Management of depression

Depression, for the purposes of this article, refers to the mental disorder known as major depressive disorder. This kind of depression is a recognized clinical condition and is becoming a common condition in developed countries, where up to 20% of the population is affected by this disorder at some stage of their lives.[1] Patients are usually assessed and managed as outpatients, and only admitted to an inpatient mental health unit if they are considered to pose a risk to themselves or others.

The three most commonly indicated treatments for depression are psychotherapy, psychiatric medication, and (in severe cases) electroconvulsive therapy. Psychiatric medication is the primary therapy for major depression.[2], though the Merck Manual suggests also using psychotherapy for best results.[3] 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. Furthermore, pathology in the parents may need to be looked for and addressed in parallel.[4]

Contents

Psychotherapy

There are a number of different psychotherapies for depression, which may be provided to individuals or groups. Psychotherapy can be delivered by a variety of mental health professionals, including psychotherapists, psychiatrists, psychologists, clinical social workers, counselors, and psychiatric nurses. With more complex and chronic forms of depression the most effective treatment is often considered to be a combination of medication and psychotherapy.[5] As mentioned earlier, psychotherapy is the treatment of choice in people under 18.[4]

The most studied form of psychotherapy for depression is cognitive behavioral therapy (CBT), 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.[6]

For the treatment of adolescent depression, one published study found that CBT without medication performed no better than placebo, and significantly worse than the antidepressant fluoxetine. However, the same article reported that CBT and fluoxetine outperformed treatment with only fluoxetine.[7] Combining fluoxetine with CBT appeared to bring no additional benefit in two different studies[8][9] or, at the most, only marginal benefit, in a fourth study.[10]

Behavior therapy for depression is sometimes referred to as behavioral activation[11] Studies exist showing behavioral activation to be superior to CBT.[12] In addition, behavioral activation appears to take less time and lead to longer lasting change.[13]

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.[14]

Interpersonal psychotherapy focuses on the social and interpersonal triggers that may cause depression. There is evidence that it is an effective treatment for depression. Here, the therapy takes a structured course with a set number of weekly sessions (often 12) as in the case of CBT, however the focus is on relationships with others. Therapy can be used to help a person develop or improve interpersonal skills in order to allow him or her to communicate more effectively and reduce stress.[15]

Psychoanalysis, a school of thought founded by Sigmund Freud that emphasizes the resolution of unconscious mental conflicts,[16] is used by its practitioners to treat clients presenting with major depression.[17] A more widely practiced technique, called psychodynamic psychotherapy, is loosely based on psychoanalysis and has an additional social and interpersonal focus.[18] In a meta-analysis of three controlled trials, psychodynamic psychotherapy was found to be as effective as medication for mild to moderate depression.[19]

Medication

To find the most effective pharmaceutical treatment, the dosages of medications must often be adjusted, different combinations of antidepressants tried, or antidepressants changed. Response rates to the first agent administered may be as low as 50%.[20] It may take anywhere from three to eight weeks after the start of medication before its therapeutic effects can be fully discovered. Patients are generally advised not to stop taking an antidepressant suddenly and to continue its use for at least four months to prevent the chance of recurrence. People with chronic depression need to take the medication for the rest of their lives.[21]

Selective serotonin reuptake inhibitors (SSRIs), such as sertraline (Zoloft, Lustral), escitalopram (Lexapro, Cipralex), fluoxetine (Prozac), paroxetine (Seroxat), and citalopram (Cipralex), 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; such a switch results in improvement in almost 50% of cases.[22] Another popular option is to switch to the atypical antidepressant bupropion (Wellbutrin) or to add bupropion to the existing therapy;[23] this strategy is possibly more effective.[24][25] It is not uncommon for SSRIs to cause or worsen insomnia; the sedating antidepressant mirtazapine (Zispin, Remeron) can be used in such cases.[26][27][28] Cognitive Behavioral Therapy for Insomnia can also help to alleviate the insomnia without additional medication. Venlafaxine (Effexor) may be moderately more effective than SSRIs;[29] however, it is not recommended as a first-line treatment because of the higher rate of side effects,[30] and its use is specifically discouraged in children and adolescents.[31] Fluoxetine is the only antidepressant recommended for people under the age of 18.[31] Evidence of effectiveness of SSRIs in those with depression complicated by dementia is lacking.[32]

Tricyclic antidepressants have more side effects than SSRIs and are usually reserved for the treatment of inpatients, for whom the tricyclic antidepressant amitriptyline, in particular, appears to be more effective.[33][34] A different class of antidepressants, the monoamine oxidase inhibitors, have historically been plagued by questionable efficacy and life-threatening adverse effects. They are still used only rarely, although newer agents of this class (RIMA), with a better side effect profile, have been developed.[35]

Augmentation

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.[36] Lithium has been used to augment antidepressant therapy in those who have failed to respond to antidepressants alone.[37] Furthermore, lithium dramatically decreases the suicide risk in recurrent depression.[38] 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 side effects.[39] There is some evidence for the addition of a thyroid hormone, triiodothyronine, in patients with normal thyroid function.[40]

Efficacy of medication and psychotherapy

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.[41][42] 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.[43][44][45] 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."[41] 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.[46]

Antidepressants in general are as effective as psychotherapy for major depression, and this conclusion holds true for both severe and mild forms of MDD.[47][48] In contrast, medication gives better results for dysthymia.[47][48] 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.[47] 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.[48]

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 a "much" or "very much" improvement in mood over the 60.6% with medication alone and the 43.2% with CBT alone.[49] Similarly, TORDIA showed a 54.8% improvement with CBT and drugs verses a 40.5% with drug therapy alone.[49]

Other medications

Numerous alternative treatments have been used to treat depression, whether medications or other kinds of intervention.

Opiates

Various opiates were commonly used as antidepressants until the mid-1950s, when they fell out of favor with medical orthodoxy due to their addictive nature, tolerance buildup issues and their side-effect profile. Today the use of opioids in treating depression is a large taboo in the medical field due to associations with drug abuse; hence, research has proceeded at a very slow rate. A small clinical trial conducted at Harvard Medical School in 1995,[50] demonstrated that a majority of treatment-refractory, unipolar, non-psychotic, major depression patients could be successfully treated with an opioid medication called Buprenorphine, which is a partial μ-agonist and potent κ antagonist. The exact mechanism of its action in depression is not known, as κ (kappa) antagonists are antidepressants in their own right.

