CASE STUDY 3
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Open Access Full Text Article
DOI: 10.2147/DHPS.S7634
Antidepressant-associated sexual dysfunction: impact, effects, and treatment
Agnes Higgins Michael Nash Aileen M Lynch School of Nursing and Midwifery Studies, Trinity College Dublin, Dublin, ireland
Correspondence: Agnes Higgins School of Nursing and Midwifery Studies, Trinity College Dublin, 24, D’Olier St, Dublin 2, ireland Tel +353 1896 3703 Fax +353 1896 3001 email ahiggins@tcd.ie
Abstract: Sexual dysfunction is a common side effect of antidepressants and can have significant impact on the person’s quality of life, relationships, mental health, and recovery. The reported
incidence of sexual dysfunction associated with antidepressant medication varies considerably
between studies, making it difficult to estimate the exact incidence or prevalence. The sexual
problems reported range from decreased sexual desire, decreased sexual excitement, diminished
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
conditions in a population that does not have a mental health problem; greater focus
on service users views and quality of life issues; and as Balon4 suggests, market-
ing competition among pharmaceutical companies. The focus of this article is to
explore the incidence, pathophysiology, and treatment of antidepressant-associated
sexual dysfunction.
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142
Higgins et al
Incidence of antidepressant- associated sexual dysfunction Pharmacotherapy of depression involves the use of antide-
pressants which modulate central neurotransmitter levels,
namely serotonin, norepinephrine, and dopamine. The main
classes of antidepressants are the tricyclic antidepressants
(TCAs), SSRIs, SNRIs, monoamine oxidase inhibitors
(MAOIs), and the atypical antidepressants.
Treatment-emergent sexual dysfunction has been
reported with virtually all of the antidepressants. The
reported incidence of sexual dysfunction associated with
antidepressant medication varies considerably between
studies, making it difficult to estimate the exact incidents
or prevalence. Rothschild6 in a review of research studies
on antidepressants and sexual function concluded that 40%
of people taking antidepressants will develop some form
of sexual dysfunction. Studies estimate that the incidence
varies from 30% of people treated with imipramine7 to
25%–73% of people treated with an SSRI,8–11 with 93%
of the men and women treated with clomipramine in
one study complaining of total or partial anorgasmia.12
Montjo-Gonzales et al10 reported an overall incidence of
58% in an unblinded study involving 344 clients who had
a history of normal sexual function before SSRI treatments.
The frequency of sexual side effects was highest for
paroxetine (65%), fluvoxamine (59%), sertaline (56%) and
fluoxetine (54%). In a multicenter, prospective, Spanish
study involving 1022 people, Montejo et al12 reported a
59.1% overall incidence of sexual dysfunction when all
antidepressants were considered as a whole. The differences
between drugs are summarized in Table 1 and were as
follows: incidence of sexual dysfunction with SSRIs and
venlafaxine (an SNRI) were high ranging between 58% and
70% – fluoxetine (57.7%), sertaline (62.9%), fluvoxamine
(62.3%), venlafaxine (67%), paroxetine (70.7%), and
citalopram (72.7%). This compared with a much lower
incidence for the newer 5-HT2 blockers (8% nefazodone
and 24% mir tazapine). Moclobemide, a reversible
MAOI, (3.9%) resulted in the lowest incidence of sexual
dysfunction. When differences between men and women
were compared, men reported a slightly higher frequency
of sexual dysfunction than women (62% and 60%). Clayton
et al,13 in an adult outpatient population (4534 women
and 1763 men) receiving antidepressant monotherapy,
reported rates of sexual dysfunction as follows: mirtazapine
and venlafaxine extended release were associated with
higher rates (36%–43%), followed by nefazodone (28%),
bupropion SR (25%) and bupropion IR (22%).
