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If
you want to taper off the Lexapro and you are not sure where to start, you can
click here and read the bestselling book, How to Get
Off Psychoactive Drugs Safely or send Jim Harper an email at
Jim@theroadback.org and he will guide you through the process of Lexapro
withdrawal.
If you
are experiencing Lexapro withdrawal brain zaps, electrical jolts in the head,
click here
Potential Lexapro side effects while taking Lexapro
click here
Lexapro belongs to a class of medications known as selective serotonin reuptake
inhibitors (SSRIs) and partial agonists of the serotonin 1A receptor. The drug
works by increasing the levels of serotonin in the brain, which is a
neurotransmitter that is responsible for regulating mood, appetite, and sleep.
One of
the primary advantages of Lexapro is its low incidence of side effects compared
to other antidepressants. While most SSRIs are associated with side effects such
as weight gain, sexual dysfunction, and drowsiness, Lexapro has been shown to
cause significantly fewer side effects in clinical trials.
Some
of the most common side effects of Lexapro include diarrhea, nausea, and
vomiting. However, these side effects are typically mild and go away on their
own after a few days. Less common side effects may include sleep disturbances,
dizziness, and dry mouth.
Lexapro is available in tablet form and is typically taken once daily with food.
The recommended starting dose is 10 milligrams (mg) per day, which can be
increased to 20 mg per day after one week. Patients who do not respond to the 20
mg dose may be increased to 40 mg per day.
Full
Description of Lexapro Escitalopram:
Lexapro is a medication that is used to treat major depressive disorder. It is
an antidepressant medication that works by increasing the levels of serotonin in
the brain. Like any medication, Lexapro can have side effects, and some people
may experience withdrawal symptoms when they stop taking it.
Withdrawal symptoms can occur when a person stops taking Lexapro suddenly, or
when they taper off the medication too quickly. Withdrawal symptoms can vary in
severity and duration, depending on the individual and how long they have been
taking the medication. Some common withdrawal symptoms of Lexapro include:
1.
Dizziness: Some people may experience dizziness or lightheadedness when they
stop taking Lexapro. This can make it difficult to perform daily activities such
as driving or working.
2.
Nausea: Nausea and vomiting are common withdrawal symptoms of Lexapro. These
symptoms can be severe and may last for several days.
3.
Insomnia: Some people may experience insomnia or difficulty sleeping when they
stop taking Lexapro. This can make it difficult to get a good night's sleep and
can lead to fatigue and other health problems.
4.
Anxiety: Lexapro is used to treat anxiety as well as depression, so it is not
surprising that some people may experience anxiety when they stop taking the
medication. This can include feelings of restlessness, nervousness, and panic.
5.
Mood swings: Lexapro can help to stabilize mood, so when people stop taking it,
they may experience mood swings or changes in their emotional state. This can
include feelings of irritability, sadness, or agitation.
6.
Headaches: Some people may experience headaches or migraines when they stop
taking Lexapro. These can be mild to severe and can make it difficult to perform
daily activities
.Flu-like symptoms: Some people may experience flu-like symptoms when they stop
taking Lexapro. These can include fever, chills, and body aches.
If you
are experiencing withdrawal symptoms from Lexapro, it is important to talk to
your doctor. Your doctor may recommend gradually tapering off the medication to
reduce the severity of withdrawal symptoms. They may also prescribe other
medications or therapies to help manage withdrawal symptoms.
In
conclusion, Lexapro withdrawal can cause a range of symptoms, from mild to
severe, and can last for several days or weeks. If you are experiencing
withdrawal symptoms, it is important to talk to your doctor to discuss the best
course of action. With the proper management and support, it is possible to
successfully stop taking Lexapro and manage any withdrawal symptoms that may
arise.
Lexapro
withdrawal
Lexapro
Withdrawal
Lexapro
Withdrawal
Lexapro
Withdrawal
Get
relief from Lexapro insomnia and Lexapro anxiety.
Lexapro withdrawal solution.
Lexapro Withdrawal
The
F.D.A. estimates 10% of the people withdrawing off an antidepressant will not be
able to succeed due to withdrawal side effects. Lexapro is not different. If you
are one of the lucky 90% that can do a successful Lexapro withdrawal you still
need to rebuild your body once off Lexapro. This site provides information what
to do for Lexapro withdrawal and after Lexapro withdrawal if you were able to
succeed on your own.
