Depression

Clinical Depression
From Wikipedia, the free encyclopedia

DepressionClassification & external resources
ICD-10
F32., F33.
ICD-9
296
OMIM
608516
DiseasesDB
3589
MedlinePlus
003213
eMedicine
med/532
Clinical depression (also called major depressive disorder, or unipolar depression when compared to bipolar disorder) is a state of intense sadness, melancholia or despair that has advanced to the point of being disruptive to an individual's social functioning and/or activities of daily living.
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. Extreme depression can culminate in its sufferers attempting or committing suicide.
Without careful assessment, delirium can easily be confused with depression and a number of other psychiatric disorders because many of the signs and symptoms are conditions present in depression, as well as other mental illnesses including dementia and psychosis.[1]

Vincent van Gogh, who himself suffered from depression and committed suicide, painted this picture in 1890 of a man seen by some as symbolizing the desperation and hopelessness felt in depression.
History
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.[2] Since these suggestions, many other causes for clinical depression have been proposed.[3]

Prevalence
Clinical depression affects about 7% - 18%[4] 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.[5] In Canada, major depression affects approximately 1.35 million people [6]. The mean age of onset, from a number of studies, is in the late 20s.[citation needed]. 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 [7].

About twice as many females as males report or receive treatment for clinical depression, due to stress and adversity, 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.[8]

According to recent studies [1], the diagnostic criteria for depression is far too broad, leading to people who are not truly clinically depressed being diagnosed due to a normal reaction to negative events.

Types of depression
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 clinical depression
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"; periods of depression may occur as discrete events or recur over the lifespan. Episodes of major or clinical depression may be further divided into mild, major or severe. Where 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 on one 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, 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.[9]

Depression with Psychotic Features - Some people with Major Depressive or Manic episode 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.

Other categories of depression
Dysthymia is a long-term, mild depression that lasts for a minimum of two years. There must be persistent depressed mood continuously for at least two years. By definition the symptoms are not as severe as with Major Depression, although those with Dysthymia are vulnerable to co-occurring episodes of Major Depression. This disorder often begins in adolescence and crosses the lifespan. People who are diagnosed with major depressive episodes and dysthymic disorder are diagnosed with double depression. Dysthymic disorder develops first and then one or more major depressive episodes happen later.

Bipolar I Disorder is an episodic illness in which moods may cycle between mania and depression. In the United States, Bipolar Disorder was previously called Manic Depression. This term is no longer favored by the medical community, however, even though depression plays a much stronger (in terms of disability and potential for suicide) role in the disorder. "Manic Depression" is still often used in the non-medical community. Bipolar II Disorder is an episodic illness that is defined primarily by depression but evidences episodes of hypomania.

Postpartum Depression or Post-Natal Depression is clinical depression that occurs within two years of childbirth. Owing to physical, mental and emotional exhaustion combined with sleep-deprivation, motherhood can "set women up", so to speak, for clinical depression.[10]

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.[11] 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.[12]

Recurrent brief depressive disorder (or recurrent brief depression) is in the ICD-10 classification. It is described as meeting the criteria for a mild, moderate or severe depressive episode; the depressive episodes have occurred about once per month over the last year; individual episodes last less than two weeks (typically less than 2-3 days), and they do not occur solely in relation to the menstrual cycle. [13] Some people are at risk of self-harm, as well as the disruption to everyday life, particularly work.

The role of anxiety in depression

Anxiety
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.[14] 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:

1. 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.
2. akathitic depression - a state of depression that presents as anxiety or suicidality and includes akathisia but does not include symptoms of panic.

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.[15] To that point, a[16] 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
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, over activity, 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.

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

Physiological causes

Genetic predisposition
The tendency to develop depression may be inherited: according to the National Institute of Mental Health[17] there is some evidence that depression may run in families, though this familial trend probably includes both biological and environmental factors.

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

Neurological
Many modern antidepressant drugs change levels of certain neurotransmitters, namely serotonin and norepinephrine (noradrenaline). However, the relationship between serotonin, SSRIs, and depression usually 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.[18] Evidence has shown the involvement of neurogenesis in depression, though the role is not exactly known.[3] Recent research has suggested that there may be a link between depression and neurogenesis of the hippocampus.[19] 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.[20] 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.[21]

Medical conditions
Certain illnesses, including cardiovascular disease,[22] 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.

Dietary
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.[23] This link has been at least partly validated by studies using dietary supplements in schools[24] and by a double-blind test in a prison. An excess of omega-6 fatty acids in the diet was shown to cause depression in rats.[25] Depression can also be caused by a magnesium deficiency or lower magnesium levels.

[edit] Sleep quality
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.

[edit] Seasonal affective disorder
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]

[edit] Postpartum depression
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.[26] About two new mothers out of a thousand experience the more serious depressive disorder Postnatal Psychosis which includes hallucinations and/or delusions.


Sociopsychological causes

Psychological factors
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]

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

Life experiences
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.

Evolution: Potential adaptive 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 psychic pain hypothesis
Psychic pain, such as depression, is analogous to physical pain. The function of physical pain is to inform the organism that it is suffering damage, to motivate it to withdraw from the source of damage, and to learn to avoid such damage-causing circumstances in the future. Analogously, depression informs the sufferer that current circumstances, such as the loss of a friend, are imposing a threat to biological fitness, it motivates the sufferer to cease activities that led to the costly situation, if possible, and it causes him or her to learn to avoid similar circumstances in the future. Proponents of this view tend to focus on low mood, and regard clinical depression as a dysfunctional extreme of low mood. See, e.g., Nesse 2000 and Keller and Nesse 2005; see also Hagen and Barrett n.d..

Rank theory
If an individual is involved in a lengthy fight for dominance in a social group and is clearly losing, depression causes the individual to back down and accept the submissive role. In doing so, the individual is protected from unnecessary harm. In this way, depression helps maintain a social hierarchy. This theory is a special case of a more general theory derived from the psychic pain hypothesis: that the cognitive response that produces modern-day depression evolved as a mechanism that allows people to assess whether they are in pursuit of an unreachable goal, and if they are, to motivate them to desist. See, e.g., Nesse 2000.

Honest signaling theory
When social partners have conflicts of interest, 'cheap' signals of need, such as crying, might not be believed. Biologists and economists have proposed that signals with inherent costs can credibly signal information when there are conflicts of interest. The symptoms of major depression, such as loss of interest in virtually all activities and suicidality, are inherently costly, but, as costly signaling theory requires, the costs differ for individuals in different states. For individuals who are not genuinely in need, the fitness cost of major depression is very high because it threatens the flow of fitness benefits. For individuals who are in genuine need, however, the fitness cost of major depression is low because the individual is not generating many fitness benefits. Thus, only an individual in genuine need can afford to suffer major depression. Major depression therefore serves as an honest, or credible, signal of need. See, e.g., Hagen 2003, Watson and Andrews 2002.

Social navigation or niche change theory
The social navigation, bargaining, or niche change hypothesis [2] suggests that depression, operationally defined as a combination of prolonged anhedonia and psychomotor retardation or agitation, provides a focused sober perspective on socially imposed constraints hindering a person’s pursuit of major fitness enhancing projects. Simultaneously, publicly displayed symptoms, which reduce the depressive's ability to conduct basic life activities, serve as a social signal of need; the signal's costliness for the depressive certifies its honesty. Finally, for social partners who find it uneconomical to respond helpfully to an honest signal of need, the same depressive symptoms also have the potential to extort relevant concessions and compromises. Depression’s extortionary power comes from the fact that it retards the flow of just those goods and services such partners have come to expect from the depressive under status quo socioeconomic arrangements.

