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Management of depression

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Management of depression is the treatment of depression that may involve a number of different therapies: medications, behavior therapy, psychotherapy, and medical devices.

Depression is a symptom of some physical diseases; a side effect of some drugs and medical treatments; and a symptom of some mood disorders such as major depressive disorder or dysthymia.[1] Physical causes are ruled out with a clinical assessment of depression that measures vitamins, minerals, electrolytes, and hormones.[2][3][4]

Though psychiatric medication is the most frequently prescribed therapy for major depression,[5] psychotherapy may be effective, either alone or in combination with medication.[6] Combining psychotherapy and antidepressants may provide a "slight advantage", but antidepressants alone or psychotherapy alone are not significantly different from other treatments, like "active intervention controls". ( e.g., sham acupuncture[clarification needed]) Given an accurate diagnosis of major depressive disorder, in general the type of treatment (psychotherapy and/or antidepressants, alternate or other treatments, or active intervention) is "less important than getting depressed patients involved in an active therapeutic program."[7]

Psychotherapy is the treatment of choice in those under the age of 18, with medication offered only in conjunction with the former and generally not as a first line agent. The possibility of depression, substance misuse or other mental health problems in the parents should be considered and, if present and if it may help the child, the parent should be treated in parallel with the child.[8]

Psychotherapy and behavior therapy

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Main article: Psychotherapy

There are a number of different psychotherapies for depression which are provided to individuals or groups by psychotherapists, psychiatrists, psychologists, clinical social workers, counselors or psychiatric nurses. With more chronic forms of depression, the most effective treatment is often considered to be a combination of medication and psychotherapy.[6][9] Psychotherapy is the treatment of choice in people under 18.[8] A meta-analysis examined the effectiveness of psychotherapy for depression across ages from younger than 13 years to older than 75 years. It summarizes results from 366 trials included 36,702 patients. It found that the best results were for young adults, with an average effect size of g=.98 (95% CI, 0.79–1.16).[10] The effects were smallest for young children (<13 years), g = .35 (95% CI, 0.15–0.55), and second largest in the oldest group, g = .97 (95% CI, 0.42–1.52). The study was not able to compare the different types of therapy to each other. Most of the studies with children used therapies originally developed with adults, which may have reduced the effectiveness. The greater benefits with young adults might be due to a large number of studies including college students, who might have an easier time learning therapy skills and techniques.[10] Most of the studies in children were done in the US, whereas in older age groups, more balanced numbers of studies came from Europe and other parts of the world as well.[10]

As the most studied form of psychotherapy for depression, cognitive behavioral therapy (CBT) is thought to work by teaching clients to learn a set of cognitive and behavioral skills, which they can employ on their own. Earlier research suggested that cognitive behavioral therapy was not as effective as antidepressant medication in the treatment of depression; however, more recent research suggests that it can perform as well as antidepressants in treating patients with moderate to severe depression.[11] Beck's treatment manual, Cognitive therapy of depression, has undergone the most research and accumulated the most evidence for its use.[12][13][14] However, a number of other CBT manuals also have evidence to support their effectiveness with depression.[15][16][17][18]

The effect of psychotherapy on patient and clinician rated improvement as well as on revision rates have declined steadily from the 1970s.[19]

A systematic review of data comparing low-intensity CBT (such as guided self-help by means of written materials and limited professional support, and website-based interventions) with usual care found that patients who initially had more severe depression benefited from low-intensity interventions at least as much as less-depressed patients.[20]

A smartphone application designed to treat depression using the principles of Cognitive Behavioral Therapy, named Rejoyn, was approved by the US FDA in 2024.[21]

For the treatment of adolescent depression, one published study found that CBT without medication performed no better than a placebo, and significantly worse than the antidepressant fluoxetine. However, the same article reported that CBT and fluoxetine outperformed treatment with only fluoxetine.[22] Combining fluoxetine with CBT appeared to bring no additional benefit in two different studies[23][24] or, at the most, only marginal benefit, in a fourth study.[25]

Behavior therapy for depression is sometimes referred to as behavioral activation.[26] In addition, behavioral activation appears to take less time and lead to longer lasting change.[27] Two well-researched treatment manuals include Social skills training for depression[28] and Behavioral activation treatment for depression.[29]

Emotionally focused therapy, founded by Sue Johnson and Les Greenberg in 1985, treats depression by identifying and processing underlying emotions. The treatment manual, Facilitating emotional change, outlines treatment techniques.[30] This kind of therapy assumes that our emotions have a strong connection to our sense of identity. It believes that if we are able to foster and understand our emotions, our sense of identity will be healed as a result.

Acceptance and commitment therapy (ACT), a mindfulness form of CBT, which has its roots in behavior analysis, also demonstrates that it is effective in treating depression, and can be more helpful than traditional CBT, especially where depression is accompanied by anxiety and where it is resistant to traditional CBT.[31][32][33]

A review of four studies on the effectiveness of mindfulness-based cognitive therapy (MBCT), a recently developed class-based program designed to prevent relapse, suggests that MBCT may have an additive effect when provided with the usual care in patients who have had three or more depressive episodes, although the usual care did not include antidepressant treatment or any psychotherapy, and the improvement observed may have reflected non-specific or placebo effects.[34] Of note, although Mindfulness-based cognitive therapy for depression prevented relapse of future depressive episodes, there is no research on whether it can cause the remission of a current depressive episode.[35]

Interpersonal psychotherapy (IPT) focuses on the social and interpersonal triggers that may cause depression. There is evidence that it is an effective treatment for depression.[36][37][38] Here, the therapy takes a fairly structured course (often 12 sessions, as in the original research versions) as in the case with CBT; however, the focus is on relationships with others. Unlike family therapy, IPT is an individual format, so it is possible to work on interpersonal themes even if other family members do not come to the session. 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.[39] In a meta-analysis of 16 studies and 4,356 patients, the average improvement in depressive symptoms was an effect size of d = 0.63 (95% CI, 0.36 to 0.90).[38] IPT combined with pharmacotherapy was more effective in preventing relapse than pharmacotherapy alone, number needed to treat = 7.63.[38]

Couples therapy is sometimes recommended for people with depression.[40] The goal of this therapy is to support the person with depression and emphasize the mutually supportive angle often associated with intimate partners and relationships, and provide mutual support for both partners and help manage any interpersonal changes in their relationship.[40]

Psychoanalysis, a school of thought founded by Sigmund Freud that emphasizes the resolution of unconscious mental conflicts,[41] is used by its practitioners to treat clients presenting with major depression.[42] A more widely practiced technique, called psychodynamic psychotherapy, is loosely based on psychoanalysis and has an additional social and interpersonal focus.[43] In a meta-analysis of three controlled trials, psychodynamic psychotherapy was found to be as effective as medication for mild to moderate depression.[44]

Shared care

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Shared decision making is an approach whereby patients and clinicians freely share important evidence when tasked with decision making and where patients are guided to consider the best available options to make an informed decision.[45] The principles are well documented, but there is a gap in that it's hard to apply them in routine clinical practice. The steps have been simplified into five steps. The first step is seeking patient participation in that the health practitioner is tasked with communicating existing choices and therefore inviting them to the decision-making process. The next step involves assisting the patient to explore and compare the treatment options by a critical analysis of the risks and benefits. The third step involves the assessment of the patient's values and what they prefer taking to account what is of paramount urgency to the patient. Step 4 involves decision making where the patient and the practitioner make a conclusive decision on the best option and arrange for subsequent follow up meetings. Finally, the fifth step involves the analysis of the patient's decision'. Five steps for you and your patients to work together to make the best possible health care decisions. The step involves monitoring of the degree of implementation, overcoming of barriers of decision implantation consequently the decisions need to be revisited and optimized thus ensuring the decision has a positive impact on health outcomes. Its success relies on the ability of the health practitioner to create a good interpersonal relationship with the patient. (Stone, 2017)[full citation needed]

Depression is a major problem globally, affecting an estimated 4.4 percent of the world population in 2017, roughly equivalent to 300 million people.[46] The depression is multifactorial and has been on the increase due to societal pressure, genetic association and increase in use of drugs (Zhang et al. 2016)[full citation needed]. incorporation of nursing in management of depression may seem important in that nursing hold a pivotal role in health care delivery where they are they are the health practitioners that have been trained to be versatile from clinical to psychological care Their incorporation shared decision making in treating depression may be important as nurses are known to have the best interpersonal relationship with the patients thus a better collaborative model can be achieved due to this fact (Williams et al. 2016)[full citation needed]. With this in mind, the nurses may serve to administer drugs in management, prepare and maintain the patient's records, interaction with other care staff to achieve optimum care, and organizing therapy sessions (Lu et al. 2019)[full citation needed].

Kathleen Walsh, 2017, recognizes that Dr. Velligan[who?] stated that SDM is of importance in demonstrating patient preferences in decision making when there is no clear approach to treatment. In addition, numerous tools can be used to make the decision making the process easier these include the Controlled Preferences Scale that informs clinicians on how to actively involve patients. She further gives the suggestion that providers need to embrace shared decision making by making sure the patients participate actively in their management thus enabling the success of the model.[47]

Medication

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See also: List of antidepressants

To find the most effective pharmaceutical drug treatment, the dosages of medications must often be adjusted, different combinations of antidepressants tried, or antidepressants changed.[citation needed] Some of the medications have side effects that affect certain people in different ways. The combinations of medication can change these side effects, so it is essential to monitor the changes that occur once we begin medication.

Selective serotonin reuptake inhibitors

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Selective serotonin reuptake inhibitors (SSRIs), such as sertraline (Zoloft, Lustral), escitalopram (Lexapro, Cipralex), fluoxetine (Prozac), paroxetine (Seroxat), and citalopram, are the primary medications considered, due to their relatively mild side effects and broad effect on the symptoms of depression and anxiety, as well as reduced risk in overdose, compared to their older tricyclic alternatives. Those who do not respond to the first SSRI tried can be switched to another. If sexual dysfunction is present prior to the onset of depression, SSRIs should be avoided.[48] Another popular option is to switch to the atypical antidepressant bupropion (Wellbutrin) or to add bupropion to the existing therapy;[49] this strategy is possibly more effective.[50][51] It is not uncommon for SSRIs to cause or worsen insomnia; the sedating noradrenergic and specific serotonergic antidepressant (NaSSA) antidepressant mirtazapine (Zispin, Remeron) can be used in such cases.[52][53][54]

For children and adolescents with moderate-to-severe depressive disorder, fluoxetine seems to be the best treatment (either with or without cognitive behavioural therapy) but more research is needed to be certain.[55][56][57][58] Sertraline, escitalopram, duloxetine might also help in reducing symptoms.[58] In the UK fluoxetine and escitalopram are the only antidepressants recommended for people under the age of 18, though, if a child or adolescent patient is intolerant to fluoxetine, another SSRI may be considered.[59]

Evidence of effectiveness of SSRIs in those with depression complicated by dementia is lacking.[60]

Norepinephrine dopamine reuptake inhibitor

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Some norepinephrine–dopamine reuptake inhibitors can be used as antidepressants.

Norepinephrine reuptake inhibitor

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Norepinephrine reuptake inhibitors (NRIs) can be used as antidepressants.