Let’s
take at how to have a successful Lexapro withdrawal first. There are two parts
that make a successful Lexapro withdrawal possible. How you reduce the Lexapro
during withdrawal and taking a few supplements that will help eliminate any
Lexapro withdrawal side effects. If you want to read the short version of how to
handle Lexapro withdrawal side effects, Click here. Page opens new browser
window.
It
does not matter what dosage of Lexapro you are taking or how long you have used
Lexapro; the reduction of Lexapro is the same. You want to reduce Lexapro by no
more than 10% and only reduce by an additional 10% every 2 weeks. This is the
safest and most successful way to become Lexapro free and not suffer during
withdrawal.
Check
with your pharmacist for compounding the Lexapro and the best option. The next
best method is to use a pill slicer and a milligram scale. Get a 7 day pill
holder and once a week cut your pills for the coming week. Roughly 90% of you
will be able to complete a Lexapro withdrawal using the method above. However,
you will most likely experience flu like symptoms, headache, brain zaps,
anxiety, and insomnia or in some cases extreme fatigue. These symptoms will
normally last 1 or 2 weeks.
In
early 1999, we began investigating the use of natural supplements to help ease
withdrawal symptoms. Over the past 20 plus years we have continued to improve
this approach and our success rate is rather high. With Lexapro withdrawal, you
should take 4 supplements. JNK Formula Complete, Neuro Day, Neuro Night and
Omega 3 Supreme.
You
can read The Program (link above) for all chapters of the bestselling book, How
to Get Off Psychoactive Drugs Safely, or just follow the instructions on each
bottle to know when to take each supplement. Take the supplements for 1 full
week before reducing the Lexapro and then you can begin your Lexapro withdrawal
reduction. It really can be this simple. If you are located in the United States
Canada, Great Britain Click here
What
is Lexapro
Lexapro is a prescription medication used to treat depression and anxiety. It
belongs to a class of drugs known as selective serotonin reuptake inhibitors
(SSRIs). The medication takes some time to build up in the body, which is why it
can take a few weeks before people begin noticing a reduction in symptoms of
depression or anxiety. If you suddenly stop taking Lexapro, however, you may
experience symptoms of withdrawal. In the United States this withdrawal is known
as Lexapro Discontinuation Syndrome but in Europe is known as Lexapro
Withdrawal. Antidepressants are among the most commonly prescribed medications
in the United States. Of the more than 60 million people who take them in a
given month, about one quarter have been taking them for more than 10 years.
Often, long- term use is linked to fear of relapse of their symptoms or
withdrawal. We have found length of time taking Lexapro WILL NOT determine how
easy or difficult it will be for you to accomplish a Lexapro withdrawal.
People
experience symptoms of Lexapro withdrawal because of the way SSRI's work in the
brain. SSRIs affect the levels of serotonin, a type of mood-regulating
neurotransmitter in the brain. When you abruptly stop taking your medication, it
doesn't give the brain enough time to adjust to the sudden change. Whether you
are stopping Lexapro because it is not working for you or you are better and
you've decided with your doctor that it makes sense to come off your medication,
the quitting process needs to be slow and gradual.
Recent
research has found that the severity of SSRI withdrawal is much worse than
previously believed. On average, about 46% of people experiencing SSRI
withdrawal symptoms describe them as severe. Severe symptoms indicate that
withdrawal can potentially interfere with your ability to meet responsibilities
at home and at work.
It was
also found that 10% of the people attempting antidepressant withdrawal, 10% quit
the Lexapro withdrawal due to a withdrawal side effect known as brain zaps. The
Omega 3 Supreme used during Lexapro withdrawal is formulated to ease this severe
withdrawal side effect.
Most
Common Symptoms
The
most common symptoms of Lexapro withdrawal—occurring in more than one in four
people—are as follows:
Dizziness
Muscle
tension
Chills
Confusion
Trouble concentrating
Trouble remembering things
Crying
The
most common symptoms of Lexapro withdrawal are dizziness, muscle tension, and
chills, which each affect about 44% of users. Many people also experience
confusion and difficulty concentrating. Once again, the supplements have been
formulated to help with these symptoms.
