored (help)
  53. ^ Anderson IM (2000). "Selective serotonin reuptake inhibitors versus tricyclic antidepressants: a meta-analysis of efficacy and tolerability". J Affect Disord. 58 (1): 19–36. PMID 10760555. {{cite journal}}: Unknown parameter |month= ignored (help)
  54. ^ Mayers AG, Baldwin DS (2005). "Antidepressants and their effect on sleep". Hum Psychopharmacol. 20 (8): 533–59. doi:10.1002/hup.726. PMID 16229049. {{cite journal}}: Unknown parameter |month= ignored (help)
  55. ^ Winokur A, DeMartinis NA, McNally DP, Gary EM, Cormier JL, Gary KA (2003). "Comparative effects of mirtazapine and fluoxetine on sleep physiology measures in patients with major depression and insomnia". J Clin Psychiatry. 64 (10): 1224–9. PMID 14658972. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  56. ^ Lawrence RW (2004). "Effect of mirtazapine versus fluoxetine on "sleep quality"". J Clin Psychiatry. 65 (8): 1149–50. PMID 15323610. {{cite journal}}: Unknown parameter |month= ignored (help)
  57. ^ Krishnan KR (2007). "Revisiting monoamine oxidase inhibitors". J Clin Psychiatry. 68 Suppl 8: 35–41. PMID 17640156.
  58. ^ 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" (htm). PLoS Medicine. Retrieved 2008-02-26. {{cite web}}: Cite has empty unknown parameter: |coauthors= (help)CS1 maint: multiple names: authors list (link)
  59. ^ Elkin I, Shea MT, Watkins JT, Imber SD, Sotsky SM, Collins JF, Glass DR, Pilkonis PA, Leber WR, Docherty JP (1989). "National Institute of Mental Health Treatment of Depression Collaborative Research Program. General effectiveness of treatments". Arch. Gen. Psychiatry. 46 (11): 971–82, discussion 983. PMID 2684085.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  60. ^ Elkin I, Gibbons RD, Shea MT, Sotsky SM, Watkins JT, Pilkonis PA, Hedeker D (1995). "Initial severity and differential treatment outcome in the National Institute of Mental Health Treatment of Depression Collaborative Research Program". J Consult Clin Psychol. 63 (5): 841–7. PMID 7593878.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  61. ^ Sotsky SM, Glass DR, Shea MT, Pilkonis PA, Collins JF, Elkin I, Watkins JT, Imber SD, Leber WR, Moyer J (1991). "Patient predictors of response to psychotherapy and pharmacotherapy: findings in the NIMH Treatment of Depression Collaborative Research Program". Am J Psychiatry. 148 (8): 997–1008. PMID 1853989.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  62. ^ Psychiatry and Behavioral Neurosciences - Outpatient Psychotherapy Groups
  63. ^ Thase, ME (1999). "When are psychotherapy and pharmacotherapy combinations the treatment of choice for major depressive disorder?". Psychiatr Q. 70 (4): 333–346. doi:10.1023/A:1022042316895.
  64. ^ Coelho HF, Canter PH, Ernst E (2007). "Mindfulness-based cognitive therapy: evaluating current evidence and informing future research". J Consult Clin Psychol. 75 (6): 1000–5. doi:10.1037/0022-006X.75.6.1000. PMID 18085916. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  65. ^ Weissman, M. M., Markowitz, J. C., & Klerman, G. L. (2000). Comprehensive guide to interpersonal psychotherapy. New York: Basic Books.
  66. ^ Dworetzky, John (1997). Psychology. Pacific Grove, CA, USA: Brooks/Cole Pub. Co. p. 602. ISBN 0-314-20412-1.