Serotonin norepinephrine reuptake inhibitor

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Venlafaxine (Effexor) from the SNRI class may be moderately more effective than SSRIs;[61] however, it is not recommended as a first-line treatment because of the higher rate of side effects,[62] and its use is specifically discouraged in children and adolescents.[63]

Tricyclic antidepressant

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Tricyclic antidepressants (TCAs) have a different side effect profile than SSRIs. In a study of inpatients the tricyclic antidepressant amitriptyline, in particular, appears to be more effective.[64][65]

Monoamine oxidase inhibitor

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Monoamine oxidase inhibitors, have historically been plagued by questionable efficacy (although early studies used dosages now considered too low) and life-threatening adverse effects. They are still used only rarely, although newer agents of this class (RIMA), with a better side effect profile, have been developed.[66]

In older patients TCAs and SSRIs are of the same efficacy.[67] However, there are differences between TCA related antidepressants and classical TCAs in terms of side effect profiles and withdrawal when compared to SSRIs.[67]

There is evidence a prominent side-effect of antidepressants, emotional blunting, is confused with a symptom of depression itself. The cited study, according to Professor Linda Gask was:

'funded by a pharmaceutical company (Servier) and two of its authors are employees of that company', which may bias the results. The study authors' note: "emotional blunting is reported by nearly half of depressed patients on antidepressants and that it appears to be common to all monoaminergic antidepressants not only SSRIs". Additionally, they note: "The OQuESA scores are highly correlated with the HAD depression score; emotional blunting cannot be described simply as a side-effect of antidepressant, but also as a symptom of depression. More emotional blunting is associated with a poorer quality of remission.[68]

NMDA antagonists

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See also: NMDA receptor antagonist

Ketamine

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Research on the antidepressant effects of ketamine infusions at subanaesthetic doses has consistently shown rapid (4 to 72 hours) responses from single doses, with substantial improvement in mood in the majority of patients and remission in some. However, these effects are often short-lived, and attempts to prolong the antidepressant effect with repeated doses and extended ("maintenance") treatment have resulted in only modest success.[69] A nasal spray formulation of esketamine, sold under the brand name Spravato, gained FDA approval in 2019 for the treatment of treatment-resistant depression when combined with an oral antidepressant.[70][71]

Zinc

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A 2012 cross-sectional study found an association between zinc deficiency and depressive symptoms among women, but not men,[72] and a 2013 meta-analysis of 17 observational studies found that blood zinc concentrations were lower in depressed subjects than in control subjects.[73] A 2012 meta-analysis found that zinc supplementation as an adjunct to antidepressant drug treatment significantly lowered depressive symptom scores of depressed patients.[74] The potential mechanisms underlying the association between low serum zinc and depression remain unclear, but may involve the regulation of neurotransmitter, endocrine and neurogenesis pathways.[75] Zinc supplementation has been reported to improve symptoms of ADHD and depression.[76][77][78] A 2013 review found that zinc supplementation may be an effective treatment in major depression.[79]

Acetyl-l-carnitine

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Acetylcarnitine levels were lower in depressed patients than controls[80] and in rats it causes rapid antidepressant effects through epigenetic mechanisms.[81] A systematic review and meta-analysis of 12 randomized controlled trials found "supplementation significantly decreases depressive symptoms compared with placebo/no intervention, while offering a comparable effect with that of established antidepressant agents with fewer adverse effects."[82]

Augmentation

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Physicians often add a medication with a different mode of action to bolster the effect of an antidepressant in cases of treatment resistance; a 2002 large community study of 244,859 depressed Veterans Administration patients found that 22% had received a second agent, most commonly a second antidepressant.[83] Stephen M. Stahl, renowned academician in psychopharmacology, has stated resorting to a dynamic psychostimulant, in particular, d-amphetamine is the "classical augmentation strategy for treatment-refractory depression".[84] However, the use of stimulants in cases of treatment-resistant depression is relatively controversial.[85][86]

It is also possible to use a benzodiazepine as to improve sleep without impairing the antidepressant response specially in patients presenting symptoms of insomnia and disturbed sleep. A randomized controlled trial found that the use of eszopiclone with fluoxetine resulted in a better remission rate.[87]

Addition of atypical antipsychotics when the patient has not responded to an antidepressant is also known to increase the effectiveness of antidepressant drugs, albeit at the cost of more frequent and potentially serious side effects.[88]

Lithium

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Lithium has been used to augment antidepressant therapy in those who have failed to respond to antidepressants alone.[89] Furthermore, lithium dramatically decreases the suicide risk in recurrent depression.[90] According to the results of the STAR-D experiment, the remission rate of lithium for treatment-resistant depression is about 15.9%.[91]

Thyroid hormones

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There is some evidence for the addition of a thyroid hormone, triiodothyronine, in patients with normal thyroid function.[92]

For TRD patients, T3 has been studied in the STAR-D study with having a remission rate of 24.7%. T4 is also being studied for this purpose and found remission rates of 21.5%–64.7% for TRD patients.[93]

Regulatory status, efficacy and tolerability of adjunctive treatments in depression

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Drug MHRA approved as an adjunct?[94] TGA approved as an adjunct?[95] FDA approved as an adjunct?[96] OR for non-response over antidepressant monotherapy[97] Mean difference for MADRS[97] Mean difference for HAM-D[97] OR for leaving the study early due to any reason[97] OR for leaving the study early due to adverse effects[97] OR for significant weight gain[97] Mean difference for weight gain (kg)[97] OR for sedation[97]
Aripiprazole No No Yes 0.48 (0.37–0.63) −3.04 (−4.09,0.00) ND 1.21 (0.86, 1.71) 2.59 (1.18, 5.71) 5.93 (2.15, 16.36) 1.07 (0.30, 1.84) 3.42 (0.66, 17.81)
Lithium[98] No No. But listed in the Australian Medicines Handbook as an accepted use of lithium treatment.[99] No 0.47 (0.27-0.81) No data No data No data No data No data No data No data
Olanzapine No No Yes (in combination with fluoxetine) 0.70 (0.48, 1.02) −2.84 (−5.84,−0.20) −7.90 (−16.63, 0.83) 1.22 (0.82, 1.83) 3.51 (1.58, 7.80) 12.14 (0.70, 208.95) 4.58 (4.06, 5.09) 3.53 (1.64, 7.60)
Quetiapine Yes Yes Yes 0.66 (0.51, 0.87) −2.67 (−4.00, −1.34) −2.67 (−3.79, −1.55) 0.75 (0.26, 2.14) 5.59 (1.47, 21.26) 3.06 (1.22, 7.68) 1.11 (0.56, 1.66) 8.79 (4.90, 15.77)
Risperidone No No No 0.57 (0.36, 0.89) −1.85 (−9.17, 5.47) −1.69 (−4.13, 0.74) 1.04 (0.59, 1.83) 2.11 (0.79, 5.68) 3.32 (0.99, 11.12) 1.80 (0.95, 2.65) 1.10 (0.31, 3.99)

Efficacy of medication and psychotherapy

[edit]

Antidepressants are statistically superior to placebo but their overall effect is low-to-moderate. In that respect they often did not exceed the National Institute for Health and Clinical Excellence criteria for a "clinically significant" effect. In particular, the effect size was very small for moderate depression but increased with severity, reaching "clinical significance" for very severe depression.[100][101] These results were consistent with the earlier clinical studies in which only patients with severe depression benefited from either psychotherapy or treatment with an antidepressant, imipramine, more than from the placebo treatment.[102][103][104] Despite obtaining similar results, the authors argued about their interpretation. One author concluded that there "seems little evidence to support the prescription of antidepressant medication to any but the most severely depressed patients, unless alternative treatments have failed to provide benefit."[100] The other author agreed that "antidepressant 'glass' is far from full" but disagreed "that it is completely empty". He pointed out that the first-line alternative to medication is psychotherapy, which does not have superior efficacy.[105]

Antidepressants in general are as effective as psychotherapy for major depression, and this conclusion holds true for both severe and mild forms of MDD.[106][107] In contrast, medication gives better results for dysthymia.[106][107] The subgroup of SSRIs may be slightly more efficacious than psychotherapy. On the other hand, significantly more patients drop off from the antidepressant treatment than from psychotherapy, likely because of the side effects of antidepressants.[106] Successful psychotherapy appears to prevent the recurrence of depression even after it has been terminated or replaced by occasional "booster" sessions. The same degree of prevention can be achieved by continuing antidepressant treatment.[107]

Two studies suggest that the combination of psychotherapy and medication is the most effective way to treat depression in adolescents. Both TADS (Treatment of Adolescents with Depression Study) and TORDIA (Treatment of Resistant Depression in Adolescents) showed very similar results. TADS resulted in 71% of their teen subjects having "much" or "very much" improvement in mood over the 61% with medication alone and 43% with CBT alone.[108] Similarly, TORDIA showed a 55% improvement with CBT and drugs versus a 41% with drug therapy alone.[108] However, a more recent meta-analysis of 34 trials of 14 drugs used with children and adolescents found that only fluoxetine produced significant benefit compared to placebo, with a medium-sized effect (standardize mean difference = .5).[109]

Treatment resistance

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The risk factors[110] for treatment resistant depression are: the duration of the episode of depression, severity of the episode, if bipolar, lack of improvement in symptoms within the first couple of treatment weeks, anxious or avoidant and borderline comorbidity and old age. Treatment resistant depression is best handled with a combination of conventional antidepressant together with atypical antipsychotics. Another approach is to try different antidepressants. It's inconclusive which approach is superior. Treatment resistant depression can be misdiagnosed if subtherapeutic doses of antidepressants is the case, patient nonadherence, intolerable adverse effects or their thyroid disease or other conditions is misdiagnosed as depression.

Experimental treatments

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Ayahuasca

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Research into ayahuasca has been recommended, given there is limited early evidence of potential antidepressant and anxiolytic effects.[111][112][113]

Chromium

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Clinical and experimental studies have reported antidepressant activity of chromium particularly in atypical depression, characterized by increased appetite and carbohydrate craving.[114]

Creatine

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The amino acid creatine, commonly used as a supplement to improve the performance of bodybuilders, has been studied for its potential antidepressant properties. A review found that creatine "has the potential to improve these disruptions [of brain metabolism] in some patients, and early clinical trials indicate that it may have efficacy as an antidepressant agent."[115] Studies on mice have found that the antidepressant effects of creatine can be blocked by dopamine receptor antagonists such as haloperidol, suggesting that the drug acts on dopamine pathways.[116]

Inositol

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Inositol, a sugar alcohol in fruits, beans, grains and nuts, was found to be significantly better than placebo in treating depression in a double-blind, controlled trial.[117] It was also reported to be reduced in human CSF in depression and found to lead to "major improvement" in 9 of 11 depressed patients in an open label trial.[118]

Magnesium

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A meta-analysis has found an association between magnesium intake and depression.[119] Magnesium was lower in serum of depressed patients than controls.[120]

A 2018 review found that Mg2+ supplementation (range 225–4000 mg) and number of weeks of treatment (range 1–12) were not related to changes in mood disorder.[119]

Essential fatty acids

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There is insufficient evidence to determine that omega-3 fatty acid has any effect on depression.[121] A 2016 review found that if trials with formulations containing mostly eicosapentaenoic acid (EPA) are separated from trials using formulations containing docosahexaenoic acid (DHA), it appeared that EPA may have an effect while DHA may not, but there was insufficient evidence to be sure.[122]

A 2020 meta-analysis showed that a high dose of omega-3 polyunsaturated fatty acid (>2 g/day) used as an adjuvent improved depressive symptoms.[123]

Dopamine receptor agonist

[edit]

Some research suggests dopamine receptor agonists, most commonly pramipexole, may be effective in treating depression. Studies are few and results are preliminary, however.[124]

N-Acetylcysteine

[edit]

A systematic review and meta-analysis of 5 studies found that N-acetylcysteine reduces depressive symptoms more than placebo and has good tolerability.[125] N-acetylecysteine may exert its benefits by replenishing the chief cellular antioxidant, glutathione, thus modulating glutamatergic, neurotropic and inflammatory pathways.[126]

Psilocybin

[edit]

Psilocybin has been shown in several studies to improve symptoms in people with treatment-resistant depression.[127] In 2018 and 2019, the FDA designated psilocybin as a "breakthrough therapy" for drug-resistant depression and major depressive disorder.[128]

St John's wort

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Main article: St John's wort

A 2008 Cochrane Collaboration meta-analysis concluded that "The available evidence suggests that the hypericum extracts tested in the included trials a) are superior to placebo in patients with major depression; b) are similarly effective as standard antidepressants; c) and have fewer side effects than standard antidepressants. The association of country of origin and precision with effects sizes complicates the interpretation."[129] The United States National Center for Complementary and Integrative Health advice is that "St. John's wort may help some types of depression, similar to treatment with standard prescription antidepressants, but the evidence is not definitive." and warns that "Combining St. John's wort with certain antidepressants can lead to a potentially life-threatening increase of serotonin, a brain chemical targeted by antidepressants. St. John's wort can also limit the effectiveness of many prescription medicines."[130]

