Major depressive disorder
Specialty	Psychiatry

Clinical depression (also called major-depressive disorder, or unipolar depression when compared to bipolar disorder) is a common mood disorder in psychology and psychiatry, in which a person's enjoyment of life and ability to function socially and in day to day matters is disrupted by intense sadness, melancholia, numbness, or despair.

Clinical depression differs from the common term depression and the everyday expression of "feeling depressed". It is diagnosed medically, and treated by therapy and possibly antidepressant drugs. There are several subtypes, some of which meet the popular perception of sadness, agitation and disruption of sleeping and eating, and others of which do not disrupt enjoyment of good things but create a highly disruptive cycle of inner paralysis and lethargy.

Clinical depression affects about 7–18% of the population on at least one occasion in their lives, before the age of 40.

Although a low mood or state of dejection that does not affect functioning is often colloquially referred to as depression, clinical depression is a clinical diagnosis and may be different from the everyday meaning of "being depressed". Many people identify the feeling of being clinically depressed as "feeling sad for no reason", or "having no motivation to do anything". A person suffering from depression may feel tired, sad, irritable, lazy, unmotivated, and apathetic. Clinical depression is generally acknowledged to be more serious than normal depressed feelings. It often leads to constant negative thinking and sometimes substance abuse or self-harm. Extreme depression can culminate in its sufferers attempting or completing suicide.

The modern idea of depression appears similar to the much older concept of melancholia. The name melancholia derives from "black bile", one of the "four humours" postulated by Galen.

Clinical depression was originally considered to be a chemical imbalance in transmitters in the brain, a theory based on observations made in the 1950s of the effects of reserpine and isoniazid in altering monoamine neurotransmitter levels and affecting depressive symptoms.^[1] Since these suggestions, many other causes for clinical depression have been proposed.^[2]

It is hard for people who have not experienced clinical depression, either personally or by regular exposure to people suffering it, to understand its emotional impact and severity, interpreting it instead as being similar to "having the blues" or "feeling down". As the list of symptoms below indicates, clinical depression is a serious, potentially lethal systemic disorder characterized by the psychiatric profession as interlocking physical, affective, and cognitive symptoms that have consequences for function and survival well beyond sad or painful feelings.

According to the DSM-IV-TR criteria for diagnosing a major depressive episode (see cautionary statement)^[3] five (or more) of the following symptoms must be present for a period of at least two weeks and represent a change from previous functioning; at least one of the symptoms is either depressed mood or loss of interest or pleasure, that is, one of the first two symptoms listed below:

• Feelings of sadness or the seeming inability to feel emotion (emptiness).
• A decrease in the amount of interest or pleasure in all, or almost all, daily activities.
• Changing appetite and marked weight gain or loss.
• Disturbed sleep patterns, such as insomnia, loss of REM sleep, or excessive sleep (hypersomnia).
• Psychomotor agitation or retardation nearly every day.
• Fatigue, mental or physical, also loss of energy.
• Intense feelings of guilt, nervousness, helplessness, hopelessness, worthlessness, isolation/loneliness and/or anxiety.
• Trouble concentrating, keeping focus or making decisions or a generalized slowing and obtunding of cognition, including memory.
• Recurrent thoughts of death (not just fear of dying), desire to just "lie down and die" or "stop breathing", recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for completing suicide.

Mnemonics commonly used to remember the DSM-IV criteria are SIGECAPS^[4] (sleep, interest [anhedonia], guilt, energy, concentration, appetite, psychomotor, suicidality), DEAD SWAMP^[5] (depressed mood, energy, anhedonia, death [thoughts of], sleep, worthlessness/guilt, appetite, mentation, psychomotor) and DIG SPACES (depressed mood, interest [lack of], guilt/worthlessness, suicidal ideation, psychomotor agitation/retardation, anorexia/weight loss, concentration difficulties, energy loss/fatigue, sleep disturbances).

The Patient Health Questionnaire (PHQ2) is a faster, two question questionnaire that may be as sensitive as the DSM-IV^[6]: "During the past month, have you often been bothered by:"

1. "little interest or pleasure in doing things?"
2. "feeling down, depressed, or hopeless?"

If either question is positive, then the SALSA questionnaire should be used for more certainty^[7]. A positive test is one of the above answers positive and two of the answers below positive:

1. Sleep disturbance nearly every day for the last 2 weeks?
2. Have you experienced little interest or pleasure in doing things nearly every day for the last 2 weeks (Anhedonia)?
3. Have you experienced Low Self esteem nearly every day for the last 2 weeks?
4. Have you experienced decreased Appetite nearly every day for the last 2 weeks?"

If the patient is diagnosed with depression, then use the Patient Health Questionnaire 9 (PHQ9) to measure severity (http://intermountainhealthcare.org/documents/61/2002_depression_phq9.pdf) and follow response to treatment. An adequate response is 50% change and a partial is 25% to 50% change.

