Antidepressant - Wikipedia

11/1/2020 Antidepressant - Wikipedia
Antidepressant
Antidepressants are medications used to treat major depressive
disorder, some anxiety disorders, some chronic pain conditions, and Antidepressant
to help manage some addictions.[1] Common side-effects of Drug class
antidepressants include dry mouth, weight gain, dizziness,
headaches, sexual dysfunction,[2][3][4][5][6] and emotional
blunting.[7][8][9] Most types of antidepressants are typically safe to
take, but may cause increased thoughts of suicide when taken by
children, adolescents, and young adults.[10] A discontinuation
syndrome can occur after stopping any antidepressant which
resembles recurrent depression.[11][12]
Some reviews of antidepressants for depression in adults find

benefit[13] while others do not.[14] Evidence of benefit in children
and adolescents is unclear.[15] There is debate in the medical
community about how much of the observed effects of
antidepressants can be attributed to the placebo effect.[16][17] Most The skeleton structure of the SNRI
research on whether antidepressant drugs work is done on people venlafaxine, a typical example of an
with very severe symptoms,[18] so the results cannot be extrapolated antidepressant.
to the general population.[19]
Class identifiers
There are methods for managing depression which do not involve Use Depressive disorders
medications or may be used in conjunction with medications.
ATC code N06A
Clinical data
Contents Drugs.com Drug Classes (https://

www.drugs.com/drug-c
Medical uses lass/antidepressants.ht
Major depressive disorder ml)
Anxiety disorders Consumer Best Buy Drugs
Eating disorders Reports
Pain
WebMD MedicineNet RxList
Other
External links
Limitations and strategies
Switching antidepressants MeSH D000928
Augmentation and combination In Wikidata
Long-term use
Adverse effects
Pregnancy
Antidepressant-induced mania
Suicide
Sexual
Changes in weight
https://en.wikipedia.org/wiki/Antidepressant 1/36
Discontinuation syndrome
Emotional blunting
Pharmacology
Types
Selective serotonin reuptake inhibitors
Serotonin–norepinephrine reuptake inhibitors
Serotonin modulators and stimulators
Serotonin antagonists and reuptake inhibitors
Norepinephrine reuptake inhibitors
Norepinephrine-dopamine reuptake inhibitors
Tricyclic antidepressants
Tetracyclic antidepressants
Monoamine oxidase inhibitors
NMDA receptor antagonists
Others
Adjuncts
Less common adjuncts
History
Isoniazid, iproniazid, and imipramine
Second generation antidepressants
Rapid-acting antidepressants
Society and culture
Prescription trends
Adherence
Social science perspective
Environmental impacts
See also
References
Further reading
External links
Medical uses
Antidepressants are used to treat major depressive disorder and of other conditions, including some
anxiety disorders, some chronic pain conditions, and to help manage some addictions. Antidepressants
are often used in combinations with one another.[1] The proponents of the monoamine hypothesis of
depression recommend choosing the antidepressant with the mechanism of action impacting the most
prominent symptoms—for example, they advocate that people with MDD who are also anxious or
irritable should be treated with SSRIs or norepinephrine reuptake inhibitors, and the ones with the loss
of energy and enjoyment of life—with norepinephrine and dopamine enhancing drugs.[20]
Major depressive disorder

The UK National Institute for Health and Care Excellence (NICE) 2009 guidelines indicate that
antidepressants should not be routinely used for the initial treatment of mild depression, because the
risk-benefit ratio is poor. The guidelines recommended that antidepressant treatment be considered for:
People with a history of moderate or severe depression,

Those with mild depression that has been present for a long period,
As a second-line treatment for mild depression that persists after other interventions,
As a first-line treatment for moderate or severe depression.
The guidelines further note that antidepressant treatment should be used in combination with
psychosocial interventions in most cases, should be continued for at least six months to reduce the risk of
relapse, and that SSRIs are typically better tolerated than other antidepressants.[21]
American Psychiatric Association treatment guidelines recommend that initial treatment should be
individually tailored based on factors that include severity of symptoms, co-existing disorders, prior
treatment experience, and the person's preference. Options may include pharmacotherapy,
psychotherapy, electroconvulsive therapy (ECT), transcranial magnetic stimulation (TMS) or light
therapy. They recommended antidepressant medication as an initial treatment choice in people with
mild, moderate, or severe major depression, that should be given to all people with severe depression
unless ECT is planned.[22]
Some reviews of antidepressants in adults with depression find benefits[19][13] while others do not.[14]
Anxiety disorders
Generalized anxiety disorder
Antidepressants are recommended by the National Institute for Health and Care Excellence (NICE) for
the treatment of generalized anxiety disorder (GAD) that has failed to respond to conservative measures
such as education and self-help activities. GAD is a common disorder of which the central feature is
excessive worry about a number of different events. Key symptoms include excessive anxiety about
multiple events and issues, and difficulty controlling worrisome thoughts that persists for at least 6
months.
Antidepressants provide a modest-to-moderate reduction in anxiety in GAD.[23] The efficacy of different