Complete Symptoms
The
following is a more complete list of symptoms associated with withdrawal:
Changes in motor control: Tremors, muscle tension, restless legs, unsteady gait,
or difficulty controlling speech and chewing movements Digestive issues: Nausea,
vomiting, cramps, diarrhea, or appetite loss Flu-like symptoms: Headache, muscle
pain, weakness, and tiredness. Instability: Dizziness, lightheadedness,
difficulty walking Mood changes: Anxiety, agitation, panic, suicidal ideation,
depression, irritability, anger, mania, or mood swings Sleep problems:
Nightmares, unusual dreams, excessive/vivid dreams, or insomnia
Unusual sensations: Brain zaps (like an electrical shock or shiver in your
brain), pins and needles, ringing in the ears, strange tastes, or
hypersensitivity to sound.
Lexapro withdrawal can take a real toll on your life, both physically and
emotionally. Antidepressants like Lexapro work by increasing serotonin levels in
your brain. When you stop taking them, it takes your brain a while to get used
to the drug’s absence. Unfortunately, the amount of time this takes can vary
widely.
Lexapro withdrawal symptoms typically arrive one to three days after your last
dose. It can start sooner (within hours) or later (more than a week). This is
why most inpatient facilities fail with Lexapro withdrawal. Insurance may pay
only 9 days of treatment and by the time you are off the plane near your city,
Lexapro withdrawal is back and in full effect. Lexapro withdrawal should never
be rushed.
Coping
& Relief
The
best way to find relief from Lexapro withdrawal is to use the supplements
mentioned above, reduce the Lexapro gradually and only continue to reduce when
you are feeling very well. If you are still experiencing symptoms of depression,
definitely send us an e-mail and we will help you adjust supplements and assist
you in finding the cause.
Taper
Off Medication Slowly
In
1999, our founder, Jim Harper, published a guideline for reducing medications.
That guideline has been adapted to all psychoactive medications by the drug
manufacturers. The most effective way to minimize symptoms of withdrawal is to
slowly taper off your medication. “Reduce the medication slowly. If withdrawal
symptoms begin go back up to the last dosage you were doing fine at, stay at
that dosage until all withdrawal has subsided. When you continue with withdrawal
reduce the medication slower than the previous reductions.
”Lexapro should only be reduced by 10%. Some people will need to reduce the
Lexapro by 5%. Reductions of the Lexapro can be made every 7 days or in some
cases every 14 days. Slow and steady wins this race.
Tapering involves adjusting your dose by a small amount, gradually decreasing
until your body gets used to lower levels of the medication. Talk to your doctor
who can then create a dose schedule and carefully monitor the process to avoid
severe symptoms. Practice Good Self-Care Taking good care of your health as you
stop taking Lexapro can also help you to better manage any withdrawal symptoms
that you experience.
Some
steps you can take that might help you cope with withdrawal symptoms include:
Do not
change your diet when tapering. This can alter metabolism rate of the Lexapro
and create a withdrawal symptom.
Follow
your doctor's tapering recommendations
Get
plenty of rest
Get
regular mild exercise
Get
support from family, friends, or support groups
If you
or someone you love shows any of the following signs or symptoms after stopping
or during a Lexapro taper, get help:
Becoming preoccupied with death, dying, or violence Engaging in risky or
self-destructive activities, such as driving drunk Feeling hopeless or trapped
Gathering the means to commit suicide, such as bullets or pills Getting affairs
in order or giving away belongings Having intense mood swings.
Planning how you would commit suicide if you were going to do it Saying goodbye
to people as if it were the last time Talking or thinking about suicide more
than normal, for example, “I wish I were dead”
1.
Withdrawal
Symptoms after Selective Serotonin Reuptake Inhibitor Discontinuation: A
Systematic Review
Background: Selective serotonin reuptake inhibitors (SSRI) are widely used in
medical practice. They have been associated with a broad range of symptoms,
whose clinical meaning has not been fully appreciated. Methods: The PRISMA
guidelines were followed to conduct a systematic review of the literature.