Rhodiola rosea

[edit]

A 2011 review reported Rhodiola rosea "is an adaptogen plant that can be especially helpful in treating asthenic or lethargic depression, and may be combined with conventional antidepressants to alleviate some of their common side effects."[114]

Saffron

[edit]

A 2013 meta-analysis found that saffron supplementation significantly reduced depression symptoms compared to placebo, and both saffron supplementation and the antidepressant groups were similarly effective in reducing depression symptoms.[131] A 2015 meta-analysis supported the "efficacy of saffron as compared to placebo in improving the following conditions: depressive symptoms (compared to anti-depressants and placebo), premenstrual symptoms, and sexual dysfunction. In addition, saffron use was also effective in reducing excessive snacking behavior."[132] Therapeutic doses of saffron exhibits no significant toxicity in both clinical and experimental investigations.[133]

SAMe

[edit]

S-Adenosyl methionine (SAMe) is available as a prescription antidepressant in Europe and an over-the-counter dietary supplement in the US. Evidence from 16 clinical trials with a small number of subjects, reviewed in 1994 and 1996 suggested it to be more effective than placebo and as effective as standard antidepressant medication for the treatment of major depression.[134][needs update]

Tryptophan and 5-HTP

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The amino acid tryptophan is converted into 5-hydroxytryptophan (5-HTP) which is subsequently converted into the neurotransmitter serotonin. Since serotonin deficiency has been recognized as a possible cause of depression, it has been suggested that consumption of tryptophan or 5-HTP may therefore improve depression symptoms by increasing the level of serotonin in the brain.[135] 5-HTP and tryptophan are sold over the counter in North America, but requires a prescription in Europe. The use of 5-HTP instead of tryptophan bypasses the conversion of tryptophan into 5-HTP by the enzyme tryptophan hydroxylase, which is the rate-limiting step in the synthesis of serotonin, and 5-HTP easily crosses the blood–brain barrier unlike tryptophan, which requires a transporter.[114]

Small studies have been performed using 5-HTP and tryptophan as adjunctive therapy in addition to standard treatment for depression. While some studies had positive results, they were criticized for having methodological flaws, and a more recent study did not find sustained benefit from their use.[136] The safety of these medications has not been well studied.[135] Due to the lack of high quality studies, preliminary nature of studies showing effectiveness, the lack of adequate study on their safety, and reports of eosinophilia–myalgia syndrome from contaminated tryptophan in 1989 and 1990,[114] the use of tryptophan and 5-HTP is not highly recommended or thought to be clinically useful.[135][136]

Medical devices

[edit]

A variety of medical devices are in use or under consideration for treatment of depression including devices that offer electroconvulsive therapy, vagus nerve stimulation, repetitive transcranial magnetic stimulation, and cranial electrotherapy stimulation. The use of such devices in the United States requires approval by the U.S. Food and Drug Administration (FDA) after field trials. In 2010 an FDA advisory panel considered the question of how such field trials should be managed. Factors considered were whether drugs had been effective, how many different drugs had been tried, and what tolerance for suicides should be in field trials.[137]

Electroconvulsive therapy

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Main article: Electroconvulsive therapy

In 2004, a meta-analytic review paper found in terms of efficacy, "a significant superiority of ECT in all comparisons: ECT versus simulated ECT, ECT versus placebo, ECT versus antidepressants in general, ECT versus tricyclics and ECT versus monoamine oxidase inhibitors."[138]

Electroconvulsive therapy (ECT) is a standard psychiatric treatment in which seizures are electrically induced in patients to provide relief from psychiatric illnesses.[139]: 1880  ECT is used with informed consent[140] as a last line of intervention for major depressive disorder.[141] Among the elderly, who often experience depression, the efficacy of ECT is difficult to determine due to the lack of trials comparing ECT to other treatments.[142]

A round of ECT is effective for about 50% of people with treatment-resistant major depressive disorder, whether it is unipolar or bipolar.[143] Follow-up treatment is still poorly studied, but about half of people who respond relapse with twelve months.[144]

Aside from effects in the brain, the general physical risks of ECT are similar to those of brief general anesthesia.[145]: 259  Immediately following treatment, the most common adverse effects are confusion and memory loss.[141][146] ECT is considered one of the least harmful treatment options available for severely depressed pregnant women.[147]

A usual course of ECT involves multiple administrations, typically given two or three times per week until the patient no longer has symptoms ECT is administered under anesthetic with a muscle relaxant.[148][unreliable medical source?] 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.[141]

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.[149]

Deep brain stimulation

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The support for the use of deep brain stimulation in treatment-resistant depression comes from a handful of case studies, and this treatment is still in a very early investigational stage.[150] In this technique electrodes are implanted in a specific region of the brain, which is then continuously stimulated.[151] A March 2010 systematic review found that "about half the patients did show dramatic improvement" and that adverse events were "generally trivial" given the younger psychiatric patient population than with movements disorders.[152] Deep brain stimulation is available on an experimental basis only in the United States; no systems are approved by the FDA for this use.[153]

Repetitive transcranial magnetic stimulation

[edit]

Transcranial magnetic stimulation (TMS) or deep transcranial magnetic stimulation is a noninvasive method used to stimulate small regions of the brain. During a TMS procedure, a magnetic field generator, or "coil" is placed near the head of the person receiving the treatment.[154]: 3  The coil produces small electric currents in the region of the brain just under the coil via electromagnetic induction. The coil is connected to a pulse generator, or stimulator, that delivers electric current to the coil.[155]

TMS was approved by the FDA for treatment-resistant major depressive disorder in 2008[156] and as of 2014 clinical evidence supports this use.[157][158] The American Psychiatric Association,[159]: 46  the Canadian Network for Mood and Anxiety Disorders,[160] and the Royal Australia and New Zealand College of Psychiatrists have endorsed rTMS for trMDD.[161]

The response rate is about 29% for TRD patients.[162] Remission rate is about 20%.[163]

Vagus nerve stimulation

[edit]

Vagus nerve stimulation (VNS) uses an implanted electrode and generator to deliver electrical pulses to the vagus nerve, one of the primary nerves emanating from the brain. It is an approved therapy for treatment-resistant depression in the EU and US and is sometimes used as an adjunct to existing antidepressant treatment. The support for this method comes mainly from open-label trials, which indicate that several months may be required to see a benefit.[150] 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 results were more favorable for one of the secondary outcomes. The authors concluded "This study did not yield definitive evidence of short-term efficacy for adjunctive VNS in treatment-resistant depression."[164]

Cranial electrotherapy stimulation

[edit]

A 2014 Cochrane review found insufficient evidence to determine whether or not Cranial electrotherapy stimulation with alternating current is safe and effective for treating depression.[165]

Transcranial direct current stimulation

[edit]

A 2016 meta-analysis of transcranial direct current stimulation (tDCS) reported some efficacy of tDCS in the treatment of acute depressive disorder with moderate effect size, and low efficacy in treatment-resistant depression, and that use of 2 mA current strength over 20 minutes per day over a short time span can be considered safe.[166]

Other treatments

[edit]

Bright light therapy

[edit]
Main article: Seasonal affective disorder
Bright light therapy is sometimes used to treat depression, especially in its seasonal form.

A meta-analysis of bright light therapy commissioned by the American Psychiatric Association found a significant reduction in depression symptom severity associated with bright light treatment. Benefit was found 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.[167] 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 in combination with antidepressants or wake therapy. A moderate statistically significant effect of light therapy was found, with response significantly better than control treatment in high-quality studies, in studies that applied morning light treatment, and with patients who respond to total or partial sleep deprivation.[168] 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.

Exercise

[edit]
Physical exercise is one recommended way to manage mild depression, such as by playing soccer.

The 2013 Cochrane Collaboration review on physical exercise for depression noted that, based upon limited evidence, it is moderately more effective than a control intervention and comparable to psychological or antidepressant drug therapies. Smaller effects were seen in more methodologically rigorous studies.[169] Three subsequent 2014 systematic reviews that included the Cochrane review in their analysis concluded with similar findings: one indicated that physical exercise is effective as an adjunct treatment with antidepressant medication;[170] the other two indicated that physical exercise has marked antidepressant effects and recommended the inclusion of physical activity as an adjunct treatment for mild–moderate depression[171] and mental illness in general. These studies also found smaller effect sizes in more methodologically rigorous studies.[172] All four systematic reviews called for more research in order to determine the efficacy or optimal exercise intensity, duration, and modality.[169][170][171][172] The evidence for brain-derived neurotrophic factor (BDNF) in mediating some of the neurobiological effects of physical exercise[173][174][175] was noted in one review which hypothesized that increased BDNF signaling is responsible for the antidepressant effect.[170] A meta-analysis of 15 studies published in 2022 suggested a curvilinear dose-response relationship between exercise and depression risk, with low levels of exercise showing the best dose-response.[176]

Meditation

[edit]
People meditating in Madison Square Park in New York City

Mindfulness meditation programs may help improve symptoms of depression, but they are no better than active treatments such as medication, exercise, and other behavioral therapies.[177]

Music therapy

[edit]

A 2009 review found that 3 to 10 sessions of music therapy (when added to standard care) resulted in a noticeable improvement in depressive symptoms, with still greater improvement after 16 to 51 sessions.[178]

A 2017 cochrane systematic review found that music therapy added to the usual treatment of depression gives better outcome than the usual treatment alone: "The effect size translates to a difference of 9.8 points on the HAM-D". It also found that there is no significant difference between active and receptive music therapy comparing depression outcome. It is also important to note that music therapy is not associated with more or fewer adverse events than treatment as usual.[179]

Occupational therapy

[edit]

Occupational therapy (OT) is a healthcare profession that involves the use of assessment and intervention to develop, recover, or maintain the meaningful activities, or occupations, of individuals, groups, or communities.[180] It is an independent health profession sometimes categorized as an allied health profession and consists of occupational therapists (OTs) and occupational therapy assistants (OTAs).[181] A person with depression may experience interruptions in sleep, difficulty completing self-care tasks, decreased motivation to participate in leisure activities, decreased concentration for school or job related work, and avoidance of social interactions. Occupational therapy practitioners possess the educational knowledge base in mental health and can contribute to the efforts in mental health promotion, prevention, and intervention.

Winston Churchill is a famous example of someone who treated his depression by occupying himself with work and other productive activities. Out of office, Churchill was prone to depression (his "black dog") as he sensed his political talents being wasted and time passing him by – in all such times, writing provided the antidote.[182]

Sleep

[edit]

Depression is sometimes associated with insomnia (difficulty in falling asleep, early waking, or waking in the middle of the night). The combination of these two results, depression and insomnia, will only worsen the situation. Hence, good sleep hygiene is important to help break this vicious circle.[183] It would include measures such as regular sleep routines, avoidance of stimulants such as caffeine and management of sleeping disorders such as sleep apnea.[184]

Smoking cessation

[edit]

Quitting smoking cigarettes is associated with reduced depression and anxiety, with the effect "equal or larger than" those of antidepressant treatments.[185]

Total/partial sleep deprivation

[edit]
Main article: Wake therapy

Sleep deprivation (skipping a night's sleep) has been found to improve symptoms of depression in 40–60% of patients. Partial sleep deprivation in the second half of the night may be as effective as an all night sleep deprivation session. Improvement may last for weeks, though the majority (50–80%) relapse after recovery sleep. Shifting or reduction of sleep time, light therapy, antidepressant drugs, and lithium have been found to potentially stabilize sleep deprivation treatment effects.[186]

Shared care

[edit]

Shared care, when primary and specialty physicians have joint management of an individual's health care, has been shown to alleviate depression outcomes.[187]

Research

[edit]

Trials are investigating whether botulinum toxin, when used to make a person appear to frown less, stops negative feedback from the face and affects depression.[188]

Psilocybin may have a beneficial role in the treatment of depression.[189][190]

A 2019 meta-analysis found that hypnotherapy may be an effective way of alleviating the symptoms of depression.[191]

No model of depression in animals that fully explains the mechanism of depression has been found as of 2019.[192]

See also

[edit]

