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Antidepressant-Associated Sexual Dysfunction: Impact, Effects, and Treatment

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Antidepressant-associated sexual dysfunction:


impact, effects, and treatment
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Drug, Healthcare and Patient Safety
8 September 2010
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Agnes Higgins Abstract: Sexual dysfunction is a common side effect of antidepressants and can have significant
Michael Nash impact on the person’s quality of life, relationships, mental health, and recovery. The reported
Aileen M Lynch incidence of sexual dysfunction associated with antidepressant medication varies considerably
between studies, making it difficult to estimate the exact incidence or prevalence. The sexual
School of Nursing and Midwifery
For personal use only.

Studies, Trinity College Dublin, problems reported range from decreased sexual desire, decreased sexual excitement, diminished
Dublin, Ireland or delayed orgasm, to erection or delayed ejaculation problems. There are a number of case
reports of sexual side effects, such as priapism, painful ejaculation, penile anesthesia, loss of
sensation in the vagina and nipples, persistent genital arousal and nonpuerperal lactation in
women. The focus of this article is to explore the incidence, pathophysiology, and treatment of
antidepressant iatrogenic sexual dysfunction.
Keywords: depression, antidepressant, iatrogenic sexual dysfunction, SSRI, SNRI

Introduction
Sexual dysfunction is a common side effect of antidepressants, particularly of selective
serotonin reuptake inhibitor (SSRIs) and serotonin norepinephrine reuptake inhibitor
(SNRIs) medications. Sexual dysfunction can have significant impact on the person’s
quality of life, quality of relationships, self esteem, and recovery and can lead to
noncompliance with antidepressant treatment with a potential for relapse of symptoms.1
Despite this and the frequency of researchers reporting antidepressant-associated sexual
dysfunction within the literature, it continues to be underreported or underemphasized
on client information leaflets, package inserts,2 and verbal information given to clients
by practitioners.3
During the 60s and 70s, reports of antidepressant-associated sexual dysfunction
were rare;4 possibly due to underreporting, lack of discussion and assessment, and
an assumption that people with mental health problems were asexual and lacked
any sexual desire.5 The increased recognition of drug induced sexual dysfunction
is multifaceted: including a greater willingness on behalf of researchers to include
questions on sexual function and sexual desire; use of antidepressants for other
Correspondence: Agnes Higgins conditions in a population that does not have a mental health problem; greater focus
School of Nursing and Midwifery
Studies, Trinity College Dublin, on service users views and quality of life issues; and as Balon4 suggests, market-
24, D’Olier St, Dublin 2, Ireland ing competition among pharmaceutical companies. The focus of this article is to
Tel +353 1896 3703
Fax +353 1896 3001
explore the incidence, pathophysiology, and treatment of antidepressant-associated
Email ahiggins@tcd.ie sexual dysfunction.

submit your manuscript | www.dovepress.com Drug, Healthcare and Patient Safety 2010:2 141–150 141
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DOI: 10.2147/DHPS.S7634 which permits unrestricted noncommercial use, provided the original work is properly cited.
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Incidence of antidepressant- Modell et  al 11 investigated through self-reported