In 2006, The Journal of European Neuropsychopharmacology published a follow-up study to the 1995 Harvard experiment, with results consistent with the original Harvard findings. Eleven severely depressed patients, refractory to all the conventional depression treatments, were given small doses of buprenorphine. Most of these patients found the buprenorphine to be of significant benefit. The researchers theorized that "Possibly, the response to opiates describes a special subtype of depressive disorders e.g. corresponding to a dysregulation of the endogenous opioid system and not of the monaminergic system."[51]

Another scientific paper was published in the American Journal of Psychiatry in 1999, detailing how researchers found Oxycodone/Oxymorphone to help 5 out of 6 "incurable" refractory severe depression patients.[52]

Buprenorphine was found to be effective as a treatment for depression in patients that had responded to neither antidepressants nor electroconvulsive therapy.[53]

Other treatments

Treatment using medical devices or equipment

A variety of medical devices are in use or under consideration for treatment of depression including devices which offer electroconvulsive therapy, vagus nerve stimulation, repetitive transcranial magnetic stimulation, and cranial electrotherapy stimulation. Use of such devices in the United States requires approval by the U.S. Food and Drug Administration (FDA) after field trials. In 2010 a 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.[55]

Electroconvulsive therapy

Electroconvulsive therapy (ECT) is a treatment where seizures are electrically induced in anesthetized patients for therapeutic effect. ECT is most often used as a "last resort" (from the perspective of hospital psychiatrists) for severe major depression which has not responded to trials of antidepressant or, less often, psychotherapy or supportive interventions.[56] It has a quicker effect than antidepressant therapy, and thus may be the treatment of choice in emergencies such as catatonic depression where the patient has ceased oral intake of fluid or nutrients, or where there is severe suicidality.[56] Some evidence suggests it is the most effective treatment for depression in the short-term[57] and one study, without a comparison group or assessment of additional treatments given, suggested that in the minority who remit it may be related to improved self-rated quality of life in both the short-term (which was correlated with the degree of amnesia) and after six months.[58] However, the first systematic documentation of the effectiveness of ECT in community practice in the 65 years of its use found much lower remission rates than in prior research, and most of those relapsed.[59] ECT on its own does not usually have a sustained benefit, as virtually all those who remit end up relapsing within 6 months following a course, even when given a placebo.[60] The relapse rate in the first six months may be reduced by the use of psychatric medications or further ECT (though the latter is not recommended by some authorities, such as NICE), but remains high.[61][62] Short-term memory loss, disorientation, headache and other adverse effects are common, as are long-term memory[63] and other neurocognitive deficits, which may persist. The American Psychiatric Association and the National Institute for Health and Clinical Excellence have concluded that the evidence they had suggested that the procedure, when administered according to their standards and without complications, does not cause brain damage in adults.[64][65]

Deep brain stimulation

Deep brain stimulation (DBS) is a neurosurgical treatment that has been used especially to treat movement disorders such as Parkinson's disease. It requires a neurosurgeon to drill a hole in the skull and insert an electrode into the patient's tissue. Then, a device located in the chest transmits a signal to the implanted electrode through wires located underneath the scalp.[66]

Clinical trials are focused on the use of DBS for epilepsy and depression but the FDA has not approved this use. It requires brain surgery and it is therefore the most invasive form of brain stimulation in the treatment of depression.[67]

Other conventional methods of treatment

St John's wort

St John's wort extract is used extensively in Europe to treat mild and moderate depression. It is a prescription antidepressant in several European countries but is classified as an herbal supplement and sold over the counter in the US. Opinions on its efficacy for major depression differ. A systematic meta-analysis of 37 trials conducted by Cochrane Collaboration indicated statistically significant weak-to-moderate effect as compared to placebo. The same meta-analysis found that St John's wort efficacy for major depression is not different from prescription antidepressants.[68] NCCAM and other NIH-affiliated organizations hold that St John's wort has minimal or no effects beyond placebo in the treatment of major depression, based primarily on one study with negative outcome conducted by NCCAM.[69][70]

SAMe

S-Adenosyl methionine (SAMe) is available as a prescription antidepressant in Europe and an over-the-counter dietary supplement in the US. Fairly strong evidence from 16 clinical trials suggests it to be more effective than placebo and as effective as standard antidepressant medication for the treatment of major depression.[71][72][73]

Repetitive transcranial magnetic stimulation

Repetitive transcranial magnetic stimulation (rTMS) use in treatment-resistant depression is supported by multiple controlled studies, and it has been approved for this indication in Europe, Canada and Australia, and now in the US.[74] A 2008 meta-analysis based on 32 trials found a robust effect of this method on depression, and it appeared similarly effective for both uncomplicated depression and depression that is resistant to medication.[75] However, it was inferior to ECT in a side-by-side randomized trial.[76]

Vagus nerve stimulation

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 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.[74] 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 the secondary outcome.[77]

Alternative treatments

Bright light therapy

A meta-analysis of bright light therapy commissioned by the American Psychiatric Association found it to be more effective than placebo—usually dim light—for both seasonal affective disorder and for nonseasonal depression, with effect sizes similar to those for conventional antidepressants. For non-seasonal depression, adding light therapy to the standard antidepressant treatment was not effective.[78] A meta-analysis of light therapy for non-seasonal depression conducted by Cochrane Collaboration, studied a different set of trials, where light was used mostly as an addition to medication or sleep deprivation. A moderate statistically significant effect of light therapy was found; however, it disappeared if a different statistical technique was used.[79] 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.

Acupuncture

A 2004 Cochrane Review concluded that based on the low quality of the evidence base there is "insufficient evidence to determine whether acupuncture is effective in the management of depression."[80] Clinical trials have shown the effect of acupuncture to be comparable with amitriptyline; in addition, specifically electroacupuncture has been found to be more effective in depressive patients with decreased excretion of 3-methyl-4-hydroxy-phenylglycol (the principal metabolite of the central neurotransmitter norepinephrine), while amitriptyline is more effective for those with inhibition in the dexamethasone suppression test.[81] Acupuncture has also been proven to prompt the body to produce greater levels of endorphins.[82]

Exercise

"A 2001 study by the Duke University in North Carolina found that exercise is a more effective treatment for depression than antidepressants, with fewer relapses and a higher recovery rate."[83] An earlier Duke study likewise found patients who completed 30 minutes of brisk exercise at least three times a week had a significantly lower incidence of relapse; "Only 8 percent of patients in the exercise group had their depression return, while 38 percent of the drug-only group and 31 percent of the exercise-plus-drug group relapsed."[84]

Vigorous exercise has significant physiological effects which help to reduce stress and counter depression. Also, by improving fitness and self-esteem, exercise may enable the sufferer to cope better with demanding events and situations and so reduce the likelihood of depressing failure.[85]

Exercise in natural surroundings such as the countryside or parks is especially recommended because contact with nature and green spaces has a positive effect upon mental health.[86] Gardening is an ideal activity of this sort, providing mental, practical and social benefits.[87] The benefits of such exercise in improving mood and self-esteem are experienced primarily in the first five minutes and are strongest in young people.[88]

Deep brain stimulation

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.[74] 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.[89]

Cold Water (Shower, Bath) Therapy

Taking cold showers according to a study led by Nikolai Shevchuk may be an effective way to help treat depression. Shevchuck believes the biological explanation as to why cold showers help with depression involves the stimulation of locus ceruleus or blue spot which is the brain's primary source of norepinephrine. Also affected are beta-endorphin levels.[90]

Tryptophan

Although tryptophan and 5-hydroxytryptophan may be more effective than placebo in alleviating depression according to the Cochrane Collaboration meta-analysis, only 2 out of 108 trials were of sufficient quality to be included in this analysis. The reviewers concluded that they were unable to recommend the drugs for use in major depression.[91]

Tryptophan is the precursor of the neurotransmitter serotonin. It has shown some promise as an antidepressant alone[92] and as an augmenter of antidepressant drugs.[92][93] Foods rich in tryptophan include chickpeas, milk products, eggs, pork, beef, chicken, fish, oats, dates, mangoes, seeds, nuts and spirulina.