Modell et al11 investigated through self-reported
anonymous questionnaires, the sexual side effects of bupro-
pion and the SSRIs (fluoxetine, paroxetine, and sertraline)
among 107 outpatients. Overall, 73% of the SSRI-treated
clients reported adverse sexual side effects; in contrast, to 14%
of clients treated with bupropion. The three SSRIs, to an equal
degree, significantly decreased libido, arousal, duration of
orgasm, and intensity of orgasm below levels experienced pre-
morbidly. In comparison, bupropion-treated clients reported
significant increases in libido, level of arousal, intensity of
orgasm, and duration of orgasm beyond levels experienced
premorbidly. Consequently, the authors concluded that adverse
sexual effects appear to be the rule rather than the exception
with SSRIs. In a similar study, Kennedy et al8 compared the
effects of moclobemide, paroxetine, sertraline, and venla-
faxine on drive/desire and arousal/orgasm. Similar to other
studies, rates of sexual dysfunction were higher for sertraline,
paroxetine, and venlafaxine, when compared with moclobe-
mide. Compared with women, men experienced a significantly
greater level of impairment in drive/desire, whereas no differ-
ence was reported in levels of arousal/orgasm. No difference
was found across the four antidepressants in men, whereas
rates of sexual dysfunction were higher in women who were
prescribed with sertraline and paroxetine.
A number of double blind comparative studies without
placebo control have also been conducted. Kavoussi et al14
in a randomized double-blind study, of 248 people with
moderate to severe depression, compared sustained-release
bupropion and sertraline on sexual function. They reported
that orgasmic dysfunction was significantly (P , 0.001)
more common in the sertraline-treated group. During the
16-week trial, 61% men and 41% of women treated with
sertaline reported orgasmic dysfunction, compared with 10%
men and 7% of women in the bupropion. Segraves et al15
also compared the effects of sustained-release bupropion and
sertraline on sexual function, in 240 people with moderate
to severe depression. They reported similar results, with a
significantly greater percentage of sertraline-treated clients
(63% and 41% of men and women, respectively) developed
sexual dysfunction compared with bupropion SR-treated
clients (15% and 7% of men and women, respectively).
Sexual dysfunction was noted as early as day 7 in sertraline-
treated clients and persisted until the end of the 16-week
treatment phase. Four clients, all of whom were treated with
sertraline, discontinued from the study prematurely because
of sexual dysfunction. Feiger et al16 compared the effects of
nefazodone with sertraline in 160 clients with major mood
disorder. Findings suggested that for men, overall satisfac-
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143
Antidepressant-induced sexual dysfunction
T ab
le 1
S um
m ar
y o f t
he s
ub cl
as se
s o f a
nt id
ep re
ss an
ts
D ru
g cl
as s
D ru
gs M
ec h
an is
m
o f
ac ti
o n
A d
ve rs
e ef
fe ct
s
(g en
er al
) S
ex u
al d
ys fu
n ct
io n
T ri
cy cl
ic
an ti de
pr es
sa nt
s (T
C A
s) Pr
o to
ty pi
ca l d
ru g:
im
ip ra
m in
e in
hi bi
ts t
he r
eu pt
ak e
of
s er
ot on
in a
nd
no re
pi ne
ph ri
ne
M an
y; m
o st
d ue
t o a
ffi ni
ty fo
r
ch o lin
er gi
c, h
is ta
m in
er gi
c an
d
ad re
ne rg
ic r
ec ep
to rs
A pp
ro xi
m at
e pr
ev al
en ce
: 3 0%
N o lo
ng er
fir
st -l in
e dr
ug s
O th
er s:
a m
it ri
pt yl
in e,
do
xe pi
n D
ec re
as ed
li bi
do , d
el ay
ed
o rg
as m
M en
: e re
ct ile
d ys
fu nc
ti o n,
de
la ye
d ej
ac ul
at io
n w
o m
en : b
re as
t en
la rg
em en
t, de
cr ea
se d
o rg
as m
Se le