Thus depression may be a social adaptation especially useful in motivating a variety of social partners, all at once, to help the depressive initiate major fitness-enhancing changes in their socioeconomic life. There are extraordinarily diverse circumstances under which this may become necessary in human social life, ranging from loss of rank or a key social ally which makes the current social niche uneconomic to having a set of creative new ideas about how to make a livelihood which begs for a new niche. The social navigation hypothesis emphasizes that an individual can become tightly ensnared in an overly restrictive matrix of social exchange contracts, and that this situation sometimes necessitates a radical contractual upheaval that is beyond conventional methods of negotiation. Regarding the treatment of depression, this hypothesis calls into question any assumptions by the clinician that the typical cause of depression is related to maladaptive perverted thinking processes or other purely endogenous sources. The social navigation hypothesis calls instead for a penetrating analysis of the depressive’s talents and dreams, identification of relevant social constraints (especially those with a relatively diffuse non-point source within the social network of the depressive), and practical social problem-solving therapy designed to relax those constraints enough to allow the depressive to move forward with their life under an improved set of social contracts.[27]

Bargaining theory
This theory is similar to the honest signaling, niche change, and social navigation theory. It basically adds one additional element to honest signaling theory. The fitness of social partners is generally correlated. When a wife suffers depression and reduces her investment in offspring, for example, the husband's fitness is also put at risk. Thus, not only do the symptoms of major depression serve as costly and therefore honest signals of need, they also compel social partners to respond to that need in order to prevent their own fitness from being reduced. See, e.g., Hagen 1999, Hagen 2003.

Diagnosis
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.

[edit] DSM-IV-TR criteria
According to the[28]DSM-IV-TR criteria for diagnosing a major depressive disorder (cautionary statement) one of the following two elements must be present for a period of at least two weeks:
Depressed mood, or
Anhedonia
It is sufficient to have either of these symptoms in conjunction with five of a list of other symptoms over a two-week period. These include:
Feelings of overwhelming sadness and/or fear, 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 committing suicide.
Feeling and/or fear of being abandoned by those close to one.
Mnemonics commonly used to remember the DSM-IV criteria are SIGECAPS[29] (sleep, interest (anhedonia), guilt, energy, concentration, appetite, psychomotor, suicidality), DEAD SWAMP[30] (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).

[edit] Patient Health Questionnaire
The Patient Health Questionnaire (PHQ2) is a faster, two question questionnaire that may be as sensitive as the DSM-IV[31]: "During the past month, have you often been bothered by:"
"little interest or pleasure in doing things?"
"feeling down, depressed, or hopeless?"
If either question is positive, then the SALSA questionnaire should be used for more certainty[32]. A positive test is one of the above answers positive and two of the answers below positive:
Sleep disturbance nearly every day for the last 2 weeks?
Have you experienced little interest or pleasure in doing things nearly every day for the last 2 weeks (Anhedonia)?
Have you experienced Low Self esteem nearly every day for the last 2 weeks?
Have you experienced decreased Appetite nearly every day for the last 2 weeks?"

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

[edit] Schedules for Clinical Assessment in Neuropsychiatry
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).

[edit] Other symptoms
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, and the belief these may be signs of serious illness.
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 you will never get better.
Excessive procrastination (What's the point?)
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 [33].
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.

[edit] Treatment
Treatment of depression varies broadly among individuals. The level, type, and methods of intervention vary dramatically. There are two primary modes of treatment that are typically used in conjunction; medication and psychotherapy. A significant number of recent studies have indicated that changes in lifestyle such as regular exercise and dietary supplements have beneficial effects.[3]
In most cases, one particular medication or combination of medications can provide significant change, although, in some cases, the condition does not respond well. Treatment-resistant depression warrants a full assessment, which may lead to the introduction of psychotherapy, a focus on lifestyle change, an increase of medication, or a change in medication.
In emergencies, hospitalization is an intervention employed to keep at-risk individuals safe until they cease to be a danger to themselves or others. An alternative treatment program is partial hospitalization, 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 often in the case of children and adolescents, academics.

[edit] Medication
Medication that relieves the symptoms of depression has been available for several decades. Typical first-line therapy for depression is the use of a selective serotonin reuptake inhibitor, such as citalopram (Celexa), fluoxetine (Prozac), paroxetine (Paxil), and sertraline (Zoloft). Under some circumstances, medication and psychotherapy may be more effective than either treatment separately.[34]

[edit] Selective serotonin reuptake inhibitors (SSRIs)
Selective serotonin reuptake inhibitors (SSRIs) are a family of antidepressants considered to be the current standard of drug treatment. It is thought that one cause of depression is an inadequate amount of serotonin, a chemical used in the brain to transmit signals between neurons. SSRIs are said to work by preventing the reuptake of serotonin by the presynaptic nerve, thus maintaining higher levels of 5-HT in the synapse. Recently, however, work by two researchers has called into question the link between serotonin deficiency and symptoms of depression, noting that the efficacy of SSRIs as treatment does not in itself prove the link.[35] Recent research indicates that these drugs may interact with transcription factors known as "clock genes",[36] which may be important for the addictive properties of drugs of abuse and possibly in obesity.[37][38]
Recent randomized controlled trials in Archives of General Psychiatry showed that up to one-third of effects of SSRI Treatment can be seen in first week. Early effects also shown to have secondary effect of reducing absolute reduction in HDRS score by 50 percent. Even more recent studies, published by the Archives of General Psychiatry note that 25% of so-called clinical depression does not meet a disease criteria and should be considered to be ordinary sadness and adjustment to the difficulties in life.
This family of drugs includes fluoxetine (Prozac), paroxetine (Paxil), escitalopram (Lexapro), citalopram (Celexa), and sertraline (Zoloft). These antidepressants typically have fewer adverse side effects than the tricyclics or the MAOIs, although such effects as drowsiness, dry mouth, nervousness, anxiety, insomnia, decreased appetite, and decreased ability to function sexually may occur. Some side effects may decrease as a person adjusts to the drug, but other side effects may be persistent. Though safer than first generation antidepressants, SSRI's may not work as often, suggesting the role of norepinephrine.

[edit] Serotonin-norepinephrine reuptake inhibitors (SNRIs)
Serotonin-norepinephrine reuptake inhibitors (SNRIs) such as venlafaxine (Effexor) and duloxetine (Cymbalta) are a newer form of antidepressant that works on both norepinephrine and 5-HT. They typically have similar side effects to the SSRIs, although there may be a withdrawal syndrome on discontinuation that may necessitate dosage tapering.

[edit] Noradrenergic and specific serotonergic antidepressants (NASSAs)
Noradrenergic and specific serotonergic antidepressants (NASSAs) form a newer class of antidepressants which purportedly work to increase norepinephrine (noradrenaline) and serotonin neurotransmission by blocking presynaptic alpha-2 adrenergic receptors while at the same time minimizing serotonin related side-effects by blocking certain serotonin receptors. The only example of this class in clinical use is mirtazapine (Avanza, Zispin, Remeron).

[edit] Norepinephrine (noradrenaline) reuptake inhibitors (NRIs)
Norepinephrine (noradrenaline) reuptake inhibitors (NRIs) such as reboxetine (Edronax) act via norepinephrine (also known as noradrenaline). NRIs are thought to have a positive effect on concentration and motivation in particular, though they have been known to increase aggression.