associated sexual dysfunction anonymous questionnaires, the sexual side effects of bupro-
Pharmacotherapy of depression involves the use of antide- pion and the SSRIs (fluoxetine, paroxetine, and sertraline)
pressants which modulate central neurotransmitter levels, among 107 outpatients. Overall, 73% of the SSRI-treated
namely serotonin, norepinephrine, and dopamine. The main clients reported adverse sexual side effects; in contrast, to 14%
classes of antidepressants are the tricyclic antidepressants of clients treated with bupropion. The three SSRIs, to an equal
(TCAs), SSRIs, SNRIs, monoamine oxidase inhibitors degree, significantly decreased libido, arousal, duration of
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(MAOIs), and the atypical antidepressants. orgasm, and intensity of orgasm below levels experienced pre-
Treatment-emergent sexual dysfunction has been morbidly. In comparison, bupropion-treated clients reported
reported with virtually all of the antidepressants. The significant increases in libido, level of arousal, intensity of
reported incidence of sexual dysfunction associated with orgasm, and duration of orgasm beyond levels experienced
antidepressant medication varies considerably between premorbidly. Consequently, the authors concluded that adverse
studies, making it difficult to estimate the exact incidents sexual effects appear to be the rule rather than the exception
or prevalence. Rothschild6 in a review of research studies with SSRIs. In a similar study, Kennedy et al8 compared the
on antidepressants and sexual function concluded that 40% effects of moclobemide, paroxetine, sertraline, and venla-
of people taking antidepressants will develop some form faxine on drive/desire and arousal/orgasm. Similar to other
of sexual dysfunction. Studies estimate that the incidence studies, rates of sexual dysfunction were higher for sertraline,
varies from 30% of people treated with imipramine7 to paroxetine, and venlafaxine, when compared with moclobe-
For personal use only.

25%–73% of people treated with an SSRI,8–11 with 93% mide. Compared with women, men experienced a significantly
of the men and women treated with clomipramine in greater level of impairment in drive/desire, whereas no differ-
one study complaining of total or partial anorgasmia. 12 ence was reported in levels of arousal/orgasm. No difference
Montjo-Gonzales et  al10 reported an overall incidence of was found across the four antidepressants in men, whereas
58% in an unblinded study involving 344 clients who had rates of sexual dysfunction were higher in women who were
a history of normal sexual function before SSRI treatments. prescribed with sertraline and paroxetine.
The frequency of sexual side effects was highest for A number of double blind comparative studies without
paroxetine (65%), fluvoxamine (59%), sertaline (56%) and placebo control have also been conducted. Kavoussi et al14
fluoxetine (54%). In a multicenter, prospective, Spanish in a randomized double-blind study, of 248 people with
study involving 1022 people, Montejo et  al12 reported a moderate to severe depression, compared sustained-release
59.1% overall incidence of sexual dysfunction when all bupropion and sertraline on sexual function. They reported
antidepressants were considered as a whole. The differences that orgasmic dysfunction was significantly (P , 0.001)
between drugs are summarized in Table  1 and were as more common in the sertraline-treated group. During the
follows: incidence of sexual dysfunction with SSRIs and 16-week trial, 61% men and 41% of women treated with
venlafaxine (an SNRI) were high ranging between 58% and sertaline reported orgasmic dysfunction, compared with 10%
70% – fluoxetine (57.7%), sertaline (62.9%), fluvoxamine men and 7% of women in the bupropion. Segraves et al15
(62.3%), venlafaxine (67%), paroxetine (70.7%), and also compared the effects of sustained-release bupropion and
citalopram (72.7%). This compared with a much lower sertraline on sexual function, in 240 people with moderate
incidence for the newer 5-HT2 blockers (8% nefazodone to severe depression. They reported similar results, with a
and 24% mirtazapine). Moclobemide, a reversible significantly greater percentage of sertraline-treated clients
MAOI, (3.9%) resulted in the lowest incidence of sexual (63% and 41% of men and women, respectively) developed
dysfunction. When differences between men and women sexual dysfunction compared with bupropion SR-treated
were compared, men reported a slightly higher frequency clients (15% and 7% of men and women, respectively).
of sexual dysfunction than women (62% and 60%). Clayton Sexual dysfunction was noted as early as day 7 in sertraline-
et  al,13 in an adult outpatient population (4534 women treated clients and persisted until the end of the 16-week
and 1763 men) receiving antidepressant monotherapy, treatment phase. Four clients, all of whom were treated with
reported rates of sexual dysfunction as follows: mirtazapine sertraline, discontinued from the study prematurely because
and venlafaxine extended release were associated with of sexual dysfunction. Feiger et al16 compared the effects of
higher rates (36%–43%), followed by nefazodone (28%), nefazodone with sertraline in 160 clients with major mood
bupropion SR (25%) and bupropion IR (22%). disorder. ­Findings suggested that for men, overall satisfac-