References

[edit]
  1. ^ Diagnostic and Statistical Manual of Mental Disorders (Fifth Edition (DSM-5) ed.). American Psychiatric Association. 2013.
  2. ^ 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.
  3. ^ 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.
  4. ^ Dale J, Sorour E, Milner G (2008). "Do psychiatrists perform appropriate physical investigations for their patients? A review of current practices in a general psychiatric inpatient and outpatient setting". Journal of Mental Health. 17 (3): 293–98. doi:10.1080/09638230701498325. S2CID 72755878.
  5. ^ Carson VB (2000). Mental health nursing: the nurse-patient journey. W.B. Saunders. p. 423. ISBN 978-0-7216-8053-8. Archived from the original on 2023-01-11. Retrieved 2016-09-24.
  6. ^ a b "Psychotherapy". The Merck Manual of Diagnosis and Therapy. Archived from the original on 2011-11-09. Retrieved 2011-11-09.
  7. ^ Khan A, Faucett J, Lichtenberg P, Kirsch I, Brown WA (July 30, 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.
  8. ^ a b NICE (2005). NICE Guidelines:depression in children and adolescents. London: NICE. p. 5. ISBN 978-1-84629-074-9. Archived from the original on 2008-09-24. Retrieved 2008-08-16.
  9. ^ Thase ME (1999). "When are psychotherapy and pharmacotherapy combinations the treatment of choice for major depressive disorder?". The Psychiatric Quarterly. 70 (4): 333–346. doi:10.1023/A:1022042316895. PMID 10587988. S2CID 45091134.
  10. ^ a b c Cuijpers P, Karyotaki E, Eckshtain D, Ng MY, Corteselli KA, Noma H, et al. (July 2020). "Psychotherapy for Depression Across Different Age Groups: A Systematic Review and Meta-analysis". JAMA Psychiatry. 77 (7): 694–702. doi:10.1001/jamapsychiatry.2020.0164. PMC 7081149. PMID 32186668.
  11. ^ Roth A, Fonagy P (2006). "Cognitive-Behavioral Therapy Alone and in Combination with medication: University of Minnesota and University of Pennsylvania–Vanderbilt University Studies". What Works for Whom?: A Critical Review of Psychotherapy Research (2nd ed.). Guilford Press. pp. 76–8. ISBN 978-1-59385-272-6.
  12. ^ Beck AT, Rush J, Shaw B, Emery G (1979). Cognitive therapy of depression. New York: Guilford Press.
  13. ^ Pagano J, Kyle BN, Johnson TL (February 2017). "A Manual by Any Other Name: Identifying Psychotherapy Manuals for Resident Training". Academic Psychiatry. 41 (1): 44–50. doi:10.1007/s40596-016-0492-4. PMID 27048607. S2CID 26071140.
  14. ^ Pagano J, Kyle BN, Johnson TL, Saeed SA (June 2017). "Training Psychiatry Residents in Psychotherapy: The Role of Manualized Treatments". The Psychiatric Quarterly. 88 (2): 285–294. doi:10.1007/s11126-016-9476-5. PMID 27785752. S2CID 3440253.
  15. ^ Beck JS (1995). Cognitive therapy: basics and beyond. New York: Guilford Press.
  16. ^ DeRubeis RJ, Beck AK (1988). "Cognitive therapy.". In Dobson KS (ed.). Handbook of cognitive behavioral therapies. New York: Guilford Press. pp. 273–306.
  17. ^ Munoz RF, Miranda J (1986). Group therapy for cognitive behavioral treatment of depression. San Francisco: San Francisco General Hospital Depression Clinic.
  18. ^ Yost EB, Beutler LE, Corbishley MA, Allender JR (1986). Group cognitive therapy: a treatment approach for depressed older adults. Elmsford: Pergamon.
  19. ^ Johnsen TJ, Friborg O (July 2015). "The effects of cognitive behavioral therapy as an anti-depressive treatment is falling: A meta-analysis". Psychological Bulletin. 141 (4): 747–768. doi:10.1037/bul0000015. PMID 25961373.
  20. ^ Bower P, Kontopantelis E, Sutton A, Kendrick T, Richards DA, Gilbody S, et al. (February 2013). "Influence of initial severity of depression on effectiveness of low intensity interventions: meta-analysis of individual patient data". BMJ. 346: f540. doi:10.1136/bmj.f540. PMC 3582703. PMID 23444423.
  21. ^ FDA Newsroom (2024-04-02). "FDA Roundup: April 2nd, 2024". FDA Press Releases. US Food and Drug Administration. Retrieved 4 April 2024. {{cite web}}: |last1= has generic name (help)
  22. ^ March J, Silva S, Petrycki S, Curry J, Wells K, Fairbank J, et al. (August 2004). "Fluoxetine, cognitive-behavioral therapy, and their combination for adolescents with depression: Treatment for Adolescents With Depression Study (TADS) randomized controlled trial". JAMA. 292 (7): 807–820. doi:10.1001/jama.292.7.807. PMID 15315995.
  23. ^ Goodyer I, Dubicka B, Wilkinson P, Kelvin R, Roberts C, Byford S, et al. (July 2007). "Selective serotonin reuptake inhibitors (SSRIs) and routine specialist care with and without cognitive behaviour therapy in adolescents with major depression: randomised controlled trial". BMJ. 335 (7611): 142. doi:10.1136/bmj.39224.494340.55. PMC 1925185. PMID 17556431.
  24. ^ Goodyer IM, Dubicka B, Wilkinson P, Kelvin R, Roberts C, Byford S, et al. (May 2008). "A randomised controlled trial of cognitive behaviour therapy in adolescents with major depression treated by selective serotonin reuptake inhibitors. The ADAPT trial". Health Technology Assessment. 12 (14): iii–iv, ix–60. doi:10.3310/hta12140. PMID 18462573.
  25. ^ Domino ME, Burns BJ, Silva SG, Kratochvil CJ, Vitiello B, Reinecke MA, et al. (May 2008). "Cost-effectiveness of treatments for adolescent depression: results from TADS". The American Journal of Psychiatry. 165 (5): 588–596. doi:10.1176/appi.ajp.2008.07101610. PMID 18413703.
  26. ^ Hopko DR, Lejuez CW, LePage JP, Hopko SD, McNeil DW (September 2003). "A brief behavioral activation treatment for depression. A randomized pilot trial within an inpatient psychiatric hospital" (PDF). Behavior Modification. 27 (4): 458–469. doi:10.1177/0145445503255489. PMID 12971122. S2CID 30950124. Archived from the original (PDF) on 2015-04-02.
  27. ^ Spates CR, Pagoto SL, Kalata A (2006). "A Qualitative And Quantitative Review of Behavioral Activation Treatment of Major Depressive Disorder". The Behavior Analyst Today. 7 (4): 508–518. doi:10.1037/h0100089. S2CID 3337916. Archived from the original on 2022-02-21. Retrieved 2019-07-14.
  28. ^ Bellack AS, Hersen M, Himmelhoch J (1981). "Social skills training for depression: a treatment manual". J Select Ab Serv Cat Select Doc Psychol. 10: 36–92.
  29. ^ Jacobson NS, Martell CR, Dimidjian S (September 2001). "Behavioral activation treatment for depression: Returning to contextual roots". Clinical Psychology: Science and Practice. 8 (3): 255–70. doi:10.1093/clipsy.8.3.255.
  30. ^ Greenberg LS, Rice LN, Elliott R (1993). Facilitating emotional change: the moment-by-moment process. New York: Guilford Press.
  31. ^ Ruiz FJ (2010). "A review of Acceptance and Commitment Therapy (ACT) empirical evidence: Correlational, experimental psychopathology, component and outcome studies". International Journal of Psychology and Psychological Therapy. 10 (1): 125–62. Archived from the original on 2012-02-23. Retrieved 2013-04-30.
  32. ^ "APA website on empirical treatments". Archived from the original on 2010-10-05. Retrieved 2009-09-01.
  33. ^ Hayes S. "State of the ACT Evidence". ContextualPsychology.org. Archived from the original on 2013-01-22. Retrieved 2013-04-30.
  34. ^ 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): 1000–1005. doi:10.1037/0022-006X.75.6.1000. PMID 18085916.
  35. ^ Segal ZV, Williams JM, Teasdale JD (2002). Mindfulness-based cognitive therapy for depression: a new approach to preventing relapse. New York: Guilford Press.
  36. ^ Klerman GL, Weissman MM, Rounsaville BJ, Chevron ES (1984). Interpersonal psychotherapy of depression. New York: Basic Books.
  37. ^ Lipsitz JD, Markowitz JC (December 2013). "Mechanisms of change in interpersonal therapy (IPT)". Clinical Psychology Review. 33 (8): 1134–1147. doi:10.1016/j.cpr.2013.09.002. PMC 4109031. PMID 24100081.
  38. ^ a b c Cuijpers P, Geraedts AS, van Oppen P, Andersson G, Markowitz JC, van Straten A (June 2011). "Interpersonal psychotherapy for depression: a meta-analysis". The American Journal of Psychiatry. 168 (6): 581–592. doi:10.1176/appi.ajp.2010.10101411. PMC 3646065. PMID 21362740.
  39. ^ Weissman MM, Markowitz JC, Klerman GL (2000). Comprehensive Guide to Interpersonal Psychotherapy. New York: Basic Books. ISBN 978-0-465-09566-7.
  40. ^ a b Barbato, Angelo; D'Avanzo, Barbara; Parabiaghi, Alberto (2018-06-08). "Couple therapy for depression". The Cochrane Database of Systematic Reviews. 6 (6): CD004188. doi:10.1002/14651858.CD004188.pub3. ISSN 1469-493X. PMC 6513419. PMID 29882960.
  41. ^ Dworetzky J (1997). Psychology. Pacific Grove, CA, USA: Brooks/Cole Pub. Co. p. 602. ISBN 978-0-314-20412-7.
  42. ^ Doidge N, Simon B, Lancee WJ, First M, Brunshaw J, Brauer L, et al. (2002). "Psychoanalytic patients in the U.S., Canada, and Australia: II. A DSM-III-R validation study". Journal of the American Psychoanalytic Association. 50 (2): 615–627. doi:10.1177/00030651020500021101. PMID 12206545. S2CID 25110425.
  43. ^ Durand VM, Barlow D (1999). Abnormal psychology: An integrative approach. Pacific Grove, CA, USA: Brooks/Cole Pub. Co. ISBN 978-0-534-34742-0.
  44. ^ de Maat S, Dekker J, Schoevers R, van Aalst G, Gijsbers-van Wijk C, Hendriksen M, et al. (June 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): 565–574. doi:10.1002/da.20305. PMID 17557313. S2CID 20373635.
  45. ^ Sanda MG, Cadeddu JA, Kirkby E, Chen RC, Crispino T, Fontanarosa J, et al. (March 2018). "Clinically Localized Prostate Cancer: AUA/ASTRO/SUO Guideline. Part I: Risk Stratification, Shared Decision Making, and Care Options". The Journal of Urology. 199 (3). Ovid Technologies (Wolters Kluwer Health): 683–690. doi:10.1016/j.juro.2017.11.095. PMID 29203269. S2CID 21405694.
  46. ^ Depression and Other Common Mental Disorders: Global Health Estimates (PDF) (Report). Geneva: World Health Organisation. 2017. p. 5. Archived (PDF) from the original on 20 January 2022. Retrieved 17 January 2022.
  47. ^ Walsh K, Sandars J (June 2017). "Shared decision-making tools: do they really involve patients?". British Journal of Hospital Medicine. 78 (6). Mark Allen Group: 304–305. doi:10.12968/hmed.2017.78.6.304. PMID 28614022. Archived from the original on 2024-02-24. Retrieved 2022-06-11.
  48. ^ Sutherland JE, Sutherland SJ, Hoehns JD (March 2003). "Achieving the best outcome in treatment of depression". The Journal of Family Practice. 52 (3): 201–209. PMID 12620174. Archived from the original on 2009-10-02.
  49. ^ 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): 203–210. doi:10.1016/j.biopsych.2005.06.027. PMID 16165100. S2CID 20997303.
  50. ^ Rush AJ, Trivedi MH, Wisniewski SR, Stewart JW, Nierenberg AA, Thase ME, et al. (March 2006). "Bupropion-SR, sertraline, or venlafaxine-XR after failure of SSRIs for depression". The New England Journal of Medicine. 354 (12): 1231–1242. doi:10.1056/NEJMoa052963. PMID 16554525.