[edit] Norepinephrine-dopamine reuptake inhibitors
Norepinephrine-dopamine reuptake inhibitors such as bupropion (Wellbutrin, Zyban) inhibit the neuronal reuptake of dopamine and norepinephrine (noradrenaline).[39]

[edit] Tricyclic antidepressants (TCAs)
Tricyclic antidepressants are the oldest and include such medications as amitriptyline and desipramine. Tricyclics block the reuptake of certain neurotransmitters such as norepinephrine (noradrenaline) and serotonin. They are used less commonly now due to the development of more selective and safer drugs. Several side effects include increased heart rate, drowsiness, dry mouth, constipation, urinary retention, blurred vision, dizziness, confusion, and sexual dysfunction. Toxicity occurs at approximately ten times normal dosages. However, tricyclic antidepressants are still used because of their high potency, especially in severe cases of clinical depression.

[edit] Monoamine oxidase inhibitor (MAOIs)
Monoamine oxidase inhibitors (MAOIs) such as phenelzine (Nardil) may be used if other antidepressant medications are ineffective. Because there are potentially fatal interactions between this class of medication and certain foods (particularly those containing Tyramine), as well as certain drugs, classic MAOIs are rarely prescribed anymore. MAOIs work by blocking the enzyme monoamine oxidase which breaks down the neurotransmitters dopamine, serotonin, and norepinephrine (noradrenaline). MAOIs can be as effective as tricyclic antidepressants, although they can have a higher incidence of dangerous side effects (as a result of inhibition of cytochrome P450 in the liver). A new generation of MAOIs has been introduced; moclobemide (Manerix), known as a reversible inhibitor of monoamine oxidase A (RIMA), acts in a more short-lived and selective manner and does not require a special diet. Additionally, Emsam is a classic MAOI (selegiline) delivered through a transdermal patch, so as to avoid interactions in the digestive tract that otherwise occur when delivered orally.

[edit] Augmentor drugs
Some antidepressants have been found to work more effectively in some patients when used in combination with another drug. Such "augmentor" drugs include tryptophan (Tryptan) and buspirone (Buspar).
Tranquillizers and sedatives, typically the benzodiazepines, may be prescribed to ease anxiety and promote sleep. Because of their high potential for fostering dependence, these medications are intended only for short-term or occasional use. Medications often are used not for their primary function but to exploit what are normally side effects. Quetiapine fumarate (Seroquel) is designed primarily to treat schizophrenia and bipolar disorder, but a frequently reported side-effect is somnolence. Therefore, this drug can be used in place of an antianxiety agent such as clonazepam (Klonopin, Rivotril).
Antipsychotics such as risperidone (Risperdal), olanzapine (Zyprexa), and Quetiapine (Seroquel) are prescribed as mood stabilizers and are also effective in treating anxiety. Their use as mood stabilizers is a recent phenomenon and is controversial with some patients. Antipsychotics (typical or atypical) may also be prescribed in an attempt to augment an antidepressant, to make antidepressant blood concentration higher, or to relieve psychotic or paranoid symptoms often accompanying clinical depression. However, they may have serious side effects, particularly at high dosages, which may include blurred vision, muscle spasms, restlessness, tardive dyskinesia, and weight gain.
Antidepressants by their nature behave similarly to psychostimulants. Antianxiety medications by their nature are depressants. Close medical supervision is critical to proper treatment if a patient presents with both illnesses because the medications tend to work against each other.
Psycho-stimulants are sometimes added to an antidepressant regimen if the patient suffers from anhedonia, hypersomnia and/or excessive eating as well as low motivation. These symptoms which are common in atypical depression can be quickly resolved with the addition of low to moderate dosages of amphetamine or methylphenidate (brand names Adderall and Ritalin, respectively) as these chemicals enhance motivation and social behavior, as well as suppress appetite and sleep. These chemicals are also known to restore sex drive. Extreme caution must be used however with certain populations. Stimulants are known to trigger manic episodes in people suffering from bipolar disorder. They are also easily abused as they are effective substitutes for Methamphetamine when used recreationally. Close supervision of those with substance abuse disorders is urged. Emotionally labile patients should avoid stimulants, as they exacerbate mood shifting.
Lithium remains the standard treatment for bipolar disorder and is often used in conjunction with other medications, depending on whether mania or depression is being treated. Lithium's potential side effects include thirst, tremors, light-headedness, and nausea or diarrhea. Some of the anticonvulsants, such as carbamazepine (Tegretol), sodium valproate (Epilim), and lamotrigine (Lamictal), are also used as mood stabilizers, particularly in bipolar disorder.

[edit] Medication failure
Approximately 30% of patients have remission of depression with medications.[40] For patients with inadequate response, either adding sustained-release bupropion(initially 200 mg per day then increase by 100 mg up to total of 400 mg per day) or buspirone (up to 60 mg per day) for augmentation as a second drug can cause remission in approximately 30% of patients[41], while switching medications can achieve remission in about 25% of patients.[42]

[edit] Dietary supplements
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 haven't already responded well to an SSRI because of their similar function: SSRIs allow the brain to use its serotonin more effectively, while 5-HTP induces production of more serotonin.[43]
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.[44][45] 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.[46])
Dehydroepiandrosterone (DHEA), available as a supplement in the U.S., has been shown to be effective in small trials.[47]
Magnesium supplementation has gathered some attention as a possible treatment for depression.[48] Some case reports demonstrate rapid recovery from major depression using magnesium treatment. "The possibility that magnesium deficiency is the cause of most major depression and related mental health problems including IQ loss and addiction is enormously important to public health and is recommended for immediate further study" [49]
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.[50]
Ginkgo Biloba Effective natural antidepressant[51] 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).[10]
Siberian Ginseng [Eleutherococcus senticosus] Although not a true panax ginseng it is a mood enhancement supplement against stress. Also popular for treating depression, insomnia, moodiness, fatigue, poor memory, lack of focus, mental tension and endurance.[10]
Zinc has had an antidepressant effect in an experiment.[52]
Biotin: a deficiency has caused a severe depression. The patient's symptoms improved after the deficiency was corrected.[53]
Vitamin B-12: Symptoms of a vitamin B-12 deficiency can include depression and other psychiatric disorders.[54]

[edit] Psychotherapy
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 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.

[edit] Transcranial magnetic stimulation
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 [55] 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,[56] with claims that the effect is not as significant once environmental conditions are controlled.

[edit] Vagus nerve stimulation
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.

[edit] Electroconvulsive therapy
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,[57] 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.

Other methods of treatment

Acupuncture
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 [58]. Other studies have found acupuncture as effective as medication, however the placebo effect was not able to be ruled out. [59]

Light therapy
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]

Exercise
It is widely believed that physical activity and exercise help depressed patients and promote quicker and better relief from depression. They are also thought to help antidepressants and psychotherapy work better and faster. It can be difficult to find the motivation to exercise if the depression is severe, but sufferers should be encouraged to take part in some form of regularly scheduled physical activity. A workout need not be strenuous; many find walking, for example, to be of great help. Exercise produces higher levels of chemicals in the brain, notably dopamine, serotonin, and norepinephrine. In general this leads to improvements in mood, which is effective in countering depression.[4]

Meditation
Meditation is increasingly seen as a useful treatment for some cases of depression.[60] 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.[61] 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]

Deep brain stimulation
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.[62] 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.

