Michelson explains that buspirone could manipulate certain serotonin receptors in an attempt to ameliorate the overload of serotonin, and that amantadine was thought to increase dopamine activity. As such, either might theoretically help with SSRI-related sexual dysfunction. However, when the double-blind test was performed, it found that the success of treatment was roughly the same regardless of whether these pills were taken or a placebo was used. One significant difference was that those on admantadine had greater energy levels than they study-mates, which did not seem to directly affect sexual functioning. Michelson and his colleagues speculated that the reason for such marked improvement in all categories was the extensive journaling and attention paid to the sexual activity. Ashton and Rosen report on "Bupropion as an antidote for serotonin reuptake inhibitor-induced sexual dysfunction"

Unlike the Michelson study, Ashton and Rosen's work on using bupropion to ameliorate the sexual dysfunctions associated with SSRIs was neither double-blind nor placebo-controlled, and so there must remain some degree on uncertainty regarding its implications for medical practice. Regardless of whether or not it is certain in its conclusions, the fact that a two-thirds majority showed positive improvements in sexual functioning when taking doses of bupropion does tend to indicate that this drug may be of some aid in reducing the negative affects of SSRIs on sexual experience.

Bupropion is itself anaminoketone antidepressant, which could theoretically be used in the place of SSRIs to treat depression. However, for patients who had successfully stabilized with another antidepressant (and might not so successfully transfer to a new drug), bupropion has already b been in use to help treat SRI-induced dysfunctions. Despite its common use, until Ashton and Rosen's work was released, there had been no studies released on the success rate of bupropion or the actual necessary dosage, which required individual doctors and patients to experiment rather blindly with it.

Ashton and Rosen found that 66% of their subjects had favorable experienced with bupropion. About 19% responded to taking 75mg shortly before sex, 26% responded to taking 150 mg shortly before sex, but a full 57% responded to taking 75 mg on a regular basis, which tends to indicate a gradual change in body chemistry. Of patients treated with paroxetine, 80% experienced positive results. Flouxetine, sertaline and venlafaxine had between 50-65% success rates, while fluvoxamine only yielded 33% success rates. That there was a significant difference in which treatments responded to bupropion might indicate that something beyond placebo affect was at work. However, further studies are in order.

Ashton & Bennet's Letter to Editor

Ashton and Bennet, whose work was neither placebo-controlled or very large in scale, chose to merely write a letter to the medical community regarding their observations of the results of using Sildenafil to treat iatrogenic male erectile dysfunction. They acknowledged that many of the former antidote options did not appear to be entirely dependable. Options they mentioned included stimulants and gingko biloba, in addition to other drugs such as cyproheptadine, yohimbine, amantadine, buspirone, and bupropion; they also mentioned the use of "drug holidays" which gave the body a short break from its treatment. The idea of merely waiting to see if the problem resolves itself (which has actually been proposed in several articles) had a very low chance of success, and only 5.8-9.8% of iatrogenic SSRI-induced sexual dysfunctions have been...

Instead, Ashton and Bennet suggested the use of Sildenafil, which is a phosphodiesterase type 5 inhibitor.
Sildenafil was released to treat male erectile dysfunction of physical, psychological, or mixed origin. Their few case studies appear to be the first to test sildenafil in the treatment of iatrogenic erectile dysfunction. In the first case, in which the gentleman was currently taking fluoxetine, bupropion had not succeeded in curing his sexual dysfunctions. sildenafil, on the other hand, was reported as working 80% to (in his words) "110%" when taken an hour before sex. In the second case study, in which the patient was using a mix of sertraline and methylphenidate, the sexual dysfunction in question had withstood attempts to treat it wit venlafaxine, bupropion, and nefazodone. In this case too, sildenafil taken one hour before sex normalized his system responses. Ashton and Bennet admit they cannot draw conclusive evidence from these studies, but suggest that they are grounds for further research.

Conclusion and Findings

It appears that all authors agree that sexual dysfunction springing from the use of SSRIs and other antidepressants are a very serious matter, and one which has not been appropriately addressed. It is somewhat ironic that although every article mentions the egregious absence of placebo-controlled studies, only one of the original studies presented used a placebo. In that single study, evidence suggested that the antidotes being used were not more effective than merely closely monitoring patient behavior and providing psychological help (which a placebo itself does) This is the biggest weakness of all of these articles -- they all work from a place of ignorance. Each article is bracketed with an admission of ignorance which suggests that the author (and science itself) does not really understand what role serotonin plays in sexual chemistry and functioning, and what actual effects antidepressants like SSRIs have on the psychology and sexuality of the patient, other than their intended affects. That sexuality is not understood by science, that it is in affect a black box, truly validates the suggest given by authors such as Rivas-Vazquez that the doctor will do best to steer away from adding more chemical treatment to the regimen and attempt to treat the problems either by using a different drug, or attempting to scale dosage, apply close monitoring, and otherwise deal with the symptoms themselves.

Of the solutions suggested, none seem truly satisfactory. Switching to non-SSRI medications may provide a certain degree of relief, though such insufficient research exists that it is difficult to say how much safer and less adverse are these drugs. Taking a "drug holiday" may or may not solve the problem. Using other drugs to balance out SSRIs seems to work well for many people, but possibly only through a placebo affect that might be more safely achieved without the use of expensive and potentially adverse drugs.

In conclusion, these articles can tell us only a little more than common sense might: if the antidepressants have negative effects, one may need to try something else, and failing that one should monitor their effects as carefully as possible in hopes of understanding them. The main point on which all the articles agree is one which the reader can wholeheartedly embrace, however: More research is absolutely necessary on the occurrence and treatment of iatrogenic sexual disorders, and this research should be controlled in a scientific way, with use of double-blind guards, large and randomized trial pools, and with the use of placebos.