Sexual dysfunction, defined as reduction in desire (i.e., libido), arousal (i.e., vaginal lubrication, erection), and/or release (i.e., orgasm, ejaculation), occurs in 30% to 50% or more of those treated with SSRIs. Patients taking SSRIs may experience one or all of these sexual disruptions. Because sexual dysfunction leads to noncompliance, nurses need to understand both underlying mechanisms and appropriate treatments. Unfortunately, both depression and its pharmacologic treatment cause sexual dysfunction, making etiology less clear.
Individuals treated for depression frequently experience sexual dysfunction as a side effect. This specific side effect commonly presents when depressed people take selective serotonin reuptake inhibitors (SSRIs). Although other antidepressants also cause sexual dysfunction, the clinical dominance of SSRIs dictates their review.
SSRIs
A class of drugs, such as fluoxetine or sertraline, that inhibit the uptake of serotonin by neurons of the central nervous system and are primarily used in the treatment of depression and obsessive compulsive disorder.
How SSRIs Cause Sexual Dysfunction
Sexual dysfunction related to SSRIs, although far from rare, remains highly unrecognized. Comparing statistics from the Physician's Desk Reference (PDR) (2002) to a number of studies supports this assertion. The PDR indicates 2% to 16% of patients taking SSRIs experience sexual dysfunction, while other sources suggest rates of 50%, 70%, or even 90% (Clayton et al., 2001; Ferguson, 2001; Hirschfeld, 1999; Keltner & Folks, 2001). One explanation for disparities between classic references such as the PDR and other sources centers on the tendency of clients to not volunteer information of such a sensitive nature. However, when directly queried about such matters, there is a sharp increase in reports of sexual dysfunction.
While this discussion provides a better understanding of how SSRIs increase serotonin, it still does not hint at the mechanisms by which these drugs cause sexual dysfunction (i.e., decreased desire, arousal, and/or release). A simple axiom illuminates our understanding of SSRI-induced sexual dysfunction-serotonin tends to diminish sexual function, while dopamine tends to enhance sexual function. Drugs that enhance serotonin or block dopamine tend to decrease sexual activity; drugs that increase dopamine or block specific serotonin receptors tend to enhance sexual activity (Montejo-- Gonzalez et al., 1997; Rosen, Lane, & Menza, 1999).
CNS serotonin cell bodies arise from the brainstem in a region called the raphe nuclei. Raphe nuclei in the midbrain project axons upward to many locations in the brain. Some of these axons project to and innervate the mesolimbic dopamine system. Stahl (1998) suggests the serotonin activation of serotonin receptors modulates (and in this case, inhibits) this pathway. Cortical-- level sexual dysfunctions such as diminished desire may well be a direct result of serotonergic inhibition. Serotonergic projections from medullary raphe nuclei travel down the spine and, when stimulated, putatively inhibit the mechanistic aspects of sexual function, such as erection, vaginal lubrication, ejaculation, and orgasm.
To this point serotonin has been globally indicted as a cause of sexual dysfunction. In reality, one or two serotonin receptor subtypes, 5HT2 and perhaps 5HT3, are primarily responsible for these disabling sexual effects (Nelson, Shah, Welge, & Keck, 2001). As you will read in the section on treatments, serotonin-enhancing agents that do not stimulate these receptors apparently do not cause significant sexual dysfunction.
Other Mechanisms Causing Sexual Dysfunction
Beyond the explanatory power of increased serotonin, other biochemical changes contribute to the demise of sexual functioning as well. For instance, drugs that block cholinergic and alpha-1 receptors may have "antisexual" properties. Cholinergic fibers help in filling the corpus cavernosum, a requisite for erection and alpha-1 receptor stimulation is required for emptying it (Montejo-Gonzalez et al., 1997). Drugs that inhibit nitric oxide synthetase, decreasing the synthesis of this necessary part of the erection process, also may cause sexual dysfunction. Lastly, drugs that elevate prolactin contribute to sexual dysfunction since prolactin inhibits both desire and performance.
Research has focused on natural, botanical ingredients which have legendary history as natural aphrodisiacs, and Horny Goat Weed is among the top performers.
Horny Goat Weed
Horny Goat Weed lowers blood pressure by dilating capillaries and blood vessels while slowing the adrenal production that can hinder blood flow to the sex organs. Men achieve better erections due to this effect and it is thought that women benefit from the increased blood flow as well and perhaps from other testosterone-like alkaloids and sterols within the plant. Research has also shown that Horny Goat Weed significantly increases testosterone in mice.