Archaic methods
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
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. However, Cannabis users who use once a week or less have been shown to have fewer symptoms of depression than non-users in one study.[63]

Adverse reactions
Aspartame was associated with a significant difference in number and severity of symptoms for patients with a history of depression in an experiment.[64] 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.[65]

Recurrence
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.[66]
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.[67]

See also
Asperger syndrome
Atypical depression
Beck Depression Inventory
Bi-polar disorder
Chemical imbalance theory
Cyclothymia
Depression (mood)
Dysthymia
Emotion and memory
Geriatric Depression Scale
Hamilton Depression Rating Scale
Hypoadrenia (also covers 'adrenal exhaustion', sometimes called 'adrenal fatigue')
List of people who have suffered from depression
Mania
Maslow's hierarchy of needs
Melancholic Depression
Post-traumatic stress disorder
Seasonal affective disorder (SAD)
Stress
Area 25 (aka Anterior cingulate cortex )

Books by psychologists and psychiatrists
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

Books by people suffering or having suffered from depression
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

Historical account
David Healy, The Antidepressant Era, Paperback Edition, Harvard University Press 1999, ISBN 0-674-03958-0

References
^ http://www.aafp.org/afp/20030301/1027.html American Family Physician, March 1, 2003 Delirium
^ Schildkraut, J.J. (1965). "The catecholamine hypothesis of affective disorders: a review of supporting evidence". Am J Psychiatry 122 (5): 509-22.
^ a b Castren, E. (2005). Is Mood Chemistry? Nat Rev Neurosci, : p6(3):241-6 PMID 15738959.
^ Bland, R.C. (1997). "Epidemiology of Affective Disorders: A Review". Can J Psychiatry 42: 367?377.
^ Types of Depression.Beyondblue
^ Blue Sky Project. [[Blue Sky Project}}
^ Blue Sky Project. [[Blue Sky Project}}
^ Murray, C.J.L.; Lopez, A.D. (1997). "Alternative projections of mortality and disability by cause 1990-2020: Global Burden of Disease Study". Lancet 349: 1498?1504.
^ http://depression.about.com/cs/diagnosis/a/atypicaldepress.htm Atypical Depression Actually Very Typical
^ a b c Fray, Kathy: "Oh Baby...Birth, Babies & Motherhood Uncensored", pages 367-381. Random House NZ, 2005, ISBN 1-86941-713-5
^ Eriksson, O., Wall, A., Marteinsdottir, I., Agren, H., Hartvig, P., Blomqvist, G., Långström, B., Naessén, T. (2006). "Mood changes correlate to changes in brain serotonin precursor trapping in women with premenstrual dysphoria". Psychiatry Res 146 (2): 107-16. PMID 16515859.
^ Eriksson, E.. "Serotonin reuptake inhibitors for the treatment of premenstrual dysphoria". Int Clin Psychopharmacol 14 Suppl 2: S27-33. PMID 10471170.
^ http://www.gpnotebook.co.uk/simplepage.cfm?ID=1268383817
^ van Praag, HM (2005). "Can Stress Cause Depression?". World J Biol Psychiatry 6 Suppl: 5-22.
^ Sapolsky, Robert M., Ph.D. (2004). Why Zebras Don't Get Ulcers. Henry Holt and Company, LLC, 291-298. ISBN 0-8050-7369-8.
^ Heim C., Newport D., Heit S., Graham Y., Wilcox M., Bonsall R., Miller A., Nemeroff C. (2000). "Pituitary-adrenal and autonomic responses to stress in women after sexual and physical abuse in childhood". JAMA 284 (5): 592-7. PMID 10918705.
^ http://depression.about.com/od/causes/a/mutantgene.htm
^ http://medicine.plosjournals.org/archive/1549-1676/2/12/pdf/10.1371_journal.pmed.0020392-L.pdf
^ Dr Helen Mayberg, quoted in http://www.sciammind.com/article.cfm?&articleID=0002AD36-CF84-14C7-8DCC83414B7F0000 Scientific American, volume 17, number 4, pp. 26-31
^ Hallowell, Edward M.; John J. Ratey (2005). Delivered from Distraction : Getting the Most out of Life with Attention Deficit Disorder. New York: Ballantine Books, p. 253–5. ISBN 0-345-44231-8.
^ see Hallowell and Ratey, 2005
^ Manev, R; Manev H (2004). "5-Lipoxygenase as a putative link between cardiovascular and psychiatric disorders". Critical Reviews in Neurobiology 16 (1?2): 181?6.
^ Lawrence, Felicity (2004). "The Ready Meal", in Kate Barker: Not on the Label. Penguin, 214. ISBN 0-14-101566-7.
^ Using Fatty Acids for Enhancing Classroom Achievement. Retrieved on January, 2004.
^ Omega-6 Levels in Brain Linked to Depression. Retrieved on May, 2006.
^ http://www.emedicine.com/med/topic3408.htm
^ Watson, PJ; Andrews PW (October 2002). "Toward a revised evolutionary adaptationist analysis of depression: the social navigation hypothesis". Journal of Affective Disorders 72: 1-14.
^ http://www.behavenet.com/capsules/disorders/mjrdepd.htm
^ Carlat DJ. The Psychiatric Review of Symptoms: A Screening Tool for Family Physicians. American Family Physician. Vol. 58/No. 7 (November 1, 1998). Available at: http://www.aafp.org/afp/981101ap/carlat.html. Accessed on: April 30, 2006.
^ Depression: major depression criteria. MedicalMnemonics.com. URL: http://www.medicalmnemonics.com/cgi-bin/return_browse.cfm?discipline=Psychiatry&browse=1. Accessed on: April 30, 2006.
^ Spitzer RL, Kroenke K, Williams JB. Validation and utility of a self-report version of PRIME-MD: the PHQ primary care study. Primary Care Evaluation of Mental Disorders. Patient Health Questionnaire. JAMA. 1999;282:1737-44. PMID 10568646
^ Brody DS, Hahn SR, Spitzer RL, Kroenke K, Linzer M, deGruy FV 3rd, Williams JB. Identifying patients with depression in the primary care setting: a more efficient method. Arch Intern Med. 1998 Dec 7-21;158(22):2469-75. PMID 9855385
^ McGlinchey J.B., Zimmerman M., Young D., & Chelminski I. (2006). Diagnosing major depressive disorder VIII: are some symptoms better than others? J Nerv Ment Dis., 194:785-90. PMID 17041292
^ Thase, ME (1999). "When are psychotherapy and pharmacotherapy combinations the treatment of choice for major depressive disorder?". Psychiatr Q. 70 (4): 333-346.
^ Lacasse J, Leo J (2005). "Serotonin and depression: a disconnect between the advertisements and the scientific literature". PLoS Med 2 (12): e392. PMID 16268734. Full text
^ Uz T, Ahmed R, Akhisaroglu M, Kurtuncu M, Imbesi M, Dirim Arslan A, Manev H (2005). "Effect of fluoxetine and cocaine on the expression of clock genes in the mouse hippocampus and striatum". Neuroscience 134 (4): 1309-16. PMID 15994025.
^ Yuferov V, Butelman E, Kreek M (2005). "Biological clock: biological clocks may modulate drug addiction". Eur J Hum Genet 13 (10): 1101-3. PMID 16094306.
^ Manev H, Uz T (2006). "Clock genes as a link between addiction and obesity". Eur J Hum Genet 14 (1): 5. PMID 16288309. Full text
^ http://www.psychiatrist.com/pcc/pccpdf/v06n04/v06n0403.pdf
^ Trivedi MH, Rush AJ, Wisniewski SR, et al (2006). "Evaluation of outcomes with citalopram for depression using measurement-based care in STAR*D: implications for clinical practice". The American journal of psychiatry 163 (1): 28-40. DOI:10.1176/appi.ajp.163.1.28. PMID 16390886.
^ Trivedi MH, Fava M, Wisniewski SR, et al (2006). "Medication augmentation after the failure of SSRIs for depression". N. Engl. J. Med. 354 (12): 1243-52. DOI:10.1056/NEJMoa052964. PMID 16554526.
^ Rush AJ, Trivedi MH, Wisniewski SR, et al (2006). "Bupropion-SR, sertraline, or venlafaxine-XR after failure of SSRIs for depression". N. Engl. J. Med. 354 (12): 1231-42. DOI:10.1056/NEJMoa052963. PMID 16554525.
^ http://intelegen.com/nutrients/5htp_5hydroxytryptophan_vs.htm
^ Delle Chiaie, Roberto; Paolo Pancheri and Pierluigi Scapicchio (2002). "Efficacy and tolerability of oral and intramuscular S-adenosyl- L-methionine 1,4-butanedisulfonate (SAMe) in the treatment of major depression: comparison with imipramine in 2 multicenter studies". Am J Clin Nutr 76 (5): 1172S?1176S.
^ Mischoulon, D; Fava M. (2002). "Role of S-adenosyl-L-methionine in the treatment of depression: a review of the evidence". Am J Clin Nutr 76 (5): 1158S?61S.
^ http://www.umm.edu/altmed/ConsSupplements/Omega3FattyAcidscs.html
^ http://ajp.psychiatryonline.org/cgi/content/full/156/4/646
^ http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15567428
^ Rapid Recovery From Depression Using Magnesium Treatment
^ http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10333988&dopt=Abstract
^ http://www.umm.edu/altmed/ConsHerbs/GinkgoBilobach.html
^ http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14730113
^ http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14730113
^ http://ajp.psychiatryonline.org/cgi/content/abstract/157/5/715
^ http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15307288&dopt=Citation
^ http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11985347&dopt=Abstract
^ http://www.breggin.com/Electroshockscientific.pbreggin.1998.pdf
^ http://www.mcmanweb.com/article-16.htm
^ http://healthpsych.psy.vanderbilt.edu/AcupunctureDepression.htm
^ http://www.wildmind.org/meditation/stress/mbsr/mbsr-abstract08.html
^ http://www.mayoclinic.com/health/meditation/HQ01070
^ http://www.neuron.org/content/article/fulltext?uid=PIIS089662730500156X (Neuron)
^ http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15964704&dopt=Abstract
^ http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8373935
^ http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11754527
^ Geddes, JR; Carney SM, Davies C, Furukawa TA, Kupfer DJ, Frank E, Goodwin GM (22 February 2003). "Relapse prevention with antidepressant drug treatment in depressive disorders: a systematic review". Lancet 361 (9358): 653?61. PMID 12606176.
^ http://cms.psychologytoday.com/articles/pto-19990301-000032.html