ct iv
e se
ro to
ni n
re
up ta
ke in
hi bi
to rs
( SS
R is
) Pr
o to
ty pi
ca l d
ru g:
Fl
uo xe
ti ne
in
hi bi
ts t
he r
eu pt
ak e
o f s
er o to
ni n
A nt
ic ho
lin er
gi c
si de
ef
fe ct
s ar
e no
t co
m m
o n
A pp
ro xi
m at
e pr
ev al
en ce
: 25
% –7
3%
Fi rs
t- lin
e dr
ug s
O th
er s:
p ar
o xe
ti ne
, s er
tr al
in e,
flu
vo xa
m in
e, e
sc it al
o pr
am ,
ci ta
lo pr
am
R is
k o f s
er o to
ni n
sy nd
ro m
e if
co
-a dm
in is
te re
d w
it h
o th
er
an ti de
pr es
sa nt
s
D ec
re as
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bi do
, d el
ay ed
/ in
ab ili
ty t
o r
ea ch
o rg
as m
, ga
la ct
o rr
he a
M en
: d el
ay ed
e ja
cu la
ti o n
an d
er ec
ti le
d ys
fu nc
ti o n
Se ro
to ni
n no
re pi
ne ph
ri ne
re
up ta
ke in
hi bi
to rs
( SN
R is
) Pr
o to
ty pi
ca l d
ru g:
v
en la
fa xi
ne
in hi
bi ts
t he
r eu
pt ak
e
o f s
er o to
ni n
an d
no re
pi ne
ph ri
ne N
au se
a, n
er vo
us ne
ss , i
ns o m
ni a
A pp
ro xi
m at
e pr
ev al
en ce
: 58
% –7
0%
O th
er : d
ul o xe
ti ne
M en
: e re
ct ile
d ys
fu nc
ti o n,
ab
no rm
al e
ja cu
la ti o n
w o m
en : d
el ay
ed o
r ab
se nt
o rg
as m
M o no
am in
e o xi
da se
in
hi bi
to rs
( M
A O
is )
Pr o to
ty pi
ca l d
ru g:
Ph
en el
zi ne
B
lo ck
s th
e en
zy m
e
m o no
am in
e o xi
da se
w
hi ch
n o rm
al ly
in ac
ti va
te s
th
e m
o no
am in
es :
se ro
to ni
n, d
o pa
m in
e, n
o re
pi ne
ph ri
ne
M an
y ad
ve rs
e re
ac ti o ns
, eg
, h yp
er te
ns iv
e cr
is is
, so
r ar
el y
us ed
in c
lin ic
al p
ra ct
ic e;
d ue
to
a ffi
ni ty
fo r
ch o lin
er gi
c an
d
ad re
ne rg
ic r
ec ep
to rs
A pp
ro xi
m at
e pr
ev al
en ce
: 4 0%
A ls
o t
ra ny
lc yp
ro m
in e
D ec
re as
ed li
bi do
, d el
ay ed
o rg
as m
N o re
pi ne
ph ri
ne
an d
do pa
m in
e
re up
ta ke
in hi
bi to
rs
Pr o to
ty pi
ca l d
ru g:
B
up ro
pi o n
in hi
bi ts
t he
r eu
pt ak
e
o f s
er o to
ni n,
no
re pi
ne ph
ri ne
an
d do
pa m
in e
A gi
ta ti o n,
in so
m ni
a, r
es tl es
sn es
s,
w ei
gh t
lo ss
A pp
ro xi
m at
e pr
ev al
en ce
: 10
% –2
5%
N o re
pi ne
ph ri
ne
re up
ta ke
in hi
bi to
rs Pr
o to
ty pi
ca l d
ru g:
R
eb o xe
ti ne
in hi
bi ts
t he
r eu
pt ak
e
o f n
o re
pi ne
ph ri
ne H
ea da
ch e,
d ry
m o ut
h,
ta ch
yc ar
di a,
h yp
o te
ns io
n,
ur in
ar y
re te
nt io
n,
co ns
ti pa
ti o n
an d
in so
m ni
a
A pp
ro xi
m at
e pr
ev al
en ce
: 5%
–1 0%
(C on
tin ue
d)
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Higgins et al
tion with sexual functioning was greater with nefazodone;
67% of men taking sertraline reported ejaculatory difficulties
compared with 19% of the nefazodone-treated group.
In women, nefazodone was superior to sertaline on measure
of ease of achieving orgasm and satisfaction with orgasmic
ability. Some years later, Ferguson et al17 in an 8-week
double-blind study, also compared nefazodone with sertra-
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.
Similar to the previous studies, sertaline-treated clients
reported more drug-related sexual dysfunction. 76% of the
sertaline-treated clients experienced reoccurrence of sexual
dysfunction (ejaculatory or orgasmic difficulty) compared
with 26% of the nefazodone-treated group. In this study, 5
of the sertaline-treated clients discontinued therapy because
of sexual dysfunction.
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
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
only 1 week of treatment in sertaline-treated clients and
continued throughout the 8-week treatment. There were
no significant differences in the occurrence of orgasmic
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
with fluoxetine treatment than with bupropine or placebo.
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.