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Table 1 Summary of the subclasses of antidepressants
Drug class Drugs Mechanism Adverse effects Sexual dysfunction
of action (general)
Dovepress

Tricyclic Prototypical drug: Inhibits the reuptake Many; most due to affinity for Approximate prevalence: 30%
antidepressants (TCAs) Imipramine of serotonin and cholinergic, histaminergic and
norepinephrine adrenergic receptors

No longer Others: amitriptyline, Decreased libido, delayed


first-line drugs doxepin orgasm
Men: erectile dysfunction,
delayed ejaculation
Women: breast enlargement,

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decreased orgasm
Selective serotonin Prototypical drug: Inhibits the reuptake Anticholinergic side Approximate prevalence:
reuptake inhibitors (SSRIs) Fluoxetine of serotonin effects are not common 25%–73%
First-line drugs Others: paroxetine, sertraline, Risk of serotonin syndrome if Decreased libido, delayed/
fluvoxamine, escitalopram, co-administered with other inability to reach orgasm,
citalopram antidepressants galactorrhea
Men: delayed ejaculation and
erectile dysfunction
Serotonin norepinephrine Prototypical drug: Inhibits the reuptake Nausea, nervousness, insomnia Approximate prevalence:
reuptake inhibitors (SNRIs) Venlafaxine of serotonin and norepinephrine 58%–70%
Other: duloxetine Men: erectile dysfunction,
abnormal ejaculation
Women: delayed or absent
orgasm
Monoamine oxidase Prototypical drug: Blocks the enzyme Many adverse reactions, Approximate prevalence: 40%
inhibitors (MAOIs) Phenelzine monoamine oxidase eg, hypertensive crisis,
which normally inactivates so rarely used in clinical practice; due
the monoamines: to affinity for cholinergic and
serotonin, dopamine, norepinephrine adrenergic receptors
Also tranylcypromine Decreased libido, delayed
orgasm
Norepinephrine Prototypical drug: Inhibits the reuptake Agitation, insomnia, restlessness, Approximate prevalence:
and dopamine Bupropion of serotonin, weight loss 10%–25%
reuptake inhibitors norepinephrine
and dopamine
Norepinephrine Prototypical drug: Inhibits the reuptake Headache, dry mouth, Approximate prevalence:
reuptake inhibitors Reboxetine of norepinephrine tachycardia, hypotension, 5%–10%
urinary retention,

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constipation and insomnia

(Continued)

143
Antidepressant-induced sexual dysfunction
Higgins et al Dovepress

tion with sexual functioning was greater with nefazodone;

Decreased libido and delayed


dysfunction may occur rarely
67% of men taking sertraline reported ejaculatory difficulties

Approximate prevalence:
Delayed orgasm, erectile

Ejaculation dysfunctions,
Sexual dysfunction
compared with 19% of the nefazodone-treated group.

anorgasmia, priapism
In women, nefazodone was superior to sertaline on measure

orgasm possible
of ease of achieving orgasm and satisfaction with orgasmic
8%–28% ability. Some years later, Ferguson et  al17 in an 8-week
double-blind study, also compared nefazodone with sertra-
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line, this time among 105 people who were experiencing


sexual dysfunction attributable to sertraline. Clients were
randomly assigned to either group following a 1-week
wash out period and a subsequent 7–10-day placebo phase.

Headache, fatigue, agranulocytosis, anemia


leukopenia, orthostatic hypotension
Similar to the previous studies, sertaline-treated clients
reported more drug-related sexual dysfunction. 76% of the

Note: Copyright © 2007. Adapted with permission from Taylor D, Paton C, Kerwin R, editors. The Maudsley Prescribing Guidelines. London, UK: Informa Healthcare; 2007.
sertaline-treated clients experienced reoccurrence of sexual
drowsiness, nausea, vomiting
nausea, sedation, dry mouth
Orthostatic hypotension,

dysfunction (ejaculatory or orgasmic difficulty) compared


with 26% of the nefazodone-treated group. In this study, 5
Seizures, acute renal
Adverse effects

of the sertaline-treated clients discontinued therapy because


failure, hepatitis,
Liver damage,

of sexual dysfunction.
(general)
For personal use only.