One of the most widely used instruments for measuring depression severity is the Beck Depression Inventory, a 21-question multiple choice survey.

Another tool, created by WHO, that can be useful in diagnosing a variety of mental disorders, including depression, is the SCAN interview (Schedules for Clinical Assessment in Neuropsychiatry).

Other symptoms often reported but not usually taken into account in diagnosis include:

• Self-loathing.
• A decrease in self-esteem.
• Inattention to personal hygiene.
• Sensitivity to noise.
• Physical aches and pains.
• Fear of "going mad".
• Change in perception of time.
• Periods of sobbing.
• Possible behavioral changes, such as aggression and/or irritability.
• A feeling that something bad is going to happen soon.
• Avoiding social situations or being late often.
• Feeling that one's situation will never improve (hopelessness).
• Excessive procrastination.

An additional indicator could be the excessive use of drugs or alcohol. Depressed adolescents are at particular risk of further destructive behaviours, such as eating disorders and self-harm.

A recent study in Journal of Nervous and Mental Disease showed that alternative symptoms of depression including diminished drive, hopelessness and helplessness, lack of reactivity, anger, psychic and somatic anxiety can be as effective as current DSM-IV criteria in diagnosis. According to this study, diminished drive has a higher diagnostic criteria than all others except for depressed mood with sensitivity of 88.2 of specificity of 69.9 ^[8]. This is only one study though, and has yet to be repeated.

Depression in children is not as obvious as it is in adults. Children may show symptoms such as:

• Loss of appetite.
• Irritability.
• Sleep problems, such as recurrent nightmares.
• Learning or memory problems where none existed before.
• Significant behavioral changes; such as withdrawal, social isolation, and aggression.

Clinical depression affects about 7–18%^[9] of the population on at least one occasion in their lives, before the age of 40. In some countries, such as Australia, one in four women and one in six men will suffer from depression.^[10] In Canada, major depression affects approximately 1.35 million people ^[11]. Because people who have one episode of depression may have more in the future, the first time a young person becomes depressed is important both as a personal and public health concern. ^[12]

About twice as many females as males report or receive treatment for clinical depression, though this imbalance is shrinking over the course of recent history; this difference seems to completely disappear after the age of 50–55. Clinical depression is currently the leading cause of disability in North America as well as other countries, and is expected to become the second leading cause of disability worldwide (after heart disease) by the year 2020, according to the World Health Organization.^[13]

Recent studies suggest that the diagnostic criteria for depression are far too broad, resulting in diagnosis of clinical depression in people who are not truly clinically depressed and who have shown normal responses to negative events. ^[14]

The diagnostic category major depressive disorder appears in the Diagnostic and Statistical Manual of Mental Disorders of the American Psychiatric Association. The term is generally not used in countries which instead use the ICD-10 system, but the diagnosis of depressive episode is very similar to an episode of major depression. Clinical depression also usually refers to acute or chronic depression severe enough to need treatment. Minor depression is a less-used term for a subclinical depression that does not meet criteria for major depression but where there are at least two symptoms present for two weeks.

Major depression or, more properly, major depressive disorder (MDD), is characterized by a severely depressed mood that persists for at least two weeks. Major depressive disorder is specified as either "a single episode" or "recurrent", depending on whether periods of depression occur as discrete events or recur within an individual's lifespan. Episodes of major or clinical depression may be further divided into mild, major or severe. If the patient has already had an episode of mania or markedly elevated mood, a diagnosis of bipolar disorder (also called bipolar affective disorder) is usually made instead of MDD; depression without periods of elation or mania is therefore sometimes referred to as unipolar depression because the mood remains at one emotional state ("pole"). The diagnosis also usually excludes cases where the symptoms are a normal result of bereavement. Diagnosticians recognize several possible subtypes of major depressive disorder. ICD-10 does not specify a melancholic subtype, but does distinguish by presence or absence of psychosis.

• Depression with melancholic features – melancholia is characterized by a loss of pleasure (anhedonia) in most or all activities, a failure of reactivity to pleasurable stimuli, a quality of depressed mood more pronounced than that of grief or loss, a worsening of symptoms in the morning hours, early morning waking, psychomotor retardation, anorexia (excessive weight loss, not to be confused with Anorexia Nervosa), or excessive guilt.

• Depression with atypical features – atypical depression is characterized by mood reactivity (paradoxical anhedonia) and positivity, significant weight gain or increased appetite ("comfort eating"),^[15] excessive sleep or somnolence (hypersomnia), leaden paralysis, or significant social impairment as a consequence of hypersensitivity to perceived interpersonal rejection. Contrary to its name, atypical depression is the most common form of depression.^[16]

• Depression with Psychotic Features – Some people with major depressive or manic episodes may experience psychotic features. They may be presented with hallucinations or delusions that are either mood-congruent (content coincident with depressive themes) or non-mood-congruent (content not coincident with depressive themes). It is clinically more common to encounter a delusional system as an adjunct to depression than to encounter hallucinations, whether visual or auditory.