Within the literature there are also a number of case
study-anecdotal accounts of other sexual side effects, such
as: priapism associated with paroxetine;20 painful ejaculation
associated with venlafaxine,21 reboxetine,22 and tricyclics;23
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 Ta bl
e 1
(C on
tin ue
d)
D ru
g cl
as s
D ru
gs M
ec h
an is
m
o f
ac ti
o n
A d
ve rs
e ef
fe ct
s
(g en
er al
) S
ex u
al d
ys fu
n ct
io n
D el
ay ed
o rg
as m
, e re
ct ile
dy
sf un
ct io
n m
ay o
cc ur
r ar
el y
C o m
bi ne
d re
up ta
ke
in hi
bi to
r an
d re
ce pt
o r
bl o ck
er T
ra zo
do ne
in
hi bi
ts t
he r
eu pt
ak e
o f s
er o to
ni n
O rt
ho st
at ic
h yp
o te
ns io
n,
na us
ea , s
ed at
io n,
d ry
m ou
th
A pp
ro xi
m at
e pr
ev al
en ce
: 8%
–2 8%
N ef
az o do
ne
in hi
bi ts
t he
r eu
pt ak
e
o f s
er o to
ni n
an d
bl o ck
s se
ro to
ni n
re ce
pt o rs
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Antidepressant-induced sexual dysfunction
of sexual side effects.27 In addition, decreased nocturnal
erections have been reported with amitriptyline.28
Over the years, several case reports have been published
on a relationship between antidepressants and nonpuerperal
lactation or galactorrhea in women. Egberts et al29 con-
cluded from their analysis of reported drug reactions to
the Netherlands Pharmacovigilance Foundation, between
1986 and 1996, that SSRIs and clomipramine were associated
with approximately eight times higher risk of nonpuerperal
lactation in women, when compared with women taking
nonserotonergic antidepressants. Although rare, withdrawal
syndromes that impact on sexuality and sexual function
have also been described. In a recent article, Leiblum and
Goldmeier30 describe persistent genital arousal disorder in
five women who attribute the onset of their sensations to
either the usage or discontinuation of an SSRI. The women
found the sensation distressing, with only brief relief from
orgasm, and reported that their genital arousal was qualita-
tively different from sexual arousal that is preceded by sexual
desire and/or subjective arousal.
There are very few studies that examine the impact of
antidepressants on people without a mental health problem.
Kowalski et al31 conducted a double-blind trial in a group of
men without psychiatric diagnosis, to compare the impact
of amitriptyline, mianserin, and placebo on nocturnal sexual
arousal. Both amitriptyline and mianserin signif icantly
decreased the amplitude and duration of nocturnal erections.
Kennedy et al32 compared the effects of moclobemide and
placebo on 60 healthy male and female adults and found no
difference in the effects on sexual interest or sexual function
in healthy volunteers. It needs to be remembered, however,
that moclobemide is an antidepressant with the lowest inci-
dence of reported sexual dysfunction in clients being treated
for depression.12
Although the research provides firm evidence that antide-
pressant medication is associated with sexual dysfunction in
both men and women, reaching any firm conclusion about the
exact prevalence is difficult. Data on the prevalence of sexual
dysfunction among the general population is scarce making it
difficult to establish a ‘normal’ baseline.33 In addition, there
are very few large studies that explored the effects of antide-
pressants on adults without depression, or who used placebo
controls. In their review of evidence of sexual dysfunction
associated with antidepressants, Montgomery et al33 describe
methodological problems such as absence of comparison
groups, inconsistent def initions of sexual dysfunction,
absence of baseline assessment of sexual functioning, and
the use of various measures of sexual functioning as well as
the questionable validity of the rating scales used. There is
also a difficulty within the studies in separating sexual dys-
function resulting from depression and that resulting from
the drugs – as depression itself is associated with decreased
libido, decreased sexual activity, and decreased erectile and
orgasmic excitement.34 Balon4 highlights that most studies
do not take into account other coexisting problems such
as substance misuse, physical health problems, and other
medications that may contribute to sexual dysfunction. The
variation in rates between studies is also possibly due to the
wide variety of measures used to measure sexual functioning,
use of different samples, and recruitment strategies. However,
a number of writers suggest that, in all probability, the dif-
ference in rates is due to substantial underreporting rather
than under occurrence.8,11
Differential effects of the various antidepressant classes and drugs In general, the mechanisms of action involve either the
inhibition of breakdown of norepinephrine or blocking the
reuptake of serotonin and norepinephrine at the presynaptic
terminal, resulting in increased neurotransmitter availability
at the synapse.