A small number of double-blind comparative studies


with placebo control have been conducted. Croft et  al1
compared the effects of sustained-release bupropion, ser-
traline, and placebo on sexual function with 360 people
5HT2 and 5HT3, histaminergic H1 and alpha1
receptors; also blocks postsynaptic serotonin

alpha2 receptors and noradrenaline reuptake


of serotonin and blocks serotonin receptors

with moderate to severe depression. Findings indicated


that people treated with sertraline experienced signifi-
cantly more sexual dysfunction throughout the duration
of the study compared with those treated with bupropion
SR or placebo. Orgasmic dysfunction occurred after
Inhibits the reuptake

Inhibits the reuptake

only 1 week of treatment in sertaline-treated clients and


Blocks presynaptic

Blocks presynaptic
alpha2-adrenergic

continued throughout the 8-week treatment. There were


Mechanism

of serotonin

no significant differences in the occurrence of orgasmic


of action

receptors

dysfunction between bupropion SR and placebo at any


time during the study. Coleman et al18 compared the sexual
function effects of bupropone, fluoxetine, and placebo in
456 people. Again, decline in sexual functioning, sexual
desire, and sexual arousal were more frequently associated
Nefazodone

Mirtazapine

with fluoxetine treatment than with bupropine or placebo.


Trazodone

Mianserin
Drugs

These findings support findings from other studies that


suggest bupropion SR is relatively free of sexual side
effects,11,19 and supports the contention that bupropion SR
may be an appropriate antidepressant for clients concerned
about sexual function.
inhibitor and receptor blocker

Within the literature there are also a number of case


study-anecdotal accounts of other sexual side effects, such
Table 1 (Continued)

Combined reuptake

as: priapism associated with paroxetine;20 painful ejaculation


associated with venlafaxine,21 reboxetine,22 and tricyclics;23
Drug class

loss of sensation in the vagina and nipples;24 penile anesthesia


associated with fluoxetine25 and sertraline;26 and spontane-
ous ejaculation with reboxetine, an SNRI known for its lack

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Dovepress Antidepressant-induced sexual dysfunction

of sexual side effects.27 In addition, decreased nocturnal the questionable validity of the rating scales used. There is
erections have been reported with amitriptyline.28 also a difficulty within the studies in separating sexual dys-
Over the years, several case reports have been published function resulting from depression and that resulting from
on a relationship between antidepressants and nonpuerperal the drugs – as depression itself is associated with decreased
lactation or galactorrhea in women. Egberts et  al29 con- libido, decreased sexual activity, and decreased erectile and
cluded from their analysis of reported drug reactions to orgasmic excitement.34 Balon4 highlights that most studies
the Netherlands Pharmacovigilance Foundation, between do not take into account other coexisting problems such
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1986 and 1996, that SSRIs and clomipramine were associated as substance misuse, physical health problems, and other
with approximately eight times higher risk of nonpuerperal medications that may contribute to sexual dysfunction. The
lactation in women, when compared with women taking variation in rates between studies is also possibly due to the
nonserotonergic antidepressants. Although rare, withdrawal wide variety of measures used to measure sexual functioning,
syndromes that impact on sexuality and sexual function use of different samples, and recruitment strategies. However,
have also been described. In a recent article, Leiblum and a number of writers suggest that, in all probability, the dif-
Goldmeier30 describe persistent genital arousal disorder in ference in rates is due to substantial underreporting rather
five women who attribute the onset of their sensations to than under occurrence.8,11
either the usage or discontinuation of an SSRI. The women
found the sensation distressing, with only brief relief from Differential effects of the various
orgasm, and reported that their genital arousal was qualita- antidepressant classes and drugs
For personal use only.