  51. ^ Trivedi MH, Fava M, Wisniewski SR, Thase ME, Quitkin F, Warden D, et al. (March 2006). "Medication augmentation after the failure of SSRIs for depression". The New England Journal of Medicine. 354 (12): 1243–1252. doi:10.1056/NEJMoa052964. PMID 16554526.
  52. ^ Mayers AG, Baldwin DS (December 2005). "Antidepressants and their effect on sleep". Human Psychopharmacology. 20 (8): 533–559. doi:10.1002/hup.726. PMID 16229049. S2CID 17912673.
  53. ^ Winokur A, DeMartinis NA, McNally DP, Gary EM, Cormier JL, Gary KA (October 2003). "Comparative effects of mirtazapine and fluoxetine on sleep physiology measures in patients with major depression and insomnia". The Journal of Clinical Psychiatry. 64 (10): 1224–1229. doi:10.4088/JCP.v64n1013. PMID 14658972.
  54. ^ Lawrence RW (August 2004). "Effect of mirtazapine versus fluoxetine on "sleep quality"". The Journal of Clinical Psychiatry. 65 (8): 1149–1150. doi:10.4088/JCP.v65n0818i. PMID 15323610.
  55. ^ "Prozac may be the best treatment for young people with depression – but more research is needed". NIHR Evidence (Plain English summary). National Institute for Health and Care Research. 2020-10-12. doi:10.3310/alert_41917. S2CID 242952585. Archived from the original on 2022-11-06. Retrieved 2022-11-06.
  56. ^ Zhou X, Teng T, Zhang Y, Del Giovane C, Furukawa TA, Weisz JR, et al. (July 2020). "Comparative efficacy and acceptability of antidepressants, psychotherapies, and their combination for acute treatment of children and adolescents with depressive disorder: a systematic review and network meta-analysis". The Lancet. Psychiatry. 7 (7): 581–601. doi:10.1016/S2215-0366(20)30137-1. PMC 7303954. PMID 32563306.
  57. ^ Boaden K, Tomlinson A, Cortese S, Cipriani A (2020-09-02). "Antidepressants in Children and Adolescents: Meta-Review of Efficacy, Tolerability and Suicidality in Acute Treatment". Frontiers in Psychiatry. 11: 717. doi:10.3389/fpsyt.2020.00717. PMC 7493620. PMID 32982805.
  58. ^ a b Hetrick SE, McKenzie JE, Bailey AP, Sharma V, Moller CI, Badcock PB, et al. (May 2021). Cochrane Common Mental Disorders Group (ed.). "New generation antidepressants for depression in children and adolescents: a network meta-analysis". The Cochrane Database of Systematic Reviews. 2021 (5): CD013674. doi:10.1002/14651858.CD013674.pub2. PMC 8143444. PMID 34029378.
  59. ^ "Overview | Depression in children and young people: identification and management | Guidance | NICE". www.nice.org.uk. 25 June 2019. Archived from the original on 2022-10-29. Retrieved 2022-11-06.
  60. ^ 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): 577–585. doi:10.1111/j.1532-5415.2011.03355.x. PMID 21453380. S2CID 2592434.
  61. ^ 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): 1217–1227. doi:10.1016/j.biopsych.2007.03.027. PMID 17588546. S2CID 45621773.
  62. ^ Cipriani A, Geddes JR, Barbui C (February 2007). "Venlafaxine for major depression". BMJ. 334 (7587): 215–216. doi:10.1136/bmj.39098.457720.BE. PMC 1790758. PMID 17272528.
  63. ^ "Depression in children and young people: identification and management in primary, community and secondary care". NHS National Institute for Health and Clinical Excellence. September 2005. Archived from the original on 2022-10-17. Retrieved 2008-08-17.
  64. ^ Anderson IM (1998). "SSRIS versus tricyclic antidepressants in depressed inpatients: a meta-analysis of efficacy and tolerability". Depression and Anxiety. 7 (S1): 11–17. doi:10.1002/(SICI)1520-6394(1998)7:1+<11::AID-DA4>3.0.CO;2-I. PMID 9597346. S2CID 25730459.
  65. ^ 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.
  66. ^ Krishnan KR (2007). "Revisiting monoamine oxidase inhibitors". The Journal of Clinical Psychiatry. 68 (Suppl 8): 35–41. PMID 17640156. Archived from the original on 2012-07-07. Retrieved 2008-08-27.
  67. ^ a b Mottram P, Wilson K, Strobl J (January 2006). "Antidepressants for depressed elderly". The Cochrane Database of Systematic Reviews. 2009 (1): CD003491. doi:10.1002/14651858.CD003491.pub2. PMC 8406818. PMID 16437456.
  68. ^ "What causes emotional blunting in people taking antidepressants?". 2018-02-08. Archived from the original on 2019-04-09. Retrieved 2018-04-25.
  69. ^ Caddy C, Giaroli G, White TP, Shergill SS, Tracy DK (April 2014). "Ketamine as the prototype glutamatergic antidepressant: pharmacodynamic actions, and a systematic review and meta-analysis of efficacy". Therapeutic Advances in Psychopharmacology. 4 (2): 75–99. doi:10.1177/2045125313507739. PMC 3952483. PMID 24688759.
  70. ^ Gastaldon C, Papola D, Ostuzzi G, Barbui C (December 2019). "Esketamine for treatment resistant depression: a trick of smoke and mirrors?". Epidemiology and Psychiatric Sciences. 29. Cambridge University Press (CUP): e79. doi:10.1017/s2045796019000751. PMC 8061126. PMID 31841104.
  71. ^ "FDA approves new nasal spray medication for treatment-resistant depression; available only at a certified doctor's office or clinic". U.S. Food and Drug Administration. 5 March 2019. Archived from the original on 23 July 2021. Retrieved 12 August 2022.
  72. ^ Maserejian NN, Hall SA, McKinlay JB (February 2012). "Low dietary or supplemental zinc is associated with depression symptoms among women, but not men, in a population-based epidemiological survey". Journal of Affective Disorders. 136 (3): 781–788. doi:10.1016/j.jad.2011.09.039. PMC 3272121. PMID 22030131.
  73. ^ Swardfager W, Herrmann N, Mazereeuw G, Goldberger K, Harimoto T, Lanctôt KL (December 2013). "Zinc in depression: a meta-analysis". Biological Psychiatry. 74 (12): 872–878. doi:10.1016/j.biopsych.2013.05.008. PMID 23806573. S2CID 381132.
  74. ^ Lai J, Moxey A, Nowak G, Vashum K, Bailey K, McEvoy M (January 2012). "The efficacy of zinc supplementation in depression: systematic review of randomised controlled trials". Journal of Affective Disorders. 136 (1–2): e31 – e39. doi:10.1016/j.jad.2011.06.022. PMID 21798601.
  75. ^ Wang J, Um P, Dickerman BA, Liu J (May 2018). "Zinc, Magnesium, Selenium and Depression: A Review of the Evidence, Potential Mechanisms and Implications". Nutrients. 10 (5): 584. doi:10.3390/nu10050584. PMC 5986464. PMID 29747386.
  76. ^ Prasad AS (June 2012). "Discovery of human zinc deficiency: 50 years later". Journal of Trace Elements in Medicine and Biology. 26 (2–3): 66–69. Bibcode:2012JTEMB..26...66P. doi:10.1016/j.jtemb.2012.04.004. PMID 22664333.
  77. ^ Chasapis CT, Loutsidou AC, Spiliopoulou CA, Stefanidou ME (April 2012). "Zinc and human health: an update". Archives of Toxicology. 86 (4): 521–534. doi:10.1007/s00204-011-0775-1. PMID 22071549. S2CID 18669835.
  78. ^ Millichap JG, Yee MM (February 2012). "The diet factor in attention-deficit/hyperactivity disorder". Pediatrics. 129 (2): 330–337. doi:10.1542/peds.2011-2199. PMID 22232312. S2CID 14925322.
  79. ^ Swardfager W, Herrmann N, McIntyre RS, Mazereeuw G, Goldberger K, Cha DS, et al. (June 2013). "Potential roles of zinc in the pathophysiology and treatment of major depressive disorder". Neuroscience and Biobehavioral Reviews. 37 (5): 911–929. doi:10.1016/j.neubiorev.2013.03.018. PMID 23567517. S2CID 1725139.
  80. ^ Nasca C, Bigio B, Lee FS, Young SP, Kautz MM, Albright A, et al. (August 2018). "Acetyl-l-carnitine deficiency in patients with major depressive disorder". Proceedings of the National Academy of Sciences of the United States of America. 115 (34): 8627–8632. Bibcode:2018PNAS..115.8627N. doi:10.1073/pnas.1801609115. PMC 6112703. PMID 30061399.
  81. ^ Nasca C, Xenos D, Barone Y, Caruso A, Scaccianoce S, Matrisciano F, et al. (March 2013). "L-acetylcarnitine causes rapid antidepressant effects through the epigenetic induction of mGlu2 receptors". Proceedings of the National Academy of Sciences of the United States of America. 110 (12): 4804–4809. Bibcode:2013PNAS..110.4804N. doi:10.1073/pnas.1216100110. PMC 3607061. PMID 23382250.
  82. ^ Veronese N, Stubbs B, Solmi M, Ajnakina O, Carvalho AF, Maggi S (Feb–Mar 2018). "Acetyl-L-Carnitine Supplementation and the Treatment of Depressive Symptoms: A Systematic Review and Meta-Analysis". Psychosomatic Medicine. 80 (2): 154–159. doi:10.1097/PSY.0000000000000537. PMID 29076953. S2CID 7649619.
  83. ^ Valenstein M, McCarthy JF, Austin KL, Greden JF, Young EA, Blow FC (July 2006). "What happened to lithium? Antidepressant augmentation in clinical settings". The American Journal of Psychiatry. 163 (7): 1219–1225. doi:10.1176/appi.ajp.163.7.1219. PMID 16816227.
  84. ^ Stahl SM (2011). The Prescriber's Guide (Stahl's Essential Psychopharmacology). Cambridge University Press. p. 39.
  85. ^ Kraus MF, Burch EA (October 1992). "Methylphenidate hydrochloride as an antidepressant: controversy, case studies, and review". Southern Medical Journal. 85 (10): 985–991. doi:10.1097/00007611-199210000-00012. PMID 1411740.
  86. ^ Orr K, Taylor D (2007). "Psychostimulants in the treatment of depression : a review of the evidence". CNS Drugs. 21 (3): 239–257. doi:10.2165/00023210-200721030-00004. PMID 17338594. S2CID 35761979.
  87. ^ Howland RH (May 2016). "Oxazepam for the Treatment of Substance Abuse and Depression: Is it Appropriate?". Journal of Psychosocial Nursing and Mental Health Services. 54 (5). SLACK, Inc.: 21–24. doi:10.3928/02793695-20160420-03. PMID 27135891.
  88. ^ Bender KJ (2008-02-01). "Evidence Grows for Value of Antipsychotics as Antidepressant Adjuncts - Psychiatric Times". Psychiatric Times. Archived from the original on 2020-06-13. Retrieved 2008-08-06.
  89. ^ Bschor T (June 2014). "Lithium in the treatment of major depressive disorder". Drugs. 74 (8). Springer Science and Business Media LLC: 855–862. doi:10.1007/s40265-014-0220-x. PMID 24825489. S2CID 12892550.
  90. ^ Guzzetta F, Tondo L, Centorrino F, Baldessarini RJ (March 2007). "Lithium treatment reduces suicide risk in recurrent major depressive disorder". The Journal of Clinical Psychiatry. 68 (3): 380–383. doi:10.4088/JCP.v68n0304. PMID 17388706.
  91. ^ Shelton RC, Osuntokun O, Heinloth AN, Corya SA (February 2010). "Therapeutic options for treatment-resistant depression". CNS Drugs. 24 (2). Springer Science and Business Media LLC: 131–161. doi:10.2165/11530280-000000000-00000. PMID 20088620. S2CID 32936223.
  92. ^ Nierenberg AA, Fava M, Trivedi MH, Wisniewski SR, Thase ME, McGrath PJ, et al. (September 2006). "A comparison of lithium and T(3) augmentation following two failed medication treatments for depression: a STAR*D report". The American Journal of Psychiatry. 163 (9): 1519–30, quiz 1665. doi:10.1176/appi.ajp.163.9.1519. PMID 16946176.
  93. ^ de Sousa RT, Zanetti MV, Brunoni AR, Machado-Vieira R (2015-10-13). "Challenging Treatment-Resistant Major Depressive Disorder: A Roadmap for Improved Therapeutics". Current Neuropharmacology. 13 (5). Bentham Science Publishers Ltd.: 616–635. doi:10.2174/1570159x13666150630173522. PMC 4761633. PMID 26467411.
  94. ^ British National Formulary (BNF) 65. Pharmaceutical Pr; 2013.
