Clinical depression (also called major depressive
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 depressed as "being blue", "feeling sad for
no reason", or "having no motivation to do anything". Clinical depression
is generally acknowledged to be more serious than normal depressed
feelings
[edit]
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.[1]
Since these suggestions, many other causes for clinical depression have
been proposed[citation
needed].
[edit]
Prevalence
Clinical depression affects about 16%[2]
of the population on at least one occasion in their lives. In some
countries, such as Australia, one in four women and one in eight men will
suffer from depression. The
mean age of
onset, from a number of studies, is in the late 20s. About twice as many
females as males report or receive treatment for clinical depression,
though this imbalance is shrinking over the course of recent history; this
difference seems to completely disappear after the age of 50 - 55, when
most females have passed the end of
menopause. It should be noted that these numbers are only for those
who report or receive treatment for depression; men are less likely to
report feeling depressed, and also less likely to seek treatment, possibly
due to gender roles[citation
needed]. 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.[3]
[edit]
Symptoms
According to the
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:
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,
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 "lay 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.
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.
Depression in children is not as obvious as it is in
adults. Here are some symptoms that children might display:
- 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.
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.
One of the most widely used instruments for
measuring depression severity is the
Beck Depression Inventory, a 21-question multiple choice survey.
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 above indicates, clinical depression is a
serious, potentially lethal systemic disorder characterized by the
psychiatric industry as interlocking physical, affective, and cognitive
symptoms that have consequences for function and survival well beyond sad
or painful feelings.
[edit]
Mnemonics
Mnemonics commonly used to remember the DSM-IV criteria are SIGECAPS[4]
(sleep, interest (anhedonia), guilt, energy, concentration, appetite,
psychomotor, suicidality) and DEAD SWAMP[5]
(depressed mood, energy, anhedonia, death (thoughts of), sleep,
worthlessness/guilt, appetite, mentation, psychomotor).
[edit]
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.
[edit]
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 as recurrent 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 their 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 on 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.
-
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.
[edit]
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.[6]
Premenstrual dysphoriais 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.[7]
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.[8]
[edit]
The role of anxiety in depression
[edit]
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, and 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[9].
This idea refers to an anxiety/depression spectrum for these two
disorders, which differs from the mainstream perspective of discrete
diagnostic categories.
Although there is no specific diagnostic category
for the comorbidity of depression and anxiety in the DSM or ICD, the
National Comorbidity Survey (US) reports that 58 percent of those with
major depression also suffer from lifetime anxiety. Supporting this
finding, two widely accepted clinical colloquialisms include
-
- agitated depression - a state of
depression that presents as anxiety and includes
akathisia, suicide, insomnia (not early morning wakefulness),
nonclinical (meaning "doesn't meet the standard for formal diagnosis")
and nonspecific panic, and a general sense of dread.
-
- akathitic depression - a state of
depression that presents as anxiety or suicidality and includes
akathisia but does not include symptoms of panic.
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.[10]
To that point, a
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.
[edit]
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.
On a final note,
researchers at the
University of California,
San
Diego, under the guidance of Hagop Akiskal MD, have found convincing
evidence for the co-occurrence of hypomanic symptoms associated with a
diagnosis of depression where the diagnosis does not meet criteria for
Bipolar Disorder.[citation
needed] Symptoms under consideration, such as
irritability, misdirected anger, and compulsivity, also may not present
sufficiently to be considered a hypomanic episode, as described by a
Bipolar II
Disorder. As noted in the Frank study [citation
needed] mentioned above, this particular course of
the disease, with the breakthrough of anxiety, may have a significant
impact on the overall course of the depression.
This idea of co-occurring anxiety and depression
is supported in a study by Giovanni Cassano MD of the
University of Pisa and his collaborators on the Spectrum Project, who
found a correlation between lifetime hypomanic and manic symptoms and the
severity of the depression.[citation
needed]
The presence of a significant number of manic/hypomanic
items in patients with recurrent unipolar depression seems to challenge
the traditional unipolar-bipolar dichotomy.
These authors, along with many other researchers[citation
needed], argue in support of a revision of the
approach to psychiatric diagnosis into what is being called the mood
spectrum, so as to "[make] more accurate diagnostic evaluation[s]." This
approach, although controversial, has begun to be given consideration by
many behavioral health professionals.