External links

• Depression at the Open Directory Project
• 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
• 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

v • d • eWHO ICD-10 Mental and behavioural disorders (F, 290-319)

Organic/symptomatic
Dementia (Alzheimer's disease, Multi-infarct dementia, Pick's disease, Creutzfeldt-Jakob disease, Huntington's disease, Parkinson's disease, AIDS dementia complex) - Delirium

Psychoactive substance
Intoxication (Drunkenness) - Physical dependence (Alcohol dependence, Opioid dependency) - Withdrawal (Benzodiazepine withdrawal, Delirium tremens) - Amnesic (Korsakoff's syndrome)

Schizophrenia, schizotypal and delusional
Schizophrenia (Disorganized schizophrenia) - Schizotypal personality disorder - Delusional disorder - Folie à deux - Schizoaffective disorder

Mood (affective)
Mania - Bipolar disorder - Clinical depression - Cyclothymia - Dysthymia

Neurotic, stress-related and somatoform
Agoraphobia - Anxiety disorder - Panic disorder - Generalized anxiety disorder - Social Anxiety Disorder - OCD - Acute stress reaction - PTSD - Adjustment disorder - Conversion disorder - Somatoform disorder - Somatization disorder - Neurasthenia

Physiological/physical behavioural
Eating disorder (Anorexia nervosa, Bulimia nervosa) - Sleep disorder (Dyssomnia, Insomnia, Hypersomnia, Parasomnia, Night terror, Nightmare) - Sexual dysfunction (Erectile dysfunction, Premature ejaculation, Vaginismus, Dyspareunia, Hypersexuality) - Postpartum depression

Adult personality and behaviour
Personality disorder - Passive-aggressive behavior - Kleptomania - Trichotillomania - Voyeurism - Factitious disorder - Munchausen syndrome

Mental retardation
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Melancholia
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"Melancholy" redirects here. For the anime series, see The Melancholy of Haruhi Suzumiya (anime).
For the record label, see Melancholia Records.

Melencolia I by Albrecht Dürer.
Melancholia (Greek μελαγχολία), in contemporary usage, is a mood disorder of non-specific depression, characterized by low levels of enthusiasm and low levels of eagerness for activity. In a modern context, "melancholy" applies only to the mental or emotional symptoms of depression or despondency; historically, "melancholia" could be physical as well as mental, and melancholic conditions were classified as such by their common cause rather than by their properties. Similarly, melancholia in ancient usage also encompassed mental disorders which would later be differentiated as schizophrenias or bipolar disorders.
Contents[hide]
1 History
2 Melancholy in Arab culture
3 The cult of melancholia
4 Notes
5 See also
6 External links
//

[edit] History
The name "melancholia" comes from the old medical theory of the four humours: disease being caused by an imbalance in one or other of the four basic bodily fluids, or humours. Personality types were similarly determined by the dominant humour in a particular person. Melancholia was caused by an excess of black bile; hence the name, which means 'black bile' (Ancient Greek μελας, melas, "black", + χολη, kholé, "bile"); a person whose constitution tended to have a preponderance of black bile had a melancholic disposition. See also: sanguine, phlegmatic, choleric
Melancholia was described as a distinct disease with particular mental and physical symptoms as early as the fifth and fourth centuries BC. Hippocrates, in his Aphorisms, characterized all "fears and despondencies, if they last a long time" as being symptomatic of melancholia.[1]
The most extended treatment of melancholia comes from Robert Burton, whose The Anatomy of Melancholy treats the subject from both a literary and a medical perspective.
Burton wrote in the 16th century that music and dance were critical in treating mental illness, especially melancholia.[2][3][4] In November 2006, Dr. Michael J. Crawford [5] and his colleagues again found that music therapy helped the outcomes of Schizophrenic patients. [6]
A famous allegorical engraving by Albrecht Dürer is entitled Melencolia I. This engraving portrays melancholia as the state of waiting for inspiration to strike, and not necessarily as a depressive affliction. Amongst other allegorical symbols, the picture includes a magic square, and a truncated rhombohedron [2]. The image in turn inspired a passage in The City of Dreadful Night by James Thomson (B.V.), and, a few years later, a sonnet by Edward Dowden.