Sex is more than a physical act. It also includes emotional
and psychological dimensions. The normal sex cycle con-
sists of four successive phases: desire, arousal, orgasm, and
resolution.35 These phases are facilitated by the interplay of
neurotransmitters, hormones, and peptides. Different classes
of antidepressants impact on all phases of the sexual response
cycle to varying degrees, and the details pertaining to each
class of antidepressant are summarized in Table 1.
The challenge is to understand how antidepressants
impact on normal sexual function. Because most antide-
pressants modulate serotonin concentration, it is generally
thought that elevated serotonin levels diminish sexual
function.37 Serotoninergic nerve terminals target dopamine
and norepinephrine pathways in the brain and inhibit their
activity,38 both of these neurotransmitters having a role in
the desire and arousal phases of the sexual response cycle.
80% of serotonin is localized in the periphery, where when
elevated, it directly reduces sensation in the anatomical
structures of the reproductive system as well as diminish-
ing erection, vaginal lubrication, ejaculation, and orgasm.39
According to Nelson et al,40 the 5HT2 and 5HT3 receptor
subtypes underlie serotoninergic-mediated sexual dysfunc-
tion. In addition, serotonin inhibits nitric oxide production,
which normally has a role in relaxing the smooth muscle of
the vasculature (including the vasculature of the reproductive
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146
Higgins et al
structures), thus enabling vasodilation and allowing sufficient
blood supply to the sexual organs during the sexual response
cycle.41
The autonomic nervous system regulates the mechanistic
aspects of sexual function (eg, orgasm and ejaculation) and
utilizes acetylcholine (parasympathetic and sympathetic
systems) and norepinephrine (sympathetic system). Many
antidepressants have some eff icacy at cholinergic and
alpha1-adrenergic receptors, thereby inhibiting the autonomic
nervous system and consequently inhibiting normal sexual
function.10
Long-term exposure may impact at the genetic level to
effect functioning of the catecholaminergic and endocrine
systems,42 such as antidepressant-associated changes to
semen quality and DNA integrity.43,44
The management of antidepressant-associated sexual dysfunction It is estimated that 30% of people treated for depression
may be noncompliant with treatment; minimization of
antidepressant-associated sexual dysfunction could be an
important factor in successful treatment and health out-
comes.18 The management of antidepressant-associated
sexual dysfunction is complex. Balon4 suggests that “given
the scarcity of evidence-based treatments the management
of sexual dysfunction is still an art rather than a science”
(p. 1506).
As stated earlier, the normal sexual response cycle consists
of four successive phases: desire, arousal, orgasm, and reso-
lution.35 The management of antidepressant-associated sexual
dysfunction should endeavor to address sexual dysfunction
equating to each stage of the sex cycle. However, this is not
entirely possible as, as Jespersen45 suggests, poor overall
sexual satisfaction is a common complaint of clients with
antidepressant-associated sexual dysfunction.
Therefore, the first stage of effective management is
a thorough assessment to ensure that the reported sexual
dysfunction is indeed a consequence of antidepressant treat-
ment. This will involve a re-evaluation of the depressive
episode, including a physical and sexual health assessment.
As Zajecka46 states, “the first step in management is to define
the actual complaint and then attempt to determine the aetiol-
ogy” (p. 35). This may not be as easy as it appears.
A thorough assessment will focus on:
• Eliminating confounding factors for sexual dysfunction, eg, age or alcohol/substance use
• Excluding a comorbid physical complaint, eg, side effects of drugs used to manage diabetes or hypertension may
be a cause of sexual dysfunction.47 Higgins48 states that
diabetes, atherosclerosis, cardiac disease, central and
peripheral nervous system disease, and alcoholism can
also contribute to sexual dysfunction.
• Excluding ongoing, or residual, symptoms of depression. Kennedy et al49 found in a sample of people with major
depression (55 male and 79 female), over 40% of men
and 50% of women reported decreased sexual interest
prior to antidepressant treatment.