tively different from sexual arousal that is preceded by sexual In general, the mechanisms of action involve either the
desire and/or subjective arousal. inhibition of breakdown of norepinephrine or blocking the
There are very few studies that examine the impact of reuptake of serotonin and norepinephrine at the presynaptic
antidepressants on people without a mental health problem. terminal, resulting in increased neurotransmitter availability
Kowalski et al31 conducted a double-blind trial in a group of at the synapse.
men without psychiatric diagnosis, to compare the impact Sex is more than a physical act. It also includes emotional
of amitriptyline, mianserin, and placebo on nocturnal sexual and psychological dimensions. The normal sex cycle con-
arousal. Both amitriptyline and mianserin significantly sists of four successive phases: desire, arousal, orgasm, and
decreased the amplitude and duration of nocturnal erections. resolution.35 These phases are facilitated by the interplay of
Kennedy et al32 compared the effects of moclobemide and neurotransmitters, hormones, and peptides. Different classes
placebo on 60 healthy male and female adults and found no of antidepressants impact on all phases of the sexual response
difference in the effects on sexual interest or sexual function cycle to varying degrees, and the details pertaining to each
in healthy volunteers. It needs to be remembered, however, class of antidepressant are summarized in Table 1.
that moclobemide is an antidepressant with the lowest inci- The challenge is to understand how antidepressants
dence of reported sexual dysfunction in clients being treated impact on normal sexual function. Because most antide-
for depression.12 pressants modulate serotonin concentration, it is generally
Although the research provides firm evidence that antide- thought that elevated serotonin levels diminish sexual
pressant medication is associated with sexual dysfunction in function.37 Serotoninergic nerve terminals target dopamine
both men and women, reaching any firm conclusion about the and norepinephrine pathways in the brain and inhibit their
exact prevalence is difficult. Data on the prevalence of sexual activity,38 both of these neurotransmitters having a role in
dysfunction among the general population is scarce making it the desire and arousal phases of the sexual response cycle.
difficult to establish a ‘normal’ baseline.33 In addition, there 80% of serotonin is localized in the periphery, where when
are very few large studies that explored the effects of antide- elevated, it directly reduces sensation in the anatomical
pressants on adults without depression, or who used placebo structures of the reproductive system as well as diminish-
controls. In their review of evidence of sexual dysfunction ing erection, vaginal lubrication, ejaculation, and orgasm.39
associated with antidepressants, Montgomery et al33 describe According to Nelson et al,40 the 5HT2 and 5HT3 receptor
methodological problems such as absence of comparison subtypes underlie serotoninergic-mediated sexual dysfunc-
groups, inconsistent definitions of sexual dysfunction, tion. In addition, serotonin inhibits nitric oxide production,
absence of baseline assessment of sexual functioning, and which normally has a role in relaxing the smooth muscle of
the use of various measures of sexual functioning as well as the vasculature (including the vasculature of the reproductive

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structures), thus enabling vasodilation and allowing sufficient • Excluding a comorbid physical complaint, eg, side effects
blood supply to the sexual organs during the sexual response of drugs used to manage diabetes or hypertension may
cycle.41 be a cause of sexual dysfunction.47 Higgins48 states that
The autonomic nervous system regulates the mechanistic diabetes, atherosclerosis, cardiac disease, central and
aspects of sexual function (eg, orgasm and ejaculation) and peripheral nervous system disease, and alcoholism can
utilizes acetylcholine (parasympathetic and sympathetic also contribute to sexual dysfunction.
systems) and norepinephrine (sympathetic system). Many • Excluding ongoing, or residual, symptoms of depression.
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antidepressants have some efficacy at cholinergic and Kennedy et al49 found in a sample of people with major
alpha1-adrenergic receptors, thereby inhibiting the autonomic depression (55 male and 79 female), over 40% of men
nervous system and consequently inhibiting normal sexual and 50% of women reported decreased sexual interest
function.10 prior to antidepressant treatment.
Long-term exposure may impact at the genetic level to The main challenge faced by practitioners is managing
effect functioning of the catecholaminergic and endocrine antidepressant-associated sexual dysfunction without compro-
systems,42 such as antidepressant-associated changes to mising the mental wellbeing of the client. This very fine balanc-
semen quality and DNA integrity.43,44 ing act may not be resolved adequately to everyone’s liking.
Noncompliance may constitute a big problem for practitioners
as this will have a positive effect on antidepressant-associated
The management of sexual dysfunction. However, the obvious complication here
antidepressant-associated
For personal use only.