Titles, abstracts, and topics were searched using the following terms:
'withdrawal symptoms' OR 'withdrawal syndrome' OR 'discontinuation syndrome' OR
'discontinuation symptoms', AND 'SSRI' OR 'serotonin' OR 'antidepressant' OR
'paroxetine' OR 'fluoxetine' OR 'sertraline' OR 'fluvoxamine' OR 'citalopram' OR
'escitalopram'. The electronic research literature databases included CINAHL,
the Cochrane Library, PubMed and Web-of-Science from inception of each database
to July 2014. Results: There were 15 randomized controlled studies, 4 open
trials, 4 retrospective investigations, and 38 case reports. The prevalence of
the syndrome was variable, and its estimation was hindered by a lack of case
identification in many studies. Symptoms typically occur within a few days from
drug discontinuation and last a few weeks, also with gradual tapering. However,
many variations are possible, including late onset and/or longer persistence of
disturbances. Symptoms may be easily misidentified as signs of impending
relapse. Conclusions: Clinicians need to add SSRI to the list of drugs
potentially inducing withdrawal symptoms upon discontinuation, together with
benzodiazepines, barbiturates, and other psychotropic drugs. The term
'discontinuation syndrome' that is currently used minimizes the potential
vulnerabilities induced by SSRI and should be replaced by 'withdrawal syndrome'.
2.
Selective
serotonin reuptake inhibitors for premenstrual syndrome
Background: Premenstrual syndrome (PMS) is a common cause of physical,
psychological and social problems in women of reproductive age. The key
characteristic of PMS is the timing of symptoms, which occur only during the two
weeks leading up to menstruation (the luteal phase of the menstrual cycle).
Selective serotonin reuptake inhibitors (SSRIs) are increasingly used as first
line therapy for PMS. SSRIs can be taken either in the luteal phase or else
continuously (every day). SSRIs are generally considered to be effective for
reducing premenstrual symptoms but they can cause adverse effects.
Objectives: The objective of this review was to evaluate the effectiveness and
safety of SSRIs for treating premenstrual syndrome.
Search methods: Electronic searches for relevant randomised controlled trials
(RCTs) were undertaken in the Cochrane Menstrual Disorders and Subfertility
Group Specialised Register, Cochrane Central Register of Controlled Trials
(CENTRAL) (The Cochrane Library), MEDLINE, EMBASE, PsycINFO, and CINAHL
(February 2013). Where insufficient data were presented in a report, attempts
were made to contact the original authors for further details.
Selection criteria: Studies were considered in which women with a prospective
diagnosis of PMS, PMDD or late luteal phase dysphoric disorder (LPDD) were
randomised to receive SSRIs or placebo for the treatment of premenstrual
syndrome.
Data collection and analysis: Two review authors independently selected the
studies, assessed eligible studies for risk of bias, and extracted data on
premenstrual symptoms and adverse effects. Studies were pooled using
random-effects models. Standardised mean differences (SMDs) with 95% confidence
intervals (CIs) were calculated for premenstrual symptom scores, using separate
analyses for different types of continuous data (that is end scores and change
scores). Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated
for dichotomous outcomes. Analyses were stratified by type of drug
administration (luteal or continuous) and by drug dose (low, medium, or high).
We calculated the number of women who would need to be taking a moderate dose of
SSRI in order to cause one additional adverse event (number needed to harm:
NNH). The overall quality of the evidence for the main findings was assessed
using the GRADE working group methods.
Main results: Thirty-one RCTs were included in the review. They compared
fluoxetine, paroxetine, sertraline, escitalopram and citalopram versus placebo.
SSRIs reduced overall self-rated symptoms significantly more effectively than
placebo. The effect size was moderate when studies reporting end scores were
pooled (for moderate dose SSRIs: SMD -0.65, 95% CI -0.46 to -0.84, nine studies,
1276 women; moderate heterogeneity (I(2) = 58%), low quality evidence). The
effect size was small when studies reporting change scores were pooled (for
moderate dose SSRIs: SMD -0.36, 95% CI -0.20 to -0.51, four studies, 657 women;
low heterogeneity (I(2)=29%), moderate quality evidence).SSRIs were effective
for symptom relief whether taken only in the luteal phase or continuously, with
no clear evidence of a difference in effectiveness between these modes of
administration. However, few studies directly compared luteal and continuous
regimens and more evidence is needed on this question.Withdrawals due to adverse
effects were significantly more likely to occur in the SSRI group (moderate
dose: OR 2.55, 95% CI 1.84 to 3.53, 15 studies, 2447 women; no heterogeneity
(I(2) = 0%), moderate quality evidence). The most common side effects associated
with a moderate dose of SSRIs were nausea (NNH = 7), asthenia or decreased
energy (NNH = 9), somnolence (NNH = 13), fatigue (NNH = 14), decreased libido
(NNH = 14) and sweating (NNH = 14). In secondary analyses, SSRIs were effective
for treating specific types of symptoms (that is psychological, physical and
functional symptoms, and irritability). Adverse effects were dose-related.The
overall quality of the evidence was low to moderate, the main weakness in the
included studies being poor reporting of methods. Heterogeneity was low or
absent for most outcomes, though (as noted above) there was moderate
heterogeneity for one of the primary analyses.