antidepressants is similar.[23]
Social anxiety disorder
Some antidepressants are used as a treatment for social anxiety disorder, but their efficacy is not entirely
convincing, as only a small proportion of antidepressants showed some efficacy for this condition.
Paroxetine was the first drug to be FDA-approved for this disorder. Its efficacy is considered beneficial,
although not everyone responds favorably to the drug. Sertraline and fluvoxamine extended release were
later approved for it as well, while escitalopram is used off-label with acceptable efficacy. However, there
isn't enough evidence to support citalopram for treating social phobia, and fluoxetine was no better than
placebo in clinical trials. SSRIs are used as a first-line treatment for social anxiety, but they don't work
for everyone. One alternative would be venlafaxine, which is a SNRI. It showed benefits for social phobia
in five clinical trials against placebo, while the other SNRIs are not considered particularly useful for this
disorder as many of them didn't undergo testing for it. As of now, it is unclear if duloxetine and
desvenlafaxine can provide benefits for social anxiety sufferers. However, another class of
antidepressants called MAOIs are considered effective for social anxiety, but they come with many
unwanted side effects and are rarely used. Phenelzine was shown to be a good treatment option, but its
use is limited by dietary restrictions. Moclobemide is a RIMA and showed mixed results but still got
approval in some European countries for social anxiety disorder. TCA antidepressants, such as
clomipramine and imipramine, are not considered effective for this anxiety disorder in particular. This
leaves out SSRIs such as paroxetine, sertraline and fluvoxamine CR as acceptable and tolerated
treatment options for this disorder.[24][25]
Obsessive–compulsive disorder
SSRIs are a second-line treatment of adult obsessive–compulsive disorder (OCD) with mild functional
impairment and as first-line treatment for those with moderate or severe impairment. In children, SSRIs
are considered as a second-line therapy in those with moderate-to-severe impairment, with close
monitoring for psychiatric adverse effects.[26] SSRIs appear useful for OCD, at least in the short term.[27]
Efficacy has been demonstrated both in short-term treatment trials of 6 to 24 weeks and in
discontinuation trials of 28 to 52 weeks duration.[28][29][30] Clomipramine, a TCA drug, is considered
effective and useful for OCD, however it is used as a second line treatment because it is less well tolerated
than the SSRIs. Despite this, it has not shown superiority to fluvoxamine in trials. All SSRIs can be used
effectively for OCD, and in some cases, SNRIs can also be tried even though none of them is approved
specifically for OCD. However, even with all these treatment options, many people remain symptomatic
after initiating the medication, and less than half of them do achieve remission.[31]
Post traumatic stress disorder
Antidepressants are one of the treatment options for PTSD, however their efficacy is not well established.
Two antidepressants are FDA approved for it, paroxetine and sertraline, they belong to the serotonin
reuptake inhibitors class. Paroxetine has slightly higher response and remission rates than sertraline for
this condition, however both drugs are not considered very helpful for every person that takes them.
Fluoxetine and venlafaxine are used off label, with fluoxetine producing unsatisfactory mixed results and
venlafaxine, while having a response rates of 78%, which is significantly higher than what paroxetine and
sertraline achieved, but it did not address all the symptoms of ptsd like the two drugs did, which is in
part due to the fact the venlafaxine is an SNRI, this class of drugs inhibit the reuptake of norepinephrine
too, this could cause some anxiety in some people. Fluvoxamine, escitalopram and citalopram were not
well tested in this disorder. MAOIs, while some of them may be helpful, are not used much because of
their unwanted side effects. This leaves paroxetine and sertraline as acceptable treatment options for
some people, although more effective antidepressants are needed.[32]
Panic disorder
Panic disorder is relatively treated well with medications compared with other disorders, several classes
of antidepressants have shown efficacy for this disorder, however SSRIs and SNRIs are used first-line.
Paroxetine, sertraline, fluoxetine are FDA approved for panic disorder, although fluvoxamine,
escitalopram and citalopram are considered effective for it. The SNRI venlafaxine is also approved for
this condition. Unlike with social anxiety and PTSD, some TCAs antidepressants, like clomipramine and
imipramine, have shown efficacy for panic disorder. Moreover, the MAOI phenelzine is considered useful
too. Panic disorder has many drugs for its treatment, however, the starting dose must be lower than the
one used for major depressive disorder because people, in the initiation of treatment, have reported an
increase in anxiety as a result of starting the medication. In conclusion, while panic disorder's treatment
options seem acceptable and useful for this condition, many people are still symptomatic after treatment
with residual symptoms.[33][34][35]
Eating disorders
Antidepressants are recommended as an alternative or additional first step to self-help programs in the
treatment of bulimia nervosa.[36] SSRIs (fluoxetine in particular) are preferred over other
antidepressants due to their acceptability, tolerability, and superior reduction of symptoms in short-term
trials. Long-term efficacy remains poorly characterized. Bupropion is not recommended for the
treatment of eating disorders due to an increased risk of seizure.[37]
Similar recommendations apply to binge eating disorder.[36] SSRIs provide short-term reductions in
binge eating behavior, but have not been associated with significant weight loss.[38]
Clinical trials have generated mostly negative results for the use of SSRIs in the treatment of anorexia
nervosa.[39] Treatment guidelines from the National Institute of Health and Care Excellence[36]
recommend against the use of SSRIs in this disorder. Those from the American Psychiatric Association
note that SSRIs confer no advantage regarding weight gain, but that they may be used for the treatment
of co-existing depressive, anxiety, or obsessive–compulsive disorders.[38]
Pain
Fibromyalgia
A 2012 meta-analysis concluded that antidepressants treatment favorably affects pain, health-related
quality of life, depression, and sleep in fibromyalgia syndrome. Tricyclics appear to be the most effective
class, with moderate effects on pain and sleep and small effects on fatigue and health-related quality of
life. The fraction of people experiencing a 30% pain reduction on tricyclics was 48% versus 28% for
placebo. For SSRIs and SNRIs the fraction of people experiencing a 30% pain reduction was 36% (20%
in the placebo comparator arms) and 42% (32% in the corresponding placebo comparator arms).
Discontinuation of treatment due to side effects was common.[40] Antidepressants including
amitriptyline, fluoxetine, duloxetine, milnacipran, moclobemide, and pirlindole are recommended by the
European League Against Rheumatism (EULAR) for the treatment of fibromyalgia based on "limited
evidence".[41]
Neuropathic pain
A 2014 meta-analysis from the Cochrane Collaboration found the antidepressant duloxetine to be
effective for the treatment of pain resulting from diabetic neuropathy.[42] The same group reviewed data
for amitriptyline in the treatment of neuropathic pain and found limited useful randomized clinical trial
data. They concluded that the long history of successful use in the community for the treatment of
fibromyalgia and neuropathic pain justified its continued use.[43] The group was concerned about the
potential for overestimating the amount of pain relief provided by amitriptyline, and highlighted that
only a small number of people will experience significant pain relief by taking this medication.[43]
Other
Antidepressants may be modestly helpful for treating people who both have depression and alcohol
dependence, however the evidence supporting this association is of low quality.[44] Buproprion is used to
help people stop smoking. Antidepressants are also used to control some symptoms of narcolepsy.[45]
Antidepressants may be used to relieve pain in people with active rheumatoid arthritis however, further
research is required.[46] Antidepressants have been shown to be superior to placebo in treating
depression in individuals with physical illness, although reporting bias may have exaggerated this
finding.[47]
Limitations and strategies
Between 30% and 50% of individuals treated with a given antidepressant do not show a response.[48][49]
Approximately one-third of people achieve a full remission, one-third experience a response and one-
third are nonresponders. Partial remission is characterized by the presence of poorly defined residual
symptoms. These symptoms typically include depressed mood, anxiety, sleep disturbance, fatigue and
diminished interest or pleasure. It is currently unclear which factors predict partial remission. However,
it is clear that residual symptoms are powerful predictors of relapse, with relapse rates 3–6 times higher
in people with residual symptoms than in those who experience full remission.[50] In addition,
antidepressant drugs tend to lose efficacy over the course of treatment.[51] According to data from the
Centers for Disease Control and Prevention, less than one-third of Americans taking one antidepressant
medication have seen a mental health professional in the previous year.[52] A number of strategies are
used in clinical practice to try to overcome these limits and variations.[53] They include switching
medication, augmentation, and combination.
Switching antidepressants
The American Psychiatric Association 2000 Practice Guideline advises that where no response is
achieved following six to eight weeks of treatment with an antidepressant, to switch to an antidepressant
in the same class, then to a different class of antidepressant. A 2006 meta-analysis review found wide
variation in the findings of prior studies; for people who had failed to respond to an SSRI antidepressant,
between 12% and 86% showed a response to a new drug. However, the more antidepressants an
individual had already tried, the less likely they were to benefit from a new antidepressant trial.[49]
However, a later meta-analysis found no difference between switching to a new drug and staying on the
old medication; although 34% of treatment resistant people responded when switched to the new drug,
40% responded without being switched.[54]
Augmentation and combination
For a partial response, the American Psychiatric Association guidelines suggest augmentation, or adding
a drug from a different class. These include lithium and thyroid augmentation, dopamine agonists, sex
steroids, NRIs, glucocorticoid-specific agents, or the newer anticonvulsants.[55]
A combination strategy involves adding another antidepressant, usually from a different class so as to
have effect on other mechanisms. Although this may be used in clinical practice, there is little evidence
for the relative efficacy or adverse effects of this strategy.[56] Other tests conducted include the use of
psychostimulants as an augmentation therapy. Several studies have shown the efficacy of combining
modafinil for treatment-resistant people. It has been used to help combat SSRI-associated fatigue.[57]
Long-term use
The effects of antidepressants typically do not continue once the course of medication ends. This results
in a high rate of relapse. A 2003 meta-analysis found that 18% of people who had responded to an
antidepressant relapsed while still taking it, compared to 41% whose antidepressant was switched for a
placebo.[58]
A gradual loss of therapeutic benefit occurs in a minority of people during the course of treatment.[59][60]
A strategy involving the use of pharmacotherapy in the treatment of the acute episode, followed by
psychotherapy in its residual phase, has been suggested by some studies.[61][62]
Adverse effects
Difficulty tolerating adverse effects is the most common reason for antidepressant discontinuation.[63]
Almost any medication involved with serotonin regulation has the potential to cause serotonin toxicity
(also known as serotonin syndrome) — an excess of serotonin that can induce mania, restlessness,
agitation, emotional lability, insomnia and confusion as its primary symptoms.[64][65] Although the
condition is serious, it is not particularly common, generally only appearing at high doses or while on
other medications. Assuming proper medical intervention has been taken (within about 24 hours) it is
rarely fatal.[66][67] Antidepressants appear to increase the risk of diabetes by about 1.3 fold.[68]
MAOIs tend to have pronounced (sometimes fatal) interactions with a wide variety of medications and
over-the-counter drugs. If taken with foods that contain very high levels of tyramine (e.g., mature cheese,
cured meats, or yeast extracts), they may cause a potentially lethal hypertensive crisis. At lower doses,
the person may only experience a headache due to an increase in blood pressure.[69]
In response to these adverse effects, a different type of MAOI has been developed: the reversible
inhibitor of monoamine oxidase A (RIMA) class of drugs. Their primary advantage is that they do not
require the person to follow a special diet, while being purportedly effective as SSRIs and tricyclics in
treating depressive disorders.[70]
Tricyclics and SSRI can cause the so-called drug-induced QT prolongation, especially in older adults;[71]
this condition can degenerate into a specific type of abnormal heart rhythm called torsades de points
which can potentially lead to sudden cardiac arrest.[72]
Pregnancy
SSRI use in pregnancy has been associated with a variety of risks with varying degrees of proof of
causation. As depression is independently associated with negative pregnancy outcomes, determining the
extent to which observed associations between antidepressant use and specific adverse outcomes reflects
a causative relationship has been difficult in some cases.[73] In other cases, the attribution of adverse
outcomes to antidepressant exposure seems fairly clear.
SSRI use in pregnancy is associated with an increased risk of spontaneous abortion of about 1.7-
fold,[74][75] and is associated with preterm birth and low birth weight.[76]
A systematic review of the risk of major birth defects in antidepressant-exposed pregnancies found a
small increase (3% to 24%) in the risk of major malformations and a risk of cardiovascular birth defects
that did not differ from non-exposed pregnancies.[77] A study of fluoxetine-exposed pregnancies found a
12% increase in the risk of major malformations that just missed statistical significance.[78] Other studies
have found an increased risk of cardiovascular birth defects among depressed mothers not undergoing
SSRI treatment, suggesting the possibility of ascertainment bias, e.g. that worried mothers may pursue
more aggressive testing of their infants.[79] Another study found no increase in cardiovascular birth
defects and a 27% increased risk of major malformations in SSRI exposed pregnancies.[75] The FDA
advises for the risk of birth defects with the use of paroxetine[80] and the MAOI should be avoided.
A 2013 systematic review and meta-analysis found that antidepressant use during pregnancy was
statistically significantly associated with some pregnancy outcomes, such as gestational age and preterm
birth, but not with other outcomes. The same review cautioned that because differences between the
exposed and unexposed groups were small, it was doubtful whether they were clinically significant.[81]
A neonate (infant less than 28 days old) may experience a withdrawal syndrome from abrupt
discontinuation of the antidepressant at birth. Antidepressants have been shown to be present in varying
amounts in breast milk, but their effects on infants are currently unknown.[82]
Moreover, SSRIs inhibit nitric oxide synthesis, which plays an important role in setting vascular tone.
Several studies have pointed to an increased risk of prematurity associated with SSRI use, and this
association may be due to an increase risk of pre-eclampsia of pregnancy.[83]
Antidepressant-induced mania
Another possible problem with antidepressants is the chance of antidepressant-induced mania or