The main challenge faced by practitioners is managing
antidepressant-associated sexual dysfunction without compro-
mising the mental wellbeing of the client. This very fine balanc-
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
sexual dysfunction. However, the obvious complication here
is for relapse into the depressive state. Therefore, practitioners
must be honest and open with the client in order to build trust,
which can empower them to make better decisions about both
their physical health and mental wellbeing.
T h e r e a r e va r i o u s p h a r m a c o l og i c a l a n d n o n -
phar macological ways of managing antidepressant-
induced sexual dysfunction.
Drug adaption In most cases, antidepressant regimes may be short term. There-
fore, clients may opt to endure the effects of sexual dysfunction
for a short period, until their treatment ends. Part of this may
stem from a perception that their ‘sex life’ not being as bad with
medication side effects as it was with their depression.
Once initiated, any medication requires a phase of adap-
tion due to the potential unintended, or unforeseen, reactions.
Drug adaption requires accommodation. Some adverse drug
reactions, eg, nausea or blurred vision, recede as the client’s
body adapts to the antidepressant. Therefore, one course of
management of antidepressant-associated sexual dysfunc-
tion is a ‘wait and see’ approach. Montejo et al12 suggest
that spontaneous and partial remission of antidepressant-
associated sexual dysfunction occurs in 10% of individuals
treated with antidepressant agents. However, this still leaves
a large proportion of individuals who will not spontaneously
recover, even partially. Therefore this approach will not be
suitable for all clients.
If antidepressant-associated sexual dysfunction emerges
rapidly then this phase may be quickly passed over for one
of the other possibilities.
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147
Antidepressant-induced sexual dysfunction
Reduction in medication dosage The first point to consider relates to the client’s medication
regime. Practitioners should ask if the client is on their
optimum dosage of antidepressant, ie, the optimum to man-
age the client’s illness, not the optimum dosage that can be
prescribed. This can give a vital space to proceeding with
reducing medication dosage.
Antidepressant-associated sexual dysfunction may be a
dose-related adverse event. Therefore reducing the dosage of
the treatment to a minimum effective dose may be an option.
However, this carries alternative risk to the client’s mental
health. While dose reduction is a management option, the
practitioner must educate the client to be aware that reduc-
tion will not have an immediate effect on the antidepressant-
associated sexual dysfunction. The rate at which the sexual
dysfunction will recede will depend on the half-life of the
particular antidepressant. If the client anticipates an immedi-
ate effect on dose reduction and it fails to materialize, the risk
is that they abstain from their antidepressant regime.
Switching medications Another strategy is switching antidepressants to one with
a less risky side effect profile. This may include switching
from an SSRI to non-SSRI antidepressant. This may give the
potential benefits of continuing to manage the depressive ill-
ness while reducing the potential for sexual dysfunction.
In a systematic review of strategies for managing sexual
dysfunction, Rudkin et al50 reported that switching from
sertraline to nefazodone was significantly less likely to
result in re-emergence of the sexual dysfunction and was not
associated with any worsening depression. Zajecka46 sug-
gests that nefazodone, bupropion, and possibly mirtazapine
have minimal or no negative impact on sexual functioning.
However, individual responses to this strategy may vary.
Firstly, the sexual dysfunction may recede but the depressive
illness reasserts itself. Secondly, the change of medication
may result in other associated side effects which may be
more debilitating as they are present throughout the client’s
day, not just when they want to have sex. Thirdly, the client
who has experienced both the depression and the sexual
dysfunction may feel that a ‘little’ depression is preferable
to sexual dysfunction.
Adjunct treatment As in most psychotropic medication regimes adjunct treatment,
introducing another drug to counteract side-effects may be
required. Clayton et al51 concluded from their double-blind
comparison study involving 42 clients with SSRI-induced
sexual dysfunction that bupropion SR was an effective antidote.
In comparison with placebo, clients treated with bupropion
SR showed a significantly greater improvement in desire and
frequency of engaging in sexual activity. Labbate et al52 found
that bupropion 75 mg q.d. reversed SSRI induced sexual dys-
function. However, this was a small case study with a sample of
six people (4 female and 2 male). Demyttenaere and Huygens22
describe the successful treatment of two clients with tamsulosin
(alpha 1A-adrenoceptor antagonist), who had experienced
antidepressant-induced painful ejaculation. Michelson et al53
concluded from their trial that neither buspirone nor amanta-
dine was more effective than placebo in improving fluoxetine-
induced sexual dysfunction in women.