• Dysthymia is a long-term, mild depression that is diagnosed when there has been a persistently depressed mood for at least two years. By definition, the symptoms are not as severe as those for major depression, although people with dysthymia are vulnerable to co-occurring episodes of major depression (sometimes referred to as "double depression"). This disorder often begins in adolescence and crosses the lifespan. Dysthymic disorder typically develops first and may be followed later by one or more major depressive episodes.

• Bipolar I disorder is an episodic illness characterized by episodes of mania, often accompanied by periods of major depression. In the United States, bipolar disorder was previously called "manic depression", though this term is no longer favored by the medical community.

• Bipolar II disorder is an episodic illness that is defined primarily by major depression accompanied by at least one episode of hypomania.

• Postpartum depression or post-natal depression is clinical depression that occurs within four weeks of childbirth. Owing to physical, mental and emotional exhaustion combined with sleep-deprivation, it has been suggested that motherhood may predispose some women to become depressed.^[17]

• Premenstrual dysphoric disorder is a pattern of recurrent depressive symptoms tied to the menstrual cycle. The premenstrual decline in brain serotonin function is strongly correlated with the concomitant worsening of self-rated cardinal mood symptoms.^[18] Of considerable clinical importance, the recent understanding of premenstrual dysphoria as depression points directly to effective treatment with Selective serotonin reuptake inhibitor (SSRI) antidepressants. Previously, disrupting ovarian cyclicity had been the only recognized treatment. A recent review of studies of a number of SSRIs has revealed that they can effectively ameliorate symptoms of premenstrual dysphoria and may actually work best when taken only during the part of the menstrual cycle when dysphoric symptoms are evident.^[19]

• Recurrent brief depressive disorder or recurrent brief depression is in the ICD-10 classification. Diagnostic criteria distinguish between mild, moderate and severe depressive episodes. Depressive episodes occur about once per month over the past year, with individual episodes lasting less than two weeks (typically less than 2–3 days); episodes do not occur solely in relation to the menstrual cycle.^[20] Some people are at risk of self-harm, as well as the disruption to everyday life, particularly work.

The different types of depression and anxiety are classified separately by the DSM-IV-TR, with the exception of hypomania, which is included in the bipolar disorder category. Despite the different categories, depression and anxiety can indeed be co-occurring (occurring together), independently (without mood congruence), or comorbid (occurring together, with overlapping symptoms, and with mood congruence). In an effort to bridge the gap between the DSM-IV-TR categories and what clinicians actually encounter, experts such as Herman Van Praag of Maastricht University have proposed ideas such as anxiety/aggression-driven depression.^[21] This idea refers to an anxiety/depression spectrum for these two disorders, which differs from the mainstream perspective of discrete diagnostic categories.

Although there is no specific diagnostic category for the comorbidity of depression and anxiety in the DSM or ICD, the National Comorbidity Survey (US) reports that 58 percent of those with major depression also suffer from lifetime anxiety. Supporting this finding, two widely accepted clinical colloquialisms include

• Agitated depression - a state of depression that presents as anxiety and includes akathisia (heightened restlessness), suicide, insomnia (not early morning wakefulness), nonclinical (meaning "doesn't meet the standard for formal diagnosis") and nonspecific panic, and a general sense of dread.

• Akathitic depression - a state of depression that presents as anxiety or suicidality and includes akathisia but does not include symptoms of panic. Some consider it a form of mixed state.

It is also clear that even mild anxiety symptoms can have a major impact on the course of a depressive illness, and the commingling of any anxiety symptoms with the primary depression is important to consider. A pilot study by Ellen Frank et al., at the University of Pittsburgh, found that depressed or bipolar patients with lifetime panic symptoms experienced significant delays in their remission.^{[citation needed]} These patients also had higher levels of residual impairment, or the ability to get back into the swing of things. On a similar note, Robert Sapolsky of Stanford University and others also argue that the relationship between stress, anxiety, and depression could be measured and demonstrated biologically.^[22] To that point, a^[23] study by Heim and Nemeroff et al., of Emory University, found that depressed and anxious women with a history of childhood abuse recorded higher heart rates and the stress hormone ACTH when subjected to stressful situations.

Hypomania, as the name suggests, is a state of mind or behavior that is "below" (hypo) mania. In other words, a person in a hypomanic state often displays behavior that has all the hallmarks of a full-blown mania (e.g., marked elevation of mood that is characterized by euphoria, overactivity, disinhibition, impulsivity, a decreased need for sleep, hypersexuality), but these symptoms, though disruptive and seemingly out of character, are not so pronounced as to be considered a diagnosably manic episode. In a psychiatric context, it is important to identify the possible presence and characteristics of manic and hypomanic episodes, since these may lead to a diagnosis of bipolar disorder, which is medically treated differently from depression.