hypomania in people with or without a diagnosis of bipolar disorder. Many cases of bipolar depression
are very similar to those of unipolar depression. Therefore, the person can be misdiagnosed with
unipolar depression and be given antidepressants. Studies have shown that antidepressant-induced
mania can occur in 20–40% of people with bipolar disorder.[84] For bipolar depression, antidepressants
(most frequently SSRIs) can exacerbate or trigger symptoms of hypomania and mania.[85]
Suicide
Studies have shown that the use of antidepressants is correlated with an increased risk of suicidal
behavior and thinking (suicidality) in those aged under 25.[86] This problem has been serious enough to
warrant government intervention by the US Food and Drug Administration (FDA) to warn of the
increased risk of suicidality during antidepressant treatment.[87] According to the FDA, the heightened
risk of suicidality occurs within the first one to two months of treatment.[88][89] The National Institute
for Health and Care Excellence (NICE) places the excess risk in the "early stages of treatment".[90] A
meta-analysis suggests that the relationship between antidepressant use and suicidal behavior or
thoughts is age-dependent.[86] Compared with placebo, the use of antidepressants is associated with an
increase in suicidal behavior or thoughts among those 25 or younger (OR=1.62). There is no effect or
possibly a mild protective effect among those aged 25 to 64 (OR=0.79). Antidepressant treatment has a
protective effect against suicidality among those aged 65 and over (OR=0.37).[86][91]
Sexual
Sexual side effects are also common with SSRIs, such as loss of sexual drive, failure to reach orgasm, and
erectile dysfunction.[92] Although usually reversible, these sexual side-effects can, in rare cases, continue
after the drug has been completely withdrawn.[93][94]
In a study of 1022 outpatients, overall sexual dysfunction with all antidepressants averaged 59.1%[95]
with SSRI values between 57% and 73%, mirtazapine 24%, nefazodone 8%, amineptine 7% and
moclobemide 4%. Moclobemide, a selective reversible MAO-A inhibitor, does not cause sexual
dysfunction,[96] and can actually lead to an improvement in all aspects of sexual function.[97]
Biochemical mechanisms suggested as causative include increased serotonin, particularly affecting 5-

