Testosterone, DHT & sexual function

Why "normal testosterone" doesn't settle it

The most common frustration in this space: a man starts TRT, his total testosterone reads squarely mid-range, and his libido or erections still aren't right. The reason is that sexual function is multi-hormone. Testosterone is necessary but not sufficient - and "testosterone" itself splits into a usable fraction (free T) and a downstream metabolite (DHT), while estradiol and prolactin pull in their own directions. A single total-T number can be perfectly normal while one of those other levers is off. Below, each hormone is tagged by how strong the evidence actually is, because the honest picture is uneven.

Free testosterone Strong evidence

This is the lever with the best data. Only ~1–4% of your testosterone is free and able to enter cells; the rest is bound, much of it locked to SHBG. And it's the free fraction that lines up with how you feel. In the European Male Ageing Study (3,369 men), free testosterone tracked sexual symptoms - low desire, erectile dysfunction, and fewer morning erections - better than total. Men with normal total but low free T carried a significantly higher symptom burden; men with low total but normal free T did not. EMAS's working threshold for symptomatic hypogonadism paired total T < 11 nmol/L (~317 ng/dL) with free T < 220 pmol/L (~6.4 ng/dL).

Practical takeaway: if your sex drive is low on a "normal" total, the first thing to check is your free testosterone - calculated from total T, SHBG, and albumin. → this is exactly the gap explained in free vs total testosterone, and you can run the numbers with the free testosterone calculator.

DHT - the potent androgen we keep overrating Mixed evidence

Dihydrotestosterone is testosterone's more potent cousin: the enzyme 5-alpha-reductase converts testosterone to DHT in tissues like the genitals and skin, and DHT binds the androgen receptor with higher avidity, so locally it's the stronger signal. Animal work backs a genuine role - in rats, DHT restored the nerve-stimulated erectile response after castration as effectively as testosterone, acting through the nitric-oxide pathway that drives erections. So it's reasonable to expect DHT matters for sexual function.

The human evidence is where it gets nuanced - and where most online claims overreach. Two findings have to sit side by side:

• Low DHT tracks symptoms. In a clinic cohort of biochemically eugonadal men (normal testosterone), higher serum DHT was associated with fewer Aging Males' Symptoms - a 0.1 nmol/L rise in DHT corresponded to a meaningfully lower odds of worse symptoms. But the same study found DHT did not independently predict erectile function once testosterone was accounted for, and the authors concluded DHT is worth measuring only after hypogonadism is ruled out - not as a first-line test.
• Giving DHT didn't help. The cleanest test of cause and effect - a 24-month randomized, placebo-controlled trial of transdermal DHT in healthy older men - found no improvement across 33 measures of sexual function and mood, and actually a small, reversible decrease in overall sexual desire (likely because exogenous DHT suppresses your own testosterone and estradiol production).

So DHT is real but not a magic dial you raise for better sex. Its most important sexual lesson is the downside of crashing it: suppressing DHT body-wide with 5-alpha-reductase inhibitors (finasteride, dutasteride) causes reduced libido or erectile dysfunction in a minority of men - under ~10% in the trial data, with a subset reporting persistent symptoms. If you're chasing libido, the DHT move isn't "add DHT" - it's don't nuke it. That's the same reason we steer away from finasteride for hair loss in men on androgens. → see minimizing hair loss without nuking your DHT.

The anecdotal flip side - read it with eyes open

Set against that flat trial result is a persistent stream of anecdotal, single-user reports - from forums and self-experimenters using injectable or transdermal DHT (or proviron, an oral DHT-derivative) - describing the opposite: firmer, more frequent erections, higher genital sensitivity, stronger drive, and occasionally a subjective sense of increased fullness or size while on it. These are real things people report, and they're worth naming rather than pretending they don't exist.

But weigh them honestly. They are n-of-1 accounts with no control group: no placebo, no blinding, no isolation of DHT from the other variables in play. Almost nobody runs DHT alone - it's typically stacked on TRT or a cycle, so any effect is hopelessly confounded with the testosterone, estradiol shifts, expectation, and the simple fact that someone optimizing hormones is usually also sleeping, training, and paying attention. There is no controlled head-to-head comparing injectable DHT against another androgen for erectile performance or size - so the gap between the glowing anecdotes and the null 24-month RCT is exactly the gap between "I felt it" and "it was shown." Treat the reports as hypotheses, not evidence, and remember that exogenous DHT still suppresses your own testosterone and estradiol - the mechanism behind the decrease in desire the controlled trial actually measured.

Estradiol and the T:E2 ratio - the hormone men wrongly fear Mixed evidence

Some testosterone aromatizes into estradiol, and a surprising amount of male libido depends on it. Estradiol is not a hormone to drive to zero: research suggests a baseline - around estradiol above ~10 pg/mL - helps maintain sexual desire even in low-testosterone men, and when testosterone is low, giving back estradiol can restore libido. The classic own-goal is over-using an aromatase inhibitor to "control estrogen," crashing estradiol, and watching libido and erections collapse.

Several studies go further and look at the testosterone-to-estradiol ratio: a low or imbalanced T:E2 correlates with reduced desire - in one cohort, roughly two-thirds of men with a low T:E ratio reported decreased libido - and some authors argue the ratio predicts erectile dysfunction and low desire better than either hormone alone. It's not unanimous; other studies find no clear link. The defensible position: keep estradiol in a healthy band, not as low as possible, and treat a badly skewed ratio as a flag worth discussing - not a number to chase. Use a sensitive (LC-MS) estradiol assay; standard assays are unreliable at male concentrations.

Prolactin - the brake on desire Strong evidence

Prolactin works against libido. The clinical and meta-analytic data show a stepwise negative effect of prolactin on male sexual desire, and it can contribute to erectile dysfunction too. It's an uncommon cause - elevated prolactin shows up in only about 2–3% of erectile-dysfunction cases - but it earns a place on the panel because it's frequently reversible: normalizing prolactin (treating the cause, sometimes with a dopamine-agonist medication) tends to restore desire, and partially restore erectile function. Notably, prolactin can blunt libido even when testosterone reads normal, so it's a classic explanation for "my T is fine but my drive is gone." Persistent low desire is a reason to check it.

Signs your problem is hormonal (and which hormone)

None of these are diagnostic on their own - they're patterns that point toward a specific test rather than away from it.

That last row matters: a large share of erectile dysfunction is vascular, neurological, psychological, or medication-driven, not hormonal. Hormones are one input. If your panel is genuinely clean, the answer is usually elsewhere - cardiovascular health, sleep, stress, SSRIs or other drugs - and that's a conversation for a clinician, not another lab draw.

What to actually test

If sexual symptoms persist on testosterone that "looks fine," a fuller fasting morning panel beats re-drawing total T: total + free testosterone (with SHBG and albumin so free can be calculated), sensitive estradiol, and prolactin, adding DHT (LC-MS) only once hypogonadism is excluded. Read it as a system - the goal is a usable free T, estradiol kept in a healthy band rather than minimized, DHT not suppressed, and prolactin not elevated. → the bloodwork guide covers the full panel and lab-day timing; free vs total T covers why the free number is the one to trust.