[edit] Melancholy in Arab culture
The Arabic word found as 'ḥuzn' and 'ḥazan' in the Qur'an and 'hüzün' in modern Turkish, refer to the pain and sorrow over a loss, death of relatives in the case of the Qur'an. Two schools further interpreted this feeling. The first sees it as a sign that one is too attached to the material world, while Sufism took it to represent a feeling of personal insuffiency, that one was not getting close enough to God and did not or could not do enough for God in this world. In [7] it is elaborated on the added meaning 'hüzün' has acquired in Turkish. Here, it denotes a sense of failure in life, lack of initiative and to retreat into oneself, symptoms quite similar to melancholia. According to [7] it has been a defining character of cultural works from Istanbul after the fall of the ottoman empire, much as melancholia has inspired art in the west.
As a parallel with physicians of classical Greece, ancient Arabic physicians also categorized 'ḥuzn' as a disease. Al-Kindi (c. 801–873 CE) links it with disease-like mental states like anger, passion, hatred and depression, while Avicenna (980 - 1037 CE) diagnosed 'ḥuzn' in a lovesick man if his pulse increased drastically when the name of the girl he loved was spoken. [8] Avicenna discuss, in remarkable similarity with Robert Burton, causes like fear of death, intrigues, love, and food and treatments combining medicine and philosophy. Including rational thought, morale, discipline, fasting and coming to terms with the catastrophe.
The various uses of 'ḥuzn' and 'hüzün' thus describe melancholy from a certain vantage point, show similarities with Female hysteria in the case of Avicenna's patient and in a religious context it is not unlike sloth, which by Dante was defined as "failure to love God with all one's heart, all one's mind and all one's soul.". Thomas Aquinas described sloth as "an oppressive sorrow, which, to wit, so weighs upon man's mind, that he wants to do nothing". [9]

[edit] The cult of melancholia
During the early 17th century, a curious cultural and literary cult of melancholia arose in England. It was believed that religious uncertainties caused by the English Reformation and a greater attention being paid to issues of sin, damnation, and salvation, led to this effect.
In music, the post-Elizabethan cult of melancholia is associated with John Dowland, whose motto was Semper Dowland, semper dolens. ("Always Dowland, always mourning.") The melancholy man, known to contemporaries as a "malcontent," is epitomized by Shakespeare's Prince Hamlet, the "Melancholy Dane." Another literary expression of this cultural mood comes from the death-obsessed later works of John Donne. Other major melancholic authors include Sir Thomas Browne, and Jeremy Taylor, whose Hydriotaphia, Urn Burial and Holy Living and Holy Dying, respectively, contain extensive meditations on death.
A similar phenomenon, though not under the same name, occurred during Romanticism, with such works as The Sorrows of Young Werther by Goethe.
In the 20th century, much of the counterculture of modernism was fueled by comparable alienation and a sense of purposelessness called "anomie."

[edit] Notes
^ Hippocrates, Aphorisms, Section 6.23
^ cf. The Anatomy of Melancholy, Robert Burton, subsection 3, on and after line 3480, "Music a Remedy":
But to leave all declamatory speeches in praise [3481]of divine music, I will confine myself to my proper subject: besides that excellent power it hath to expel many other diseases, it is a sovereign remedy against [3482] despair and melancholy, and will drive away the devil himself. Canus, a Rhodian fiddler, in [3483]Philostratus, when Apollonius was inquisitive to know what he could do with his pipe, told him, "That he would make a melancholy man merry, and him that was merry much merrier than before, a lover more enamoured, a religious man more devout." Ismenias the Theban, [3484]Chiron the centaur, is said to have cured this and many other diseases by music alone: as now they do those, saith [3485]Bodine, that are troubled with St. Vitus's Bedlam dance. [1]
^ "Humanities are the Hormones: A Tarantella Comes to Newfoundland. What should we do about it?" by Dr. John Crellin, MUNMED, newsletter of the Faculty of Medicine, Memorial University of Newfoundland, 1996.
^ Aung, Steven K.H., Lee, Mathew H.M. (2004). "Music, Sounds, Medicine, and Meditation: An Integrative Approach to the Healing Arts". Alternative & Complementary Therapies 10 (5): 266-270. DOI:10.1089/act.2004.10.266.
^ Dr. Michael J. Crawford page at Imperial College London, Faculty of Medicine, Department of Psychological Medicine.
^ Crawford, Mike J.; Talwar, Nakul, et al. (November 2006). "Music therapy for in-patients with schizophrenia: Exploratory randomised controlled trial". The British Journal of Psychiatry (2006) 189: 405-409. DOI:10.1192/bjp.bp.105.015073. PMID 17077429.
^ a b 'Istanbul', chapter 10, (2003) Orhan Pamuk
^ Avicenna, Fi'l-Ḥuzn, (About Ḥuzn)
^ "Summa Theologica", Thomas Aquinas

[edit] See also
Depression (mood)
Dysthymia
Nostalgia
Saudade

[edit] External links
Grunwald Center website: Durer's Melencolia and clinical depression, iconography and printmaking techniques
"Dürer's Melancholia": sonnet by Edward Dowden
Melancholy and abstraction, on the Berlin exhibition "Melancholy: Genius and Madness in Art"
Diderot's historic writing on Melancholy - translated into English
Retrieved from "http://en.wikipedia.org/wiki/Melancholia"

Dysthymia
From Wikipedia, the free encyclopedia

Classification & external resources
ICD-10
F34.1
ICD-9
300.4

Dysthymia is a mood disorder that falls on the depression spectrum. It is typically characterized by a lack of enjoyment or pleasure, clinically referred to as anhedonia, that continues for an extended period. Dysthymia differs from major depression in that it is both longer-lasting and less disabling. Dysthymia can prevent a person from functioning effectively, disrupt sleep patterns, and interfere with activities of daily living (ADLs). Many dysthymia sufferers have a more specific subtype called Atypical depression. [citation needed] Dysthymia sufferers exhibit fairly mild symptoms on a day-to-day basis. Over a lifetime the disorder may have more severe effects, such as a high rate of suicide, work impairment, and social isolation. The psychiatric term describing a personality with opposite characterstics to dysthymia is hyperthymia.

Diagnostic criteria
The Diagnostic and Statistical Manual of Mental Disorders (DSM), published by the American Psychiatric Association, characterizes Dysthymic disorder as a chronic depression, but with less severity than a major depression. The essential symptom involves the individual feeling depressed almost daily for at least two years, but without the criteria necessary for a major depression. Low energy, disturbances in sleep or in appetite, and low self-esteem typically contribute to the clinical picture as well. Sufferers have often experienced dysthymia for many years before it is diagnosed. People around them come to believe that the sufferer is 'just a moody person.' Note the following diagnostic criteria:

• On the majority of days for 2 years or more, the patient reports depressed mood or appears depressed to others for most of the day.
• When depressed, the patient has 2 or more of:

• Appetite decreased or increased
• Sleep decreased or increased
• Fatigue or low energy
• Poor self-image
• Reduced concentration or indecisiveness
• Feels hopeless
• During this 2 year period, the above symptoms are never absent longer than 2 consecutive months.
• During the first 2 years of this syndrome, the patient has not had a Major Depressive Episode.
• The patient has had no Manic, Hypomanic or Mixed Episodes.
• The patient has never fulfilled criteria for Cyclothymic Disorder.
• The disorder does not exist solely in the context of a chronic psychosis (such as Schizophrenia or Delusional Disorder).
• The symptoms are not directly caused by a general medical condition or the use of substances, including prescription medications.
• The symptoms cause clinically important distress or impair work, social or personal functioning.

Treatment
As with other forms of depression, a number of treatments exist for dysthymia. Doctors most commonly use psychotherapy, including cognitive therapy, to help change the mind-set of the individual affected. Additionally doctors may prescribe a variety of antidepressant medications For mild or moderate depression, the American Psychiatric Association in its 2000 Treatment Guidelines for Patients with Major Depressive Disorder advises psychotherapy alone or in combination with an antidepressant as possibly appropriate.

