Efforts to find a biological treatment for diminished sexual desire or diminished arousal in women by looking for a Viagra® equivalent is misdirected. This misdirection is partly related to the misunderstanding, if not misrepresentation, of Viagra® (or Cialis® or Levitra®). Viagra® doesn't increase sexual desire in men; all it does is increase arterial blood flow into the penis while interfering with venous return. This process results in a mechanical erection but it has little or nothing to do with desire. Any stimulation to the penis of an individual on Viagra® will generate an erection, regardless of to whom the penis is attached or to whom it is inserted.
Although the clitoris has a penis-like physiology, its relatively small size makes Viagra® ineffective in women. With enough stimulation of the clitoris, though, most women, except those with an arousal disorder, will get the same engorged (i.e., "erectile") effect that Viagra® produces in a man's penis.
The new, highly touted drug -Flibanserin-might increase desire by an entirely different mechanism: it reduces brain serotonin, the affection-generating hormone, and simultaneously increases dopamine and norepinephrine, the novelty-seeking, passionate hormones. It is the same hormonal reshuffling that one experiences with the novelty of falling in love, which invariably leads to increased sexual desire in both sexes. Typically, though, passion and affection don't mix.
Biologically, the major way to increase actual sexual desire in men and women is through increasing testosterone levels, which can be done by administering exogenous testosterone (often by a skin patch.) But this can have a potential cost. In both genders testosterone may have deleterious effects (e.g. increased risk of certain cancers in men; masculinization in women) that may outweigh its potential benefits.
One good thing came out of Flibanserin research: There now is a trend to acknowledge that the source of sexual desire is the brain, not the sex organs.
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