Low fructose diet

Fructose malabsorption is poor absorption of fructose and fructans in the intestines. Subjects with this condition show a significantly higher score in the Beck Depression Inventory than normal fructose absorbers.[94] Some minerals and amino acids (among others, tryptophan) are also poorly absorbed. Because of the inadequate supply of precursor molecules, some hormones and neurotransmitters (among others, serotonin) may not be synthesized in sufficient quantities.[95] Treatment is a diet that is low in fructose, fructans and sorbitol. Depression scores were reduced by 65.2% after four weeks on this diet.[96]

Omega-3 fatty acids

Omega-3 fatty acids have been studied in clinical trials for major depression primarily as an adjunctive to antidepressant therapy. A systematic review of 18 such trials found little evidence of a beneficial effect.[97]

DHEA

Dehydroepiandrosterone (DHEA), a metabolic precursor for several hormones including estrogen and testosterone, has been promoted as a remedy for many ailments. Sold in the 1970s and 1980s as a weight-loss aid, it was subsequently banned for over-the-counter sale, but then unbanned, and is currently available as a supplement in the US. It has been shown to be more effective than placebo in two small double-blind trials: in one as an adjunct to antidepressant treatment,[98] and as monotherapy in another.[99] However, a larger placebo-controlled randomized clinical trial reported in the New England Journal of Medicine in 2006 found that DHEA supplementation in elderly men and women had no beneficial effects on quality of life.[100]

Chromium picolinate

Chromium picolinate was found to be equivalent to placebo for atypical depression overall but possibly efficacious in the sub-group of patients with severe carbohydrate craving.[101]

Zinc

Zinc supplementation was found in a small study to augment the effect of antidepressants.[102]

Serum levels of zinc are found to be low in depressed patients and supplementation with zinc has been demonstrated to be of benefit.[103] Most of the zinc found in the human body is located in the brain, mainly in the hippocampus and cerebral cortex area. Lack of zinc influences zinc homeostasis and leads to a change in learning, behavior, mood swings, mental function and epilepsy. Zinc is found in beans, meat, nuts, oysters, whole grains and seeds.

Lithium

In the late 1800s there was a vogue for consumption of lithia water which contained a significant quantity of lithium. Some claimed that this cured depression, but its effectiveness is not clear.[104]

In May 2009, the BBC reported that a Japanese study of lithium in drinking water in the Japan prefecture of Oita, which has a population of more than one million, revealed that the suicide rate was significantly lower in those areas with the highest levels of lithium.[105]

Lithium is also used as the standard drug to treat different mood disorders including depression. See Lithium pharmacology.

Magnesium

Magnesium deficiency is common and may cause depression. Supplementation or changes in diet may therefore be helpful.[106] Foodstuffs rich in magnesium include whole grains, beans and seeds, halibut and spinach.

Cranial electrotherapy stimulation

Cranial electrotherapy stimulation (CES, electrosleep) devices currently on the market have been granted marketing authorization by the FDA based on the legacy waiver, that is because a sufficiently similar device had been marketed before 1976, when the new regulations requiring controlled testing were introduced.[107] The FDA considers them to be the class III devices—"devices for which insufficient information exists to ... provide reasonable assurance of safety and effectiveness"[108] The effects of CES on depression were inconclusive or negative in multiple double-blind studies of psychiatric patients.[109][110][111][112][113] In one of them, four out of six clinically depressed patients dropped out of the study because of the massive worsening of depressive symptoms, with two of them becoming actively suicidal.[113] One of the authors of the latter study cautioned that CES "should not be used as a treatment of choice" for the patients with the primary diagnosis of depression, "and should be used with caution if this diagnosis is suspected."[114] Nevertheless, the CES practitioners continue to employ it as a treatment of choice for depression.[115][116]

Inositol (Vitamin B8)

Inositol or Vitamin B8 has been tested as a treatment for depression in four RCTs, but there is insufficient evidence of therapeutic benefit.[117]

Kanna

Kanna (Sceletium tortuosum) is a succulent herb commonly found in South Africa. In doses as low as 50 mg, users have reported improvements in mood, decreased anxiety, relaxation and a sense of well-being. It contains about 1-1.5% alkaloids and those which are believed to be psychoactive include mesembrine, mesembrenone, mesembrenol and tortuosamine.[118]

There is about 0.3% mesembrine in the leaves and 0.86% in the stems of the plant.[119] This has been shown to be a potent serotonin reuptake inhibitor.[120]

Flower remedies

Bach flower remedies and Australian bush flower essences are prepared from various flowers. Current clinical evidence does not support any hypothesized action or efficacy beyond placebo effects.[121]

Meditation

Mindfulness meditation has been shown to be of medical benefit in a number of ways, including lowering blood pressure and stress levels. The most helpful and gentle form of meditation for a clinically depressed person may be the repetition—silently or aloud—of a mantra.[122][123]

Neurofeedback

Neurofeedback is a form of biofeedback therapy in which brain activity is monitored using an EEG. The output is presented to the patient who is then able to see any variation in the brain waves associated with depression and may then develop some ability to reduce them, so improving their mood. The resulting direct control of mental state is thought to be similar to that achieved by the mental exercises of yoga.[124][125]

Reiki

Reiki is a form of energy medicine which originated in 1922 by Mikao Usui. In the UK, it has been recommended as a complementary medicine for pain management, anxiety and depression by NHS Trusts and Princess of Wales's Foundation of Integrative Medicine, but there is no scientifically satisfactory evidence of its efficacy in the treatment of any medical disorder. Furthermore, reiki's putative mechanism of action postulates a form of energy whose existence has never been scientifically validated.[126]

Religion

Numerous studies and clinical trials have looked at the relationship between religion and depression. These have looked at the matter from Buddhist, Christian and Muslim perspectives. These indicate that religious faith helps to prevent the onset of depression and assists recovery if depression should still occur.[127]

Sleep

Depression is commonly associated with poor sleep (difficulty going to sleep, early waking, and general lassitude during the day). The interaction of the two results in each condition worsening. Good sleep hygiene is therefore important to help break this vicious circle.[128] This would include measures such as regular bed times, avoidance of stimulants such as caffeine and management of disturbances such as sleep apnea. Ironically, sleep deprivation (such as wake therapy) is a temporary treatment for depression.[129]

Qigong

The traditional Chinese exercise of Qigong and related martial arts such as T'ai chi can help to prevent and relieve depression.[130]

Music Therapy

Studies have demonstrated that music can bring about different moods, conditioned by different emotional states. Music has the property of facilitating self-expression and in this way giving vent to disturbing emotional upheavals and dissipating them. Music has been proven that it can reach the sub-cortical centers of the brain and thereby helps to integrate the personality that is being disrupted by unhealthy emotions. Researchers have shown that music therapy is effective in patients. It has been shown that clinically depressed patients who were made to listen to soft, dissonant-free, melodic music gradually became more emotional and rhythmical.[131]

Green/White Tea

A frequent consumption of green tea was associated with a lower prevalence of depressive symptoms in a Japanese study.[132] Researchers conducted a cross-sectional study in 1,058 community-dwelling elderly Japanese individuals 70 years of age. The prevalence of mild and severe depressive symptoms was 34.1 percent and 20.2 percent, respectively. After adjustment for confounding factors, the odds ratios for mild and severe depressive symptoms when higher green tea consumption was compared with green tea consumption of one cup/day were: two to three cups green tea/day and four cups green tea/day. Similar relations were also observed in the case of severe depressive symptoms.

