Depression often co-exists with sexual dysfunction, and the medical treatment of depression can further worsen sexual symptoms or cause de-novo sexual dysfunction in a person who did not experience it prior to treatment. There are many drugs that can adversely affect sexual response. Among antidepressants, this effect is commonly observed with selective serotonin reuptake inhibitors (SSRI).

Numerous strategies for the treatment of SSRI-related sexual dysfunction have been studied, including: awaiting spontaneous remission of sexual dysfunction; reducing the dose of medication; taking a ?drug holiday?; adding another drug to help reverse sexual symptoms; changing antidepressants; or initially starting with a different antidepressant that is known to have fewer or no sexual side effects. Overall, it is important to address sexual health when caring for a patient in order to improve drug compliance and the patient’s well being.

Female sexual dysfunction is highly prevalent, affecting 43% of American women. [1] Based on data from the National Health and Social Life Survey: (1) a third of women lack sexual interest, (2) nearly a fourth do not experience orgasm, (3) approximately 20% report lubrication difficulties, and (4) 20% find sex not pleasurable. Female sexual dysfunction is a multifactorial problem combining biological, psychological, and interpersonal causes. [2]

Relationship Between Depression and Sexual Dysfunction: Depression is a common disorder with a prevalence of 6-11.8% in women. [3] Unipolar depression is twice as common in women as men. A core symptom of depression is anhedonia, which is defined as markedly diminished interest or pleasure in all, or almost all activities. Anhedonia includes loss of libido. In one study, it was found that 70% of depressed patients had a loss of sexual interest while not on medication, and they reported that the severity of this loss of interest was worse than the other symptoms of depression. [4] Despite these important findings, several myths exist about sexual dysfunction and depression. [5] One myth is that depressed patients do not care about their sexual function. In a door-to-door epidemiologic survey in the United Kingdom of over 6,000 people, 70% reported that having a good sex life was fairly or very important to them. [6] Among the 1,140-person subsample of people reporting depression, 75% reported that having a good sex life was fairly or very important to them. These findings suggest that depressed patients value sexual health as much as non-depressed patients.

{mosbanner:id=1:right:0}Another myth is that most patients will continue to take their medications even if they are experiencing sexual dysfunction, as long as the drug is effectively treating their depression. In a study of sexual dysfunction caused by clomipramine, an antidepressant, approximately 96% of patients developed difficulty in achieving orgasm. [7] It was later discovered that some patients were secretly reducing their dose of clomipramine in order to regain sexual function.

A third myth is that patients will spontaneously report sexual dysfunction to their physician. Patients often do not spontaneously report sexual dysfunction to their doctors because of the personal nature of sexual behavior or because of fear, shame, or ignorance. [8] Gender may also influence spontaneous reporting of sexual dysfunction, with men more likely to report problems than women. Physicians may also hesitate to ask patients directly because of their own discomfort with the topic; lack of knowledge about sexual dysfunction; wishing to avoid appearing intrusive or seductive; and/or feeling that they do not have enough time to address a complex issue such as sexual dysfunction. In order to fully care for a patient, it is necessary to obtain a sexual history. In the previously mentioned study regarding clomipramine, it was shown to be essential to ask patients directly about sexual function. [7] The percentage of patients with sexual dysfunction elicited by questionnaire was 36% and the percentage of patients elicited by a direct interview was 96%.

The fourth and final myth is that all antidepressants cause sexual dysfunction at the same rate. In a prospective multicenter study of 1,022 outpatients, the overall incidence of sexual dysfunction was 59.1% when all antidepressants were considered. [9] The incidence of any type of sexual dysfunction was different among the different drugs: (1) fluoxetine (Prozac, Elli Lily & Company, Indianapolis, IN) 57.7%, (2) sertraline (Zoloft, Pfizer, New York, NY) 62.9%, (3) fluvoxamine (Luvox, Solvay, Marietta, GA) 62.3%, (4) paroxetine (Paxil, SmithKline Beecham, Philadelphia, PA) 70.7%, (5) citalopram (Celexa, Forest, St. Louis, MO) 72.7%, (6) venlafaxine (Effexor, Wyeth-Ayerst, Philadelphia, PA) 67.3%, (7) mirtazapine (Remeron, Organon, West Orange, NJ) 24.4%, (8) nefazodone (Serzone, Bristol-Meyers Squibb, Princeton, NJ) 8%, (9) amineptine (6.9%), (10) moclobemide (3.9%). (table 4) The incidence of sexual dysfunction is high with SSRIs (medications 1-5) and venlafaxine, which is a serotonin-norepinephrine reuptake inhibitor (SNRI).

Mechanism of SSRI-Induced Sexual Dysfunction: SSRIs can be associated with most forms of sexual dysfunction, but the main effects of SSRIs involve sexual arousal, orgasm, and libido. [10] With sexual stimulation and arousal, the erectile tissue of the clitoris and the smooth muscle of the vaginal wall engorge. The increased blood flow to the vagina triggers a process called transudation, providing lubrication. SSRIs cause sexual dysfunction by inhibiting the production of nitric oxide, which is the main mediator of both the male and female sexual arousal response. [11] (figure 1) This leads to complaints of vaginal dryness, diminished genital sensation, and often times orgasmic difficulty.

The effect of SSRIs on libido may be the result of multiple factors that impact the central nervous system, especially the mesolimbic system. [12] Dopamine is believed to be one of the neurotransmitters that positively affects libido. Selective serotonin reuptake blockade, as seen with SSRIs, has been implicated in reducing dopamine activity via the serotonin-2 (5-HT2) receptor. SSRIs have also been associated with increasing prolactin levels, which may have effects on the central nervous system, resulting in decreased libido.