HT2 and 5-HT3 receptors; decreased dopamine; decreased norepinephrine; blockade of cholinergic and
α1adrenergic receptors; inhibition of nitric oxide synthetase; and elevation of prolactin levels.[98]
Mirtazapine is reported to have fewer sexual side effects, most likely because it antagonizes 5-HT2 and 5-
HT3 receptors and may, in some cases, reverse sexual dysfunction induced by SSRIs by the same
mechanism.[99]
Bupropion, a weak NDRI and nicotinic antagonist, may be useful in treating reduced libido as a result of
SSRI treatment.[100]
Changes in weight
Changes in appetite or weight are common among antidepressants, but are largely drug-dependent and
related to which neurotransmitters they affect. Mirtazapine and paroxetine, for example, may be
associated with weight gain and/or increased appetite,[101][102][103] while others (such as bupropion and
venlafaxine) achieve the opposite effect.[104][105]
The antihistaminic properties of certain TCA- and TeCA-class antidepressants have been shown to
contribute to the common side effects of increased appetite and weight gain associated with these classes
of medication.
Discontinuation syndrome
Antidepressant discontinuation syndrome, also called antidepressant withdrawal syndrome, is a

condition that can occur following the interruption, reduction, or discontinuation of antidepressant
medication.[106] The symptoms may include flu-like symptoms, trouble sleeping, nausea, poor balance,
sensory changes, and anxiety.[106][12][107] The problem usually begins within three days and may last for
several months.[106][107] Rarely psychosis may occur.[106]
A discontinuation syndrome can occur after stopping any antidepressant including selective serotonin
re-uptake inhibitors (SSRIs), serotonin–norepinephrine reuptake inhibitors (SNRIs), and tricyclic
antidepressants (TCAs).[106][12] The risk is greater among those who have taken the medication for
longer and when the medication in question has a short half-life.[106] The underlying reason for its
occurrence is unclear.[106] The diagnosis is based on the symptoms.[106]
Methods of prevention include gradually decreasing the dose among those who wish to stop, though it is
possible for symptoms to occur with tapering.[106][11][107] Treatment may include restarting the
medication and slowly decreasing the dose.[106] People may also be switched to the long acting
antidepressant fluoxetine which can then be gradually decreased.[11]
Approximately 20–50% of people who suddenly stop an antidepressant develop an antidepressant