Another important point is that hypomania is a diagnostic category that includes both anxiety and depression. It often presents as a state of anxiety that occurs in the context of a clinical depression. Patients in a hypomanic state often describe a sense of extreme generalized or specific anxiety, recurring panic attacks, night terrors, guilt, and agency (as it pertains to codependence and counterdependence). All of this happens while they are in a state of retarded or somnolent depression. This is the type of depression in which a person is lethargic and unable to move through life. The terms retarded and somnolent are shorthand for states of depression that include lethargy, hypersomnia, a lack of motivation, a collapse of ADLs (activities of daily living), and social withdrawal. This is similar to the shorthand used to describe an "agitated" or "akathitic" depression.

In considering the hypomania-depression connection, a distinction should be made between anxiety, panic, and stress. Anxiety is a physiological state that is caused by the sympathetic nervous system. Anxiety does not need an outside influence to occur. Panic is related to the "fight or flight" mechanism. It is a reaction, induced by an outside stimulus, and is a product of the sympathetic nervous system and the cerebral cortex. More plainly, panic is an anxiety state that we are thinking about. Finally, stress is a psychosocial reaction, influenced by how a person filters nonthreatening external events. This filtering is based on one's own ideas, assumptions, and expectations. Taken together, these ideas, assumptions, and expectations are called social constructionism

Current theories regarding the risk factors and causes of clinical depression can be broadly classified into two categories, Physiological and Sociopsychological:

The tendency to develop depression may be inherited: according to the National Institute of Mental Health^[24] there is some evidence that depression may run in families, though this familial trend probably includes both biological and environmental factors.

Many modern antidepressant drugs change levels of certain neurotransmitters, namely serotonin and norepinephrine (noradrenaline). However, the relationship between serotonin, SSRIs, and depression is typically greatly oversimplified when presented to the public, though this may be due to the lack of scientific knowledge regarding the mechanisms of action.^[25] Evidence has shown the involvement of neurogenesis in depression, though the role is not exactly known.^[2] Recent research has suggested that there may be a link between depression and neurogenesis of the hippocampus.^[26] This horseshoe-shaped structure is a center for both mood and memory. Loss of neurons in the hippocampus is found in depression and correlates with impaired memory and dysthymic mood. That is why treatment usually results in an increase of serotonin levels in the brain which would in turn stimulate neurogenesis and therefore increase the total mass of the hippocampus and restores mood and memory, therefore assisting in the fight against the mood disorder. ^{[citation needed]}

In about one-third of individuals diagnosed with attention-deficit hyperactivity disorder (ADHD), a developmental neurological disorder, depression is recognized as comorbid.^[27] Dysthymia, a form of chronic, low-level depression, is particularly common in adults with undiagnosed ADHD who have encountered years of frustrating ADHD-related problems with education, employment, and interpersonal relationships.^[28]

Certain illnesses, including cardiovascular disease,^[29] hepatitis, mononucleosis, hypothyroidism, and organic brain damage caused by degenerative conditions such as Parkinson disease, Multiple Sclerosis or by traumatic blunt force injury may contribute to depression, as may certain prescription drugs such as hormonal contraception methods and steroids.

The increase in depression in industrialised societies has been linked to diet, particularly to reduced levels of omega-3 fatty acids in intensively farmed food and processed foods.^[30] This link has been at least partly validated by studies using dietary supplements in schools^[31] and by a double-blind test in a prison.^{[citation needed]} An excess of omega-6 fatty acids in the diet was shown to cause depression in rats.^[32] Depression can also be caused by a magnesium deficiency or lower magnesium levels.

Poor sleep quality co-occurs with major depression. Major depression leads to alterations in the function of the hypothalamus and pituitary causing excessive release of cortisol which can lead to poor sleep quality. Individuals suffering from Major Depression have been found to have an abnormal sleep architecture, often entering REM sleep sooner than usual, along with highly emotionally-charged dreaming. Antidepressant drugs, which often function as REM sleep suppressants, may serve to dampen abnormal REM activity and thus allow for a more restorative sleep to occur.

Seasonal affective disorder (SAD) is a type of depressive disorder that occurs in the winter when daylight hours are short. It is believed that the body's production of melatonin, which is produced at higher levels in the dark, plays a major part in the onset of SAD and that many sufferers respond well to bright light therapy, also known as phototherapy.^{[citation needed]}

Postpartum depression refers to the intense, sustained, and sometimes disabling depression experienced by women after giving birth. Postpartum depression, which has incidence rate of 10-15%, typically sets in within three months of labor and can last for as long as three months.^[33] About two new mothers out of a thousand experience the more serious depressive disorder Postnatal Psychosis which includes hallucinations and/or delusions.