  67. ^ Doidge N, Simon B, Lancee WJ; et al. (2002). "Psychoanalytic patients in the U.S., Canada, and Australia: II. A DSM-III-R validation study". J Am Psychoanal Assoc. 50 (2): 615–27. PMID 12206545. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  68. ^ Durand, Vincent Mark; Barlow, David (1999). Abnormal psychology: an integrative approach. Pacific Grove, CA, USA: Brooks/Cole Pub. Co. ISBN 0-534-34742-8.{{cite book}}: CS1 maint: multiple names: authors list (link)
  69. ^ de Maat S, Dekker J, Schoevers R; et al. (2007). "Short Psychodynamic Supportive Psychotherapy, antidepressants, and their combination in the treatment of major depression: a mega-analysis based on three Randomized Clinical Trials". Depress Anxiety. doi:10.1002/da.20305. PMID 17557313. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  70. ^ "Electroconvulsive therapy discussion hosted at the MGH". Retrieved 2007-06-05.
  71. ^ McCall WV, Prudic J, Olfson M, Sackeim H. Health-related quality of life following ECT in a large community sample. J Affect Disord. 2006 Feb;90(2-3):269-74. PMID 16412519
  72. ^ American Psychiatric Association. "Electroconvulsive Therapy (ECT)". Retrieved 2007-12-29.
  73. ^ National Institute for Clinical Excellence (2003-04). Guidance on the use of electrocunvulsive therapy (PDF). London. ISBN 1-84257-282-2. {{cite book}}: Check date values in: |date= (help); Cite has empty unknown parameter: |coauthors= (help)
  74. ^ Being prepared for a crisis with a psychiatric advance directive
  75. ^ Linde K, Mulrow CD, Berner M, Egger M (2005). "St John's wort for depression". Cochrane Database Syst Rev (2): CD000448. doi:10.1002/14651858.CD000448.pub2. PMID 15846605.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  76. ^ St. John's Wort and Depression NCCAM on St John's wort and depression]
  77. ^ How is depression detected and treated? NIMH on depression, including a section on St John's wort
  78. ^ Mischoulon D, Fava M (2002). "Role of S-adenosyl-L-methionine in the treatment of depression: a review of the evidence". Am. J. Clin. Nutr. 76 (5): 1158S – 61S. PMID 12420702. {{cite journal}}: Unknown parameter |month= ignored (help)
  79. ^ Bressa GM (1994). "S-adenosyl-l-methionine (SAMe) as antidepressant: meta-analysis of clinical studies". Acta Neurol. Scand., Suppl. 154: 7–14. PMID 7941964.
  80. ^ a b c Marangell LB, Martinez M, Jurdi RA, Zboyan H (2007). "Neurostimulation therapies in depression: a review of new modalities". Acta Psychiatr Scand. 116 (3): 174–81. doi:10.1111/j.1600-0447.2007.01033.x. PMID 17655558. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  81. ^ Schutter DJ (2008). "Antidepressant efficacy of high-frequency transcranial magnetic stimulation over the left dorsolateral prefrontal cortex in double-blind sham-controlled designs: a meta-analysis". Psychol Med: 1–11. doi:10.1017/S0033291708003462. PMID 18447962. {{cite journal}}: Unknown parameter |month= ignored (help)
  82. ^ Eranti S, Mogg A, Pluck G; et al. (2007). "A randomized, controlled trial with 6-month follow-up of repetitive transcranial magnetic stimulation and electroconvulsive therapy for severe depression". Am J Psychiatry. 164 (1): 73–81. doi:10.1176/appi.ajp.164.1.73. PMID 17202547. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  83. ^ Rush AJ, Marangell LB, Sackeim HA; et al. (2005). "Vagus nerve stimulation for treatment-resistant depression: a randomized, controlled acute phase trial". Biol. Psychiatry. 58 (5): 347–54. doi:10.1016/j.biopsych.2005.05.025. PMID 16139580. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  84. ^ Golden RN, Gaynes BN, Ekstrom RD; et al. (2005). "The efficacy of light therapy in the treatment of mood disorders: a review and meta-analysis of the evidence". Am J Psychiatry. 162 (4): 656–62. doi:10.1176/appi.ajp.162.4.656. PMID 15800134. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  85. ^ Tuunainen A, Kripke DF, Endo T (2004). "Light therapy for non-seasonal depression". Cochrane Database Syst Rev (2): CD004050. doi:10.1002/14651858.CD004050.pub2. PMID 15106233.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  86. ^ Smith, CA (2005). "Acupuncture for Depression". Cochrane Database of Systematic Reviews. 2005 (2): CD004046. doi:10.1002/14651858.CD004046.pub2. {{cite journal}}: |access-date= requires |url= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  87. ^ Merritt, Richard (2000-09-22). "Study: Exercise Has Long-Lasting Effect on Depression". Duke University News. Retrieved 2007-10-20.
