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Erectile Dysfunction Tests: What Needs to Be Checked and Why It Matters
Erectile Dysfunction Tests: What Needs to Be Checked and Why It Matters
What tests are needed when erectile dysfunction is first assessed — and why starting treatment without investigation is where problems begin. Mr Ollandini, Consultant Urological Surgeon and Andrologist, London.
The most expensive mistake in erectile dysfunction treatment is not choosing the wrong medication. It is starting treatment before you know what you are treating.
Men who cycle through PDE5 inhibitors without response are often not treatment failures. They are often assessment failures. The first prescription often came without any meaningful investigation. There may have been a hormonal issue, a metabolic condition, or a nutritional deficiency quietly running in the background. The medication was blamed. Trust in treatment evaporated.
A thorough assessment does two things. It identifies causes that are directly treatable — sometimes reversibly so. And it ensures that when treatment begins, it begins in the best possible position to work.
This page maps the full diagnostic landscape: from the clinical interview through the blood panel most workups include, the tests many workups omit, the specialist investigations reserved for specific situations, and a brief account of what the field tried in the past and why it moved on.
What tests are done for erectile dysfunction?
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Author —Published —Last update 18 March 2026Next review 18 March 2027Version —
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What I am actually trying to establish
The clinical interview: why talking is the first test
The history I take when you come to see me is not a formality before the real tests begin. It is the real test — the one that tells me most of what I need to know, and that determines which investigations are actually indicated.
I am listening for pattern. When did this start? Did it come on gradually over months, or did it appear suddenly? Does it happen in all situations or only in some? Does it work when you are alone? How are things in the relationship? Are there other symptoms — fatigue, changes in libido, mood, sleep, urinary function? What medications are you taking?
These questions are not casual conversation. Each answer narrows or opens the differential. Gradual onset suggests vascular or hormonal disease developing over time. Sudden onset, particularly if situational, points more towards psychological drivers. Erections that work reliably when alone but fail with a partner suggest a very different picture from erections that fail in all contexts.
I also ask about lifestyle in detail: diet, exercise, alcohol, smoking, recreational drugs, stress. These are modifiable contributors that can shift the clinical picture significantly, and optimising them before starting pharmacological treatment often improves results.
The sexual and psychosocial history requires a particular kind of directness. Most patients have never been asked these questions by a doctor. I ask them clearly, without euphemism, and without implied judgement about who you have sex with or how.
Knowledge check
What is the most important first step in assessing erectile dysfunction?
The two errors I see most often
Two opposite errors damage patients in this field — and both stem from skipping a proper assessment.
The first: a referral letter arrives stating that the patient "denies psychological factors." On direct questioning, it becomes clear this conclusion came from a GP asking: "Do you think it's physical or psychological?" — a question the patient understood as is this real or are you making it up? The answer was defensive, not clinical. In the consulting room, I hear a history of a previous abusive relationship, and erectile difficulties that began precisely when a new relationship started to feel serious. The patient is not consciously aware of the connection. The aetiology is psychogenic — and sending him for vascular investigations first would have been a waste of time and a delay in getting him to the right support.
The second: a referral for psychosexual assessment arrives for a patient who is a poorly controlled diabetic, hypertensive, obese, and a smoker. He is convinced the cause is psychological. It is not. Referring him to a psychosexual therapist before addressing a dense organic substrate would produce poor results and erode his confidence in treatment.
Both errors produce the same outcome: the patient's trust in the therapeutic process is spent before treatment has properly begun.
The lesson is not that one type of aetiology matters more. It is that a systematic approach is mandatory in every case — including in young men who appear to have an obvious psychological cause, and including in older men with extensive comorbidities who are certain it is all in their heads. Erection problems in a young man can reveal early metabolic disease. Missing that is not a minor oversight — it can be clinically significant.
In most new presentations of erectile dysfunction, a baseline assessment including blood tests is appropriate. Starting treatment without any investigation is common — and often where problems begin.
The tests below are common baseline investigations in a thorough first assessment, particularly where an organic or mixed cause is suspected.
The test that everyone orders — and the one most frequently done incorrectly.
Testosterone is secreted in a diurnal pattern, with peak levels in the morning. A valid measurement requires a fasting early-morning sample, ideally between 07:00 and 10:00. Results taken at random times of day are unreliable and can produce falsely low readings in men whose levels are entirely normal.
A single low result is not sufficient for a diagnosis of testosterone deficiency. Current EAU guidelines require confirmation on at least two separate occasions, under the same conditions, before treatment is initiated. Testosterone levels are affected by acute illness, poor sleep, significant psychological stress, and alcohol consumption in the preceding 24–48 hours. Many men who are told they have low testosterone based on a single afternoon sample do not.