is for relapse into the depressive state. Therefore, practitioners


sexual dysfunction must be honest and open with the client in order to build trust,
It is estimated that 30% of people treated for depression which can empower them to make better decisions about both
may be noncompliant with treatment; minimization of their physical health and mental wellbeing.
antidepressant-associated sexual dysfunction could be an There are various phar macological and non-
important factor in successful treatment and health out- pharmacological ways of managing antidepressant-
comes.18 The management of antidepressant-associated induced sexual dysfunction.
sexual dysfunction is complex. Balon4 suggests that “given
the scarcity of evidence-based treatments the management Drug adaption
of sexual dysfunction is still an art rather than a science” In most cases, antidepressant regimes may be short term. There-
(p. 1506). fore, clients may opt to endure the effects of sexual dysfunction
As stated earlier, the normal sexual response cycle consists for a short period, until their treatment ends. Part of this may
of four successive phases: desire, arousal, orgasm, and reso- stem from a perception that their ‘sex life’ not being as bad with
lution.35 The management of antidepressant-associated sexual medication side effects as it was with their depression.
dysfunction should endeavor to address sexual dysfunction Once initiated, any medication requires a phase of adap-
equating to each stage of the sex cycle. However, this is not tion due to the potential unintended, or unforeseen, reactions.
entirely possible as, as Jespersen45 suggests, poor overall Drug adaption requires accommodation. Some adverse drug
sexual satisfaction is a common complaint of clients with reactions, eg, nausea or blurred vision, recede as the client’s
antidepressant-associated sexual dysfunction. body adapts to the antidepressant. Therefore, one course of
Therefore, the first stage of effective management is management of antidepressant-associated sexual dysfunc-
a thorough assessment to ensure that the reported sexual tion is a ‘wait and see’ approach. Montejo et  al12 suggest
dysfunction is indeed a consequence of antidepressant treat- that spontaneous and partial remission of antidepressant-
ment. This will involve a re-evaluation of the depressive associated sexual dysfunction occurs in 10% of individuals
episode, including a physical and sexual health assessment. treated with antidepressant agents. However, this still leaves
As Zajecka46 states, “the first step in management is to define a large proportion of individuals who will not spontaneously
the actual complaint and then attempt to determine the aetiol- recover, even partially. Therefore this approach will not be
ogy” (p. 35). This may not be as easy as it appears. suitable for all clients.
A thorough assessment will focus on: If antidepressant-associated sexual dysfunction emerges
• Eliminating confounding factors for sexual dysfunction, rapidly then this phase may be quickly passed over for one
eg, age or alcohol/substance use of the other possibilities.

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Reduction in medication dosage sexual dysfunction that bupropion SR was an effective antidote.
The first point to consider relates to the client’s medication In comparison with placebo, clients treated with bupropion
regime. Practitioners should ask if the client is on their SR showed a significantly greater improvement in desire and
optimum dosage of antidepressant, ie, the optimum to man- frequency of engaging in sexual activity. Labbate et al52 found
age the client’s illness, not the optimum dosage that can be that bupropion 75 mg q.d. reversed SSRI induced sexual dys-
prescribed. This can give a vital space to proceeding with function. However, this was a small case study with a sample of
reducing medication dosage. six people (4 female and 2 male). Demyttenaere and Huygens22
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Antidepressant-associated sexual dysfunction may be a describe the successful treatment of two clients with tamsulosin
dose-related adverse event. Therefore reducing the dosage of (alpha 1A-adrenoceptor antagonist), who had experienced
the treatment to a minimum effective dose may be an option. antidepressant-induced painful ejaculation. Michelson et al53
However, this carries alternative risk to the client’s mental concluded from their trial that neither buspirone nor amanta-
health. While dose reduction is a management option, the dine was more effective than placebo in improving fluoxetine-
practitioner must educate the client to be aware that reduc- induced sexual dysfunction in women.
tion will not have an immediate effect on the antidepressant- There is evidence from systematic review of randomized,
associated sexual dysfunction. The rate at which the sexual controlled trials into the management of antidepressant-
dysfunction will recede will depend on the half-life of the induced sexual dysfunction that the addition of sildenafil
particular antidepressant. If the client anticipates an immedi- (Viagra) will improve erectile dysfunction in men.50,54 The
ate effect on dose reduction and it fails to materialize, the risk benefit to women has yet to be comprehensively proven. One
For personal use only.