Low self-esteem and self-defeating or distorted thinking are connected with depression. Although it is not clear which is the cause and which is the effect, it is known that depressed persons who are able to make corrections in their thinking patterns can show improved mood and self-esteem (Cognitive Behavioral Therapy).^{[citation needed]} Psychological factors related to depression include the complex development of one's personality and how one has learned to cope with external environmental factors such as stress.^{[citation needed]}

Events such as the death of a parent, issues with biological development, school related problems, abandonment or rejection, neglect, chronic illness, and physical, psychological, or sexual abuse can also increase the likelihood of depression later in life. Post-traumatic stress disorder (PTSD) includes depression as one of its major symptoms.^{[citation needed]}

Job loss, poverty, financial difficulties, gambling addiction, eating disorders, long periods of unemployment, the loss of a spouse or other family member, rape, divorce or the end of a committed relationship, involuntary celibacy, inability to have proper sex or premature ejaculation or other traumatic events may trigger depression. Long-term stress at home, work, or school can also be involved.

For more details on this topic, see Evolutionary advantages of clinical depression

Evolutionary analyses examine the ways in which depression as a response to certain environmental stimuli may act as an adaptive advantage and increase genetic fitness, either of the individual or the society as a whole. See, e.g., Nesse 2006

The treatment of depression is highly individualized to the patient, based on the patient's unique combination of biological, psychological and social health factors and the severity of their condition.^[34] The three most conventional treatments for depression include medication, psychotherapy, and Electroconvulsive therapy, however new treatments and less conventional options are also available, including self help, life style changes, and vagus nerve stimulation.^[34]

If there is an imminent threat of suicide or the patient is a danger to other, hospitalization is an employed as an intervention method to keep at-risk individuals safe until they cease to be a danger to themselves or others. At-risk individuals may also be played in a partial hospitalization therapy, in which the patient sleeps at home but spends most of the day in a psychiatric hospital setting. This intensive treatment usually involves group therapy, individual therapy, medication management, and is used often in the case of children and adolescents.

Sufferers of moderate and severe depression often benefit from the use of antidepressant medications. Selective serotonin reuptake inhibitors, such as citalopram (Celexa), fluoxetine (Prozac), paroxetine (Paxil), and sertraline (Zoloft), are the primarily medications considered for patients, having fewer side affects that the older monoamine oxidase inhibitors (MAOIs). However, MAOIs may be the best medication for a small number of patients, however those patients will have to avoid a variety of foods and decongestant medications to reduce the changes of a hypertensive crisis. ^[35]

A patient's doctor may have to change the antidepressant taken, adjust the dosages of medications, or try different combinations of antidepressants before finding the most effective option for the patient. It may take anywhere from 3 to 8 weeks after the start of medication before its therapeutic affects 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 change of recurrence. For patients that have chronic depression, medication may need to be continued for the remainder of their life.^[35]

In psychotherapy, or counseling, one receives assistance in understanding and resolving habits or problems that may be contributing to or the cause of the depression. This may be done individually or with a group and is conducted by mental health professionals such as psychiatrists, psychologists, clinical social workers, or psychiatric nurses.

Effective psychotherapy may result in different habitual thinking and action which leads to a lower relapse rate than antidepressant drugs alone. Medication, however, may yield quicker results and be strongly indicated in a crisis. Medication and psychotherapy are generally complementary, and both may be used at the same time.

It is important to ask about potential therapists' training and approach; a very close bond often forms between practitioner and client, and it is important that the client feel understood by the clinician. Moreover, some approaches have been convincingly demonstrated to be much more effective in treating depression.

Counselors can help a person make changes in thinking patterns, deal with relationship problems, detect and deal with relapses, and understand the factors that contribute to depression.

There are many counseling approaches, but all are aimed at improving one's personal and interpersonal functioning. Cognitive behavioral therapy (CBT) has been demonstrated in carefully controlled studies to be among the foremost of the recent wave of methods which achieve more rapid and lasting results than traditional "talk therapy" analysis. Cognitive therapy, often combined with behavioral therapy, focuses on how people think about themselves and their relationships. It helps depressed people learn to replace negative depressive thoughts with realistic ones, as well as develop more effective coping behaviors and skills. 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. Interpersonal psychotherapy focuses on the social and interpersonal triggers that cause their depression. Narrative therapy gives attention to each person's "dominant story" by means of therapeutic conversations, which also may involve exploring unhelpful ideas and how they came to prominence. Possible social and cultural influences may be explored if the client deems it helpful. Behavioral therapy is based on the assumption that behaviors are learned. This type of therapy attempts to teach people more healthful types of behaviors. Supportive therapy encourages people to discuss their problems and provides them with emotional support. The focus is on sharing information, ideas, and strategies for coping with daily life. Family therapy helps people live together more harmoniously and undo patterns of destructive behavior.