[edit]
Causes of depression
No specific cause for depression has been
identified, but a number of factors are believed to be involved.
-
Heredity – The tendency to develop depression may be inherited;
there is some evidence that this disorder may run in families. "Running
in families" may indicate an environmental cause, however. For example,
religion "runs in families". A 2004
press release from the
National Institute of Mental Health declares "major depression is
thought to be 40–70 percent heritable, but likely involves an
interaction of several genes with environmental events".
[1]
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.
-
Physiology – There may be changes or imbalances in chemicals that
transmit information in the brain, called
neurotransmitters. Many modern
antidepressant
drugs increase levels of certain neurotransmitters, such as
serotonin and
norepinephrine. Although the causal relationship is unclear, it is
known that antidepressant medications can relieve certain symptoms of
depression, although critics point out that the relationship between
serotonin,
SSRIs, and depression usually is typically greatly oversimplified
when presented to the public (see
here). Recent research has suggested that there may be a link
between depression and
neurogenesis of the
hippocampus.[citation
needed] 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 dysthemic mood. The
hippocampus regains mass when exposed to treatments that increase brain
serotonin, and when regrown, mood and memory tend to be restored.
-
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.
-
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.[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,
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.
- Life experiences – Job loss,
poverty,
financial difficulties,
gambling addiction, long periods of
unemployment, the
loss of a
spouse or other family member, divorce or the end of a committed
relationship,
involuntary celibacy, or other
traumatic events may trigger depression. Long-term
stress at home, work, or school can also be involved. Bullying in
late adolescence is also thought to be a contributing factor.
- Medical conditions – Certain illnesses,
including cardiovascular disease,[11]
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.
Gender dysphoria can also cause depression.
- Diet – 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.[12]
This link has been at least partly validated by studies using
dietary supplements in schools[13]
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.[14]
- Alcohol and other drugs – Alcohol can have a
negative effect on mood, and misuse of alcohol,
benzodiazepine-based tranquilizers, and sleeping medications can all
play a major role in the length and severity of depression.
-
Postpartum depression (also known as postnatal depression) –
Dr. Ruta M Nonacs writes that while many women experience some mood
changes after giving birth, "10-15% of women experience a more disabling
and persistent form of mood disturbance (e.g., postpartum depression,
postpartum psychosis)".[2]
When it occurs, the onset typically is within three months after
delivery, and it may last for several months. About two new mothers out
of a thousand experience the more serious depressive disorder Postnatal
Psychosis which includes hallucinations and/or delusions.
- Living with a depressed person – Those living
with someone suffering from depression experience increased anxiety and
life disruption, increasing the possibility of also becoming depressed.[citation
needed]
- Evolutionary biological hypotheses of
depression – Evolutionary analyses usually consider possible functions
for depressed mood as well as clinical depression.
-
- 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 mate, 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 signalling 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
[3] 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.[15]
-
-
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.
[edit]
Treatment
Treatment of depression varies broadly and is
different for each individual. Various types and combinations of
treatments may have to be tried, but without hope in a complete solution
to the problem. There are two primary modes of treatment, typically used
in conjunction:
medication and
psychotherapy. A third treatment,
electroconvulsive therapy (ECT), may be used when chemical treatment
fails.
Other alternative treatments used for depression
include exercise and the use of vitamins, herbs, or other nutritional
supplements.[citation
needed]
The effectiveness of treatment often depends on
factors such as the amount of optimism and hope the sufferer is able to
maintain, the control s/he has over stressors, the severity of symptoms,
the amount of time the sufferer has been depressed, the results of
previous treatments, and the degree of support of family, friends, and
significant others.[citation
needed]
Although treatment is generally effective[citation
needed], in some cases the condition does not
respond. Treatment-resistant depression warrants a full assessment, which
may lead to the addition of psychotherapy, higher medication dosages,
changes of medication or combination therapy, a trial of
ECT/electroshock, or even a change in the diagnosis, with subsequent
treatment changes. Although this process helps many, some people's
symptoms continue unabated.
In emergencies,
psychiatric hospitalization is used simply to keep suicidal people
safe until they cease to be dangers to themselves. Another treatment
program is
partial hospitalization, in which the patient sleeps at home but
spends the day, either five or seven days a week, in a psychiatric
hospital setting in intense treatment. This treatment usually involves
group therapy,
individual therapy,
psychopharmacology, and academics (in child and adolescent programs).