Total testosterone is the standard first measurement. Free testosterone (calculated or measured) is additionally useful in men with altered sex hormone-binding globulin (SHBG) — including those with obesity, diabetes, thyroid disease, or liver disease — because SHBG changes can produce normal total testosterone with functionally low free testosterone, or vice versa.
In clinical practice, symptomatic men with levels below 12 nmol/L on a properly conducted test warrant further assessment. Men with levels below 8 nmol/L are likely to benefit from replacement if symptoms are consistent.
Testosterone deficiency rarely causes erectile dysfunction in isolation. Its primary role is in libido and the health of erectile tissue. If testosterone is low in a man with ED, correcting it is part of the picture — but it is rarely the whole answer.
Knowledge check
Which testosterone sample is clinically valid for assessing erectile dysfunction?
If testosterone is low or borderline: LH and FSH
Once a low or borderline testosterone is confirmed, adding LH and FSH maps the axis and determines the type of hypogonadism — which has direct implications for management.
They distinguish primary from secondary (hypogonadotrophic) hypogonadism. Primary hypogonadism — failure at the testicular level — produces low testosterone with elevated LH and FSH, as the pituitary attempts to compensate. Secondary hypogonadism — failure at the hypothalamic or pituitary level — produces low testosterone with low or inappropriately normal gonadotrophins.
Secondary hypogonadism raises the possibility of a pituitary lesion and requires prolactin measurement and, in some cases, MRI. It also has fertility implications: men who want to father children cannot simply be started on testosterone replacement without a full fertility discussion, since exogenous testosterone suppresses the gonadotrophic axis and can cause azoospermia.
Diabetes is one of the most common organic causes of erectile dysfunction, operating through both vascular and neurological mechanisms. Chronic hyperglycaemia causes endothelial dysfunction (reducing nitric oxide bioavailability), accelerates atherosclerosis, and damages the small nerve fibres responsible for the erectile reflex.
In men with established diabetes, severity and duration correlate with erectile dysfunction severity. But the more clinically important group is men with undiagnosed diabetes or impaired glucose tolerance (pre-diabetes), who present with erectile dysfunction as the first prominent symptom. A workup that omits glycaemic assessment misses these cases entirely.
HbA1c reflects average glucose over the preceding 8–12 weeks and is the preferred screening test. A result in the pre-diabetic range (HbA1c 42–47 mmol/mol, or fasting glucose 6.1–6.9 mmol/L) is clinically significant — not a reason for reassurance, but a prompt for lifestyle intervention and metabolic monitoring that can directly influence erectile function.
Dyslipidaemia — particularly elevated LDL and low HDL — contributes to erectile dysfunction through endothelial mechanisms shared with diabetes and hypertension. Atherosclerotic plaques reduce arterial inflow; endothelial dysfunction impairs nitric oxide release.
Total cholesterol alone is insufficient. The full profile — LDL, HDL, triglycerides, total:HDL ratio — is needed. The pattern matters: normal total cholesterol with low HDL and elevated triglycerides (the metabolic syndrome lipid pattern) carries meaningfully elevated cardiovascular risk that a single figure obscures.
Erectile dysfunction typically precedes cardiac symptoms by two to five years. A lipid profile at first presentation is part of a cardiovascular risk assessment that the erectile complaint has opened the door to.
A full blood count, urea and electrolytes, and liver function tests provide general health screening and are part of a thorough first assessment, particularly where an organic or mixed cause is suspected.
Anaemia can contribute to fatigue and reduced sexual function. Renal impairment affects drug metabolism — relevant when prescribing PDE5 inhibitors. Liver disease alters SHBG and drug handling, and some hepatic conditions are associated with secondary hypogonadism. Elevated liver enzymes may point towards alcohol-related disease, which is independently associated with erectile dysfunction and warrants a more detailed alcohol history.
Hypothyroidism is a reversible cause of erectile dysfunction that is consistently under-recognised in andrological assessment. The mechanisms are multiple: hypothyroidism reduces testosterone by suppressing SHBG and the HPG axis, causes peripheral neuropathy, and contributes to fatigue and depression that independently impair sexual function.
A TSH is a single, inexpensive blood test. Elevated TSH with normal fT4 indicates subclinical hypothyroidism. Elevated TSH with low fT4 indicates overt primary hypothyroidism. Both TSH and fT4 low indicates secondary hypothyroidism, warranting pituitary investigation.
Hyperthyroidism can also affect erectile function, typically alongside high libido, weight loss, heat intolerance, and palpitations.
