Sex and SSRIs (selective serotonin re-uptake inhibitors)
Depression and sexual difficulties are both very common and can be inter- related: If a person is experiencing depression, this can lower sexual interest but also antidepressants can have a negative impact on a person’s sexual functioning (treatment- emergent sexual dysfunction, TESD).
Sometimes there can be a positive association between treatment and sexual function: as a person’s mood improves so too can their level of sexual desire.
Both SSRIs and SNRIs (Serotonin- norepinephrine reuptake inhibitors) have commonly been associated with sexual side effects in up to 40-60% of individuals.1,2 Despite their selectivity, this is likely due to some of their effects on other neurotransmitter systems (eg norepinephrine and dopamine) and hormones (such as testosterone). 3
Studies have shown a gross under recognition of sexual side effects by healthcare professionals (HCPs) as compared to their patients (20x under recognition in the HCPs) with sexual side effects being a major reasons why patients discontinue their medications. 4
The common sexual side effects associated with SSRIs and SNRIs are as follows5:
- Reduction in sexual desire
- Erectile difficulties (ED)
- Difficulties reaching orgasm / not being able to reach orgasm
- And very rarely: Post SSRI sexual dysfunction / syndrome (this condition occurs despite stopping the medication. Symptoms include: ED, poor arousal including vaginal dryness, orgasmic difficulties with overall reduction in sexual pleasure, genital numbness and low desire)5
For the majority of people, stopping the SSRI means their side effects will fully resolve.
If you are about to start a patient on an SSRI it is important to discuss sexual side effects with them. There is evidence that some SSRIs may be more likely to cause sexual side effects than others.3 For example paroxetine (known to be the most effective at delaying ejaculation in men with early ejaculation) and citalopram may cause more sexual side effects than fluoxetine or sertraline. Side effects may be minimised by using the lowest effective dose. Treatment breaks and altered timing of doses have been discussed in the literature as a way of reducing side effects but different SSRIs have different half lives eg fluoxetine has a long half life (4-6 days), so these approaches would not be effective in this case. In addition, these ‘drug holidays’ risk causing a relapse in depressive symptoms or symptoms of discontinuation syndrome, indeed Paroxetine has a short half-life, approx. 21 hours (so there is a need for careful tapering when this drug is being discontinued).
If a patient is experiencing troublesome side effects watchful waiting in the first instance may be a reasonable approach as the sexual side effect could spontaneously settle in approximately 10% of cases (or partially remit in 11%)7. Another option is to switch to alternative antidepressant, for example vortioxetine8. Vortioxetine inhibits the reuptake of serotonin (5-HT) and is an antagonist at 5HT3 and an agonist at 5-HT1a receptors. A switch study has shown a significant improving in TESD when switching from an SSRI to Vortioxetine8. (Although current NICE guidance states that Vortioxetine is only recommended for treatment of major depressive illness as a third line agent9.) Bupropion and mirtazepine have also been associated with fewer sexual side effects3 (although due to its unselective nature mirtazepine can cause other unpleasant side effects such as weight gain and nausea3). Adding in another medication to assist with the sexual problem may be appropriate eg prescribing a PDE5i for those experiencing ED can be effective. 10 The 5-HT2 antagonist, trazodone has also been cited as a possible helpful addition with some small studies showing a possible improvement in sexual functioning in patients with TESD (note the rates of priapism with trazadone are greater than with PDE5i, although still not common). 11
It is also important to keep an open mind when a patient is presenting with possible TESD and think about other possible pathology causing (or adding to) the sexual problems eg Diabetes, cardiovascular disease or relationship issues and investigate / manage accordingly.
Dr Ali Mears, Consultant Physician in Sexual Medicine – The Havelock Clinic
References
Waldinger MD. . Psychiatric disorders and sexual dysfunction. Handb Clin Neurol. 2015; 130: 469- 89.
Higgins A, Nash M, Lynch A. Antidepressant-associated sexual dysfunction: impact, effects, and treatment. Drug Healthc Patient Saf. 2010; 2: 141–150.
Jing E, Straw- Wilson K. Sexual dysfunction in selective serotonin reuptake inhibitors (SSRIs) and potential solutions: A narrative literature review. Meant Health Clin. 2016 Jul; 6(4): 191–196.
Zimmerman M, Galione JN, Attiullah N, et al. Underrecognition of clinically significant side effects in depressed outpatients. J Clin Psychiatry. 2010;71(4):484-490.
Serretti A, Chiesa A. Treatment-emergent sexual dysfunction related to antidepressants: a meta-analysis. J Clin Psychopharmacol. 2009;29:259-266.
Reisman, Y. Sexual Consequences of Post-SSRI Syndrome. Sexual Medicine Reviews. 2017; 5(4): 429-433.
Montejo AL, Llorca G, Izquierdo JA et al. Incidence of sexual dysfunction associated with antidepressant agents: a prospective multicentre study of 1022 outpatients. Journal of Clinical Psychiatry 2001; 62(Suppl.3): 10-120
Jacobsen, PL, Mahableshwarkar AR, Chen Y, Chrones L, Clayton A. Effect of Vortioxetine vs. Escitalopram on sexual functioning in adults with well treated major depressive disorder experiencing SSRI- induced sexual dysfunction. J Sex Med. 2015; 12(10): 2036-2048
Vortioxetine for treating major depressive episodes. Technology appraisal guidance [TA367] Published date: 25 November 2015. https://www.nice.org.uk/guidance/TA367 [accessed 2nd September 2020]
Rudkin L et al. Strategies for managing sexual dysfunction induced by antidepressant medication. Cochrane Database Syst Rev 2004;CD003382.
Stryer R, Spivak B, Strous R, Shiloh. Trazodone for the Treatment of Sexual Dysfunction Induced by Serotonin Reuptake Inhibitors: A Preliminary Open-Label Study. Clinical neuropharmacology. 2008 32(2):82-4