discontinuation syndrome.[106][12][107] The condition is generally not serious.[106] Though about half of
people with symptoms describe them as severe.[107] Some restart antidepressants due to the severity of
the symptoms.[107]
Emotional blunting
SSRIs appear to cause emotional blunting, or numbness in some people who take them. This is a
reduction in extremes of emotion, both positive and negative. While the person may feel less depressed,
they may also feel less happiness or empathy. This may be cause for a dose reduction or medication
change. The mechanism is unknown.[108][109]
Pharmacology
The earliest and probably most widely accepted scientific theory of antidepressant action is the
monoamine hypothesis (which can be traced back to the 1950s), which states that depression is due to an
imbalance (most often a deficiency) of the monoamine neurotransmitters (namely serotonin,
norepinephrine and dopamine).[110] It was originally proposed based on the observation that certain
hydrazine anti-tuberculosis agents produce antidepressant effects, which was later linked to their
inhibitory effects on monoamine oxidase, the enzyme that catalyses the breakdown of the monoamine
neurotransmitters.[110] All currently marketed antidepressants have the monoamine hypothesis as their
theoretical basis, with the possible exception of agomelatine which acts on a dual melatonergic-
serotonergic pathway.[110] Despite the success of the monoamine hypothesis it has a number of
limitations: for one, all monoaminergic antidepressants have a delayed onset of action of at least a week;
and secondly, there are a sizeable portion (>40%) of depressed patients that do not adequately respond
to monoaminergic antidepressants.[111][112] A number of alternative hypotheses have been proposed,
including the glutamate, neurogenic, epigenetic, cortisol hypersecretion and inflammatory
hypotheses.[111][112][113][114]
Types
Selective serotonin reuptake inhibitors
Selective serotonin reuptake inhibitors (SSRIs) are believed to

increase the extracellular level of the neurotransmitter serotonin by
limiting its reabsorption into the presynaptic cell, increasing the
level of serotonin in the synaptic cleft available to bind to the
postsynaptic receptor. They have varying degrees of selectivity for
the other monoamine transporters, with pure SSRIs having only
weak affinity for the norepinephrine and dopamine transporters.
SSRIs are the most widely prescribed antidepressants in many

countries.[115] The efficacy of SSRIs in mild or moderate cases of Blister pack of Prozac (fluoxetine), a
depression has been disputed.[116][117][118][119] selective serotonin reuptake
inhibitor
Serotonin–norepinephrine reuptake inhibitors
Serotonin–norepinephrine reuptake inhibitors (SNRIs) are potent inhibitors of the reuptake of serotonin
and norepinephrine. These neurotransmitters are known to play an important role in mood. SNRIs can
be contrasted with the more widely used selective serotonin reuptake inhibitors (SSRIs), which act
mostly upon serotonin alone.
The human serotonin transporter (SERT) and norepinephrine

transporter (NET) are membrane proteins that are responsible for
the reuptake of serotonin and norepinephrine. Balanced dual
inhibition of monoamine reuptake can possibly offer advantages
over other antidepressants drugs by treating a wider range of
symptoms.[120]
SNRIs are sometimes also used to treat anxiety disorders, obsessive–

compulsive disorder (OCD), attention deficit hyperactivity disorder
(ADHD), chronic neuropathic pain, and fibromyalgia syndrome
(FMS), and for the relief of menopausal symptoms.
The chemical structure of

Serotonin modulators and stimulators venlafaxine (Effexor), an SNRI
Serotonin modulator and stimulators (SMSs), sometimes referred to