3.
Kappa opioid
receptor in nucleus accumbens regulates depressive-like behaviors following
prolonged morphine withdrawal in mice
Prolonged withdrawal from opioids leads to negative emotions. Kappa opioid
receptor (KOR) plays an important role in opioid addiction and affective
disorders. However, the underlying mechanism of KOR in withdrawal-related
depression is still lacking. We found that escitalopram treatment had a limited
effect in improving depression symptoms in heroin-dependent patients. In mice,
we demonstrated prolonged (4 weeks) but not acute (24 h) withdrawal from
morphine induced depressive-like behaviors. The number of c-Fos positive cells
and the expression of KOR in the nucleus accumbens (NAc), were significantly
increased in the prolonged morphine withdrawal mice. Conditional KOR knockdown
in NAc significantly improved depressive-like behaviors. Repeated but not acute
treatment with the KOR antagonist norBNI improved depressive-like behaviors and
reversed PSD95, synaptophysin, p-ERK, p-CREB, and BDNF in NAc. This study
demonstrated the important role of striatal KOR in morphine withdrawal-related
depressive-like behaviors and offered therapeutic potential for the treatment of
withdrawal-related depression.
4.
Are all
antidepressants the same? The consumer has a point
Background: Although a large variety of antidepressants agents (AD) with
different mechanisms of action are available, no significant differences in
efficacy and safety have been shown. However, there have been few attempts to
incorporate data on subjective experiences under different AD.
Method: We conducted a qualitative and quantitative analysis of the posts from
the website www.askapatient.com from different AD. We reviewed a random sample
of 1000 posts.
Result: After applying the inclusion and exclusion criteria, we included a final
sample of 450 posts, 50 on each of the most used AD: sertraline, citalopram,
paroxetine, escitalopram, fluoxetine, venlafaxine, duloxetine, mirtazapine, and
bupropion. Bupropion, citalopram, and venlafaxine had the higher overall
satisfaction ratings. Sertraline, paroxetine, and fluoxetine had high reports of
emotional blunting, while bupropion very few. Overall satisfaction with AD
treatment was inversely associated with the presence of the following
side-effects: suicidality, irritability, emotional blunting, cognitive
disturbances, and withdrawal symptoms. After adjusting for confounders, only
emotional blunting was shown to be more frequently reported by users of
serotonergic agents, as compared to non-serotoninergic agents.
Conclusion: This research points out that the subjective experience of patients
under treatment should be taken into consideration when selecting an AD as
differences between agents were evident. In contrast to the more frequent
treatment decisions, users might prefer receiving a non-serotoninergic agent
over a serotonergic one due to their lower propensity to produce emotional
blunting.
5.
Escitalopram
Ameliorates Cognitive Impairment in D-Galactose-Injected Ovariectomized Rats:
Modulation of JNK, GSK-3β, and ERK Signalling Pathways
Though selective serotonin reuptake inhibitors (SSRIs) have been found to
increase cognitive performance in some studies on patients and animal models of
Alzheimer's disease (AD), other studies have reported contradictory results, and
the mechanism of action has not been fully described. This study aimed to
examine the effect of escitalopram, an SSRI, in an experimental model of AD and
to determine the involved intracellular signalling pathways. Ovariectomized rats
were administered D-galactose (150 mg/kg/day, i.p) over ten weeks to induce AD.
Treatment with escitalopram (10 mg/kg/day, p.o) for four weeks, starting from
the 7th week of D-galactose injection, enhanced memory performance and
attenuated associated histopathological changes. Escitalopram reduced
hippocampal amyloid β 42, β-secretase, and p-tau, while increasing α-secretase
levels. Furthermore, it decreased tumor necrosis factor-α, nuclear factor-kappa
B p65, and NADPH oxidase, while enhancing brain-derived neurotrophic factor,
phospho-cAMP response element binding protein, and synaptophysin levels.
