In Reply We agree with Goldstein et al that it is a clinician鈥檚 task to diligently and routinely help patients to evaluate benefits, risks, and appropriateness of therapeutic options. When available, meta-analyses, not clinical opinion, should be the basis of such a risk and benefit analysis.

Being clinicians as well as scientists, we know that reduced or absent sexual desire can be extremely distressing. Contrary to what Goldstein et al suggest however, hypoactive sexual desire disorder (HSDD) is far from undisputed; HSDD is based on the conceptualization of sexual desire as a spontaneous internal drive. Toates^1(p102) summarized the evidence for this concept as, 鈥淚f an intrinsic drive arising in the body tissue exists, no one has been able so far to identify its biological basis.鈥� Current Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition² nomenclature has abandoned HSDD and instead regards sexual arousal and desire as emerging from sexually rewarding stimuli in an appropriate context.^3,4 Also, evidence for flibanserin鈥檚 mechanism of action is lacking. Flibanserin is presented as a drug that restores the balance between excitatory and inhibitory activity of the brain to a healthy level by enhancing levels of dopamine and norepinephrine and by reducing serotonin levels.⁵ Yet, there is no diagnostic test to establish the presence of such an imbalance, nor is there scientific evidence that women鈥檚 problems with sexual desire are caused by such an imbalance, nor that flibanserin restores this imbalance to a healthy level.