Various clinically used or experimental drugs enhance sexual interest or potency as a side effect in humans.
Levodopa (L-dopa) is a natural intermediate in the biosynthesis of catecholamines in the brain and peripheral adrenergic nerve terminals. In the biologic sequence of events it is converted to dopamine, which in turn serves as a substrate of the neurotransmitter norepinephrine. Levodopa is used successfully in the treatment of Parkinson’s syndrome, a disease characterized by dopamine deficiency. When levodopa is administered to an individual with this syndrome, the symptoms of Parkinson’s disease are ameliorated, presumably because the drug is converted to dopamine and thereby counteracts the deficiency. Individuals treated with levodopa, especially older men, have been observed to experience a sexual rejuvenation. This effect has led to the belief that levodopa stimulates sexual powers. Consequently, studies with younger men complaining of decreased erectile ability have shown that levodopa increases libido and the incidence of penile erections. Overall, however, these effects are short lived and do not reflect continued satisfactory sexual function and potency. Thus, levodopa is not a true aphrodisiac. The increased sexual activity experienced by parkinsonian patients treated with levodopa may reflect improved well-being and partial recovery of normal sexual functions that were impaired by Parkinson’s disease.
Amyl nitrite, a drug used in the past to treat angina pectoris, is alleged to enhance sexual activity in humans. As a vasodilator and smooth muscle stimulant, amyl nitrite has been reported to intensify the orgasmic experience for men if inhaled at the moment of orgasm. This effect is probably the result of relaxation of smooth muscles and consequent vasodilation of the genitourinary tract. No effects of amyl nitrite on libido have been reported, but a loss of erection or delayed ejaculation may result. Women generally experience negative effects on orgasm when taking this drug.
Much has been said about the positive effects of vitamin E (α-tocopherol) on sexual performance and ability in humans. Unfortunately, there is little scientific rationale to substantiate such claims. The primary reasons for attributing a positive role in sexual performance to vitamin E come from experiments on vitamin E deficiency in laboratory animals. In such experiments the principal manifestation of this deficiency is infertility, although the reasons for this condition differ in males and females. In female rats there is no loss in ability to produce apparently healthy ova, nor is there any defect in the placenta or uterus. However, fetal death occurs shortly after the first week of embryonic life, and fetuses are reabsorbed. This situation can be prevented if vitamin E is administered any time up to day 5 or 6 of embryonic life. In the male rat the earliest observable effect of vitamin E deficiency is immobility of spermatozoa, with subsequent degeneration of the germinal epithelium. Secondary sex organs are not altered and sexual vigor is not diminished, but vigor may decrease if the deficiency continues.
Because of experimental results such as these, vitamin E has been conjectured to restore potency or to preserve fertility, sexual interest, and endurance in humans. No evidence supports these contentions, but because sexual performance is often influenced by mental attitude, a person who believes vitamin E may improve sexual prowess may actually find improvement. The only established therapeutic use for vitamin E is for the prevention or treatment of vitamin E deficiency, a condition that is rare in humans.
Sildenafil increases the release of nitric oxide and increases the levels of cyclic guanosine mono-phosphate (cGMP), a smooth muscle relaxant. Sildenafil enhances the effects of nitric oxide by inhibiting phosphodiesterase 5, an enzyme found primarily in the penis that degrades cGMP. As a result, increased levels of cGMP in the corpus cavernosum enhance smooth muscle relaxation, the inflow of blood, and erection. Sildenafil has no effect in the absence of sexual stimulation.
This is an exciting new era in the treatment of erectile dysfunction. Since the development of such a highly effective oral preparation as sildenafil, much more research activity will be generated to produce competing therapies. Locally applied, rapidly absorbed preparations will almost certainly have a role to play. Combination therapy has to date not been extensively studied. The potential of utilizing centrally acting drugs or sildenafil in combination with locally applied preparations in the more clinically challenging patient is an exciting therapeutic opportunity. Much as been achieved in the past 15 years in the field of andrological research and much will be achieved in the very near future for the benefit of patients.