  88. ^ Shaw K, Turner J, Del Mar C (2002). "Tryptophan and 5-hydroxytryptophan for depression". Cochrane Database Syst Rev (1): CD003198. doi:10.1002/14651858.CD003198. PMID 11869656.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  89. ^ Appleton KM, Hayward RC, Gunnell D; et al. (2006). "Effects of n-3 long-chain polyunsaturated fatty acids on depressed mood: systematic review of published trials". Am. J. Clin. Nutr. 84 (6): 1308–16. PMID 17158410. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  90. ^ Wolkowitz OM, Reus VI, Keebler A; et al. (1999). "Double-blind treatment of major depression with dehydroepiandrosterone". Am J Psychiatry. 156 (4): 646–9. PMID 10200751. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  91. ^ Schmidt PJ, Daly RC, Bloch M; et al. (2005). "Dehydroepiandrosterone monotherapy in midlife-onset major and minor depression". Arch. Gen. Psychiatry. 62 (2): 154–62. doi:10.1001/archpsyc.62.2.154. PMID 15699292. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  92. ^ Docherty JP, Sack DA, Roffman M, Finch M, Komorowski JR (2005). "A double-blind, placebo-controlled, exploratory trial of chromium picolinate in atypical depression: effect on carbohydrate craving". J Psychiatr Pract. 11 (5): 302–14. PMID 16184071. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  93. ^ Nowak G, Siwek M, Dudek D, Zieba A, Pilc A (2003). "Effect of zinc supplementation on antidepressant therapy in unipolar depression: a preliminary placebo-controlled study" (PDF). Pol J Pharmacol. 55 (6): 1143–7. PMID 14730113.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  94. ^ FDA > CDRH > CFR Title 21 Database Search
  95. ^ FDA 515(i) Reclassification Letter to Manufacturers
  96. ^ Levitt EA, James NM, Flavell P (1975). "A clinical trial of electrosleep therapy with a psychiatric inpatient sample". Aust N Z J Psychiatry. 9 (4): 287–90. PMID 769773. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  97. ^ a b Passini FG, Watson CG, Herder J (1976). "The effects of cerebral electric therapy (electrosleep) on anxiety, depression, and hostility in psychiatric patients". J. Nerv. Ment. Dis. 163 (4): 263–6. PMID 972328. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link) Cite error: The named reference "pmid972328" was defined multiple times with different content (see the help page).
  98. ^ Philip P, Demotes-Mainard J, Bourgeois M, Vincent JD (1991). "Efficiency of transcranial electrostimulation on anxiety and insomnia symptoms during a washout period in depressed patients. A double-blind study". Biol. Psychiatry. 29 (5): 451–6. PMID 2018818. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  99. ^ Moore JA, Mellor CS, Standage KF, Strong H (1975). "A double-blind study of electrosleep for anxiety and insomnia". Biol. Psychiatry. 10 (1): 59–63. PMID 1091305.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  100. ^ a b Feighner JP, Brown SL, Olivier JE (1973). "Electrosleep therapy. A controlled double blind study". J. Nerv. Ment. Dis. 157 (2): 121–8. PMID 4724809.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  101. ^ Feighner JP (1971). "Electrosleep Therapy: Current Usage in Psychiatry". Calif. Med. 115 (3): 44. Retrieved 2007-12-02.