I include TSH in the first panel for all new ED presentations. It costs almost nothing, it is rapidly reversible when abnormal, and I have seen it change management often enough that excluding it from the first-line screen makes no sense to me. This is my practice, not universal standard — many GP-led assessments would reserve it for symptomatic cases — but at a specialist level I consider it baseline.
PSA is not part of the core erectile dysfunction workup, but is often worth considering in men over 50, in men with lower urinary tract symptoms, or where a future testosterone discussion makes a baseline helpful.
The pragmatic reason: if testosterone deficiency is identified and treatment is being considered, a baseline PSA is required before starting. Measuring it at the first assessment avoids a separate step later. It also opens the door to a prostate discussion and voiding history where relevant.
I do not routinely include it in younger men with no urinary symptoms and a clearly psychogenic or lifestyle aetiology. In those cases, it would be doing the test because it is possible, not because it will change management.
The extended panel: when I go further
The following tests are not part of most standard erectile dysfunction panels. I do not request them in every patient. But in selected cases, they explain what the standard workup does not.
If you have been through a full assessment and nothing has been found, or if the clinical pattern does not fit the standard picture, these are the next layer to consider.
Hyperprolactinaemia suppresses the hypothalamic-pituitary-gonadal axis, reducing GnRH pulsatility and consequently LH, FSH, and testosterone. The clinical presentation is typically low libido and erectile dysfunction, sometimes with gynaecomastia. The cause may be a prolactin-secreting pituitary adenoma (prolactinoma), which requires MRI and specialist endocrine input, or drug-induced hyperprolactinaemia — a common and frequently missed cause.
Medications that elevate prolactin include antipsychotics (both typical and atypical, particularly risperidone and amisulpride), metoclopramide, domperidone, some antidepressants, and antihypertensives including methyldopa and verapamil. In any man presenting with erectile dysfunction and low libido who is on these medications, prolactin should be measured.
A mildly elevated result in an anxious patient in a clinic setting is not diagnostic — venepuncture itself can raise prolactin transiently. A sustained elevation on a repeat fasted, calm-conditions sample is significant.
I measure prolactin routinely in any man with unexplained secondary hypogonadism, and in men on medications known to raise it.
Vitamin D deficiency is extremely common in the United Kingdom. Population surveys consistently find that a substantial proportion of adults have levels below the threshold for adequacy, particularly in winter months and among men who spend limited time outdoors. It is also the marker most consistently absent from erectile dysfunction workups.
The mechanism is not fully established, but there is a plausible biological pathway. Vitamin D receptors (VDRs) are expressed in vascular endothelium and smooth muscle, including in the corpora cavernosa. Deficiency is associated with reduced nitric oxide synthase activity, endothelial dysfunction, and arterial stiffness — the same vascular processes that underlie vasculogenic erectile dysfunction. Cross-sectional studies have demonstrated an association between low vitamin D and erectile dysfunction, with effect sizes that survive adjustment for other cardiovascular risk factors.
More practically: severe deficiency can produce fatigue, mood disturbance, and musculoskeletal aches that are easily misattributed to depression or a psychological aetiology for sexual dysfunction.
Optimising vitamin D does not reliably resolve erectile dysfunction in isolation. But in men with a clear vascular or unexplained mixed pattern — particularly those where standard tests are unremarkable — it is one of the additional tests I consider early.
The Man Whose Vitamin D Was 14
He was 38, stable relationship of four years. Erections were fine when alone but increasingly unreliable during sex — not absent, but fading at the wrong moment.
His GP had been thorough in a particular way. He had been told the problem was anxiety and referred for psychosexual counselling. No blood tests had been run.
When he came to see me, the pattern was partly situational — but not entirely. He was more tired than he should be, had stopped going to the gym without a clear reason, and concentration at work had slipped. None of this had been connected to the erectile complaint.
I ran the full panel. Testosterone low-normal. HbA1c fine. Lipids unremarkable. TSH normal. 25-hydroxyvitamin D: 14 nmol/L. Severe deficiency.
I started high-dose supplementation and asked him to return in twelve weeks before making any decision about psychological referral or pharmacological treatment.
At twelve weeks, he needed neither. Erectile function had improved substantially. The fatigue had cleared. He felt like himself again.
Had he gone to psychosexual therapy first with a vitamin D of 14, progress would likely have been modest and unnecessarily confusing. Trust in the therapeutic process might have been spent while the underlying problem remained uncorrected.
In men with a clear vascular pattern but a normal standard panel — normal lipids, normal glucose, no established cardiovascular disease — I sometimes look further at markers of endothelial function. Homocysteine is one of them.
