Is low testosterone the main cause of erectile dysfunction?

No. Most ED has vascular, neurological, or psychological roots. Hormonal causes are a minority — but they are over-represented among men under 40 with ED, and they are the subset where the cause is often reversible. A hormone panel is not a complete ED workup; it rules in or rules out the hormonal third.

Why include prolactin?

Hyperprolactinaemia is one of the few reversible, medication-treatable causes of low testosterone, low libido and ED. Prolactin elevations are silent until you measure them. Missing prolactin means treating the symptom (low T, ED) without addressing the cause (a possible pituitary adenoma or medication side effect).

What does estradiol have to do with ED?

Both extremes matter. Very low estradiol — often after aggressive aromatase-inhibitor use — is associated with low libido and erectile difficulties. Elevated estradiol, often paired with high body fat or exogenous testosterone, can cause similar symptoms via different mechanisms. Aiming for a 'low' E2 in men is a common mistake.

Will treating the hormones fix my ED?

If the cause is hormonal, often yes. If the cause is vascular or psychological — and many ED cases are — fixing hormones won't fix the symptom. The point of a panel is not to assume hormonal cause. The point is to rule it in or out so you don't waste time treating the wrong thing.

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Erectile dysfunctionHormonesTestosteroneDiagnostics

Erectile dysfunction and your hormones: what a panel actually shows

Erectile dysfunction is rarely just about testosterone. Here is which hormones a panel measures, what each one means for ED, and when the result points at something fixable.

FutureKit Medical & Science Team

In-house research, written against ESHRE and AUA clinical guidance

Published 2026-04-29

KEY TAKEAWAYS

What to remember before reading on.

1
Hormonal causes account for only a minority of ED cases — but the ones they do explain are often the most fixable.
2
Six markers cover the hormonal landscape: Total + Free Testosterone, FSH, LH, SHBG, Prolactin, Estradiol. Prolactin is the one most often missed and most worth catching.
3
Symptoms come from free testosterone and downstream tissue, not the headline number. Two men with identical total-T can feel completely different.
4
ED with an upstream hormonal cause usually responds to treating the cause — not to PDE5 inhibitors alone.

What a hormone panel can and can't tell you about ED

Erectile dysfunction has many possible causes. They tend to cluster into three categories:

Vascular — atherosclerosis, microvascular disease, venous leak, smoking-related endothelial damage.
Neurological / psychological — performance anxiety, depression, antidepressant side effects, pelvic-nerve injury, MS.
Hormonal — low testosterone, hyperprolactinaemia, thyroid disease, low or high estradiol, secondary hypogonadism from opioids or steroids.

A six-marker hormone panel addresses the third category. It will not detect a vascular cause and it will not unpick a psychological one. What it does well — and what most GP encounters miss — is rule the hormonal third in or out cleanly.

The hormonal subset is small but disproportionate. Among men under 40 with ED, hormonal causes are over-represented. Among men of any age with the combination of low libido + ED + fatigue, hormonal causes climb further. And the subset is over-represented in another way: it is the subset where the underlying cause is most often reversible.

What each marker tells you

The Hormone Panel 01 measures six markers. Read in this order, they answer different ED-relevant questions.

Total + Free Testosterone. The headline number plus the bioavailable fraction. Free testosterone is what acts on tissue. A normal-looking total testosterone with high SHBG can leave free T inadequate and produce libido and erectile symptoms despite a "normal" T result.

SHBG. Decides how much of total testosterone is bioavailable. Very high SHBG often masks an effectively low free T. Very low SHBG is associated with insulin resistance and metabolic syndrome — which carries its own ED risk via the vascular route.

LH. Localises the cause if testosterone is low. Low T with high LH is primary (testicular). Low T with low LH is secondary (pituitary or hypothalamic) — and the secondary causes include the most fixable ones.

FSH. Less direct on ED, more relevant for fertility. But a high FSH alongside low T tells you the testicular failure is not subtle.

Prolactin. The most underappreciated marker for ED. Hyperprolactinaemia — sometimes from a benign pituitary adenoma, often from antidepressants, opioids, or antipsychotics — directly suppresses GnRH and the entire male axis. The result is low libido + ED + low T. Treating the prolactin elevation often resolves the downstream symptoms. Missing it means treating the wrong end.

Estradiol. Both extremes matter. Very low E2 (often after AI overuse, or after rapid weight loss) reduces libido and causes erectile difficulties. Elevated E2 — often with high body fat — does the same via different mechanisms. The mid-range is where you want to be.

Three patterns worth knowing

If you see your panel result and want to know what to focus on, these three patterns are the highest-yield.

Pattern 1: Low T + low LH + elevated prolactin. Strong signal for hyperprolactinaemia-driven secondary hypogonadism. Look at medications first (SSRIs, opioids, methadone, antipsychotics — especially risperidone). If no medication explains it, an MRI of the pituitary may be warranted. Treatable; ED resolves alongside the underlying cause in most cases.

Pattern 2: Low free T + high SHBG + normal-looking total T. Classic "your numbers say you're fine but you don't feel fine." High SHBG can be driven by hyperthyroidism, ageing, or alcohol. Treating the SHBG driver — or accepting that the bioavailable T is the relevant figure — is the move.

Pattern 3: Low T + high LH + high FSH. Primary testicular failure. Causes include past chemotherapy, varicocele, undescended testes, post-orchitis, Klinefelter. Testosterone replacement may be appropriate; the cause itself is generally not reversible.

If your pattern doesn't match one of these — and most don't — the panel result still narrows the workup substantially. A clinician with the panel in hand can plan the next step in 5 minutes; a clinician without it has to start from scratch.

What the panel doesn't replace

Three things a hormone panel does not do:

A vascular workup. ED often has vascular causes. Panel doesn't help with those.
A medication review. Many ED cases are driven by SSRIs, beta-blockers, finasteride, opioids, antipsychotics. A medication review with your GP should run in parallel.
A specialist consultation. For men with persistent ED and a normal panel, a urologist or andrologist is the right next stop. Bring the panel; it lets them skip the part of the workup most often skipped.

Taking action

If you are reading this because ED has been ongoing or recent, the order of operations:

Run a six-marker panel. Two morning samples, fasted, before 10 am, two to four weeks apart. The Hormone Panel 01 covers all six markers from a finger-prick at home.
Review medications and lifestyle. SSRIs, finasteride, alcohol, stimulants, sleep, weight — all move ED probabilities.
If hormones are normal, see a clinician for the vascular and medication side. A panel rules out the hormonal third — that's worth a lot in narrowing the next conversation.

The panel is €89, finger-prick at home, ISO-certified German lab, physician-reviewed in 3–5 working days. If you'd rather start with a screen, the 30-second quick check tells you whether testing now is the right move.

Sources cited: AUA male sexual dysfunction guideline, ESHRE male infertility guideline — full entries on /science.

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