  95. ^ "Therapeutic Goods Administration. TGA eBusiness Services [Internet]". Australian Government Department of Health and Ageing. Archived from the original on 21 April 2013. Retrieved 13 September 2013.
  96. ^ Drugs@FDA. "FDA Approved Drug Products". Archived from the original on 14 August 2012. Retrieved 13 September 2013.
  97. ^ a b c d e f g h Komossa K, Depping AM, Gaudchau A, Kissling W, Leucht S (December 2010). Leucht S (ed.). "Second-generation antipsychotics for major depressive disorder and dysthymia". The Cochrane Database of Systematic Reviews (12): CD008121. doi:10.1002/14651858.CD008121.pub2. PMID 21154393.
  98. ^ Bauer M, Dopfmer S (October 1999). "Lithium augmentation in treatment-resistant depression: meta-analysis of placebo-controlled studies". Journal of Clinical Psychopharmacology. 19 (5): 427–434. doi:10.1097/00004714-199910000-00006. PMID 10505584.
  99. ^ Rossi, S, ed. (2013). Australian Medicines Handbook (2013 ed.). Adelaide: The Australian Medicines Handbook Unit Trust. ISBN 978-0-9805790-9-3.
  100. ^ 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.
  101. ^ Turner EH, Matthews AM, Linardatos E, Tell RA, Rosenthal R (January 2008). "Selective publication of antidepressant trials and its influence on apparent efficacy". The New England Journal of Medicine. 358 (3): 252–260. doi:10.1056/NEJMsa065779. PMID 18199864.
  102. ^ Elkin I, Shea MT, Watkins JT, Imber SD, Sotsky SM, Collins JF, et al. (November 1989). "National Institute of Mental Health Treatment of Depression Collaborative Research Program. General effectiveness of treatments". Archives of General Psychiatry. 46 (11): 971–82, discussion 983. doi:10.1001/archpsyc.1989.01810110013002. PMID 2684085.
  103. ^ Elkin I, Gibbons RD, Shea MT, Sotsky SM, Watkins JT, Pilkonis PA, Hedeker D (October 1995). "Initial severity and differential treatment outcome in the National Institute of Mental Health Treatment of Depression Collaborative Research Program". Journal of Consulting and Clinical Psychology. 63 (5): 841–847. doi:10.1037/0022-006X.63.5.841. PMID 7593878.
  104. ^ Sotsky SM, Glass DR, Shea MT, Pilkonis PA, Collins JF, Elkin I, et al. (August 1991). "Patient predictors of response to psychotherapy and pharmacotherapy: findings in the NIMH Treatment of Depression Collaborative Research Program". The American Journal of Psychiatry. 148 (8): 997–1008. doi:10.1176/ajp.148.8.997. PMID 1853989.
  105. ^ Turner EH, Rosenthal R (March 2008). "Efficacy of antidepressants". BMJ. 336 (7643): 516–517. doi:10.1136/bmj.39510.531597.80. PMC 2265347. PMID 18319297.
  106. ^ a b c Cuijpers P, van Straten A, van Oppen P, Andersson G (November 2008). "Are psychological and pharmacologic interventions equally effective in the treatment of adult depressive disorders? A meta-analysis of comparative studies". The Journal of Clinical Psychiatry. 69 (11): e1 – e11. doi:10.4088/jcp.v69n1102. PMID 18945396.
  107. ^ a b c Imel ZE, Malterer MB, McKay KM, Wampold BE (October 2008). "A meta-analysis of psychotherapy and medication in unipolar depression and dysthymia". Journal of Affective Disorders. 110 (3): 197–206. doi:10.1016/j.jad.2008.03.018. PMID 18456340.
  108. ^ a b Van Voorhees BW, Smith S, Ewigman B (November 2008). "Treat depressed teens with medication and psychotherapy". The Journal of Family Practice. 57 (11): 735–79a. PMC 3183842. PMID 19006622.
  109. ^ Cipriani A, Zhou X, Del Giovane C, Hetrick SE, Qin B, Whittington C, et al. (August 2016). "Comparative efficacy and tolerability of antidepressants for major depressive disorder in children and adolescents: a network meta-analysis". Lancet. 388 (10047): 881–890. doi:10.1016/S0140-6736(16)30385-3. hdl:11380/1279478. PMID 27289172. S2CID 19728203. Archived from the original on 2021-10-27. Retrieved 2020-11-30.
  110. ^ Serretti A, Fabbri C (September 2014). "Factors that predispose patients to treatment-resistant depression". Psychiatric Times. 31 (9). Archived from the original on 2018-04-25. Retrieved 2018-04-25.
  111. ^ Nunes AA, Dos Santos RG, Osório FL, Sanches RF, Crippa JA, Hallak JE (2016-05-26). "Effects of Ayahuasca and its Alkaloids on Drug Dependence: A Systematic Literature Review of Quantitative Studies in Animals and Humans". Journal of Psychoactive Drugs. 48 (3). Informa UK Limited: 195–205. doi:10.1080/02791072.2016.1188225. hdl:11449/159021. PMID 27230395. S2CID 5840140.
  112. ^ Carbonaro TM, Gatch MB (September 2016). "Neuropharmacology of N,N-dimethyltryptamine". Brain Research Bulletin. 126 (Pt 1). Elsevier BV: 74–88. doi:10.1016/j.brainresbull.2016.04.016. PMC 5048497. PMID 27126737.
  113. ^ Frecska E, Bokor P, Winkelman M (2016-03-02). "The Therapeutic Potentials of Ayahuasca: Possible Effects against Various Diseases of Civilization". Frontiers in Pharmacology. 7. Frontiers Media SA: 35. doi:10.3389/fphar.2016.00035. PMC 4773875. PMID 26973523.
  114. ^ a b c d Iovieno N, Dalton ED, Fava M, Mischoulon D (May 2011). "Second-tier natural antidepressants: review and critique". Journal of Affective Disorders. 130 (3): 343–357. doi:10.1016/j.jad.2010.06.010. PMID 20579741.
  115. ^ Kious BM, Kondo DG, Renshaw PF (August 2019). "Creatine for the Treatment of Depression". Biomolecules. 9 (9): 406. doi:10.3390/biom9090406. PMC 6769464. PMID 31450809.
  116. ^ Cunha MP, Machado DG, Capra JC, Jacinto J, Bettio LE, Rodrigues AL (November 2012). "Antidepressant-like effect of creatine in mice involves dopaminergic activation". Journal of Psychopharmacology. 26 (11): 1489–1501. doi:10.1177/0269881112447989. PMID 22674968. S2CID 23293173.
  117. ^ Levine J, Barak Y, Gonzalves M, Szor H, Elizur A, Kofman O, Belmaker RH (May 1995). "Double-blind, controlled trial of inositol treatment of depression". The American Journal of Psychiatry. 152 (5): 792–4. doi:10.1176/ajp.152.5.792. PMID 7726322.
  118. ^ Levine J, Gonsalves M, Babur I, Stier S, Elizur A, Kofman O, Belmaker RH (January 1993). "Inositol 6 g daily may be effective in depression but not in schizophrenia". Human Psychopharmacology: Clinical and Experimental. 8 (1): 49–53. doi:10.1002/hup.470080109. S2CID 144478254.
  119. ^ a b Phelan D, Molero P, Martínez-González MA, Molendijk M (July 2018). "Magnesium and mood disorders: systematic review and meta-analysis". BJPsych Open. 4 (4). Royal College of Psychiatrists: 167–179. doi:10.1192/bjo.2018.22. PMC 6034436. PMID 29897029.
  120. ^ You HJ, Cho SE, Kang SG, Cho SJ, Na KS (October 2018). "Decreased serum magnesium levels in depression: a systematic review and meta-analysis". Nordic Journal of Psychiatry. 72 (7): 534–541. doi:10.1080/08039488.2018.1538388. PMID 30444158. S2CID 53564501.
  121. ^ Appleton KM, Voyias PD, Sallis HM, Dawson S, Ness AR, Churchill R, Perry R (November 2021). "Omega-3 fatty acids for depression in adults". The Cochrane Database of Systematic Reviews. 2021 (11). Wiley: CD004692. doi:10.1002/14651858.cd004692.pub5. PMC 8612309. PMID 34817851.
  122. ^ Hallahan B, Ryan T, Hibbeln JR, Murray IT, Glynn S, Ramsden CE, et al. (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. PMC 9406129. PMID 27103682.
  123. ^ Luo XD, Feng JS, Yang Z, Huang QT, Lin JD, Yang B, et al. (May 2020). "High-dose omega-3 polyunsaturated fatty acid supplementation might be more superior than low-dose for major depressive disorder in early therapy period: a network meta-analysis". BMC Psychiatry. 20 (1). Springer Science and Business Media LLC: 248. doi:10.1186/s12888-020-02656-3. PMC 7238659. PMID 32434488.
  124. ^ Dunlop BW, Nemeroff CB (March 2007). "The role of dopamine in the pathophysiology of depression". Archives of General Psychiatry. 64 (3): 327–337. doi:10.1001/archpsyc.64.3.327. PMID 17339521. S2CID 26550661.
  125. ^ Fernandes BS, Dean OM, Dodd S, Malhi GS, Berk M (April 2016). "N-Acetylcysteine in depressive symptoms and functionality: a systematic review and meta-analysis". The Journal of Clinical Psychiatry. 77 (4): e457 – e466. doi:10.4088/JCP.15r09984. PMID 27137430. S2CID 40688371.
  126. ^ Dean O, Giorlando F, Berk M (March 2011). "N-acetylcysteine in psychiatry: current therapeutic evidence and potential mechanisms of action". Journal of Psychiatry & Neuroscience. 36 (2): 78–86. doi:10.1503/jpn.100057. PMC 3044191. PMID 21118657.
  127. ^ Daws RE, Timmermann C, Giribaldi B, Sexton JD, Wall MB, Erritzoe D, et al. (April 2022). "Increased global integration in the brain after psilocybin therapy for depression". Nature Medicine. 28 (4): 844–851. doi:10.1038/s41591-022-01744-z. hdl:10044/1/95521. PMID 35411074. S2CID 248099554.
  128. ^ Marks M (11 October 2021). "A Strategy for Rescheduling Psilocybin". Scientific American. Archived from the original on 13 August 2022. Retrieved 13 August 2022.
  129. ^ Linde K, Berner MM, Kriston L (October 2008). "St John's wort for major depression". The Cochrane Database of Systematic Reviews. 2008 (4): CD000448. doi:10.1002/14651858.CD000448.pub3. PMC 7032678. PMID 18843608.
  130. ^ "St John's Wort and depression". 2011-11-21. Archived from the original on 2015-02-05. Retrieved January 25, 2014.
  131. ^ Hausenblas HA, Saha D, Dubyak PJ, Anton SD (November 2013). "Saffron (Crocus sativus L.) and major depressive disorder: a meta-analysis of randomized clinical trials". Journal of Integrative Medicine. 11 (6): 377–383. doi:10.3736/jintegrmed2013056. PMC 4643654. PMID 24299602.
  132. ^ Hausenblas HA, Heekin K, Mutchie HL, Anton S (July 2015). "A systematic review of randomized controlled trials examining the effectiveness of saffron (Crocus sativus L.) on psychological and behavioral outcomes". Journal of Integrative Medicine. 13 (4): 231–240. doi:10.1016/S2095-4964(15)60176-5. PMC 5747362. PMID 26165367.
  133. ^ Bostan HB, Mehri S, Hosseinzadeh H (February 2017). "Toxicology effects of saffron and its constituents: a review". Iranian Journal of Basic Medical Sciences. 20 (2): 110–121. doi:10.22038/ijbms.2017.8230. PMC 5339650. PMID 28293386.
  134. ^ Mischoulon D, Fava M (November 2002). "Role of S-adenosyl-L-methionine in the treatment of depression: a review of the evidence". The American Journal of Clinical Nutrition. 76 (5): 1158S – 1161S. doi:10.1093/ajcn/76.5.1158s. PMID 12420702.
  135. ^ a b c Shaw K, Turner J, Del Mar C (2002). "Tryptophan and 5-hydroxytryptophan for depression". The Cochrane Database of Systematic Reviews. 2010 (1): CD003198. doi:10.1002/14651858.CD003198. PMC 8711266. PMID 11869656.
  136. ^ a b Ravindran AV, da Silva TL (September 2013). "Complementary and alternative therapies as add-on to pharmacotherapy for mood and anxiety disorders: a systematic review". Journal of Affective Disorders. 150 (3): 707–719. doi:10.1016/j.jad.2013.05.042. PMID 23769610.
  137. ^ Walker EP (8 October 2010). "FDA Panel Looks at Trials of Devices to Treat Depression". Washington: MedPage Today. Archived from the original on 12 October 2010. Retrieved 9 October 2010.