Elevated plasma homocysteine is an independent cardiovascular risk factor associated with endothelial dysfunction, oxidative stress, and impaired nitric oxide bioavailability through mechanisms distinct from those captured by the lipid profile. Its relevance to erectile dysfunction follows from these vascular effects. Several studies have demonstrated elevated homocysteine in men with vasculogenic erectile dysfunction compared with matched controls, with the association persisting after adjustment for other risk factors.
The additional clinical value is treatability. Elevated homocysteine caused by folate, B6, or B12 deficiency responds to supplementation. When homocysteine is elevated, B12 and folate should be checked alongside it.
This is not a first-line test. It is a second-pass investigation in men where the vascular picture deserves closer scrutiny and standard tests have not provided an answer.
Vitamin B12 deficiency causes peripheral and autonomic neuropathy through impaired myelin synthesis. In the context of erectile dysfunction, this matters because nerve function — both somatic and autonomic — is required for the erectile reflex. Subclinical B12 deficiency can impair both without producing overt neurological symptoms that would prompt investigation.
At-risk groups are identifiable: men on long-term metformin (which impairs ileal B12 absorption through a well-established mechanism, often producing progressive deficiency over years of use), men on proton pump inhibitors, those with pernicious anaemia or autoimmune gastritis, strict vegans, and men over 65 in whom gastric atrophy reduces intrinsic factor production.
In any of these groups, B12 measurement is part of a thorough assessment. It is also directly relevant when homocysteine is elevated, since B12 is a cofactor in the remethylation of homocysteine to methionine, and deficiency is one of the most common causes of raised homocysteine.
B12 deficiency is correctable. In a neurogenic or mixed-aetiology presentation where the standard panel is unremarkable, missing it is a missed opportunity.
Assessing penile blood flow
Not every man with erectile dysfunction needs a penile Doppler scan. When the history is clear — a young man with situational difficulties, obvious performance anxiety, and no vascular risk factors — ordering a Doppler adds cost, anxiety, and waiting time without changing management.
I order one when the pattern suggests a vascular contribution that needs characterising: gradual onset, difficulties in all situations, known cardiovascular risk factors, failure of first-line treatment, or when Peyronie's disease is present alongside the erectile complaint and vascular assessment will change the surgical planning conversation.
In which of these men is a penile Doppler scan most clearly indicated?
Nocturnal penile tumescence (NPT) testing measures erections during sleep. Healthy men experience periodic erections during REM sleep driven by central mechanisms largely independent of psychological state. A man with psychogenic erectile dysfunction typically has preserved nocturnal erections; a man with significant organic disease does not.
The RigiScan device is worn overnight on two to three consecutive nights, recording number, duration, rigidity, and tumescence of nocturnal events at the base and tip of the penis. A normal RigiScan in a man with erectile dysfunction in a partnered context is a strong pointer towards psychogenic aetiology. An abnormal result supports organic disease.
Limitations are real: the test is prone to false negatives in men with disrupted sleep architecture — shift workers, untreated obstructive sleep apnoea, or men on sedative medications. The anxiety of wearing a device can suppress nocturnal erections in some men. Results require clinical context rather than mechanical threshold application.
I use it selectively: when the organic versus psychogenic distinction is genuinely unresolved despite full history and investigation, and when the result would materially change management. It is not a routine first-line test.
Specialist tests: the full landscape
Most men with erectile dysfunction will never need any of the investigations in this section. They exist, they have specific indications, and they are performed in a small number of carefully selected cases. Understanding when they are — and equally when they are not — appropriate is part of what a comprehensive assessment involves.
Dynamic infusion cavernosometry and cavernosography (DICC) directly assesses venous outflow from the corpora cavernosa. Under pharmacological erection, saline is infused at a measured rate; the flow required to maintain intracavernosal pressure at a defined threshold quantifies the degree of venous leak. Cavernosography adds contrast imaging to visualise leaking venous channels.
It is more specific than Doppler, which infers venous competence from flow measurements rather than measuring outflow directly.
Current EAU guidelines reserve DICC for a very narrow indication: young men with suspected congenital or traumatic venous leak who are being evaluated specifically for surgical or interventional management. Outside this context — which represents a small minority — DICC is not recommended. Penile Doppler is adequate for clinical decision-making in the vast majority of cases.
DICC is an invasive procedure with risks including priapism, infection, and haematoma. Its routine use has not been supported by guidelines for over a decade. If it has been suggested as a first-line investigation, that warrants scrutiny.