While milder forms of depression can be successfully treated with medication or psychotherapy alone, with more complex and chronic forms the most effective treatment is often a combination of medication and psychotherapy.^[36]

Electroconvulsive therapy (ECT), also known as electroshock or electroshock treatment, uses short bursts of a controlled current of electricity (typically fixed at 0.9 ampere) into the brain to induce a brief, artificial seizure while the patient is under general anesthesia.

In contrast to direct electroshock of years ago, most countries now allow ECT to be administered only under anaesthesia. In a typical regimen of treatment, a patient receives three treatments per week over three or four weeks. Repeat sessions may be needed. Short-term memory loss, disorientation, and headache are very common side effects. Detailed neuropsychological testing in clinical studies has not been able to prove permanent effects on memory. ECT offers the benefit of a very fast response; however, this response has been shown not to last unless maintenance electroshock or maintenance medication is used. Whereas antidepressants usually take around a month to take effect, the results of ECT have been shown to be much faster. For this reason, it is the treatment of choice in emergencies (e.g., in catatonic depression in which the patient has ceased oral intake of fluid or nutrients).

There remains much controversy over electroshock. Advocacy groups and scientific critics, such as Dr Peter Breggin, ^[37] call for restrictions on its use or complete abolishment. Like all forms of psychiatric treatment, electroshock can be given without a patient's consent, but this is subject to legal conditions dependent on the jurisdiction. In Oregon patient consent is necessary by statute.

In studies, acupuncture appears to be helpful in reducing depression; one study by the National Institute of Health found a 43% decrease in depression by those receiving acupuncture specifically targeting depression.^[38] Other studies have found acupuncture as effective as medication; however, the placebo effect was not able to be ruled out. ^[39]

Bright light (both sunlight and artificial light) is shown to be effective in seasonal affective disorder, and sometimes may be effective in other types of depression, especially atypical depression or depression with "seasonal phenotype" (overeating, oversleeping, weight gain, apathy).^{[citation needed]}

Studies have indicated that changes in lifestyle, such as regular exercise, when used in conjunction with medication with non-suicidal can have beneficial effects in the prevention of depression returning. Patients that completed 30 minutes of brisk exercise at least 3 times a week were found to have a significantly lower incidence of relapse.^[40]

Meditation is increasingly seen as a useful treatment for some cases of depression.^[41] The current professional opinion on meditation is that it represents at least a complementary method of treating depression, a view that has been endorsed by the Mayo Clinic.^[42] Since the late 1990s, much research has been carried out to determine how meditation affects the brain (see the main article on meditation). Although the effects on the mind are complex, they are often quite positive, encouraging a calm, reflective, and rational state of mind that can be of great help against depression.^{[citation needed]}

Though still experimental, a new form of treatment called deep brain stimulation offers some hope in the relief of treatment resistant clinical depression. Published in the journal Neuron (2005), Helen Mayberg described the implanting of electrodes in a region of the brain known as Area 25.^[43] The electrodes act in an inhibitory fashion, on an otherwise overactive region of the brain. Further research is required before it becomes available as a method of treatment, but it offers hope for those suffering from treatment resistant depression.

Insulin shock therapy is an old and largely abandoned treatment of severe depressions, psychoses, catatonic states, and other mental disorders. It consists of induction of hypoglycemic coma by intravenous infusion of insulin.

Atropinic shock therapy, also known as atropinic coma therapy, is an old and rarely used method. It consists of induction of atropinic coma by rapid intravenous infusion of atropine.

Atropinic shock treatment is considered safe, but it entails prolonged coma (4–5 hours), with careful monitoring and preparation, and it has many unpleasant side effects, such as blurred vision.

Self-medication is the use of drugs or alcohol to treat a perceived or real malady, usually of a psychological nature. Typically the use of non-prescription chemicals are taken with the intent of the user to alter a mood state for a temporary amount of time. In one study, cannabis users who use once a week or less were shown to have fewer symptoms of depression.^[44]

5-HTP supplements are claimed to provide more raw material to the body's natural serotonin production process. There is a reasonable indication that 5-HTP may not be effective for those who have not already responded well to an SSRI because of their similar function: SSRIs prolong serotonin concentrations in the synapse, while 5-HTP induces production of more serotonin.^[45]

S-adenosyl methionine (SAM-e) is a derivative of the amino acid methionine that is found throughout the human body, where it acts as a methyl donor and participates in other biochemical reactions. It is available as a prescription antidepressant in Europe and an over-the-counter dietary supplement in the United States. Clinical trials have shown SAM-e to be as effective as standard antidepressant medication, with fewer side effects; however, some studies have reported an increased incidence of mania resulting from SAM-e use compared to other antidepressants.^[46][47] Its mode of action is unknown.