Moreover, escitalopram diminished the protein expression of the phosphorylated
forms of c-Jun N-terminal kinase (JNK)/c-Jun, while increasing those of
phosphoinositide 3-kinase (PI3K), protein kinase B (Akt), glycogen synthase
kinase-3β (GSK-3β), extracellular signal-regulated kinase (ERK) and its upstream
kinases MEK and Raf-1. In conclusion, escitalopram ameliorated
D-galactose/ovariectomy-induced AD-like features through modulation of
PI3K/Akt/GSK-3β, Raf-1/MEK/ERK, and JNK/c-Jun pathways.
7.
Calcium-dependent intracellular signal pathways in primary cultured adipocytes
and ANK3 gene variation in patients with bipolar disorder and healthy controls
Bipolar disorder (BD) is a chronic psychiatric disorder of public health
importance affecting >1% of the Swedish population. Despite progress, patients
still suffer from chronic mood switches with potential severe consequences.
Thus, early detection, diagnosis and initiation of correct treatment are
critical. Cultured adipocytes from 35 patients with BD and 38 healthy controls
were analysed using signal pathway reporter assays, that is, protein kinase C
(PKC), protein kinase A (PKA), mitogen-activated protein kinases (extracellular
signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK)), Myc, Wnt and
p53. The levels of activated target transcriptional factors were measured in
adipocytes before and after stimulation with lithium and escitalopram.
Variations were analysed in the loci of 25 different single-nucleotide
polymorphisms (SNPs). Activation of intracellular signals in several pathways
analysed were significantly higher in patients than in healthy controls upon
drug stimulation, especially with escitalopram stimulation of PKC, JNK and Myc,
as well as lithium-stimulated PKC, whereas no meaningful difference was observed
before stimulation. Univariate analyses of contingency tables for 80 categorical
SNP results versus diagnoses showed a significant link with the ANK3 gene
(rs10761482; likelihood ratio χ(2)=4.63; P=0.031). In a multivariate ordinal
logistic fit for diagnosis, a backward stepwise procedure selected ANK3 as the
remaining significant predictor. Comparison of the escitalopram-stimulated PKC
activity and the ANK3 genotype showed them to add their share of the diagnostic
variance, with no interaction (15% of variance explained, P<0.002). The study is
cross-sectional with no longitudinal follow-up. Cohorts are relatively small
with no medication-free patients, and there are no 'ill patient' controls. It
takes 3 to 4 weeks of culture to expand adipocytes that may change epigenetic
profiles but remove the possibility of medication effects. Abnormalities in the
reactivity of intracellular signal pathways to stimulation and the ANK3 genotype
may be associated with pathogenesis of BD. Algorithms using biological patterns
such as pathway reactivity together with structural genetic SNP data may provide
opportunities for earlier detection and effective treatment of BD.
8.
Gastrointestinal side effects associated with antidepressant treatments in
patients with major depressive disorder: A systematic review and meta-analysis
Gastrointestinal side effects (SEs) are frequently observed in patients with
major depressive disorder (MDD) while taking antidepressants and may lead to
treatment discontinuation. The aim of this meta-analysis is to provide
quantitative measures on short-term rates of gastrointestinal SEs in MDD
patients treated with second-generation antidepressants. An electronic search of
the literature was conducted by using MEDLINE, ISI Web of Science - Web of
Science Core Collection, and Cochrane Library databases. Eligible studies had to
focus on the use of at least one of 15 antidepressants commonly used in MDD
(i.e., agomelatine, bupropion, citalopram, desvenlafaxine, duloxetine,
escitalopram, fluoxetine, fluvoxamine, levomilnacipran, mirtazapine, paroxetine,
reboxetine, sertraline, venlafaxine, and vortioxetine) and report data on
treatment-emergent gastrointestinal SEs (i.e. nausea/vomiting, diarrhoea,
constipation, abdominal pain, dyspepsia, anorexia, increased appetite and dry
mouth) within 12 weeks of treatment. Overall, 304 studies were included in the
meta-analyses. All the considered antidepressants showed higher rates of
gastrointestinal SEs than placebo. Escitalopram and sertraline were shown to be
the least tolerated antidepressants on the gastrointestinal tract, being
associated with all the considered SEs with the exception of constipation and
increased appetite, while mirtazapine was shown to be the antidepressant with
fewer side effects on the gut, being only associated with increased appetite. In
conclusion, commonly used antidepressants showed different profiles of
gastrointestinal SEs, possibly related to their mechanisms of action. The
specific tolerability profile of each compound should be considered by
clinicians when prescribing antidepressants in order to improve adherence to
treatment and increase positive outcomes in patients with MDD.