There is evidence from systematic review of randomized,
controlled trials into the management of antidepressant-
induced sexual dysfunction that the addition of sildenafil
(Viagra) will improve erectile dysfunction in men.50,54 The
benefit to women has yet to be comprehensively proven. One
randomized placebo controlled trial involving 98 women
experiencing antidepressant induced sexual dysfunction con-
cluded that sildenafil significantly reduced the adverse sexual
effects, such as delayed orgasm responses and inadequate
lubrication.55 However, the clinical benefit and risk have yet
to be proven in large studies.
Alcantara56 states that drugs that act as 5-HT2-receptor
agonists may cause sexual dysfunction by inhibiting the
release of dopamine and noradrenaline. They suggest that
5-HT2 antagonism or strategies that increase noradrenergic
or dopaminergic transmission may be useful in reversing
sexual dysfunction.
Adjunct treatments should only be considered following a
thorough physical assessment of the client and a medication
review to address any contraindications with current psychotro-
pic medications. Both sildenafil and bupropion have potential
side effects. Sildenafil is associated with visual disturbances,
palpitations, hypotension, and priapism, and bupropion may
cause dry mouth, insomnia, gastrointestinal disturbances, and
tremor.57 Individuals might perceive these side effects as more
debilitating than sexual dysfunction. Therefore it is important
that they have all the information on potential effects of adjunct
treatments so that they can make informed decisions.
Conflicting evidence on the nature of herbal supplements
such as ginkgo biloba as an adjunct treatment exists. In an
open trial, ginkgo biloba was found to be effective in treating
antidepressant induced sexual dysfunction generally having a
positive effect on all four phases of the sexual response cycle:
desire, excitement, orgasm, and resolution.58 The authors
also note that women were more responsive to the sexually
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148
Higgins et al
enhancing effects of ginkgo biloba than men. However,
a group placebo controlled double blind trial of ginkgo biloba
found no significant difference in sexual functioning in any
phase, although the placebo group showed improved orgasm
satisfaction.59 While its mode of action is not yet known,60
further trials of herbal supplements may be appropriate.
Drug holiday A drug holiday is a high-risk treatment option where medication
is omitted on the day of or prior to, anticipated sexual activity.
While drug holidays are contentious and might not appeal to
many practitioners, some evidence does exist which suggests
stopping antidepressant medication on a temporary basis might
be a potential strategy. In a trial of a drug holiday for SSRI-
induced sexual dysfunction, Rothschild61 instructed 30 outpa-
tients to discontinue their SSRIs after their Thursday morning
dose and then restart at their previous dose on Sunday at 12:00
noon over four weekends. They found that clients taking sertra-
line and paroxetine reported a significant improvement in their
sexual functioning, ie, improved libido and sexual satisfaction,
but not by those taking fluoxetine. Furthermore, there were no
statistically significant increases in mean Hamilton depression
scores after discontinuation of the SSRIs.
Keltner et al41 suggests that drug holidays may impair
therapeutic efficacy and lead to withdrawal symptoms. Drug
holidays may be seen as an exercise in manipulating antide-
pressant half-life. Drugs such as fluoxetine, with a longer
half-life, will need a longer drug holiday to ensure adequate
excretion for sexual activity to occur. However, the longer
the drug holiday the higher the risk of depressive symptoms
recurring. Short half-life drugs, eg, venlafaxine, may be
better with regards to facilitating sexual activity; however,
again the risk of depressive symptoms reasserting themselves
increases due to the short half life. Drug holidays also carry
the risk of the client experiencing withdrawal symptoms
associated with their particular medication. In this event such
withdrawal symptoms may render the individual unable to
engage in sexual activity.
A drug holiday is a precursor to sexual activity. Therefore
the mechanization of scheduling sexual activity so that the
drug holiday can be introduced may be another drawback of
this approach. Timetabling is no substitute for romance that
partners may appreciate as part of their sexual cycle. Setting
deadlines like this may also increase ‘performance’ anxiety
which might further compound the problem. The partner will
also need to be educated about the condition if drug holidays
are to be introduced as they may be able to give corroborative
information regarding their effectiveness.