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Depression Medications

Selective Serotonin Reuptake Inhibitors
Selective serotonin reuptake inhibitor (SSRI) medications affect the levels of serotonin in the brain. For many people, these medications are the first choice to treat depression. Examples of these medications are fluoxetine (Prozac, Prozac Weekly, Sarafem), sertraline (Zoloft), paroxetine (Paxil, Paxil CR), escitalopram (Lexapro), fluvoxamine, and citalopram (Celexa).

How do SSRIs work?
The antidepressant action of SSRIs is not thoroughly understood but is possibly due to the ability of SSRIs to block the uptake of serotonin, thereby providing higher levels of serotonin at the brain receptor site.

Who should not use these medications?
Individuals who are allergic to SSRIs
Individuals who are currently taking, or have taken within the past 2 weeks, thioridazine (Mellaril), pimozide (Orap), or monoamine oxidase inhibitors (MAOIs) such as phenelzine (Nardil) and tranylcypromine (Parnate)
Individuals must not take MAOIs or thioridazine for at least 5 weeks after stopping SSRIs.Use
SSRIs may be administered as oral tablets, capsules, or liquid once or twice a day.

Prozac Weekly is administered once each week.
Do not discontinue these medications abruptly, but gradually taper use to avoid withdrawal-like symptoms such as agitation, anxiety, confusion, dizziness, headache, and insomnia.

Elderly individuals typically require lower doses of SSRIs.Children: Fluoxetine (Prozac) is the only SSRI approved by the FDA for treatment of depression in children aged 8-18 years.
Drug or food interactions: Tell the doctor what medications are currently being taken because many medicines interact with SSRIs. Do not take any nonprescription or herbal medications without first consulting the doctor or pharmacist. The following are examples of interactions, but they do not represent a complete list.

When an SSRI is administered with 5-HT1 agonists, such as sumatriptan or zolmitriptan, weakness and incoordination, although rare, have been reported.

SSRIs may increase the blood levels and risk of toxicity of certain medications, including the following:

• Highly protein-bound medicines such as warfarin (Coumadin) and digoxin
• Antiarrhythmic medicines such as propafenone (Rythmol) or flecainide (Tambocor)
• Beta blockers such as propranolol (Inderal) or metoprolol (Lopressor, Toprol XL)
• Tricyclic antidepressants such as amitriptyline (Elavil)
• Benzodiazepines such as alprazolam (Xanax), diazepam (Valium), midazolam (Versed), or
• triazolam (Halcion)
• Carbamazepine (Tegretol)
• Cisapride (Propulsid)
• Clozapine (Clozaril)
• Cyclosporine (Neoral, Sandimmune)
• Haloperidol (Haldol)
• Thioridazine (Mellaril)
• Phenytoin (Dilantin)
• Pimozide (Orap)
• Theophylline (Theo-Dur, TheoBid)

The following substances may increase toxicity of SSRIs:

• Alcohol or other drugs that depress the central nervous system
• Diuretics (water pills)
• MAOIs (may cause serious, and sometimes fatal, reactions)
• St. John’s wort
• Decongestants such as pseudoephedrine (Sudafed)
• Lithium
• Sibutramine (Meridia)
• Zolpidem (Ambien) or other medications used for insomnia

Side Effects: This is NOT a complete list of side effects reported with SSRIs. A doctor, health care provider, or pharmacist can discuss a more complete list of side effects.

• Photosensitivity (increased risk of sunburn) (Use protective clothing, such as long sleeves and hats, and sunscreen to decrease the risk of sunburn.)
• Rash
• Nausea
• Dry mouth
• Constipation
• Low blood sodium levels (in people who are dehydrated or taking diuretics)
• Low blood sugar levels
• Drowsiness (Caution is advised when operating machinery, driving, or performing other tasks that require alertness.)
• Sexual dysfunction such as delayed ejaculation, erectile difficulties, and impotence (in men) and difficulty reaching climax or orgasm (in women)
• Withdrawal-like symptoms in newborns (Women who take SSRIs in late pregnancy [third trimester] may have newborns who require prolonged hospitalization due to withdrawal-like symptoms such as shortness of breath, constant crying, feeding difficulty, or low blood sugar levels.)
• Manic episodes in persons with bipolar disorder (If not combined with a mood-stabilizing medication, SSRIs may induce manic episodes in individuals with bipolar disorder [manic depression].)
• Kidney or liver impairment precautions (The doctor may draw blood samples to check for kidney or liver impairment before prescribing SSRIs.)

Tricyclic Antidepressants
Tricyclic antidepressants (TCAs) are often prescribed in severe cases of depression or when SSRI medications do not work. Tricyclic antidepressants include:

• amitriptyline (Elavil),
• amoxapine (Asendin),
• desipramine (Norpramin),
• doxepin (Adapin, Sinequan, Zonalon),
• imipramine (Tofranil),
• nortriptyline (Aventyl, Pamelor),
• protriptyline (Vivactil), and
• trimipramine (Surmontil).

How do TCAs work? TCAs block the uptake of serotonin and norepinephrine, thereby providing higher levels of these neurotransmitters at the brain receptor site. Besides increasing norepinephrine and serotonin, amoxapine also increases the neurotransmitter dopamine.

• Who should not use these medications?
• Individuals who have allergic reactions to TCAs
• Individuals in the acute recovery phase following a heart attack
• Individuals with glaucoma
• Individuals with urine retention
• Individuals who are currently taking or have taken MAOIs within the past 2 weeks (Phenelzine [Nardil], and tranylcypromine [Parnate], are examples of MAOIs.) (Do not start taking MAOIs for at least 2 weeks after stopping TCAs. This is a general warning; see drug and food interactions for low-dose use together.)
• Individuals taking some medications that alter heart rhythm such as thioridazine (Mellaril) or cisapride (Propulsid)Use

Tricyclic antidepressants are taken orally by tablet, capsule, or oral solution.
Elderly individuals and adolescents often require lower doses.Elderly: Elderly individuals require lower doses. Elderly individuals are more susceptible to sedative effects and may feel faint when standing up, therefore increasing the risk of falls and injuries.

Children: The following TCAs are approved in the United States for treating adolescents with depression who are older than 12 years:

• Amitriptyline
• Desipramine
• Doxepin
• Nortriptyline
• Protriptyline
• Trimipramine
• Amoxapine (approved for persons older than 16 years)

Drug or food interactions: Tell the doctor what medications are currently being taken because many medicines interact with TCAs. Do not take any nonprescription or herbal medications without first consulting the doctor or pharmacist. The following are examples of interactions, but they do not represent a complete list.

TCAs may increase the blood levels and/or risk of toxicity of the following medications:

• MAOIs (These may cause serious and sometimes fatal reactions; some TCAs have been used safely with MAOIs, but the dose of TCAs must be increased very slowly and the person must strictly adhere to MAOI dietary restrictions.)
• Sympathomimetics such as pseudoephedrine (Sudafed)
  The following substances may increase the toxicity of TCAs:
  Alcohol or other drugs that depress the central nervous system such as medications taken for insomnia
• Medications, such as antihistamines (Benadryl), that may produce similar side effects
• Antifungal medications such as ketoconazole (Nizoral) or fluconazole (Diflucan)
• SSRIs, venlafaxine, and nefazodone (may increase risk for serotonin syndrome—symptoms include hypertension, fever, muscle tremor, or confusion)
• Tramadol (Ultram) (may increase risk of seizures)
• Medications such as cisapride, thioridazine, quinidine, antihistamines, erythromycin, dofetilide, and pimozide that also increase the risk for abnormal heart rhythm
• Valproic acid
• Other interactions include the following:
  
• TCAs may decrease the ability for clonidine to lower blood pressure levels.
• Carbamazepine may decrease TCA effectiveness.
• St. John’s wort may decrease TCA effectiveness and increase the risk of serotonin syndrome.