References

  1. ^ "Beyond Blue". http://www.beyondblue.org.au. Retrieved 2007-04-30. 
  2. ^ Carson VB (2000). Mental health nursing: the nurse-patient journey W.B. Saunders. ISBN 9780721680538. pp 423.
  3. ^ The Merck Manual of Diagnosis and Therapy
  4. ^ a b NICE (2005). NICE Guidelines:depression in children and adolsecents. London: NICE. pp. 5. ISBN 1-84629-074-0. http://www.nice.org.uk/Guidance/CG28/QuickRefGuide/pdf/English. Retrieved 2008-08-16. 
  5. ^ Thase, ME (1999). "When are psychotherapy and pharmacotherapy combinations the treatment of choice for major depressive disorder?". Psychiatric Quarterly 70 (4): 333–46. doi:10.1023/A:1022042316895. PMID 10587988. 
  6. ^ Roth, Anthony; Fonagy, Peter (2005) [1996]. What Works for Whom? Second Edition: A Critical Review of Psychotherapy Research. Guilford Press. pp. 78. ISBN 159385272X. 
  7. ^ March J, Silva S, Petrycki S, 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): 807–20. doi:10.1001/jama.292.7.807. PMID 15315995. 
  8. ^ Goodyer I, Dubicka B, Wilkinson P, 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". British Medical Journal 335 (7611): 142. doi:10.1136/bmj.39224.494340.55. PMC 1925185. PMID 17556431. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1925185. 
  9. ^ Goodyer IM, Dubicka B, Wilkinson P, 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 Technol Assess 12 (14): 1–80. PMID 18462573. http://www.hta.ac.uk/execsumm/summ1214.htm. 
  10. ^ Domino ME, Burns BJ, Silva SG, et al. (May 2008). "Cost-effectiveness of treatments for adolescent depression: results from TADS". American Journal of Psychiatry 165 (5): 588–96. doi:10.1176/appi.ajp.2008.07101610. PMID 18413703. 
  11. ^ Hopko, D. R., Lejuez, C. W., Lepage, J. P., Hopko, S. D., & McNeil, D. W. (2004). "A Brief Behavioral Activation Treatment for Depression". Behavior Modification 27 (4): 458–469. doi:10.1177/0145445503255489. PMID 12971122. http://web.utk.edu/~dhopko/BAinpatient.pdf. 
  12. ^ Dimidjian, S., et al. (2006). "Randomized Trial of Behavioral Activation, Cognitive Therapy, and Antidepressant Medication in the Acute Treatment of Adults With Major Depression". Journal of Consulting and Clinical Psychology 74 (4): 658–670. doi:10.1037/0022-006X.74.4.658. PMID 16881773. 
  13. ^ Spates, C. R., Pagoto, S. and Kalata, A. (2006). A Qualitative And Quantitative Review of Behavioral Activation Treatment of Major Depressive Disorder. The Behavior Analyst Today, 7(4), 508-518 [1]
  14. ^ Coelho HF, Canter PH, Ernst E (December 2007). "Mindfulness-based cognitive therapy: Evaluating current evidence and informing future research". Journal of Consulting and Clinical Psychology 75 (6): 1000–05. doi:10.1037/0022-006X.75.6.1000. PMID 18085916. 
  15. ^ Weissman MM, Markowitz JC, Klerman GL (2000). Comprehensive Guide to Interpersonal Psychotherapy. New York: Basic Books. ISBN 0-465-09566-6. 
  16. ^ Dworetzky J (1997). Psychology. Pacific Grove, CA, USA: Brooks/Cole Pub. Co. pp. 602. ISBN 0-314-20412-1. 
  17. ^ Doidge N, Simon B, Lancee WJ, et al. (2002). "Psychoanalytic patients in the US, Canada, and Australia: II. A DSM-III-R validation study". Journal of the American Psychoanalytic Association 50 (2): 615–27. doi:10.1177/00030651020500021101. PMID 12206545. 
  18. ^ Durand VM, Barlow D (1999). Abnormal psychology: An integrative approach. Pacific Grove, CA, USA: Brooks/Cole Pub. Co. ISBN 0-534-34742-8. 
  19. ^ de Maat S, Dekker J, Schoevers R, 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): 565–74. doi:10.1002/da.20305. PMID 17557313. 
  20. ^ Depression Guideline Panel. Depression in primary care. Vol. 2. Treatment of major depression. Clinical practice guideline. No. 5. Rockville, MD: Agency for Health Care Policy and Research, 1999.
  21. ^ Mayo Clinic Staff (2006-03-06). "Depression" (PDF). National Institute of Mental Health (NIMH). http://www.nimh.nih.gov/health/publications/depression/nimhdepression.pdf. Retrieved 2007-10-20. 
  22. ^ Sutherland JE, Sutherland SJ, Hoehns JD (March 2003). "Achieving the best outcome in treatment of depression". Journal of Family Practice 52 (3): 201–09. PMID 12620174. http://www.jfponline.com/Pages.asp?AID=1406. 
  23. ^ Zisook S, Rush AJ, Haight BR, Clines DC, Rockett CB (2006). "Use of bupropion in combination with serotonin reuptake inhibitors". Biological Psychiatry 59 (3): 203–10. doi:10.1016/j.biopsych.2005.06.027. PMID 16165100. 
  24. ^ Rush AJ, Trivedi MH, Wisniewski SR, et al. (2006). "Bupropion-SR, sertraline, or venlafaxine-XR after failure of SSRIs for depression". New England Journal of Medicine 354 (12): 1231–42. doi:10.1056/NEJMoa052963. PMID 16554525. 
  25. ^ Trivedi MH, Fava M, Wisniewski SR, Thase ME, Quitkin F, Warden D, Ritz L, Nierenberg AA, Lebowitz BD, Biggs MM, Luther JF, Shores-Wilson K, Rush AJ (2006). "Medication augmentation after the failure of SSRIs for depression". New England Journal of Medicine 354 (12): 1243–52. doi:10.1056/NEJMoa052964. PMID 16554526. 
  26. ^ Mayers AG, Baldwin DS (December 2005). "Antidepressants and their effect on sleep". Human Psychopharmacology 20 (8): 533–59. doi:10.1002/hup.726. PMID 16229049. 
  27. ^ 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". Journal of Clinical Psychiatry 64 (10): 1224–29. doi:10.4088/JCP.v64n1013. PMID 14658972. 
  28. ^ Lawrence RW (August 2004). "Effect of mirtazapine versus fluoxetine on "sleep quality"". Journal of Clinical Psychiatry 65 (8): 1149–50. doi:10.4088/JCP.v65n0818i. PMID 15323610. http://article.psychiatrist.com/?ContentType=START&ID=10001013. 