  138. ^ Pagnin D, de Queiroz V, Pini S, Cassano GB (2004). "Efficacy of ECT in depression: a meta-analytic review". The Journal of ECT. 20 (1): 13–20. doi:10.1097/00124509-200403000-00004. PMID 15087991. S2CID 25843283.
  139. ^ Rudorfer MV, Henry ME, Sackeim HA (2003). "Electroconvulsive therapy" (PDF). In Tasman A, Kay J, Lieberman JA (eds.). Psychiatry (Second ed.). Chichester: John Wiley & Sons Ltd. pp. 1865–1901. Archived (PDF) from the original on 2007-08-10. Retrieved 2013-11-03.
  140. ^ Beloucif S (April 2013). "Informed consent for special procedures: electroconvulsive therapy and psychosurgery". Current Opinion in Anesthesiology. 26 (2): 182–5. doi:10.1097/ACO.0b013e32835e7380. PMID 23385317. S2CID 36643014.
  141. ^ a b c "FDA Executive Summary" (PDF). U.S. Food and Drug Administration. Archived (PDF) from the original on 2015-09-24. Retrieved 2019-12-16. Prepared for the January 27–28, 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."
  142. ^ Van der Wurff FB, Stek ML, Hoogendijk WL, Beekman AT (2003). "Electroconvulsive therapy for the depressed elderly". The Cochrane Database of Systematic Reviews. 2015 (2): CD003593. doi:10.1002/14651858.CD003593. PMC 8722425. PMID 12804479.
  143. ^ Dierckx B, Heijnen WT, van den Broek WW, Birkenhäger TK (March 2012). "Efficacy of electroconvulsive therapy in bipolar versus unipolar major depression: a meta-analysis". Bipolar Disorders. 14 (2): 146–50. doi:10.1111/j.1399-5618.2012.00997.x. PMID 22420590. S2CID 44280002.
  144. ^ 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.
  145. ^ Surgeon General (1999). "Chapter 4". Mental Health: A Report of the Surgeon General. Archived from the original on 2007-01-12. Retrieved 2015-01-07.
  146. ^ American Psychiatric Association, et al. (Committee on Electroconvulsive Therapy) (2001). Weiner RD (ed.). The practice of electroconvulsive therapy: recommendations for treatment, training, and privileging (2nd ed.). Washington, DC: American Psychiatric Publishing. ISBN 978-0-89042-206-9. Archived from the original on 2024-02-24. Retrieved 2016-09-24.
  147. ^ Pompili M, Dominici G, Giordano G, Longo L, Serafini G, Lester D, Amore M, Girardi P (December 2014). "Electroconvulsive treatment during pregnancy: a systematic review". Expert Review of Neurotherapeutics. 14 (12): 1377–90. doi:10.1586/14737175.2014.972373. PMID 25346216. S2CID 31209001.
  148. ^ "5 Outdated Beliefs About ECT". 2016-05-17. Archived from the original on 2013-08-08. Retrieved 2013-11-03.
  149. ^ Abbott CC, Gallegos P, Rediske N, Lemke NT, Quinn DK (March 2014). "A review of longitudinal electroconvulsive therapy: neuroimaging investigations". Journal of Geriatric Psychiatry and Neurology. 27 (1): 33–46. doi:10.1177/0891988713516542. PMC 6624835. PMID 24381234.
  150. ^ a b Marangell LB, Martinez M, Jurdi RA, Zboyan H (September 2007). "Neurostimulation therapies in depression: a review of new modalities". Acta Psychiatrica Scandinavica. 116 (3): 174–81. doi:10.1111/j.1600-0447.2007.01033.x. PMID 17655558. S2CID 38081703.
  151. ^ Underwood E (November 2013). "Short-circuiting depression". Science. 342 (6158): 548–51. Bibcode:2013Sci...342..548U. doi:10.1126/science.342.6158.548. PMID 24179199.
  152. ^ Lakhan SE, Callaway E (March 2010). "Deep brain stimulation for obsessive-compulsive disorder and treatment-resistant depression: systematic review". BMC Research Notes. 3: 60. doi:10.1186/1756-0500-3-60. PMC 2838907. PMID 20202203.
  153. ^ "Brain Stimulation Therapies". National Institute of Mental Health. U.S. Department of Health and Human Services. Archived from the original on 2013-11-13. Retrieved 2013-11-21.
  154. ^ "Transcranial magnetic stimulation for treating and preventing migraine". NiCE. January 2014. Archived from the original on 2015-10-04.
  155. ^ Miller MC (26 July 2012). "Magnetic stimulation: a new approach to treating depression?". Harvard Health Publications. Archived from the original on 29 October 2017. Retrieved 2 January 2015.
  156. ^ Melkerson MN (2008-12-16). "Special Premarket 510(k) Notification for NeuroStar® TMS Therapy System for Major Depressive Disorder" (PDF). Food and Drug Administration. Archived (PDF) from the original on 2010-03-31. Retrieved 2010-07-16.
  157. ^ 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)" (PDF). Clinical Neurophysiology. 125 (11): 2150–2206. doi:10.1016/j.clinph.2014.05.021. PMID 25034472. S2CID 206798663. Archived (PDF) from the original on 2022-07-23. Retrieved 2022-07-26.
  158. ^ George MS, Post RM (April 2011). "Daily left prefrontal repetitive transcranial magnetic stimulation for acute treatment of medication-resistant depression". The American Journal of Psychiatry. 168 (4): 356–64. doi:10.1176/appi.ajp.2010.10060864. PMID 21474597.
    (6) Gaynes BN, Lux L, Lloyd S, Hansen RA, Gartlehner G, Thieda P, Brode S, Swinson Evans T, Jonas D, Crotty K, Viswanathan M, Lohr KN (September 2011). "Nonpharmacologic Interventions for Treatment-Resistant Depression in Adults. Comparative Effectiveness Review Number 33. (Prepared by RTI International-University of North Carolina (RTI-UNC) Evidence-based Practice Center)" (PDF). AHRQ Publication No. 11-EHC056-EF. Rockville, Maryland: Agency for Healthcare Research and Quality. p. 36. Archived from the original (PDF) on 2012-05-16. Retrieved 2011-10-11.
  159. ^ Gelenberg AJ, Freeman MP, Markowitz JC, Rosenbaum JF, Thase ME, Trivedi MH, Van Rhoads RS, eds. (2010). "Practice Guidelines for the Treatment of Patients with Major Depressive Disorder" (PDF). American Psychiatric Association (3rd ed.). Archived (PDF) from the original on 2017-06-23. Retrieved 2015-01-02.
  160. ^ Kennedy SH, Lam RW, Parikh SV, Patten SB, Ravindran AV (October 2009). "Canadian Network for Mood and Anxiety Treatments (CANMAT) clinical guidelines for the management of major depressive disorder in adults. Introduction" (PDF). Journal of Affective Disorders. 117 (Suppl 1): S1-2. doi:10.1016/j.jad.2009.06.043. PMID 19682750. Archived from the original (PDF) on 2015-08-23.
  161. ^ Practice and Partnerships Committee (2013). "Position Statement 79. Repetitive Transcranial Magnetic Stimulation". The Royal Australian and New Zealand College of Psychiatrists. Archived from the original on 2017-08-29. Retrieved 2015-01-02.
  162. ^ Cheng CM, Li CT, Tsai SJ (2021). "Current Updates on Newer Forms of Transcranial Magnetic Stimulation in Major Depression". Major Depressive Disorder. Advances in Experimental Medicine and Biology. Vol. 1305. Singapore: Springer Singapore. pp. 333–349. doi:10.1007/978-981-33-6044-0_18. ISBN 978-981-336-043-3. ISSN 0065-2598. PMID 33834408. S2CID 233194002.
  163. ^ Tasman A, Kay J, Lieberman JA, First MB, Riba MB, eds. (2015-03-23). Psychiatry. Chichester, UK: John Wiley & Sons, Ltd. doi:10.1002/9781118753378. ISBN 978-1-118-75337-8.
  164. ^ Rush AJ, Marangell LB, Sackeim HA, George MS, Brannan SK, Davis SM, Howland R, Kling MA, Rittberg BR, Burke WJ, Rapaport MH, Zajecka J, Nierenberg AA, Husain MM, Ginsberg D, Cooke RG (September 2005). "Vagus nerve stimulation for treatment-resistant depression: a randomized, controlled acute phase trial". Biological Psychiatry. 58 (5): 347–54. doi:10.1016/j.biopsych.2005.05.025. PMID 16139580. S2CID 22066326. Archived from the original on 2019-02-27. Retrieved 2019-07-14.
  165. ^ Kavirajan HC, Lueck K, Chuang K (July 2014). "Alternating current cranial electrotherapy stimulation (CES) for depression". The Cochrane Database of Systematic Reviews. 2014 (7): CD010521. doi:10.1002/14651858.CD010521.pub2. PMC 10554095. PMID 25000907.
  166. ^ Palm U, Hasan A, Strube W, Padberg F (December 2016). "tDCS for the treatment of depression: a comprehensive review". European Archives of Psychiatry and Clinical Neuroscience. 266 (8): 681–694. doi:10.1007/s00406-016-0674-9. PMID 26842422. S2CID 1104287.
  167. ^ Golden RN, Gaynes BN, Ekstrom RD, Hamer RM, Jacobsen FM, Suppes T, et al. (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): 656–662. doi:10.1176/appi.ajp.162.4.656. PMID 15800134.
  168. ^ Tuunainen A, Kripke DF, Endo T (2004). Tuunainen A (ed.). "Light therapy for non-seasonal depression". The Cochrane Database of Systematic Reviews. 2004 (2): CD004050. doi:10.1002/14651858.CD004050.pub2. PMC 6669243. PMID 15106233.
  169. ^ a b Cooney GM, Dwan K, Greig CA, Lawlor DA, Rimer J, Waugh FR, et al. (September 2013). "Exercise for depression". The Cochrane Database of Systematic Reviews. 2013 (9): CD004366. doi:10.1002/14651858.CD004366.pub6. PMC 9721454. PMID 24026850. Exercise is moderately more effective than a control intervention for reducing symptoms of depression, but analysis of methodologically robust trials only shows a smaller effect in favour of exercise. When compared to psychological or pharmacological therapies, exercise appears to be no more effective, though this conclusion is based on a few small trials.
  170. ^ a b c Mura G, Moro MF, Patten SB, Carta MG (December 2014). "Exercise as an add-on strategy for the treatment of major depressive disorder: a systematic review". CNS Spectrums. 19 (6): 496–508. doi:10.1017/S1092852913000953. PMID 24589012. S2CID 32304140. Considered overall, the studies included in the present review showed a strong effectiveness of exercise combined with antidepressants. ... Conclusions
    This is the first review to have focused on exercise as an add-on strategy in the treatment of MDD. Our findings corroborate some previous observations that were based on few studies and which were difficult to generalize.41,51,73,92,93 Given the results of the present article, it seems that exercise might be an effective strategy to enhance the antidepressant effect of medication treatments. Moreover, we hypothesize that the main role of exercise on treatment-resistant depression is in inducing neurogenesis by increasing BDNF expression, as was demonstrated by several recent studies.
