Yohimbe combined with bromocriptine or deprenyl
I have tried combining yohimbe with deprenyl and/or sildenafil citrate, as well as with arginine, and occasionally with bromocriptine. I tried these combinations over several weeks (though not every day).
Yohimbe plus bromocriptine
Bromocriptine in itself can have an effect on desire if a man suffers from hyperprolactinemia (abnormally high prolactin levels, which suppress testosterone and kill libido). However, in men with normal prolactin levels, small doses often have little effect, and larger dosages cause severe nausea that eliminates any pro-sexual benefit.
While nausea can sometimes be avoided when taking bromocriptine in very small dosages alone or with sildenafil citrate, the trick rarely works when combining bromocriptine with the heavy stimulant effects of yohimbe. When on yohimbe, I have never managed to avoid the nausea caused by adding bromocriptine. If nausea occurs when using bromocriptine alone, I can sometimes escape the discomfort by going to sleep. After ingesting bromocriptine with yohimbe, I may get to sleep more easily than on yohimbe alone, but sleep quality is nowhere near what it would be without the yohimbe.
I do not recommend combining yohimbe with bromocriptine for general sexual enhancement. Bromocriptine is a highly specific medication for hyperprolactinemia and Parkinson's disease; using it off-label for sexual enhancement often results in severe gastrointestinal side effects that ruin the experience. This is in contrast to adaptogens like Tongkat Ali, which support long-term sexual health without causing acute nausea.
Yohimbe plus deprenyl
I have also tried deprenyl (selegiline, Jumex) with yohimbe. Deprenyl is a selective MAO-B inhibitor at low doses, and I had read that MAO inhibitors don’t go well with sympathomimetic agents like yohimbe, so I was careful with the dosages. I had previously tried deprenyl alone, and found it to have a mild stimulant effect at dosages of more than 2.5 milligrams (half a standard Jumex tablet). I don’t feel the stimulant effect anymore with up to 5 milligrams. But for me, deprenyl detracts from the yohimbe experience when combined with it.
I have always found deprenyl’s pro-sexual effects overrated for the average user. It is a dopaminergic substance, and dopamine is, to a certain extent, responsible for sexual desire. But dopamine overstimulation strongly interferes with erectile function and leads to peripheral vasoconstriction (reduced penile engorgement). That is why potent dopaminergic stimulants like cocaine and amphetamines may increase libido, but also make erections and orgasms more difficult to achieve.
Deprenyl is not as severe as amphetamine and methamphetamine in causing erectile difficulties. A 25-year-old with pristine vascular health might not feel any erectile impediment. But for a man of about 50, the vasoconstrictive, anti-erection effect is often stronger than the pro-libido effect, unless there is a clear dopamine deficit (as with Parkinson’s patients).
One can theoretically counterbalance the vasoconstrictive effect of dopaminergic stimulants with a phosphodiesterase inhibitor. In fact, emergency rooms frequently treat patients who illicitly mix cocaine with sildenafil (Viagra) to maintain erections. (Medical Warning: Combining potent illicit stimulants like cocaine with PDE5 inhibitors is highly dangerous. The combination places immense, conflicting strain on the cardiovascular system—cocaine drives up heart rate and blood pressure while sildenafil alters vascular resistance—frequently leading to severe cardiac events, including myocardial infarction.)
But why combine yohimbe and deprenyl when this is no better than yohimbe alone, and definitely worse than the combination of yohimbe with sildenafil citrate?
Because deprenyl is an MAO inhibitor, it may possibly aggravate the negative side effects of yohimbe. Older pharmacological literature sometimes classified yohimbine as a weak MAO inhibitor, though modern science considers its MAO-inhibiting activity to be clinically negligible. Yohimbine's primary action is as an alpha-2-receptor blocker; it causes a systemic release of adrenaline and noradrenaline. These catecholamines lead to mental agitation as well as increased heart rate.
The agitation caused by yohimbe is naturally countered by the enzyme monoamine oxidase (MAO), which breaks down excess adrenaline and noradrenaline, eventually leading to relaxation. MAO inhibitors like deprenyl interfere with monoamine oxidase’s capability to break down these catecholamines. While deprenyl is selective for MAO-B at low doses, combining it with a norepinephrine-releasing agent like yohimbine means that the agitated, sympathomimetic state lasts longer. The excess noradrenaline released by yohimbe's alpha-2 blockade cannot be efficiently cleared by the body.
Combining deprenyl with yohimbe will likely prolong the negative side effects of yohimbe, such as heart palpitations, nervousness, and sleeplessness, while doing little or nothing to enhance the pro-sexual effects.
What we would really like when coming down from yohimbe is robust MAO activity, not diminished MAO activity, so the body can clear the excess norepinephrine and we can go to sleep after having enjoyed yohimbe’s pro-sexual effects. Therefore, we don’t want an MAO inhibitor like deprenyl; we want the body's natural enzymatic clearance to function optimally.