  29. ^ Papakostas GI, Thase ME, Fava M, Nelson JC, Shelton RC (December 2007). "Are antidepressant drugs that combine serotonergic and noradrenergic mechanisms of action more effective than the selective serotonin reuptake inhibitors in treating major depressive disorder? A meta-analysis of studies of newer agents". Biological Psychiatry 62 (11): 1217–27. doi:10.1016/j.biopsych.2007.03.027. PMID 17588546. 
  30. ^ Cipriani A, Geddes JR, Barbui C (2007). "Venlafaxine for major depression". British Medical Journal 334 (7587): 215 (editorial). doi:10.1136/bmj.39098.457720.BE. PMC 1790758. PMID 17272528. http://www.bmj.com/cgi/content/full/334/7587/215?grp=1. Retrieved 2008-09-13. 
  31. ^ a b "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. http://www.nice.org.uk/Guidance/CG28. Retrieved 2008-08-17. 
  32. ^ Nelson, JC; Devanand, DP (2011 Apr). "A systematic review and meta-analysis of placebo-controlled antidepressant studies in people with depression and dementia.". Journal of the American Geriatrics Society 59 (4): 577–85. doi:10.1111/j.1532-5415.2011.03355.x. PMID 21453380. 
  33. ^ Anderson IM (1998). "SSRIS versus tricyclic antidepressants in depressed inpatients: A meta-analysis of efficacy and tolerability". Depression and Anxiety 7 Suppl 1: 11–17. doi:10.1002/(SICI)1520-6394(1998)7:1+<11::AID-DA4>3.0.CO;2-I. PMID 9597346. 
  34. ^ 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. http://linkinghub.elsevier.com/retrieve/pii/S0165-0327(99)00092-0. 
  35. ^ Krishnan KR (2007). "Revisiting monoamine oxidase inhibitors". Journal of Clinical Psychiatry 68 Suppl 8: 35–41. PMID 17640156. http://article.psychiatrist.com/?ContentType=START&ID=10003141. 
  36. ^ Valenstein M, McCarthy JF, Austin KL, Greden JF, Young EA, Blow FC (2006). "What happened to lithium? Antidepressant augmentation in clinical settings". American Journal of Psychiatry 163 (7): 1219–25. doi:10.1176/appi.ajp.163.7.1219. PMID 16816227. 
  37. ^ Bauer M, Dopfmer S (1999). "Lithium augmentation in treatment-resistant depression: Meta-analysis of placebo-controlled studies". Journal of Clinical Psychopharmacology 19 (5): 427–34. doi:10.1097/00004714-199910000-00006. PMID 10505584. 
  38. ^ Guzzetta F, Tondo L, Centorrino F, Baldessarini RJ (March 2007). "Lithium treatment reduces suicide risk in recurrent major depressive disorder". J Clin Psychiatry 68 (3): 380–83. doi:10.4088/JCP.v68n0304. PMID 17388706. http://article.psychiatrist.com/?ContentType=START&ID=10002980. 
  39. ^ Bender KJ (2008-02-01). "Evidence Grows for Value of Antipsychotics as Antidepressant Adjuncts - Psychiatric Times". Psychiatric Times. http://www.psychiatrictimes.com/display/article/10168/1147436. Retrieved 2008-08-06. 
  40. ^ Nierenberg AA, Fava M, Trivedi MH, Wisniewski SR, Thase ME, McGrath PJ, Alpert JE, Warden D, Luther JF, Niederehe G, Lebowitz B, Shores-Wilson K, Rush AJ (2006). "A comparison of lithium and T(3) augmentation following two failed medication treatments for depression: A STAR*D report". American Journal of Psychiatry 163 (9): 1519–30. doi:10.1176/appi.ajp.163.9.1519. PMID 16946176. 
  41. ^ 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 Med. 5 (2): e45. doi:10.1371/journal.pmed.0050045. PMC 2253608. PMID 18303940. http://medicine.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pmed.0050045&ct=1. 
  42. ^ Turner EH, Matthews AM, Linardatos E, Tell RA, Rosenthal R (January 2008). "Selective publication of antidepressant trials and its influence on apparent efficacy". N. Engl. J. Med. 358 (3): 252–60. doi:10.1056/NEJMsa065779. PMID 18199864. 
  43. ^ Elkin I, Shea MT, Watkins JT, Imber SD, Sotsky SM, Collins JF, Glass DR, Pilkonis PA, Leber WR, Docherty JP (1989). "National Institute of Mental Health Treatment of Depression Collaborative Research Program. General effectiveness of treatments". Archives of General Psychiatry 46 (11): 971–82; discussion 983. PMID 2684085. 
  44. ^ Elkin I, Gibbons RD, Shea MT, Sotsky SM, Watkins JT, Pilkonis PA, Hedeker D (1995). "Initial severity and differential treatment outcome in the National Institute of Mental Health Treatment of Depression Collaborative Research Program". Journal of Consulting and Clinical Psychology 63 (5): 841–47. doi:10.1037/0022-006X.63.5.841. PMID 7593878. 
  45. ^ Sotsky SM, Glass DR, Shea MT, Pilkonis PA, Collins JF, Elkin I, Watkins JT, Imber SD, Leber WR, Moyer J (1991). "Patient predictors of response to psychotherapy and pharmacotherapy: Findings in the NIMH Treatment of Depression Collaborative Research Program". American Journal of Psychiatry 148 (8): 997–1008. PMID 1853989. 
  46. ^ Turner EH, Rosenthal R (March 2008). "Efficacy of antidepressants". BMJ 336 (7643): 516–7. doi:10.1136/bmj.39510.531597.80. PMC 2265347. PMID 18319297. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2265347. 
  47. ^ a b c Cuijpers P, van Straten A, van Oppen P, Andersson G (August 2008). "Are Psychological and Pharmacologic Interventions Equally Effective in the Treatment of Adult Depressive Disorders? A Meta-Analysis of Comparative Studies". Journal of Clinical Psychiatry: e1–e11. http://www.psychiatrist.com/abstracts/abstracts.asp?abstract=oap/ej08r04112.htm. 
  48. ^ 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". J Affect Disord 110 (3): 197–206. doi:10.1016/j.jad.2008.03.018. PMID 18456340. 
  49. ^ a b Van Voorhees, Benjamin W., et al. "Treat depressed teens with medication and psychotherapy. Cover story)." Journal of Family Practice 57.11 (Nov. 2008): 735-739. Academic Search Premier. EBSCO. Pikes Peak Community College. PPCC, Lib, Colorado Springs, Co. 27 June 2009 <http://search.ebscohost.com.libdb.ppcc.edu/login.aspx?direct=true&db=a9h&AN=35265823&site=ehost-live>
  50. ^ J Clin Psychopharmacol 1995 Feb; 15(1):49-57 "Buprenorphine (Temgesic) as an antidepressant". Opioids.com. http://opioids.com/buprenorphine/buprefdep.html. Retrieved 2008-11-06. 
