Sexual Performance

Sexual performance is one of those topics where guys will sit on a problem for years before saying anything, and then when they finally bring it up, it’s at the very end of an appointment that was nominally about something else. Sleep. Mood. Blood pressure. “Oh, one more thing.” The one more thing is almost always the actual thing.

This is partly cultural and partly how the system is set up. Nobody’s primary care doctor has fifteen minutes to spend on erections. Urology feels like a big deal to see. Psychiatry doesn’t get raised because most guys don’t think of this as a head problem. So it sits. And while it sits, the original problem (which is often pretty fixable) gets layered with a performance anxiety problem that wasn’t there at the start.

Roughly half of men over forty have some degree of erectile dysfunction. Premature ejaculation affects something like one in three men at some point. Those numbers haven’t really moved in decades. You are not in a small or weird group.

Sorting vascular from psychogenic before you do anything else

Before reaching for a prescription pad, the question worth answering is whether the plumbing is the problem or whether the brain is the problem. The rough-and-dirty test most clinicians use is morning erections. If you’re waking up with erections, or getting them during the night, or getting them reliably with masturbation but not with a partner, the hardware works. The wiring works. What’s failing is the part of the system that involves another person being in the room, which is a psychological problem with a physical symptom, not a vascular problem.

If morning erections have disappeared, if firmness has gradually faded over years, if you can’t get one in any context, the differential shifts toward vascular. That usually means small-vessel disease, the same biology that drives heart attacks and strokes, just showing up earlier in a smaller artery. ED in a 50-year-old man is often the first warning shot from his cardiovascular system, which is why a real workup includes glucose, lipids, blood pressure, and sometimes testosterone. The dick is an early-warning system. Pay attention to it.

I had a guy a couple of years ago, late forties, came in convinced he was depressed because his sex life had cratered. Sleep was fine. Mood was fine when I pressed on it. His erections had quietly degraded over about eighteen months and he’d built a story around being broken, started avoiding his wife, ended up sleeping in the guest room “because of snoring.” Workup found uncontrolled blood pressure and prediabetes. Tadalafil 5mg daily, statin from his PCP, thirty minutes of walking a day. Six months later he wasn’t depressed. He’d never been depressed. He’d been scared.

PDE5 inhibitors and the daily-vs-PRN question

Sildenafil, tadalafil, vardenafil. Viagra, Cialis, Levitra. They all work the same way, which is to block an enzyme that breaks down the signal that tells blood vessels in the penis to relax. They don’t create desire. They don’t create erections out of nothing. They amplify what’s there when arousal happens. If you take one and just sit there, nothing dramatic occurs. This confuses people who expect them to work like a switch.

The practical differences are duration and dosing. Sildenafil lasts about four hours, kicks in at thirty to sixty minutes, and gets blunted by a heavy meal. Vardenafil is similar. Tadalafil lasts up to thirty-six hours (where the “weekend pill” name came from) and has a daily-dose option at 2.5 to 5mg.

The daily tadalafil case is underused. For guys who hate the planning, who don’t want to take a pill and watch the clock, who want sex to feel spontaneous again, low-dose daily tadalafil is often the better answer than PRN sildenafil. It also helps urinary symptoms in older men. PRN makes more sense for younger guys with infrequent activity who don’t want a daily med. Both are reasonable.

The pill doesn’t create desire. It amplifies what’s there. If desire isn’t there, no PDE5 inhibitor in the world is going to fix that.

Contraindications worth knowing: nitrates plus a PDE5 inhibitor can drop blood pressure dangerously. Don’t combine them. Severe cardiovascular disease where exercise itself is risky is a relative contraindication, because sex is exercise. Outside of that, these drugs have one of the safer track records in medicine.

Premature ejaculation and the underused SSRI angle

Premature ejaculation is the other half of this conversation and it gets way less airtime, partly because it’s even more embarrassing to bring up and partly because there’s no advertised pill for it in the US the way there is for ED.

Dapoxetine, a short-acting SSRI made specifically for PE, is approved in most of Europe and Asia but not in the US. So what American clinicians actually do is use off-label SSRIs. Sertraline 50 to 100mg daily, or paroxetine 20mg daily, both delay ejaculation as a side effect that happens to be useful here. Some guys do PRN dosing, taking paroxetine 20mg about four hours before sex, which works for some and not for others. The daily approach is more reliable.

Topical lidocaine sprays applied ten minutes before are a reasonable adjunct, sometimes enough on their own. Behavioral approaches (the stop-start technique, the squeeze technique) work for some couples and are worth trying alongside medication, not instead of it.

The first conversation worth having is about what’s actually happening. A lot of guys who think they have PE are within the normal range and have absorbed an expectation from pornography that has nothing to do with real human sexual response. The clinical definition involves ejaculation within about a minute of penetration, consistently, with distress. If you’re going ten minutes and feeling like you should be going thirty, that’s a different conversation.

When SSRIs cause the problem instead of solving it

SSRIs and SNRIs cause sexual side effects in something like 50 to 70 percent of users. Delayed orgasm, reduced libido, sometimes ED, sometimes anorgasmia. This is the single most common reason people quit antidepressants, and most of the time their prescriber doesn’t ask about it, so the patient just stops taking the medication and the depression comes back.

The rescue strategies, roughly in order of how aggressive they are: drop the dose if the depression is well-controlled (sometimes 25mg of sertraline is enough where 100mg was overkill); switch to bupropion, which is the antidepressant that does not cause sexual side effects and sometimes mildly enhances function; add bupropion 150 to 300mg on top of the SSRI if switching isn’t an option; add PRN sildenafil specifically for the SSRI-induced ED, which has reasonable data behind it. None of these are perfect. All of them are better than silently quitting your medication.

When to involve urology versus psychiatry

Urology gets involved when the workup points clearly vascular and PDE5 inhibitors aren’t enough, when there’s a structural issue like Peyronie’s, when injectables or vacuum devices or implants enter the conversation, when testosterone is genuinely low and replacement is being considered. Urologists handle the plumbing-and-hardware end.

Psychiatry comes in when performance anxiety has built on top of what was originally a physical problem, when SSRIs caused the issue, when depression or anxiety is the real driver, when the issue started after a specific event. Sometimes it’s both, and the right answer is two clinicians who are talking to each other.

What I’d push back on is the assumption that this is a problem you have to live with quietly because mentioning it is embarrassing. The number of guys I’ve watched fix this in a few months after sitting on it for years is not small. The hard part is the first sentence. After that, it’s just medicine.