Omega-3 fatty acids (found naturally in oily fish, flax seeds, hemp seeds, walnuts, and canola oil) have also been found to be effective when used as a dietary supplement (although only fish-based omega-3 fatty acids have shown antidepressant efficacy.^[48]) In addition to the total amount of omega 3 oils in the body, the level of omega 6 fatty acids have also been found to be implicated. An excess of omega 6 appears to be associated with depression.^[49]

Dehydroepiandrosterone (DHEA), available as a supplement in the U.S., has been shown to be effective in small trials.^[50]

Magnesium supplementation has gathered some attention as a possible treatment for depression.^[51] Some case reports demonstrate rapid recovery from major depression using magnesium treatment.^[52]

St John's Wort Except under medical supervision, St. John's Wort should not be used with SSRIs or MAOIs due to the risk of serotonin syndrome.^[53]

Ginkgo Biloba Effective natural antidepressant^[54] said to stabilise cell membranes, inhibiting lipid breakdown and aiding cell use of oxygen and glucose - so subsequently a mental and vascular stimulant that improves neurotransmitter production. Also popular for treating mental concentration (such as for Alzheimer's and stroke patients).^[17]

Siberian Ginseng [Eleutherococcus senticosus] Although not a true panax ginseng it is claimed by some to be a mood enhancement supplement against stress. The claims are that it is effective for treating depression, insomnia, moodiness, fatigue, poor memory, lack of focus, mental tension and endurance.^[17] There is little or no scientific evidence to support these claims.

Zinc has had an antidepressant effect in an experiment.^[55]

Biotin: a deficiency has caused a severe depression. The patient's symptoms improved after the deficiency was corrected.^[56]

B vitamins: Symptoms of a deficiency in vitamins such as vitamin B6, B12 and others can include depression and other psychiatric disorders.^[57]

Chromium: Evidence has emerged that supplementing with high doses of chromium (ie: in doses of several hundred to 100 mg) exerts antidepressant effects ^[58]. It has been found to enhance the availability of serotonin and norepinephrine. Chromium in the form of chromium picolinate has generated some controversy as it has been shown to increase damage to DNA in the ovary cells of hamsters, possible increasing the risk of cancer.^[59]

Rhodiola Rosea: Rhodiola is a herb growing in cold climates that has just recently been introduced to the west. It has been shown to help alleviate depression and fatigue. It is believed to elevate extracellular levels of monoamines and beta-endorphins. ^[60]

Repetitive transcranial magnetic stimulation (rTMS) is under study as a possible treatment for depression. Initially designed as a tool for physiological studies of the brain, this technique shows promise as a means of alleviating depression. In this therapy, a powerful magnetic field is used to stimulate the left prefrontal cortex, an area of the brain that typically shows abnormal activity in depressed people. ^{[citation needed]}

Recent work ^[61] in Poland suggested that weak, variable magnetic fields may offer relief from depression in those who have not responded to medication. However, some of the existing work has been questioned,^[62] with claims that the effect is not as significant once environmental conditions are controlled.

Vagus nerve stimulation therapy is a treatment used since 1997 to control seizures in epileptic patients and has recently been approved for treating resistant cases of treatment-resistant depression (TRD). The VNS Therapy device is implanted in a patient's chest with wires that connect it to the vagus nerve, which it stimulates to reach a region of the brain associated with moods. The device delivers controlled electrical currents to the vagus nerve at regular intervals.

Aspartame was associated with a significant difference in number and severity of symptoms for patients with a history of depression in an experiment.^[63] However, the main findings of this 1993 study have not been replicated since, and its methodology has been criticized on the basis that unrelated symptoms were aggregated artificially, thereby boosting the statistical difference between the aspartame and the placebo conditions.^[64]

Recurrence is more likely if treatment has not resulted in full remission of symptoms.⁴ In fact, current guidelines for antidepressant use recommend 4 to 6 months of continuing treatment after symptom resolution to prevent relapse.

Combined evidence from many randomized controlled trials indicates that continuing antidepressant medications after recovery substantially reduces (halves) the chances of relapse. This preventive effect probably lasts for at least the first 36 months of use.^[65]

Anecdotal evidence suggests that chronic disease is accompanied by recurrence after prolonged treatment with antidepressants (tachyphylaxis). Psychiatric texts suggest that physicians respond to recurrence by increasing dosage, complementing the medication with a different class, or changing the medication class entirely. The reason for recurrence in these cases is as poorly understood as the change in brain physiology induced by the medications themselves. Possible reasons may include aging of the brain or worsening of the condition. Most SSRI psychiatric medications were developed for short-term use (a year or less) but are widely prescribed for indefinite periods.^[66]

• Emotion and memory
• Geriatric Depression Scale
• Hamilton Depression Rating Scale
• List of people who have suffered from depression