  51. ^ "Coretext results for SELECT * from tblPublications where recNo = 8086". Coretext.org. http://www.coretext.org/show_detail.asp?recno=8086. Retrieved 2008-11-06. 
  52. ^ American Journal of Psychiatry, 156:2017, December 1999 "Use of µ-opiate agonists oxycodone and oxymorphone to treat major depression". Opioids.com. http://opioids.com/antidepressant/opiate.html. Retrieved 2008-11-06. 
  53. ^ Nyhuis, Peter W ; Markus Gastpar ; Norbert Scherbaum (October 2008). "Opiate treatment in depression refractory to antidepressants and electroconvulsive therapy.". J Clin Psychopharmacol. 28 (5): 593–5. doi:10.1097/JCP.0b013e31818638a4. PMID 18794671. 
  54. ^ "Drug treats depression in hours'". BBC. 2006-08-07. http://news.bbc.co.uk/1/hi/health/5253800.stm. Retrieved 2006-09-17. 
  55. ^ "FDA Panel Looks at Trials of Devices to Treat Depression" article by Emily P. Walker, Washington Correspondent, MedPage Today Published: October 08, 2010, accessed October 9, 2010
  56. ^ a b American Psychiatric Association (April 2000). "Practice guideline for the treatment of patients with major depressive disorder". American Journal of Psychiatry 157 (Supp 4): 1–45. PMID 10767867. http://www.guideline.gov/summary/summary.aspx?doc_id=2605#s23. 
  57. ^ The UK ECT Review Group (2003). "Efficacy and safety of electroconvulsive therapy in depressive disorders: A systematic review and meta-analysis". The Lancet 361 (9360): 799–808. doi:10.1016/S0140-6736(03)12705-5. PMID 12642045. http://linkinghub.elsevier.com/retrieve/pii/S0140673603127055. 
  58. ^ McCall WV, Prudic J, Olfson M, Sackeim H (February 2006). "Health-related quality of life following ECT in a large community sample". Journal of Affective Disorders 90 (2–3): 69–74. doi:10.1016/j.jad.2005.12.002. PMID 16412519. 
  59. ^ Prudic J, Olfson M, Marcus SC, Fuller RB, Sackeim HA (2004). "Effectiveness of electroconvulsive therapy in community settings". Biol. Psychiatry 55 (3): 301–12. doi:10.1016/j.biopsych.2003.09.015. PMID 14744473. 
  60. ^ Sackeim HA, Haskett RF, Mulsant BH, Thase ME, Mann JJ, Pettinati HM, Greenberg RM, Crowe RR, Cooper TB, Prudic J.(2001) Continuation pharmacotherapy in the prevention of relapse following electroconvulsive therapy: a randomized controlled trial. JAMA. 2001 Mar 14;285(10):1299-307.
  61. ^ Tew JD, Mulsant BH, Haskett RF, Joan P, Begley AE, Sackeim HA (2007). "Relapse During Continuation Pharmacotherapy after Acute Response to ECT: A Comparison of Usual Care versus Protocolized Treatment". Annals of Clinical Psychiatry 19 (1): 1–4. doi:10.1080/10401230601163360. PMID 17453654. 
  62. ^ Kellner CH, Knapp RG, Petrides G, et al. (December 2006). "Continuation Electroconvulsive Therapy vs Pharmacotherapy for Relapse Prevention in Major Depression: A Multisite Study From the Consortium for Research in Electroconvulsive Therapy (CORE)". Archives of General Psychiatry 63 (12): 1337–44. doi:10.1001/archpsyc.63.12.1337. PMID 17146008. 
  63. ^ Barlow 2005, p. 239
  64. ^ American Psychiatric Association. "Electroconvulsive Therapy (ECT)". http://www.psych.org/research/apire/training_fund/clin_res/index.cfm. Retrieved 2007-12-29. 
  65. ^ National Institute for Clinical Excellence (2003) (PDF). Guidance on the use of electroconvulsive therapy. London: National Institute for Health and Clinical Excellence. ISBN 1-84257-282-2. http://www.nice.org.uk/nicemedia/pdf/59ectfullguidance.pdf. 
  66. ^ "Can a Shock to the Brain Cure Depression?". http://discovermagazine.com/2010/jan-feb/20. Retrieved 2010-07-02. 
  67. ^ "Deep Brain Stimulation". http://www.mayoclinic.com/health/deep-brain-stimulation/MY00184. Retrieved 2010-07-02. 
  68. ^ Linde K, Mulrow CD, Berner M, Egger M (2005). Linde, Klaus. ed. "St John's wort for depression". Cochrane Database Syst Rev (2): CD000448. doi:10.1002/14651858.CD000448.pub2. PMID 15846605. 
  69. ^ St. John's Wort and Depression NCCAM on St John's wort and depression]
  70. ^ How is depression detected and treated? NIMH on depression, including a section on St John's wort
  71. ^ Mischoulon D, Fava M (November 2002). "Role of S-adenosyl-L-methionine in the treatment of depression: a review of the evidence". Am. J. Clin. Nutr. 76 (5): 1158S–61S. PMID 12420702. http://www.ajcn.org/cgi/pmidlookup?view=long&pmid=12420702. 
  72. ^ Bressa GM (1994). "S-adenosyl-l-methionine (SAMe) as antidepressant: meta-analysis of clinical studies". Acta Neurol. Scand., Suppl. 154: 7–14. doi:10.1111/j.1600-0404.1994.tb05403.x. PMID 7941964. 
  73. ^ "Investigating SAMe". Geriatric Times. 2001. http://www.geriatrictimes.com/g010923.html. Retrieved 2006-12-08. 
  74. ^ a b c Marangell LB, Martinez M, Jurdi RA, Zboyan H (September 2007). "Neurostimulation therapies in depression: a review of new modalities". Acta Psychiatr Scand 116 (3): 174–81. doi:10.1111/j.1600-0447.2007.01033.x. PMID 17655558. 
  75. ^ Schutter DJ (April 2008). "Antidepressant efficacy of high-frequency transcranial magnetic stimulation over the left dorsolateral prefrontal cortex in double-blind sham-controlled designs: a meta-analysis". Psychol Med 39 (1): 1–11. doi:10.1017/S0033291708003462. PMID 18447962. 
  76. ^ Eranti S, Mogg A, Pluck G, et al. (January 2007). "A randomized, controlled trial with 6-month follow-up of repetitive transcranial magnetic stimulation and electroconvulsive therapy for severe depression". Am J Psychiatry 164 (1): 73–81. doi:10.1176/appi.ajp.164.1.73. PMID 17202547. 
  77. ^ Rush AJ, Marangell LB, Sackeim HA, et al. (September 2005). "Vagus nerve stimulation for treatment-resistant depression: A randomized, controlled acute phase trial". Biological Psychiatry 58 (5): 347–54. doi:10.1016/j.biopsych.2005.05.025. PMID 16139580. 