is that they abstain from their antidepressant regime. randomized placebo controlled trial involving 98 women
experiencing antidepressant induced sexual dysfunction con-
Switching medications cluded that sildenafil significantly reduced the adverse sexual
Another strategy is switching antidepressants to one with effects, such as delayed orgasm responses and inadequate
a less risky side effect profile. This may include switching lubrication.55 However, the clinical benefit and risk have yet
from an SSRI to non-SSRI antidepressant. This may give the to be proven in large studies.
potential benefits of continuing to manage the depressive ill- Alcantara56 states that drugs that act as 5-HT2-receptor
ness while reducing the potential for sexual dysfunction. agonists may cause sexual dysfunction by inhibiting the
In a systematic review of strategies for managing sexual release of dopamine and noradrenaline. They suggest that
dysfunction, Rudkin et  al50 reported that switching from 5-HT2 antagonism or strategies that increase noradrenergic
sertraline to nefazodone was significantly less likely to or dopaminergic transmission may be useful in reversing
result in re-emergence of the sexual dysfunction and was not sexual dysfunction.
associated with any worsening depression. Zajecka46 sug- Adjunct treatments should only be considered following a
gests that nefazodone, bupropion, and possibly mirtazapine thorough physical assessment of the client and a medication
have minimal or no negative impact on sexual functioning. review to address any contraindications with current psychotro-
However, individual responses to this strategy may vary. pic medications. Both sildenafil and bupropion have potential
Firstly, the sexual dysfunction may recede but the depressive side effects. Sildenafil is associated with visual disturbances,
illness reasserts itself. Secondly, the change of medication palpitations, hypotension, and priapism, and bupropion may
may result in other associated side effects which may be cause dry mouth, insomnia, gastrointestinal disturbances, and
more debilitating as they are present throughout the client’s tremor.57 Individuals might perceive these side effects as more
day, not just when they want to have sex. Thirdly, the client debilitating than sexual dysfunction. Therefore it is important
who has experienced both the depression and the sexual that they have all the information on potential effects of adjunct
dysfunction may feel that a ‘little’ depression is preferable treatments so that they can make informed decisions.
to sexual dysfunction. Conflicting evidence on the nature of herbal supplements
such as ginkgo biloba as an adjunct treatment exists. In an
Adjunct treatment open trial, ginkgo biloba was found to be effective in treating
As in most psychotropic medication regimes adjunct treatment, antidepressant induced sexual dysfunction generally having a
introducing another drug to counteract side-effects may be positive effect on all four phases of the sexual response cycle:
required. Clayton et  al51 concluded from their double-blind desire, excitement, orgasm, and resolution.58 The authors
comparison study involving 42 clients with SSRI-induced also note that women were more responsive to the sexually

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enhancing effects of ginkgo biloba than men. However, Cognitive behavioral therapy
a group placebo controlled double blind trial of ginkgo biloba Counseling therapies such as cognitive behavioral therapy
found no significant difference in sexual functioning in any (CBT) may be used in a biopsychosocial approach to sexual
phase, although the placebo group showed improved orgasm dysfunction. CBT focuses on current issues that are causing
satisfaction.59 While its mode of action is not yet known,60 present problems. As such, it can help people change how
further trials of herbal supplements may be appropriate. they think in order to increase positive coping. CBT breaks
problems down so that individuals can see the links between
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Drug holiday thoughts, feelings, and behavior.