• Beck, A. T., Rush, A. J., Shaw, B. F., Emery, G. (1987). Cognitive therapy of depression. New York: Guilford.
• Burns, David D. (1999). Feeling Good : The New Mood Therapy. Avon.
• Griffin, J., Tyrrell, I. (2004) How to lift Depression – Fast. HG Publishing. ISBN 1-899398-41-4
• Jacobson, Edith: "Depression; Comparative Studies of Normal, Neurotic, and Psychotic Conditions", International Universities Press, 1976, ISBN 0-8236-1195-7
• Klein, D. F., & Wender, P. H. (1993). Understanding depression: A complete guide to its diagnosis and treatment. New York: Oxford University Press.
• Kramer, Peter D. (2005). Against Depression. New York: Viking Adult.
• Plesman, J. (1986). Getting off the Hook, Sydney Australia. A self-help book available on the internet.
• Rowe, Dorothy (2003). Depression: The way out of your prison. London: Brunner-Routledge.
• Sarbadhikari, S. N. (ed.) (2005) Depression and Dementia: Progress in Brain Research, Clinical Applications and Future Trends. Hauppauge, Nova Science Publishers. ISBN 1-59454-114-0.
• Weissman, M. M., Markowitz, J. C., & Klerman, G. L. (2000). Comprehensive guide to interpersonal psychotherapy. New York: Basic Books.
• Bieling, Peter J. & Anthony, Martin M. (2003) Ending The Depression Cycle. New Harbinger Publications. ISBN 1572243333

• Wurtzel, Elizabeth. (1997) Prozac Nation: Young and Depressed in America: A Memoir. Riverhead Books. ISBN 1-57322-512-6
• Lewinsohn, P. M., Munoz, R. F, Youngren, M. A., Zeiss, A. M. (1992). Control your depression. New York: Fireside/Simon&Schuster.
• Mays, John Bentley. (1995). In the Jaws of the Black Dogs: A Memoir of Depression. Toronto, Canada: Penguin Books. ISBN 0-14-024650-9
• Nesaule, Agate. (1995). A Woman in Amber: Healing the Trauma of War and Exile New York: Penguin Books. ISBN 1-56947-046-4 (hc.); ISBN 0-14-026190-7 (pbk.)
• Sealey, Robert (2002). Finding Care for Depression, Mental Episodes & Brain Disorders, Toronto: Sear Publications www.searpubl.ca
• Shields, Brooke. (2005). Down Came the Rain: My Journey Through Postpartum Depression. Hyperion. ISBN 1-4013-0189-4.
• Smith, Jeffery. (2001). Where the Roots Reach for Water: A Personal and Natural History of Melancholia. New York: North Point Press.
• Solomon, Andrew. (2001). The Noonday Demon: An Atlas of Depression. New York: Scribner.
• Styron, William. (1992). Darkness Visible: A Memoir of Madness. New York: Vintage Books/Random House.
• Wolpert, Lewis. (2001). Malignant sadness: The anatomy of depression. London: Faber and Faber.
• Tolle, Eckhart. (1999). The Power of Now: A Guide to Spiritual Enlightenment, New World Library. ISBN 1-57731-152-3 (hc.); ISBN 1-57731-480-8 (pbk.)
• Plath, Sylvia. (1963). The Bell Jar. Perennial. ISBN 0-06-093018-7
• Maschio, Jill. (2006). When Your Mind Is Clear, the Sun Shines All the Time: A Guidebook for Overcoming Depression Norman, OK: Illumines Publishing. ISBN 0-9777483-4-0

• Healy, David. (1999). The Antidepressant Era, Paperback Edition, Harvard University Press. ISBN 0-674-03958-0

• Template:Dmoz
• National Alliance on Mental Illness Depression support, advocacy, and education
• National Depressive and Manic Depressive Association - National Depressive and Manic Depressive Association
• Depression Research News - ScienceDaily's Depression Research News
• Recovering From Depression
• Depression: Signs, Symptoms, Causes, and Treatment Strategies
• Hell and Back - Chris Rose, a reporter for the New Orleans Times-Picayune, describes his personal experience with depression and an eventual recovery from it in his newspaper article titled "Hell And Back" (Sunday, October 22, 2006). The book also makes reference to the book Darkness Visible: A Memoir of Madness, in which the writer William Styron recounts his own descent into and recovery from depression. Rose's depression followed his extended coverage of Hurricane Katrina.
• beyondblue, The Australian National Depression Initiative
• Bibliography of scholarly, peer-reviewed histories of depression
• Free guide to learning skills to overcome depression
• MoodGYM Free training program to overcome depression.
• Depression Treatment at Columbia University Research Studies Involving Free Treatment for Depression.
• Substance Abuse and Mental Health Services (SAMHSA), US Department of Health and Human Services (HHS)

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