  78. ^ Golden RN, Gaynes BN, Ekstrom RD, et al. (April 2005). "The efficacy of light therapy in the treatment of mood disorders: a review and meta-analysis of the evidence". American Journal of Psychiatry 162 (4): 656–62. doi:10.1176/appi.ajp.162.4.656. PMID 15800134. 
  79. ^ Tuunainen A, Kripke DF, Endo T (2004). Tuunainen, Arja. ed. "Light therapy for non-seasonal depression". Cochrane Database Syst Rev (2): CD004050. doi:10.1002/14651858.CD004050.pub2. PMID 15106233. 
  80. ^ Smith, CA; PPJ Hay (2004-03-17). Smith, Caroline A. ed. "Acupuncture for depression". Cochrane Database of Systematic Reviews 2005 (2): CD004046. doi:10.1002/14651858.CD004046.pub2. PMID 15846693. http://www.cochrane.org/reviews/en/ab004046.html. Retrieved 2008-05-02. 
  81. ^ World Health Organisation, Acupuncture: Review and Analysis of Reports on Controlled Clinical Trials, 2002
  82. ^ "ABC Australia Science News on acupuncuture". http://www.abc.net.au/science/news/stories/s27924.htm. 
  83. ^ "How to beat the winter blues". The Independent (London). 2007-11-13. http://www.independent.co.uk/life-style/health-and-wellbeing/healthy-living/how-to-beat-the-winter-blues-400175.html. Retrieved 2010-05-26. 
  84. ^ Merritt, Richard (2000-09-22). "Study: Exercise Has Long-Lasting Effect on Depression". Duke University News. http://dukenews.duke.edu/2000/09/exercise922.html. Retrieved 2007-10-20. 
  85. ^ Keith W. Johnsgard (2004). Conquering Depression and Anxiety Through Exercise. Amherst, N.Y.: Prometheus Books. ISBN 9781591021926. http://books.google.com/?id=A6oIAAAACAAJ 
  86. ^ Nick Higham (23 May 2008). Putting a spring in your step. BBC. http://news.bbc.co.uk/1/hi/sci/tech/7417516.stm 
  87. ^ Gardening aids mentally ill. BBC. 1 May 1999. http://news.bbc.co.uk/1/hi/health/332459.stm 
  88. ^ 'Green' exercise quickly 'boosts mental health'. BBC. 1 May 2010. http://news.bbc.co.uk/1/hi/health/8654350.stm 
  89. ^ Lakhan SE, Callaway H (2010). "Deep brain stimulation for obsessive-compulsive disorder and treatment-resistant depression: systematic review". BMC Research Notes 2010 (3): 60. doi:10.1186/1756-0500-3-60. PMC 2838907. PMID 20202203. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2838907. 
  90. ^ Adapted cold shower as a potential treatment for depression? Medical Hypotheses , Volume 70 , Issue 5 , Pages 995 - 1001 N . Shevchuk Med Hypotheses. 2008;70(5):995-1001. Epub 2007 Nov 13 http://www.ncbi.nlm.nih.gov/pubmed/17993252
  91. ^ Shaw K, Turner J, Del Mar C (2002). Shaw, Kelly A. ed. "Tryptophan and 5-hydroxytryptophan for depression". Cochrane Database Systematic Reviews (1): CD003198. doi:10.1002/14651858.CD003198. PMID 11869656. 
  92. ^ a b Thomson J, Rankin H, Ashcroft GW, Yates CM, McQueen JK, Cummings SW (1982). "The treatment of depression in general practice: a comparison of L-tryptophan, amitriptyline, and a combination of L-tryptophan and amitriptyline with placebo". Psychological medicine 12 (4): 741–51. doi:10.1017/S0033291700049047. PMID 7156248. 
  93. ^ Levitan RD, Shen JH, Jindal R, Driver HS, Kennedy SH, Shapiro CM (2000). "Preliminary randomized double-blind placebo-controlled trial of tryptophan combined with fluoxetine to treat major depressive disorder: antidepressant and hypnotic effects". Journal of psychiatry & neuroscience : JPN 25 (4): 337–46. PMC 1407729. PMID 11022398. http://www.cma.ca/index.cfm/ci_id/12652/la_id/1.htm. 
  94. ^ Ledochowski M, Sperner-Unterweger B, Widner B, Fuchs D (1998). "Fructose malabsorption is associated with early signs of mental depression". Eur. J. Med. Res. 3 (6): 295–8. PMID 9620891. 
  95. ^ Tryptophan, Serotonin, and Melatonin: Basic Aspects and applications, By Gerald Huether
  96. ^ Ledochowski, M.; B. Widner, H. Bair, T. Probst, D. Fuchs (2000). "Fructose- and Sorbitol-reduced Diet Improves Mood and Gastrointestinal Disturbances in Fructose Malabsorbers" (PDF). Scandinavian Journal of Gastroenterology (University of Innsbruck, Innsbruck, Austria: Dept. of Clinical Nutrition, Institute of Medical Chemistry and Biochemistry, and Dept. of Gastroenterology) 35 (10): 1048–1052. doi:10.1080/003655200451162. PMID 11099057. http://www.fructose.at/pdf/works/11099057.pdf. Retrieved November 27, 2008. 
  97. ^ Appleton KM, Hayward RC, Gunnell D, et al. (December 2006). "Effects of n-3 long-chain polyunsaturated fatty acids on depressed mood: systematic review of published trials". Am. J. Clin. Nutr. 84 (6): 1308–16. PMID 17158410. http://www.ajcn.org/cgi/pmidlookup?view=long&pmid=17158410. 
  98. ^ Wolkowitz OM, Reus VI, Keebler A, et al. (April 1999). "Double-blind treatment of major depression with dehydroepiandrosterone". American Journal of Psychiatry 156 (4): 646–49. PMID 10200751. http://ajp.psychiatryonline.org/cgi/pmidlookup?view=long&pmid=10200751. 
  99. ^ Schmidt PJ, Daly RC, Bloch M, et al. (February 2005). "Dehydroepiandrosterone monotherapy in midlife-onset major and minor depression". Archives of General Psychiatry 62 (2): 154–62. doi:10.1001/archpsyc.62.2.154. PMID 15699292. 
  100. ^ Nair, K. S.; Rizza, R. A.; O'Brien, P. et al. (2006). "DHEA in elderly women and DHEA or testosterone in elderly men". N. Engl. J. Med. 355 (16): 1647–59. doi:10.1056/NEJMoa054629. PMID 17050889. 
  101. ^ Docherty JP, Sack DA, Roffman M, Finch M, Komorowski JR (September 2005). "A double-blind, placebo-controlled, exploratory trial of chromium picolinate in atypical depression: effect on carbohydrate craving". J Psychiatr Pract 11 (5): 302–14. doi:10.1097/00131746-200509000-00004. PMID 16184071. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=1527-4160&volume=11&issue=5&spage=302. 