  102. ^ Shealy CN (2003). "Transcutaneous electrical nerve stimulation: the treatment of choice for pain and depression". J Altern Complement Med. 9 (5): 619–23. doi:10.1089/107555303322524463. PMID 14629839. {{cite journal}}: Unknown parameter |month= ignored (help)
  103. ^ Shealy CN, Thomlinson P (2008). "Safe Effective Nondrug Treatment of Chronic Depression: A Review of Research on Low-Voltage Cranial Electrical Stimulation and Other Adjunctive Therapies". Complementary Health Practice Review. 13 (2): 92–99. doi:10.1177/1533210108317232.
  104. ^ Geddes JR, Carney SM, Davies C; et al. (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. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  105. ^ Psychology Today: Skirmish or Siege?
  106. ^ Mead Mathews. "How did pre-twentieth century theories of the aetiology of depression develop?". Priory Medical Journal. Available at: http://www.priory.com/homol/dephist.htm
  107. ^ http://www.priory.com/homol/dephist.htm
  108. ^ http://www.priory.com/homol/dephist.htm
  109. ^ http://72.14.205.104/search?q=cache:-6640GTpnZUJ:www.mind.org.uk/Information/Factsheets/History%2Bof%2Bmental%2Bhealth/Notes%2Bon%2Bthe%2BHistory%2Bof%2BMental%2BHealth%2BCare.htm
  110. ^ http://72.14.205.104/search?q=cache:-6640GTpnZUJ:www.mind.org.uk/Information/Factsheets/History%2Bof%2Bmental%2Bhealth/Notes%2Bon%2Bthe%2BHistory%2Bof%2BMental%2BHealth%2BCare.htm
  111. ^ http://72.14.205.104/search?q=cache:-6640GTpnZUJ:www.mind.org.uk/Information/Factsheets/History%2Bof%2Bmental%2Bhealth/Notes%2Bon%2Bthe%2BHistory%2Bof%2BMental%2BHealth%2BCare.htm
  112. ^ http://72.14.205.104/search?q=cache:-6640GTpnZUJ:www.mind.org.uk/Information/Factsheets/History%2Bof%2Bmental%2Bhealth/Notes%2Bon%2Bthe%2BHistory%2Bof%2BMental%2BHealth%2BCare.htm
  113. ^ http://72.14.205.104/search?q=cache:-6640GTpnZUJ:www.mind.org.uk/Information/Factsheets/History%2Bof%2Bmental%2Bhealth/Notes%2Bon%2Bthe%2BHistory%2Bof%2BMental%2BHealth%2BCare.htm
  114. ^ http://72.14.205.104/search?q=cache:-6640GTpnZUJ:www.mind.org.uk/Information/Factsheets/History%2Bof%2Bmental%2Bhealth/Notes%2Bon%2Bthe%2BHistory%2Bof%2BMental%2BHealth%2BCare.htm
  115. ^ http://72.14.205.104/search?q=cache:-6640GTpnZUJ:www.mind.org.uk/Information/Factsheets/History%2Bof%2Bmental%2Bhealth/Notes%2Bon%2Bthe%2BHistory%2Bof%2BMental%2BHealth%2BCare.htm
  116. ^ http://www.priory.com/homol/dephist.htm
  117. ^ Schildkraut, J.J. (1965). "The catecholamine hypothesis of affective disorders: a review of supporting evidence". Am J Psychiatry. 122 (5): 509–22.
  118. ^ Castren, E. (2005). Is Mood Chemistry? Nat Rev Neurosci, : p6(3):241-6 PMID 15738959.
  119. ^ Healy, David. (1999). The Antidepressant Era, Paperback Edition, Harvard University Press. ISBN 0-674-03958-0
  120. ^ http://www.priory.com/homol/dephist.htm
  121. ^ Oxford Concise Dictionary of Quotations, 5th Edition. Oxford University Press. 2006. ISBN 13: 978-0-19-861417-3. {{cite book}}: Check |isbn= value: invalid character (help)
  122. ^ Robinson DJ. Reel Psychiatry:Movie Portrayals of Psychiatric Conditions. Port Huron, Michigan: Rapid Psychler Press. pp. p. 69-70. ISBN 1-894328-07-8. {{cite book}}: |pages= has extra text (help)
  123. ^ Robinson (Reel Psychiatry) p. 67-68


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