more simply as "serotonin modulators", are a type of drug with a multimodal action specific to the
serotonin neurotransmitter system. To be precise, SMSs simultaneously modulate one or more serotonin
receptors and inhibit the reuptake of serotonin. The term was coined in reference to the mechanism of
action of the serotonergic antidepressant vortioxetine, which acts as a serotonin reuptake inhibitor (SRI),
partial agonist of the 5-HT1A receptor, and antagonist of the 5-HT3 and 5-HT7 receptors.[121][122][123]
However, it can also technically be applied to vilazodone, which is an antidepressant as well and acts as
an SRI and 5-HT1A receptor partial agonist.[124]
An alternative term is serotonin partial agonist/reuptake inhibitor (SPARI), which can be applied only to
vilazodone.[125]
Serotonin antagonists and reuptake inhibitors
Serotonin antagonist and reuptake inhibitors (SARIs) while mainly used as antidepressants, are also
anxiolytics and hypnotics. They act by antagonizing serotonin receptors such as 5-HT2A and inhibiting
the reuptake of serotonin, norepinephrine, and/or dopamine. Additionally, most also act as α1-
adrenergic receptor antagonists. The majority of the currently marketed SARIs belong to the
phenylpiperazine class of compounds. They include trazodone and nefazodone.
Norepinephrine reuptake inhibitors
Norepinephrine reuptake inhibitors (NRIs or NERIs) are a type of drug that acts as a reuptake inhibitor
for the neurotransmitter norepinephrine (noradrenaline) by blocking the action of the norepinephrine
transporter (NET). This in turn leads to increased extracellular concentrations of norepinephrine.
NRIs are commonly used in the treatment of conditions like ADHD and narcolepsy due to their
psychostimulant effects and in obesity due to their appetite suppressant effects. They are also frequently
used as antidepressants for the treatment of major depressive disorder, anxiety and panic disorder.
Additionally, many drugs of abuse such as cocaine and methylphenidate possess NRI activity, though it is
important to mention that NRIs without combined dopamine reuptake inhibitor (DRI) properties are not
significantly rewarding and hence are considered to have a negligible abuse potential.[126][127] However,
norepinephrine has been implicated as acting synergistically with dopamine when actions on the two
neurotransmitters are combined (e.g., in the case of NDRIs) to produce rewarding effects in
psychostimulant drugs of abuse.[128]
Norepinephrine-dopamine reuptake inhibitors
The only drug used of this class for depression is bupropion.[100]
Tricyclic antidepressants
The majority of the tricyclic antidepressants (TCAs) act primarily as serotonin–norepinephrine reuptake
inhibitors (SNRIs) by blocking the serotonin transporter (SERT) and the norepinephrine transporter
(NET), respectively, which results in an elevation of the synaptic concentrations of these
neurotransmitters, and therefore an enhancement of neurotransmission.[129][130] Notably, with the sole
exception of amineptine, the TCAs have negligible affinity for the dopamine transporter (DAT), and
therefore have no efficacy as dopamine reuptake inhibitors (DRIs).[129]
Although TCAs are sometimes prescribed for depressive disorders, they have been largely replaced in
clinical use in most parts of the world by newer antidepressants such as selective serotonin reuptake
inhibitors (SSRIs), serotonin–norepinephrine reuptake inhibitors (SNRIs) and norepinephrine reuptake
inhibitors (NRIs). Adverse effects have been found to be of a similar level between TCAs and SSRIs.[131]
Tetracyclic antidepressants
Tetracyclic antidepressants (TeCAs) are a class of antidepressants that were first introduced in the 1970s.
They are named after their chemical structure, which contains four rings of atoms, and are closely related
to the tricyclic antidepressants (TCAs), which contain three rings of atoms.
Monoamine oxidase inhibitors
Monoamine oxidase inhibitors (MAOIs) are chemicals which inhibit the activity of the monoamine
oxidase enzyme family. They have a long history of use as medications prescribed for the treatment of
depression. They are particularly effective in treating atypical depression.[132] They are also used in the
treatment of Parkinson's disease and several other disorders.
Because of potentially lethal dietary and drug interactions, monoamine oxidase inhibitors have
historically been reserved as a last line of treatment, used only when other classes of antidepressant
drugs (for example selective serotonin reuptake inhibitors and tricyclic antidepressants) have failed.
MAOIs have been found to be effective in the treatment of panic disorder with agoraphobia,[133] social
phobia,[134][135][136] atypical depression[137][138] or mixed anxiety and depression,
bulimia,[139][140][141][142] and post-traumatic stress disorder,[143] as well as borderline personality
disorder.[144] MAOIs appear to be particularly effective in the management of bipolar depression
according to a retrospective-analysis.[145] There are reports of MAOI efficacy in obsessive–compulsive
disorder (OCD), trichotillomania, dysmorphophobia, and avoidant personality disorder, but these
reports are from uncontrolled case reports.[146]
MAOIs can also be used in the treatment of Parkinson's disease by targeting MAO-B in particular
(therefore affecting dopaminergic neurons), as well as providing an alternative for migraine prophylaxis.
Inhibition of both MAO-A and MAO-B is used in the treatment of clinical depression and anxiety
disorders.
NMDA receptor antagonists
NMDA receptor antagonists like ketamine and esketamine are rapid-acting antidepressants and seem to
work via blockade of the ionotropic glutamate NMDA receptor.[147]
Others
See the list of antidepressants and management of depression for other drugs that are not specifically
characterized.
Adjuncts
Adjunct medications are an umbrella category of substances that increase the potency or "enhance"
antidepressants.[148] They work by affecting variables very close to the antidepressant, sometimes
affecting a completely different mechanism of action. This may be attempted when depression
treatments have not been successful in the past.
Common types of adjunct medication techniques generally fall into the following categories:
Two or more antidepressants taken together

From the same class (affecting the same area of the brain, often at a much higher level)
From different classes (affecting multiple parts of the brain not covered simultaneously by either
drug alone)
An antipsychotic combined with an antidepressant, particularly atypical antipsychotics such as
aripiprazole (Abilify), quetiapine (Seroquel), olanzapine (Zyprexa), and risperidone (Risperdal).[149]
It is unknown if undergoing psychological therapy at the same time as taking anti-depressants enhances
the anti-depressive effect of the medication.[150]
Less common adjuncts
Lithium has been used to augment antidepressant therapy in those who have failed to respond to
antidepressants alone.[151] Furthermore, lithium dramatically decreases the suicide risk in recurrent
depression.[152] There is some evidence for the addition of a thyroid hormone, triiodothyronine, in
patients with normal thyroid function.[153]
Psychopharmacologists have also tried adding a stimulant, in particular, d-amphetamine.[154] However,

the use of stimulants in cases of treatment-resistant depression is relatively controversial.[155][156] A
review article published in 2007 found psychostimulants may be effective in treatment-resistant
depression with concomitant antidepressant therapy, but a more certain conclusion could not be drawn
due to substantial deficiencies in the studies available for consideration, and the somewhat contradictory
nature of their results.[156]
History
Before the 1950s, opioids and amphetamines were commonly used

as antidepressants.[157][158] Their use was later restricted due to their
addictive nature and side effects.[157] Extracts from the herb St
John's wort have been used as a "nerve tonic" to alleviate
depression.[159]
Isoniazid, iproniazid, and imipramine