  102. ^ Nowak G, Siwek M, Dudek D, Zieba A, Pilc A (2003). "Effect of zinc supplementation on antidepressant therapy in unipolar depression: a preliminary placebo-controlled study" (PDF). Pol J Pharmacol 55 (6): 1143–7. PMID 14730113. http://www.if-pan.krakow.pl/pjp/pdf/2003/6_1143.pdf. 
  103. ^ Gabriel Nowak, Bernadeta Szewczyk, Andrzej Pilc (2005). "Zinc and depression." (PDF). Pharmacological Reports. http://www.if-pan.krakow.pl/pjp/pdf/2005/6_713.pdf 
  104. ^ Bryan L. Court, Court, Gerald E. Nelson, L. Court Bryan (1996). Bipolar Puzzle Solution. Taylor & Francis. pp. 57. ISBN 9781560324935. http://books.google.com/?id=qq1DZjH0K6cC 
  105. ^ "Lithium in water 'curbs suicide'". BBC News. 2009-05-01. http://news.bbc.co.uk/2/hi/health/8025454.stm. Retrieved 2010-05-26. 
  106. ^ G. Eby, K. Eby (2006). "Rapid recovery from major depression using magnesium treatment.". Medical Hypotheses 67 (2): 362–370. doi:10.1016/j.mehy.2006.01.047. PMID 16542786. http://linkinghub.elsevier.com/retrieve/pii/S0306987706001034 
  107. ^ FDA > CDRH > CFR Title 21 Database Search
  108. ^ FDA 515(i) Reclassification Letter to Manufacturers
  109. ^ Levitt EA, James NM, Flavell P (December 1975). "A clinical trial of electrosleep therapy with a psychiatric inpatient sample". Aust N Z J Psychiatry 9 (4): 287–90. doi:10.3109/00048677509159864. PMID 769773. 
  110. ^ Passini FG, Watson CG, Herder J (October 1976). "The effects of cerebral electric therapy (electrosleep) on anxiety, depression, and hostility in psychiatric patients". J. Nerv. Ment. Dis. 163 (4): 263–66. doi:10.1097/00005053-197610000-00005. PMID 972328. 
  111. ^ Philip P, Demotes-Mainard J, Bourgeois M, Vincent JD (March 1991). "Efficiency of transcranial electrostimulation on anxiety and insomnia symptoms during a washout period in depressed patients. A double-blind study". Biol. Psychiatry 29 (5): 451–6. doi:10.1016/0006-3223(91)90267-P. PMID 2018818. 
  112. ^ Moore JA, Mellor CS, Standage KF, Strong H (1975). "A double-blind study of electrosleep for anxiety and insomnia". Biol. Psychiatry 10 (1): 59–63. PMID 1091305. 
  113. ^ a b Feighner JP, Brown SL, Olivier JE (1973). "Electrosleep therapy. A controlled double blind study". J. Nerv. Ment. Dis. 157 (2): 121–8. PMID 4724809. 
  114. ^ Feighner JP (1 September 1971). "Electrosleep Therapy: Current Usage in Psychiatry". Calif. Med. 115 (3): 44. PMC 1518073. PMID 18730592. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1518073. Retrieved 2007-12-02. 
  115. ^ Shealy CN (October 2003). "Transcutaneous electrical nerve stimulation: the treatment of choice for pain and depression". J Altern Complement Med 9 (5): 619–23. doi:10.1089/107555303322524463. PMID 14629839. 
  116. ^ Shealy CN, Thomlinson P (2008). "Safe Effective Nondrug Treatment of Chronic Depression: A Review of Research on Low-Voltage Cranial Electrical Stimulation and Other Adjunctive Therapies". Complementary Health Practice Review 13 (2): 92–99. doi:10.1177/1533210108317232. http://chp.sagepub.com/cgi/content/abstract/13/2/92. 
  117. ^ Taylor, M.J.; Wilder, H.; Bhagwagar, Z.; Geddes, J. (2004). Taylor, Matthew J. ed. "Inositol for depressive disorders". Cochrane Database Syst Rev 2 (2): CD004049. doi:10.1002/14651858.CD004049.pub2. PMID 15106232. 
  118. ^ Journal of Ethnopharmacology 1996 Mar; 50(3): 119-30 Psychoactive constituents of the genus Sceletium N.E.Br. and other Mesembryanthemaceae: a review.
  119. ^ www.plantzafrica.com
  120. ^ Pharmaceutical compositions containing mesembrine and related compounds. U.S. Patent 6,288,104 (PDF)
  121. ^ E. Ernst (December 30, 2002). ""Flower remedies": a systematic review of the clinical evidence". Wiener Klinische Wochenschrift 114 (23–24): 963–966. PMID 12635462. 
  122. ^ Benson, Dr. Herbert (1996). Timeless Healing. ISBN 0684814412. 
  123. ^ Bricklin, Mark (1983). Natural Healing. ISBN 0670902047. 
  124. ^ James Strohecker, Nancy Shaw Strohecker, David E. Bresler (1999). "2,4,10". Natural Healing for Depression. New York: Perigee Book. ISBN 9780399525377. http://books.google.com/?id=R60NAAAACAAJ 
  125. ^ Paul G. Swingle (2008). Biofeedback for the Brain. New Brunswick, N.J.: Rutgers University Press. ISBN 9780813542874. http://books.google.com/?id=uqPqRIb9wCAC 
  126. ^ Lee, M. S.; M. H. Pittler, E. Ernst (2008). "Effects of reiki in clinical practice: a systematic review of randomised clinical trials". International Journal of Clinical Practice 62 (6): 947–954. doi:10.1111/j.1742-1241.2008.01729.x. PMID 18410352. 
  127. ^ Harold George Koenig (2005). Faith And Mental Health. Philadelphia: Templeton Foundation Press. ISBN 9781932031911. http://books.google.com/?id=B9bSdb7bLckC 
  128. ^ (PDF) Depression. NICE. December 2004. http://www.nice.org.uk/nicemedia/pdf/CG023NICEguideline.pdf 
  129. ^ Wirz-Justice, A.; Benedetti, F.; Berger, M.; Lam, R.W.; Martiny, K.; Terman, M.; Wu, J.C. (July 2005). "Chronotherapeutics (light and wake therapy) in affective disorders". Psychological Medicine 35 (7): 939–44. doi:10.1017/S003329170500437X. PMID 16045060. 
  130. ^ Tsang, Hector W. H.; Chan, Edward P.; Cheung, W. M. (September 2008). "Effects of mindful and non-mindful exercises on people with depression: A systematic review". British Journal of Clinical Psychology (British Psychological Society) 47 (Pt 3): 303–322. doi:10.1348/014466508X279260. PMID 18237457. http://www.ingentaconnect.com/content/bpsoc/bjcp/2008/00000047/00000003/art00005 
  131. ^ Edward Podolsky (2006). Music Therapy. Kessinger Publishing, LLC. ISBN 1428637192, 9781428637191. http://books.google.com/?id=63TKNdIYf1cC 
  132. ^ Kaijun Niu et al. (2009). "Green tea consumption is associated with depressive symptoms in the elderly". Am J Clin Nutr. 90 (6): 1615–22. doi:10.3945/ajcn.2009.28216. PMID 19828710. http://www.ajcn.org/cgi/content/abstract/90/6/1615.