Sexual dysfunction in women: Can we talk about it?
ABSTRACT
Sexual dysfunction in women is common and often goes unreported and untreated. Its management is part of patient-centered primary care. Primary care providers are uniquely positioned to identify and assess sexual health concerns of their patients, provide reassurance regarding normal sexual function, and treat sexual dysfunction or refer as appropriate.
KEY POINTS
- Sexual dysfunction in women is complex and often multifactorial and has a significant impact on quality of life.
- Primary care providers can assess the problem, provide education on sexual health and normal sexual functioning, and manage biological factors affecting sexual function, including genitourinary syndrome of menopause in postmenopausal women and antidepressant-induced sexual dysfunction.
- Treatment may require a multidisciplinary team, including a psychologist or sex therapist to manage the psychological, sociocultural, and relational factors affecting a woman’s sexual health, and a physical therapist to manage pelvic floor disorders.
DEPRESSION AND ANTIDEPRESSANT-INDUCED SEXUAL DYSFUNCTION
Depression increases the risk of sexual dysfunction, and vice versa.
A meta-analysis that included 12 studies involving almost 15,000 patients confirmed that depression increased the risk of sexual dysfunction, and sexual dysfunction increased the risk of depression.43 This interaction may be related to the overlap in affected neurotransmitters and neuroendocrine systems.44
In the Sequenced Treatment Alternatives to Relieve Depression trial, Ishak et al45 found that patients treated with a selective serotonin reuptake inhibitor (SSRI) who experienced remission of depression had a lower prevalence of impaired sexual satisfaction and much greater improvements in sexual satisfaction than did those who remained depressed. The severity of depressive symptoms predicted impairment in sexual satisfaction, which in turn predicted poorer quality of life. The authors suggested that physicians encourage patients to remain on SSRI treatment, given that improvement in depressive symptoms is likely to improve sexual satisfaction.
Antidepressant-induced sexual dysfunction
As many as 70% of patients taking an SSRI or serotonin-norepinephrine reuptake inhibitor (SNRI) experience antidepressant-induced sexual dysfunction, though this is difficult to estimate across studies of different medications due to differences in methods and because many patients only report it when directly asked about it.46
Treatment of antidepressant-induced sexual dysfunction includes not only optimal management of depression but reassessment of the antidepressant treatment. If using only nondrug treatments for the mood disorder is not feasible, switching to (or ideally, starting with) an antidepressant with fewer sexual side effects such as mirtazapine, vilazodone, or bupropion is an option.46
A drug holiday (suspending antidepressant treatment for 1 or 2 days) has been suggested as a means of treating antidepressant-induced sexual dysfunction, but this may result in poorer control of depressive symptoms and discontinuation symptoms, and it encourages medication noncompliance.46,47
Treatment with a phosphodiesterase type 5 inhibitor (eg, sildenafil) has been studied in women with antidepressant-induced sexual dysfunction, with modest results.48
A Cochrane review reported that treatment with bupropion shows promise at higher doses (300 mg daily).49
Exercise for 20 minutes 3 times weekly is associated with improvement in antidepressant-induced sexual dysfunction when the exercise is performed immediately before sexual activity.50
LOW SEXUAL DESIRE
Hypoactive sexual desire disorder is defined as persistent or recurrent deficiency or absence of sexual fantasies and desire for sexual activity associated with marked distress and not due exclusively to a medication, substance abuse, or a medical condition.
Low or decreased sexual desire is the most commonly reported sexual health concern in women of all ages, with an unadjusted prevalence of 39.7%. When the criterion of personal distress is included, the prevalence is 8.9% in women ages 18 to 44, 12.3% in women ages 45 to 64, and 7.4% in women ages 65 and older.1
Multiple biological, psychological, and social factors may contribute to the problem. Identifying the ones that are present can help in planning treatment. A multifaceted approach may be appropriate.
Mindfulness and cognitive behavioral therapy for low sexual desire
Mindfulness-based cognitive therapy is designed to improve awareness, focusing on and accepting the present moment, and directing attention away from and lessening self-criticism and evaluation of one’s sexual responsiveness.
Mindfulness-based therapy has been associated with improvements in sexual desire and associated distress.51 Similarly, the effectiveness of cognitive behavioral therapy for treating hypoactive sexual desire disorder is supported by 3 controlled trials, although concerns exist about the adequacy of these trials, and further study is needed.52
Androgen therapy in women
In randomized controlled trials in women with low sexual desire who were either naturally or surgically menopausal, sexual function improved with testosterone therapy that resulted in mostly supraphysiologic total testosterone levels (which may not reflect free testosterone levels) with or without concurrent estrogen treatment.53–57
Testosterone is not approved by the US Food and Drug Administration (FDA) for use in women, primarily because of the lack of long-term safety and efficacy data (ie, beyond 24 months). However, studies have shown no evidence of increased risk of endometrial cancer or cardiovascular disease with testosterone dosed to achieve physiologic premenopausal levels.58 Data on breast cancer risk are less clear, but observational studies over the last decade do not support an association with testosterone use in women.58 There is no clearly defined androgen deficiency syndrome in women, and androgen levels do not reliably correlate with symptoms.59
The Endocrine Society59 guidelines endorse the use of testosterone in postmenopausal women with hypoactive sexual desire disorder. They say to aim for the midnormal premenopausal range and suggest discontinuing the drug if there is no response in 6 months. They recommend checking testosterone levels at baseline, after 3 to 6 weeks of therapy, and every 6 months to monitor for excessive use, to avoid supraphysiologic dosing and to evaluate for signs of androgen excess (eg, acne, hair growth). The use of products formulated for men or those formulated by pharmacies is discouraged; however, no FDA-approved products are currently available for use in women in the United States.
Flibanserin
A postsynaptic serotonin 5-HT1A receptor agonist and 5-HT2A receptor agonist, flibanserin was approved by the FDA in 2015 for treatment of hypoactive sexual desire disorder in premenopausal women. Its mechanism of action is likely through an effect on neurotransmitters that suppresses serotonin (which has sexually inhibitory effects) and promotes dopamine and norepinephrine (which have excitatory effects).60
The efficacy of flibanserin has been demonstrated in 3 randomized controlled trials, with significant increases in the number of sexually satisfying events and in sexual desire scores and a decrease in distress associated with low sexual desire.17–19 While the increase in sexually satisfying events was modest (about 1 extra event per month), some have suggested that the frequency of sexual activity may not be the best measure of sexual function in women.61 Further, responders to this drug showed a return to near-normal premenopausal frequencies of sexual activity in a separate analysis.61
The drug is generally well tolerated, with common adverse effects being somnolence, dizziness, and fatigue.18,19 Flibanserin has been associated with orthostatic hypotension with alcohol use and carries a boxed warning highlighting this potential interaction.62 Use of this drug is contraindicated in women who drink alcohol or take medications that are moderate or strong inhibitors of CYP-3A4 (eg, some antiretroviral drugs, antihypertensive drugs, antibiotics, and fluconazole, which can increase systemic exposure to flibanserin and potential side effects), and in those with liver impairment.