  171. ^ 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): 259–272. doi:10.1111/sms.12050. PMID 23362828. S2CID 29351791. Physical activity has also become increasingly and firmly associated with improvements in mental health and psychological well-being (Mutrie, 2000; Landers & Arent, 2007). In particular, exercise is believed to be effective in preventing depression and also to significantly reduce depressive symptoms in clinical as well as in nonclinical populations (O'Neal et al., 2000; Landers & Arent, 2007). Several correlational studies show that exercise is negatively related to depressive symptoms (e.g., Galper et al., 2006; Hassmén et al., 2000). Moreover, a considerably large number of intervention studies have by now investigated the effect of various exercise programs on depression and the vast majority of them indicate that exercise significantly reduces depression (e.g., Blumenthal et al., 2007; Martinsen et al., 1985; Singh et al., 1997). ... To date, it is not possible to determine exactly how effective exercise is in reducing depression symptoms in clinical and nonclinical depressed populations, respectively. However, the results from the present meta-analysis as well as from seven earlier meta-analyses (North et al., 1990; Craft & Landers, 1998; Lawlor & Hopker, 2001; Stathopoulou et al., 2006; Mead et al., 2009; Rethorst et al., 2009; Krogh et al., 2011) indicate that exercise has a moderate to large antidepressant effect. Some meta-analytic results (e.g., Rethorst et al., 2009) suggest that exercise may be even more efficacious for clinically depressed people. ... In short, our final conclusion is that exercise may well be recommended for people with mild and moderate depression who are willing, motivated, and physically healthy enough to engage in such a program.
  172. ^ a b Rosenbaum S, Tiedemann A, Sherrington C, Curtis J, Ward PB (September 2014). "Physical activity interventions for people with mental illness: a systematic review and meta-analysis". The Journal of Clinical Psychiatry. 75 (9): 964–974. doi:10.4088/JCP.13r08765. PMID 24813261. This systematic review and meta-analysis found that physical activity reduced depressive symptoms among people with a psychiatric illness. The current meta-analysis differs from previous studies, as it included participants with depressive symptoms with a variety of psychiatric diagnoses (except dysthymia and eating disorders). ... This review provides strong evidence for the antidepressant effect of physical activity; however, the optimal exercise modality, volume, and intensity remain to be determined. ... Conclusion
    Few interventions exist whereby patients can hope to achieve improvements in both psychiatric symptoms and physical health simultaneously without significant risks of adverse effects. Physical activity offers substantial promise for improving outcomes for people living with mental illness, and the inclusion of physical activity and exercise programs within treatment facilities is warranted given the results of this review.
  173. ^ Denham J, Marques FZ, O'Brien BJ, Charchar FJ (February 2014). "Exercise: putting action into our epigenome". Sports Medicine. 44 (2): 189–209. doi:10.1007/s40279-013-0114-1. PMID 24163284. S2CID 30210091. Aerobic physical exercise produces numerous health benefits in the brain. Regular engagement in physical exercise enhances cognitive functioning, increases brain neurotrophic proteins, such as brain-derived neurotrophic factor (BDNF), and prevents cognitive diseases [76–78]. Recent findings highlight a role for aerobic exercise in modulating chromatin remodelers [21, 79–82]. ... These results were the first to demonstrate that acute and relatively short aerobic exercise modulates epigenetic modifications. The transient epigenetic modifications observed due to chronic running training have also been associated with improved learning and stress-coping strategies, epigenetic changes and increased c-Fos-positive neurons ... Nonetheless, these studies demonstrate the existence of epigenetic changes after acute and chronic exercise and show they are associated with improved cognitive function and elevated markers of neurotrophic factors and neuronal activity (BDNF and c-Fos). ... The aerobic exercise training-induced changes to miRNA profile in the brain seem to be intensity-dependent [164]. These few studies provide a basis for further exploration into potential miRNAs involved in brain and neuronal development and recovery via aerobic exercise.
  174. ^ Phillips C, Baktir MA, Srivatsan M, Salehi A (2014). "Neuroprotective effects of physical activity on the brain: a closer look at trophic factor signaling". Frontiers in Cellular Neuroscience. 8: 170. doi:10.3389/fncel.2014.00170. PMC 4064707. PMID 24999318. Moreover, recent evidence suggests that myokines released by exercising muscles affect the expression of brain-derived neurotrophic factor synthesis in the dentate gyrus of the hippocampus, a finding that could lead to the identification of new and therapeutically important mediating factors. ... Studies have demonstrated the intensity of exercise training is positively correlated with BDNF plasma levels in young, healthy individuals (Ferris et al., 2007). Resistance exercise has also been shown to elevate serum BDNF levels in young individuals (Yarrow et al., 2010). Moreover, it has been shown that moderate levels of physical activity in people with AD significantly increased plasma levels of BDNF (Coelho et al., 2014). ... In humans, it has been shown that 4 h of rowing activity leads to increased levels of plasma BDNF from the internal jugular (an indicator of central release from the brain) and radial artery (an indicator of peripheral release; Rasmussen et al., 2009). Seifert et al. (2010) reported that basal release of BDNF increases following 3 months endurance training in young and healthy individuals, as measured from the jugular vein. These trends are augmented by rodent studies showing that endurance training leads to increased synthesis of BDNF in the hippocampal formation (Neeper et al., 1995, 1996). ... Both BDNF and IGF-1 play a significant role in cognition and motor function in humans. ... Multiple large-scale studies in humans have shown that serum levels of IGF-1 are correlated with fitness and as well as body mass indices (Poehlman and Copeland, 1990). Furthermore, animal studies have shown that exercise in rats is associated with increased amounts of IGF-1 in the CSF.
  175. ^ Heinonen I, Kalliokoski KK, Hannukainen JC, Duncker DJ, Nuutila P, Knuuti J (November 2014). "Organ-specific physiological responses to acute physical exercise and long-term training in humans". Physiology. 29 (6): 421–436. doi:10.1152/physiol.00067.2013. PMID 25362636. The Effects of Long-Term Exercise Training
    [A] physically active lifestyle has been shown to lead to higher cognitive performance and delayed or prevented neurological conditions in humans (71, 101, 143, 191). ... The production of brain-derived neurotrophic factor (BDNF), a key protein regulating maintenance and growth of neurons, is known to be stimulated by acute exercise (145), which may contribute to learning and memory. BDNF is released from the brain already at rest but increases two- to threefold during exercise, which contributes 70–80% of circulating BDNF (145).
  176. ^ Pearce M, Garcia L, Abbas A, Strain T, Schuch FB, Golubic R, et al. (June 2022). "Association Between Physical Activity and Risk of Depression: A Systematic Review and Meta-analysis". JAMA Psychiatry. 79 (6): 550–559. doi:10.1001/jamapsychiatry.2022.0609. PMC 9008579. PMID 35416941.
  177. ^ Goyal M, Singh S, Sibinga EM, Gould NF, Rowland-Seymour A, Sharma R, et al. (March 2014). "Meditation programs for psychological stress and well-being: a systematic review and meta-analysis". JAMA Internal Medicine. 174 (3): 357–368. doi:10.1001/jamainternmed.2013.13018. PMC 4142584. PMID 24395196.
  178. ^ Gold C, Solli HP, Krüger V, Lie SA (April 2009). "Dose-response relationship in music therapy for people with serious mental disorders: systematic review and meta-analysis". Clinical Psychology Review. 29 (3): 193–207. doi:10.1016/j.cpr.2009.01.001. PMID 19269725.
  179. ^ Aalbers S, Fusar-Poli L, Freeman RE, Spreen M, Ket JC, Vink AC, et al. (November 2017). "Music therapy for depression". The Cochrane Database of Systematic Reviews. 2017 (11). Wiley: CD004517. doi:10.1002/14651858.cd004517.pub3. PMC 6486188. PMID 29144545.
  180. ^ "What is Occupational Therapy". Canadian Association of Occupational Therapists | Association canadienne des ergothérapeutes. Archived from the original on 2017-06-06. Retrieved 2017-05-24.
  181. ^ "What is Occupational Therapy". Canadian Association of Occupational Therapists | Association canadienne des ergothérapeutes. Archived from the original on 2017-06-06. Retrieved 2017-05-24.
  182. ^ Jenkins, Roy (2001). Churchill. London: Macmillan Press. p. 466, 819. ISBN 978-03-30488-05-1.
  183. ^ "Depression: Management of depression in primary and secondary care, Clinical Guideline 23" (PDF). National Collaborating Centre for Mental Health. London: National Institute for Clinical Excellence (NICE). December 2004. Archived from the original (PDF) on 10 February 2012.
  184. ^ Wirz-Justice A, Benedetti F, Berger M, Lam RW, Martiny K, Terman M, Wu JC (July 2005). "Chronotherapeutics (light and wake therapy) in affective disorders". Psychological Medicine. 35 (7): 939–944. doi:10.1017/S003329170500437X. PMID 16045060.
  185. ^ 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: g1151. doi:10.1136/bmj.g1151. PMC 3923980. PMID 24524926.
  186. ^ Giedke H, Schwärzler F (October 2002). "Therapeutic use of sleep deprivation in depression". Sleep Medicine Reviews. 6 (5): 361–377. doi:10.1053/smrv.2002.0235. PMID 12531127.
  187. ^ Smith SM, Cousins G, Clyne B, Allwright S, O'Dowd T (February 2017). "Shared care across the interface between primary and specialty care in management of long term conditions". The Cochrane Database of Systematic Reviews. 2017 (2): CD004910. doi:10.1002/14651858.CD004910.pub3. PMC 6473196. PMID 28230899.
  188. ^ Schulze J, Neumann I, Magid M, Finzi E, Sinke C, Wollmer MA, Krüger TH (March 2021). "Botulinum toxin for the management of depression: An updated review of the evidence and meta-analysis". Journal of Psychiatric Research. 135: 332–340. doi:10.1016/j.jpsychires.2021.01.016. PMID 33578275. S2CID 231911095.
  189. ^ Goldberg SB, Pace BT, Nicholas CR, Raison CL, Hutson PR (February 2020). "The experimental effects of psilocybin on symptoms of anxiety and depression: A meta-analysis". Psychiatry Research. 284: 112749. doi:10.1016/j.psychres.2020.112749. PMID 31931272. S2CID 209527316.
  190. ^ Vargas AS, Luís Â, Barroso M, Gallardo E, Pereira L (September 2020). "Psilocybin as a New Approach to Treat Depression and Anxiety in the Context of Life-Threatening Diseases-A Systematic Review and Meta-Analysis of Clinical Trials". Biomedicines. 8 (9): 331. doi:10.3390/biomedicines8090331. PMC 7554922. PMID 32899469.
  191. ^ Milling LS, Valentine KE, McCarley HS, LoStimolo LM (January 2019). "A Meta-Analysis of Hypnotic Interventions for Depression Symptoms: High Hopes for Hypnosis?". The American Journal of Clinical Hypnosis. 61 (3): 227–243. doi:10.1080/00029157.2018.1489777. PMID 34874235. S2CID 149965049.
  192. ^ Hao Y, Ge H, Sun M, Gao Y (September 2019). "Selecting an Appropriate Animal Model of Depression". International Journal of Molecular Sciences. 20 (19): 4827. doi:10.3390/ijms20194827. PMC 6801385. PMID 31569393.
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