A drug holiday is a high-risk treatment option where medication While CBT is a recognized nonpharmacological inter-
is omitted on the day of or prior to, anticipated sexual activity. vention for a range of psychiatric disorders including
While drug holidays are contentious and might not appeal to depression,62 there is little evidence of effectiveness of CBT
many practitioners, some evidence does exist which suggests for antidepressant-associated sexual dysfunction. Indeed
stopping antidepressant medication on a temporary basis might while CBT alone may not be wholly appropriate for manag-
be a potential strategy. In a trial of a drug holiday for SSRI- ing the sexual dysfunction, it may be useful in managing
induced sexual dysfunction, Rothschild61 instructed 30 outpa- negative feelings that may have a hugely negative impact
tients to discontinue their SSRIs after their Thursday morning on the individual’s self esteem and self image. Feelings of
dose and then restart at their previous dose on Sunday at 12:00 sexual inadequacy may further compound any depressive
noon over four weekends. They found that clients taking sertra- illness and may put the client at risk of noncompliance. In
For personal use only.

line and paroxetine reported a significant improvement in their CBT, clients can talk about the emotional impact of the
sexual functioning, ie, improved libido and sexual satisfaction, sexual dysfunction and get psychological and emotional
but not by those taking fluoxetine. Furthermore, there were no support, while still adhering to treatment regimes. Another
statistically significant increases in mean Hamilton depression key factor in CBT will be education of the client regarding
scores after discontinuation of the SSRIs. their sexual dysfunction. This may help reduce catastrophic
Keltner et  al41 suggests that drug holidays may impair thinking and even prepare for possible future events should
therapeutic efficacy and lead to withdrawal symptoms. Drug they arise.
holidays may be seen as an exercise in manipulating antide- A CBT action plan would seek to challenge these
pressant half-life. Drugs such as fluoxetine, with a longer negative thoughts in order to enhance self image and self
half-life, will need a longer drug holiday to ensure adequate esteem. This approach requires both tact and expertise
excretion for sexual activity to occur. However, the longer as the problem may be seen to be the medication not the
the drug holiday the higher the risk of depressive symptoms sexual dysfunction. Part of this overall psycho-education
recurring. Short half-life drugs, eg, venlafaxine, may be should involve the partner who may be equally affected. Sex
better with regards to facilitating sexual activity; however, therapy or ‘couples’ counseling would be another alterna-
again the risk of depressive symptoms reasserting themselves tive, which again would focus not on the core problem of
increases due to the short half life. Drug holidays also carry sexual dysfunction but on how the couple can cope with
the risk of the client experiencing withdrawal symptoms its consequences. The unaffected partner will also need
associated with their particular medication. In this event such education so that they can be reassured that the sexual
withdrawal symptoms may render the individual unable to dysfunction is not related to a disinterest in them but as a
engage in sexual activity. result of medication.
A drug holiday is a precursor to sexual activity. Therefore The overall management of sexual dysfunction will
the mechanization of scheduling sexual activity so that the involve pre- and post-test sexual dysfunction and depres-
drug holiday can be introduced may be another drawback of sion surveys. This will test the efficacy of any intervention
this approach. Timetabling is no substitute for romance that in reducing sexual dysfunction and how interventions affect
partners may appreciate as part of their sexual cycle. Setting the depressive illness. The conundrum for managing sexual
deadlines like this may also increase ‘performance’ anxiety dysfunction is what is more important in antidepressant
which might further compound the problem. The partner will treatment – the threshold for efficacious treatment of depres-
also need to be educated about the condition if drug holidays sion or managing the threshold of adverse drug reactions
are to be introduced as they may be able to give corroborative such as sexual dysfunction. This will evidentially need to be
information regarding their effectiveness. decided on a case by case basis.

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