[edit]
Medication
Medication that relieves the symptoms of
depression has been available for several decades. These drugs are listed
in order of historical development. Typical first-line therapy for
depression is the use of an
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.[16]
Monoamine oxidase inhibitors (MAOIs) such as Nardil may be used if
other antidepressant medications are ineffective. Because there are
potentially fatal interactions between this class of medication and
certain foods and drugs, they are rarely prescribed anymore. MAOI's are
used to block the enzyme monoamine oxidase which breaks down
neurotransmitters such as serotonin and norepinephrine. MAOI's are as
effective as tricyclics, if not slightly more effective
[citation
needed]. A new MAOI has recently been introduced.
Moclobemide (Manerix), known as a
reversible inhibitor of monoamine oxidase A (RIMA), follows a very
specific chemical pathway and does not require a special diet.
Tricyclic antidepressants are the oldest and include such
medications as
amitriptyline and
desipramine. Tricyclics block the reuptake of certain
neurotransmitters such as norepinephrine and serotonin. They are used less
commonly now because of their side effects, which include increased
heart rate,
drowsiness, dry mouth,constipation, urinary retention, blurred
vision,dizziness, confusion, and sexual dysfunction. Most importantly,
they have a high potential to be lethal in moderate overdose. However,
tricyclic antidepressants are still used because of their high potency,
especially in severe cases of clinical depression.
Selective serotonin reuptake inhibitors (SSRIs) are a family of
antidepressant 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 reabsorption of
serotonin by the nerve cell, thus maintaining the levels the brain needs
to function effectively, although two researchers recently demonstrated
that this is a marketing technique rather than a scientific portrayal of
how the drugs actually work.
[4]. Recent research indicates that these drugs may interact with
transcription factors known as "clock genes"[5],
which may be important for the addictive properties of drugs of abuse and
possibly in obesity[6][7].
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.
Norepinephrine 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.[citation
needed]
Norepinephrine-dopamine reuptake inhibitors such as
bupropion (Wellbutrin, Zyban) inhibit the neuronal reuptake of
dopamine
and
norepinephrine (noradrenaline)[8].
Serotonin-norepinephrine reuptake inhibitors (SNRIs) such as
venlafaxine (Effexor) and
duloxetine (Cymbalta) are a newer form of antidepressant that works on
both noradrenaline and serotonin. They typically have similar side effects
to the SSRIs, although there may be a withdrawal syndrome on
discontinuation that may necessitate dosage tapering.
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]
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.[citation
needed]
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.[17][18]
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
[9].
Dehydroepiandrosterone (DHEA), available as a supplement in the
U.S., has been shown to be effective in small trials
[10].
Chocolate improves mood, probably by raising
serotonin.
[11]. Indeed, chocolate contains
serotonin and there are case reports of interactions between chocolate
and antidepressant drugs[12].
Magnesium supplementation has gathered some attention as a
possible treatment for depression
[13][14].
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."
[15]
St John's Wort [Hypericum perforatum] Traditionally used by 'wise
women' and midwives for hundreds of years, to 'chase away the devil' of
melancholia and anxiety. It is a mood-enhancing herbal substance which
acts like an antidepressant and increases the availability of serotonin,
norepinephrine and dopamine at the neuron synapses.[citation
needed] Also popular for treating insomnia, mood
swings, fatigue, PMS and menopause. Except under medical supervision, St.
John's Wort should not be used with SSRIs or MAOIs due to the risk of
serotonin syndrome.[16]
Ginkgo Biloba Effective natural antidepressant
[17] 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).[6]
Siberian Ginseng [Eleutherococcus senticosus] Although not a true
panax ginseng it is a mood enhancement supplment against stress. Also
popular for treating depression, insomnia, moodiness, fatigue, poor
memory, lack of focus, mental tension and endurance.[6]
Zinc has
had an antidepressant effect in an experiment
[18].
Biotin:
a deficiency has caused a severe depression. The patient's symptoms
improved after the deficiency was corrected.
[19]
Vitamin B-12: Symptoms of a vitamin B-12 deficiency can include
depression and other psychiatric disorders.
[20]
The amino acids
phenylalanine and
tyrosine
have also a favorable effect on easy forms of depression. They enhance the
neurotransmitters dopamine and noradrenalin.[citation
needed]
[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 street speed when used recreationaly. 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]
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
behaviour 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.