St John's wort
In 1951, Irving Selikoff and Edward H. Robitzek, working out of Sea
View Hospital on Staten Island, began clinical trials on two new anti-
tuberculosis agents developed by Hoffman-LaRoche, isoniazid and
iproniazid. Only patients with a poor prognosis were initially treated; nevertheless, their condition
improved dramatically. Selikoff and Robitzek noted "a subtle general stimulation ... the patients
exhibited renewed vigor and indeed this occasionally served to introduce disciplinary problems."[160] The
promise of a cure for tuberculosis in the Sea View Hospital trials was excitedly discussed in the
mainstream press.
In 1952, learning of the stimulating side effects of isoniazid, the Cincinnati psychiatrist Max Lurie tried it
on his patients. In the following year, he and Harry Salzer reported that isoniazid improved depression in
two-thirds of their patients and coined the term antidepressant to refer to its action.[161] A similar
incident took place in Paris, where Jean Delay, head of psychiatry at Sainte-Anne Hospital, heard of this
effect from his pulmonology colleagues at Cochin Hospital. In 1952 (before Lurie and Salzer), Delay, with
the resident Jean-Francois Buisson, reported the positive effect of isoniazid on depressed patients.[162]
The mode of antidepressant action of isoniazid is still unclear. It is speculated that its effect is due to the
inhibition of diamine oxidase, coupled with a weak inhibition of monoamine oxidase A.[163]
Selikoff and Robitzek also experimented with another anti-tuberculosis drug, iproniazid; it showed a
greater psychostimulant effect, but more pronounced toxicity.[164] Later, Jackson Smith, Gordon
Kamman, George E. Crane, and Frank Ayd, described the psychiatric applications of iproniazid. Ernst
Zeller found iproniazid to be a potent monoamine oxidase inhibitor.[165] Nevertheless, iproniazid
remained relatively obscure until Nathan S. Kline, the influential head of research at Rockland State
Hospital, began to popularize it in the medical and popular press as a "psychic energizer".[165][166] Roche
put a significant marketing effort behind iproniazid.[165] Its sales grew until it was recalled in 1961, due
to reports of lethal hepatotoxicity.[165]
The antidepressant effect of a tricyclic, a three ringed compound, was first discovered in 1957 by Roland
Kuhn in a Swiss psychiatric hospital. Antihistamine derivatives were used to treat surgical shock and
later as neuroleptics. Although in 1955 reserpine was shown to be more effective than placebo in
alleviating anxious depression, neuroleptics were being developed as sedatives and antipsychotics.
Attempting to improve the effectiveness of chlorpromazine, Kuhn – in conjunction with the Geigy
Pharmaceutical Company – discovered the compound "G 22355", later renamed imipramine.
Imipramine had a beneficial effect in patients with depression who showed mental and motor
retardation. Kuhn described his new compound as a "thymoleptic" "taking hold of the emotions," in
contrast with neuroleptics, "taking hold of the nerves" in 1955–56. These gradually became established,
resulting in the patent and manufacture in the US in 1951 by Häfliger and SchinderA.[167]
Second generation antidepressants
Antidepressants became prescription drugs in the 1950s. It was estimated that no more than 50 to 100
individuals per million suffered from the kind of depression that these new drugs would treat, and
pharmaceutical companies were not enthusiastic in marketing for this small market. Sales through the
1960s remained poor compared to the sales of tranquilizers,[168] which were being marketed for different
uses.[169] Imipramine remained in common use and numerous successors were introduced. The use of
monoamine oxidase inhibitors (MAOI) increased after the development and introduction of "reversible"
forms affecting only the MAO-A subtype of inhibitors, making this drug safer to use.[169][170]
By the 1960s, it was thought that the mode of action of tricyclics was to inhibit norepinephrine reuptake.
However, norepinephrine reuptake became associated with stimulating effects. Later tricyclics were
thought to affect serotonin as proposed in 1969 by Carlsson and Lindqvist as well as Lapin and
Oxenkrug.
Researchers began a process of rational drug design to isolate antihistamine-derived compounds that
would selectively target these systems. The first such compound to be patented was zimelidine in 1971,
while the first released clinically was indalpine. Fluoxetine was approved for commercial use by the US
Food and Drug Administration (FDA) in 1988, becoming the first blockbuster SSRI. Fluoxetine was
developed at Eli Lilly and Company in the early 1970s by Bryan Molloy, Klaus Schmiegel, David T. Wong
and others.[171][172] SSRIs became known as "novel antidepressants" along with other newer drugs such
as SNRIs and NRIs with various selective effects.[173]
St John's wort fell out of favor in most countries through the 19th and 20th centuries, except in
Germany, where Hypericum extracts were eventually licensed, packaged and prescribed. Small-scale
efficacy trials were carried out in the 1970s and 1980s, and attention grew in the 1990s following a meta-
analysis.[174] It remains an over-the-counter drug (OTC) supplement in most countries. Of concern are
lead contaminant; on average, lead levels in women in the United States taking St. John's wort are
elevated about 20%.[175] Research continues to investigate its active component hyperforin, and to
further understand its mode of action.[176][177]
Rapid-acting antidepressants
Esketamine (brand name Spravato), the first rapid-acting antidepressant to be approved for clinical
treatment of depression, was introduced for this indication in March 2019 in the United States.[147]
Research
A 2016 placebo randomized controlled trial evaluated the rapid antidepressant effects of the psychedelic
ayahuasca in treatment-resistant depression with positive outcome.[178][179] In 2018 the FDA granted
Breakthrough Therapy Designation for psilocybin-assisted therapy for treatment-resistant depression
and in 2019, the FDA granted Breakthrough Therapy Designation for psilocybin therapy treating major
depressive disorder.[180]
Society and culture
Prescription trends
In the United States, antidepressants were the most commonly prescribed medication in 2013.[181] Of the
estimated 16 million "long term" (over 24 months) users, roughly 70 percent are female.[181] As of 2017,
about 16.5% of white people in the United States took antidepressants compared with 5.6% of black
people in the United States.[182]
In the UK, figures reported in 2010 indicated that the number of antidepressants prescribed by the
National Health Service (NHS) almost doubled over a decade.[183] Further analysis published in 2014
showed that number of antidepressants dispensed annually in the community went up by 25 million in
the 14 years between 1998 and 2012, rising from 15 million to 40 million. Nearly 50% of this rise
occurred in the four years after the 2008 banking crash, during which time the annual increase in
prescriptions rose from 6.7% to 8.5%.[184] These sources also suggest that aside from the recession, other
factors that may influence changes in prescribing rates may include: improvements in diagnosis, a
reduction of the stigma surrounding mental health, broader prescribing trends, GP characteristics,
geographical location and housing status. Another factor that may contribute to increasing consumption
of antidepressants is the fact that these medications now are used for other conditions including social
anxiety and posttraumatic stress disorder.
United States: The most commonly prescribed antidepressants in

