By David Warmflash
The subject of libido always gets a lot of attention, and recent decades have produced a variety of libido-enhancing drugs. In addition to sildenafil, (Viagra) some 24 drugs are on the market for treating male sexual dysfunction.
For all the approved drugs, the mechanism of action involves dilation of blood vessels within the erectile tissue. Some of these same agents are given to women, based on the rationale that female genital tissues, such as the clitoris, are affected by blood circulation, just like male tissues.
But there’s a problem. For years, we’ve known that the brain is actually the most important sexual organ of all. Sexuality researchers emphasize that in women arousal in the brain tends to dominate the sexual experience. This perspective has led to the hypothesis that female sexual dysfunction more often has an etiology in the brain, rather than in genital blood flow. Medically, the condition is termed hypoactive sexual desire disorder (HSDD), which affects an estimated 10 percent of women, and generally the usual blood flow enhancing drugs are not very effective.
Consequently, a brain-active libido drug, flibanserin, is being promoted and investigated, and studies thus far are promising. Over the last years, popular media, including the Washington Post, have published opinion pieces expressing concerns about reported low efficacy and possible serious side effects, particularly hypotension and syncope. Regarding low efficacy, the Washington Post piece notes that “Only about 10–12 percent of women in trials benefitted from taking the drug”, based on the FDA briefing document (PDF) connected with the drug’s ongoing FDA review. However, studies testing flibanserin in which women were asked to report specific details on changes both in their sexual desire and quantity and quality of their orgasms have revealed an increase—almost a doubling—in the frequency of satisfying sexual events, along with the intensity of sexual desire. Reported adverse events include fatigue, somnolence, dizziness, and nausea. As far as hypotension and syncope, however, the FDA briefing document (PDF) notes these effects as being likely, only with excessive levels of flibanserin.
Flibanserin is hypothesized to increase sexual desire and pleasure by changing the balance of the neurotransmitters norepinephrine, dopamine, and serotonin (5-HT). HSDD is thought to result from 5-HT levels being too high and dopamine and norepinephrine levels being too low. Specifically flibanserin is a 5-HT(1A) receptor agonist/5-HT(2A) antagonist. When given to patients, serotonin levels decrease and there’s an added effect, in that dopamine and norepinephrine levels go up, and so the neurochemistry all makes sense.
Nevertheless, the drug still awaits FDA approval as an HSDD treatment. This is because the studies thus far have been fairly small, and so reviewers remain skeptical as to the efficacy, not because of hypotension and syncope. Additionally, flibanserin may not work well in women on medication for depression and obsessive compulsive disorder, or it may interfere with those agents, which increase 5-HT levels. So while the neurochemistry seems to make sense, the situation gets complicated when more drugs are added to the mix, as it often does regardless of the condition being treated.