Cognitive behavioral therapy Counseling therapies such as cognitive behavioral therapy
(CBT) may be used in a biopsychosocial approach to sexual
dysfunction. CBT focuses on current issues that are causing
present problems. As such, it can help people change how
they think in order to increase positive coping. CBT breaks
problems down so that individuals can see the links between
thoughts, feelings, and behavior.
While CBT is a recognized nonpharmacological inter-
vention for a range of psychiatric disorders including
depression,62 there is little evidence of effectiveness of CBT
for antidepressant-associated sexual dysfunction. Indeed
while CBT alone may not be wholly appropriate for manag-
ing the sexual dysfunction, it may be useful in managing
negative feelings that may have a hugely negative impact
on the individual’s self esteem and self image. Feelings of
sexual inadequacy may further compound any depressive
illness and may put the client at risk of noncompliance. In
CBT, clients can talk about the emotional impact of the
sexual dysfunction and get psychological and emotional
support, while still adhering to treatment regimes. Another
key factor in CBT will be education of the client regarding
their sexual dysfunction. This may help reduce catastrophic
thinking and even prepare for possible future events should
they arise.
A CBT action plan would seek to challenge these
negative thoughts in order to enhance self image and self
esteem. This approach requires both tact and expertise
as the problem may be seen to be the medication not the
sexual dysfunction. Part of this overall psycho-education
should involve the partner who may be equally affected. Sex
therapy or ‘couples’ counseling would be another alterna-
tive, which again would focus not on the core problem of
sexual dysfunction but on how the couple can cope with
its consequences. The unaffected partner will also need
education so that they can be reassured that the sexual
dysfunction is not related to a disinterest in them but as a
result of medication.
The overall management of sexual dysfunction will
involve pre- and post-test sexual dysfunction and depres-
sion surveys. This will test the efficacy of any intervention
in reducing sexual dysfunction and how interventions affect
the depressive illness. The conundrum for managing sexual
dysfunction is what is more important in antidepressant
treatment – the threshold for efficacious treatment of depres-
sion or managing the threshold of adverse drug reactions
such as sexual dysfunction. This will evidentially need to be
decided on a case by case basis.
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Antidepressant-induced sexual dysfunction
Conclusion Depression is a common mental health problem for which
a key intervention is antidepressant medication. Although
there is extensive evidence that antidepressants, especially
the SSRI group, cause sexual dysfunction in both men and
women, estimating the exact prevalence is difficult. The sex-
ual problems reported are extensive, ranging from decreased
sexual desire, decreased sexual excitement, diminished or
delayed orgasm, to erection or delayed ejaculation problems.
In addition, there are a number of anecdotal accounts and
case reports of sexual side effects, such as priapism, painful
ejaculation, penile anesthesia, decreased nocturnal erections,
and spontaneous ejaculation in men; and loss of sensation
in the vagina and nipples, persistent genital arousal, and
nonpuerperal lactation or galactorrhea in women.
Tackling the problem of antidepressant-induced sexual dys-
function is complex and requires partnership between research
and practice. While some evidence regarding pharmacological
management of antidepressant-associated sexual dysfunction
exists, Taylor et al54 suggest that this is rather limited and insuf-
ficient to formulate a clinical guideline. The first step in manag-
ing antidepressant-induced sexual dysfunction is assessment.
For many practitioners this may be challenging given the taboo
that surrounds sex and sexual health. Taking a sexual history
might be awkward for clinicians and clients alike. However
as clinicians make this a routine part of their practice for this
specific client group, they will enhance their skills and practice,
transforming their awkwardness into expertise, which will
ensure clients feel well attended to and able to discuss issues
openly. Initial awkwardness will be a small price to pay for
enhancing clinical practice and the quality of client care in this
area. Waiting for clients to break the silence and raise their con-
cerns may leave many clients isolated, confused, and distressed
or fearful – not just of the drugs, but of engaging in intimate
relationships. Good assessment will generate good information
that will enhance effective clinical decision making.
Treating and managing antidepressant-induced sexual
dysfunction requires a holistic approach as sufferers may be
skeptical of pharmacological only remedies. There is evi-
dence that bupropion and nefazodone, compared with SSRI
group, are far less likely to cause sexual dysfunction, and that
sildenafil will improve erectile dysfunction in men. However,
nonpharmacological interventions such as sex therapy, CBT,
and homeopathic remedies should be considered within
practice and in further research.
Disclosure The authors report no conflicts of interest in this work.
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