the US retail market in 2010 were:[185]
Drug name Drug class Total prescriptions

Sertraline SSRI 33,409,838
Citalopram SSRI 27,993,635
Fluoxetine SSRI 24,473,994
Escitalopram SSRI 23,000,456
Trazodone SARI 18,786,495 Structural formula of the SSRI
sertraline
Venlafaxine (all formulations) SNRI 16,110,606
Bupropion (all formulations) NDRI 15,792,653
Duloxetine SNRI 14,591,949
Paroxetine SSRI 12,979,366
Amitriptyline TCA 12,611,254
Venlafaxine XR SNRI 7,603,949
Bupropion XL NDRI 7,317,814
Mirtazapine TeCA 6,308,288
Venlafaxine ER SNRI 5,526,132
Bupropion SR NDRI 4,588,996
Desvenlafaxine SNRI 3,412,354
Nortriptyline TCA 3,210,476
Bupropion ER NDRI 3,132,327
Venlafaxine SNRI 2,980,525
Bupropion NDRI 753,516
Netherlands: In the Netherlands, paroxetine is the most prescribed antidepressant, followed by

amitriptyline, citalopram and venlafaxine.[186]
Adherence
As of 2003, worldwide, 30 to 60% of people didn't follow their practitioner's instructions about taking
their antidepressants,[187] and as of 2013 in the US, it appeared that around 50% of people did not take
their antidepressants as directed by their practitioner.[188]
When people fail to take their antidepressants, there is a greater risk that the drug won't help, that
symptoms get worse, that they miss work or are less productive at work, and that the person may be
hospitalized.[189] This also increases costs for caring for them.[189]
Social science perspective
Some academics have highlighted the need to examine the use of antidepressants and other medical
treatments in cross-cultural terms, due to the fact that various cultures prescribe and observe different
manifestations, symptoms, meanings and associations of depression and other medical conditions within
their populations.[190][191] These cross-cultural discrepancies, it has been argued, then have implications
on the perceived efficacy and use of antidepressants and other strategies in the treatment of depression
in these different cultures.[190][191] In India, antidepressants are largely seen as tools to combat
marginality, promising the individual the ability to reintegrate into society through their use—a view and
association not observed in the West.[190]
Environmental impacts
Because most antidepressants function by inhibiting the reuptake of neurotransmitters serotonin,

dopamine, and norepinepherine[192] these drugs can interfere with natural neurotransmitter levels in
other organisms impacted by indirect exposure.[193] Antidepressants fluoxetine and sertraline have been
detected in aquatic organisms residing in effluent dominated streams.[194] The presence of
antidepressants in surface waters and aquatic organisms has caused concern because ecotoxicological
effects to aquatic organisms due to fluoxetine exposure have been demonstrated.[195]
Coral reef fish have been demonstrated to modulate aggressive behavior through serotonin.[196]
Artificially increasing serotonin levels in crustaceans can temporarily reverse social status and turn
subordinates into aggressive and territorial dominant males.[197]
Exposure to fluoxetine has been demonstrated to increase serotonergic activity in fish, subsequently
reducing aggressive behavior.[198] Perinatal exposure to fluoxetine at relevant environmental
concentrations has been shown to lead to significant modifications of memory processing in 1-month-old
cuttlefish.[199] This impairment may disadvantage cuttlefish and decrease their survival. Somewhat less
than 10% of orally administered fluoxetine is excreted from humans unchanged or as
glucuronide.[200][201]
See also
Management of depression
Antidepressants in Japan
Atypical antidepressant
Depression and natural therapies
Listening to Prozac by Peter Kramer
Anatomy of an Epidemic by Robert Whittaker

List of investigational antidepressants
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Further reading
Stahl SM (1997). Psychopharmacology of Antidepressants. Informa Healthcare. ISBN 978-1-85317-
513-8.
External links
Media related to Antidepressants at Wikimedia Commons
▶ Antidepressants
▶ Drug classes defined by psychological effects
▶ Drugs by psychological effects
▶ Psychoactive drugs
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Some reviews of antidepressants for depression in adults find

Contents Drugs.com Drug Classes (https://

Major depressive disorder

People with a history of moderate or severe depression,

Generalized anxiety disorder

Antidepressants provide a modest-to-moderate reduction in anxiety in GAD.[23] The efficacy of different

Social anxiety disorder

Post traumatic stress disorder

Limitations and strategies

Augmentation and combination

Another possible problem with antidepressants is the chance of antidepressant-induced mania or

Biochemical mechanisms suggested as causative include increased serotonin, particularly affecting 5-

Antidepressant discontinuation syndrome, also called antidepressant withdrawal syndrome, is a

Approximately 20–50% of people who suddenly stop an antidepressant develop an antidepressant

Selective serotonin reuptake inhibitors

Selective serotonin reuptake inhibitors (SSRIs) are believed to

SSRIs are the most widely prescribed antidepressants in many

Serotonin–norepinephrine reuptake inhibitors

The human serotonin transporter (SERT) and norepinephrine

SNRIs are sometimes also used to treat anxiety disorders, obsessive–

The chemical structure of

Serotonin modulator and stimulators (SMSs), sometimes referred to

Serotonin antagonists and reuptake inhibitors

Norepinephrine reuptake inhibitors

Norepinephrine-dopamine reuptake inhibitors

The only drug used of this class for depression is bupropion.[100]

Monoamine oxidase inhibitors

NMDA receptor antagonists

Two or more antidepressants taken together

Less common adjuncts

Psychopharmacologists have also tried adding a stimulant, in particular, d-amphetamine.[154] However,

Before the 1950s, opioids and amphetamines were commonly used

Isoniazid, iproniazid, and imipramine

Second generation antidepressants

Society and culture

United States: The most commonly prescribed antidepressants in

Drug name Drug class Total prescriptions

Netherlands: In the Netherlands, paroxetine is the most prescribed antidepressant, followed by

Social science perspective

Because most antidepressants function by inhibiting the reuptake of neurotransmitters serotonin,

Anatomy of an Epidemic by Robert Whittaker

This page was last edited on 19 October 2020, at 15:50 (UTC).

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