Side Effects: This is NOT a complete list of possible side effects reported with TCAs. A doctor, health care provider, or pharmacist can discuss a more complete list of side effects.

• Confusion, agitation, or hallucinations (Contact a doctor immediately if these occur.)
• Severe diarrhea, fever, sweating, muscle stiffness, or tremors (These may be symptoms of neuroleptic malignant syndrome. Contact a doctor immediately.)
• Rapid or abnormal heartbeat or fainting (Contact a doctor immediately if these occur.)
• Changes in sexual interest or ability
• Manic episodes in persons with bipolar disorder (If not combined with a mood-stabilizing medication, SSRIs may induce manic episodes in individuals with bipolar disorder [manic depression].)
• Drowsiness (Caution is advised when operating machinery, driving, or performing other tasks that require alertness.)
• Photosensitivity (increased risk of sunburn) (Use protective clothing, such as long sleeves and hats, and sunscreen to decrease the risk of sunburn.)
• Rash
• Nausea
• Dry mouth
• Urine retention
• Blurred vision
• Constipation
• Lightheadedness when standing up from a sitting or lying position (Stand up gradually from lying down or sitting positions.)
• Seizures (TCAs lower the threshold for seizures, that is, seizures may occur more easily in the person taking TCAs. Caution is advised for individuals prone to seizures or those who have a history of seizures.)

Monoamine Oxidase Inhibitors
Monoamine oxidase inhibitors (MAOIs) include:

1. isocarboxazid (Marplan),
2. phenelzine (Nardil), and
3. tranylcypromine (Parnate).

These medications are rarely used because of strict dietary requirements and life-threatening drug and food interactions. Because of these drug and food interactions, MAOIs may not be taken with many other types of medicines, and some foods that are high in tyramine, dopamine, or tryptophan must be avoided as well.

How do MAOIs work? These drugs inhibit monoamine oxidase. Monoamine oxidase is an enzyme in the body that is responsible for metabolizing (breaking down) neurotransmitters such as norepinephrine, epinephrine, dopamine, and serotonin. The result of MAOIs is an increase in the concentration of neurotransmitters. Some of these neurotransmitters increase blood pressure.

Who should not use these medications? In many circumstances, the use of MAOIs is dangerous.

• Individuals who are allergic to MAOIs
• Individuals with diseases, such as pheochromocytoma or hypertension, that cause increased blood pressure
• Individuals with diseases, such as heart failure or other heart disease, severe impaired renal function, and stroke or other cerebrovascular disease, in which increased blood pressure is likely to aggravate the condition
• Individuals with a history of headache
• Individuals with liver disease
• Individuals using other drugs that may elevate blood pressure or cause additive effects (see drug interactions)
• Individuals consuming foods with high tyramine content—MAOIs may lead to dangerously elevated blood pressure (see food interactions)

Use

• MAOIs are administered orally.
• MAOIs are rarely the first antidepressant drug prescribed, but they are an option when initial treatments do not work or are not tolerated.
• MAOIs are not a good choice for elderly or debilitated individuals.
• Children: Phenelzine is not approved for children younger than 16 years. Tranylcypromine is not approved for children or adolescents.

Drug or food interactions: Tell the doctor what medications are currently being taken because many drugs interact with MAOIs. Do not take any nonprescription or herbal medications without first consulting the doctor or pharmacist. The following are examples of interactions, but they do not represent a complete list.

• The risk for serotonin syndrome may be increased by SSRIs, TCAs, atomoxetine (Strattera), duloxetine, dextromethorphan (in many cough syrups), dexfenfluramine, 5-HT1 agonists (such as sumatriptan or zolmitriptan), venlafaxine (Effexor), St. John’s wort, or ginkgo. Serotonin syndrome is a serious side effect and may be fatal. Symptoms include fever, muscle stiffness, and changes in mental status such as confusion or hallucinations.
  The risk of neuroleptic malignant syndrome (restlessness, sweating, fever, confusion, and muscle stiffness) may increase with lithium and tramadol (Ultram).
• Morphine, meperidine (Demerol), and other narcotic pain relievers may cause hypotension and depress the central nervous system and respirations.
• The following drugs may increase the risk of hypertensive crisis when taken with MAOIs or within 2 weeks of stopping MAOIs:
  
• Decongestants such as pseudoephedrine (Sudafed)
• Stimulants such as
  amphetamine, cocaine, methamphetamine, or ephedrine (ma huang, ephedra)
• Cyclobenzaprine (Flexeril)
• Dopamine, methyldopa (Aldomet), or levodopa (Sinemet)
• Epinephrine (EpiPen)
• Methylphenidate (Ritalin) or Adderall
• Buspirone
  
• MAOIs may increase side effects of the following drugs:
  
• Bupropion
  - Increases risk of seizures, agitation, and psychotic changes
• Antidiabetic agents - Increases risk for low blood sugar levels, depression, and seizures
• Mirtazapine - May increase risk for seizures
• Carbamazepine - May result in high blood pressure, fever, and seizures

• Do not eat foods high in tyramine, dopamine, or tryptophan while taking MAOIs or for 2 weeks after discontinuing MAOIs. Tyramine, dopamine, and tryptophan are chemicals that can interact with MAOIs and cause hypertensive crisis, which is an extremely dangerous side effect. Foods high in these chemicals should be avoided. They include the following:
  
• Dairy products Cheese, particularly Blue, Camembert, Cheddar, Emmenthaler,
  Stilton, and Swiss, which contain very high amounts of tyramine, Yogurt
• Meat and fish products

o Anchovies
o Beef or chicken liver
o Other meats or fish that have not been refrigerated, are fermented, or are spoiled
o Caviar
o Fermented
o sausages such as bologna, pepperoni, salami, and summer sausage
o Game meat
o Meats prepared with tenderizer
o Herring
o Shrimp paste

• Alcoholic beverages
  
• Beer
• Red wine, especially Chianti
• Sherry
• Distilled spirits and
• liqueurs
• Fruits and vegetables
• Fruits such as bananas, raspberries, dried fruits, and overripe fruits (especially avocados and figs)
• Bean cure, miso soup, sauerkraut, soy sauce, and yeast extracts (such as Marmite)
• Foods containing other chemicals that increase blood pressure
• Broad beans (fava beans)
• Caffeine containing beverages such as coffee, tea, and cola
• Chocolate
• Ginseng

Side Effects: This is NOT a complete list of side effects reported with MAOIs. A doctor, health care provider, or pharmacist can discuss a more complete list of side effects.

• Hypertensive crisis (Hypertensive crisis is the most serious reaction and involves dramatic increases in blood pressure and requires immediate care from the doctor. The hypertensive crisis usually occurs within several hours after ingestion of a drug or food that interacts with MAOIs. Hypertensive crisis can be fatal. Symptoms include severe headache, rapid heart rate, chest pain, neck stiffness, nausea, vomiting, sweating [may include a fever or cold, clammy skin], dilated pupils, and eye sensitivity to light.)
  Manic episodes in persons with bipolar disorder (If not combined with a mood-stabilizing drug, MAOIs may induce manic episodes in individuals with bipolar disorder [manic depression].)
• Increased heart rate or blood pressure in people with hyperthyroid conditions

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