Neurophysiological testing of the pudendal pathway assesses the somatic nerve supply to the genitalia. Somatosensory evoked potentials (SEPs) record cortical responses to electrical stimulation of the dorsal penile nerve; bulbocavernous reflex (BCR) latency measures the reflex arc from glans to the bulbocavernosus muscle via the sacral cord.
These tests are indicated in men with suspected neurogenic erectile dysfunction in the context of known or suspected spinal cord pathology, multiple sclerosis, diabetic neuropathy with peripheral nerve involvement, or after pelvic or perineal trauma. They are not indicated in idiopathic or vasculogenic erectile dysfunction without a neurological history.
Penile biothesiometry — measuring vibration perception threshold at the glans and shaft — is a simpler office test for peripheral sensory neuropathy, useful in diabetic men where neuropathy is suspected as a contributing mechanism.
Selective arteriography provides anatomical mapping of the penile arterial supply. It is used almost exclusively in young men (typically under 45) with erectile dysfunction following pelvic or perineal trauma — a cycling accident, a road collision, a straddle injury — where focal arterial damage is suspected and revascularisation surgery is being considered.
In this narrow group, arteriography identifies the lesion and guides surgical planning. Outside it, there is no indication for arteriography in erectile dysfunction assessment. It is invasive, requires arterial access, contrast administration, and radiation exposure, and its outcomes in non-traumatic vascular disease do not justify its use.
Biopsy of the corpus cavernosum — typically to assess smooth muscle to connective tissue ratio — is a research tool rather than a routine clinical investigation. Smooth muscle content of the corpora predicts pharmacological treatment response: men with severe fibrosis and low smooth muscle content are unlikely to respond to PDE5 inhibitors or injection therapy and are more directly candidates for prosthetic surgery.
In clinical practice, this assessment is rarely done. The information it provides can generally be inferred from clinical pattern, response to pharmacological testing, and Doppler findings. Its principal use has been in research settings evaluating penile rehabilitation after radical prostatectomy, and in the assessment of severe Peyronie's disease with cavernosal fibrosis.
Two examples from the history of erectile dysfunction diagnostics are worth knowing — not as curiosities, but as a reminder that rigour is not optional, and that the existence of a procedure is not evidence of its effectiveness.
A row of postage stamps was wrapped around the penis before sleep. If the perforations were torn in the morning, a nocturnal erection had occurred — suggesting that the erectile mechanism was intact and the cause was likely psychological. If intact, organic disease was suspected.
Published in peer-reviewed journals, used in urology clinics throughout the 1980s and early 1990s. Economical, non-invasive, and not entirely without logic. Superseded by the RigiScan, which quantified what the stamp test could only indicate. The snap gauge — a ring of plastic films designed to break at calibrated pressures — was a slightly more sophisticated variant with the same basic premise and the same eventual fate.
Surgical ligation of penile outflow veins was performed for two decades on the basis that, if blood was escaping too quickly, the exit routes could be tied off. It was a logical idea. It was not an effective one.
Long-term results were consistently poor: initial responses, where they occurred, were not maintained. Collateral venous channels opened. Erectile function deteriorated further in many patients. Both the EAU and the AUA now explicitly recommend against venous ligation.
This was not ancient medicine — it was performed within living clinical memory, by competent surgeons, on the basis of plausible pathophysiology. The fact that a procedure has been done for twenty years in reputable centres is not evidence that it works. It is evidence that it was believed to work. Those are not the same thing.
In 1889, the French neurologist Charles Édouard Brown-Séquard reported to the Société de Biologie in Paris that he had been injecting himself subcutaneously with extracts prepared from the testicles of dogs and guinea pigs. He described dramatic improvements in physical strength, mental clarity, and sexual function. The paper was published in The Lancet.
The effects were almost certainly placebo. His preparation contained negligible bioavailable testosterone by any modern measure. But the underlying observation — that something in testicular tissue had a systemic effect — was not entirely wrong. The experiment opened a line of enquiry that led to the isolation of testosterone as a chemical compound in 1929, its synthesis from cholesterol by Adolf Butenandt in 1935, and the Nobel Prize in Chemistry in 1939.
Brown-Séquard was 72 when he published his self-experiment. He died five years later. He had inadvertently founded andrology.
What you may have been told — and what the evidence shows
Myth vs Fact
Myth
Myth: I still get morning erections, so my ED must be purely psychological.
Fact
Fact: Morning erections are a useful data point — they suggest your neurovascular pathways are at least partially intact. But they do not exclude mixed aetiology, organic contributors, or the need for a proper blood panel. They are one piece of information, not a complete picture.
Myth
Myth: My testosterone came back normal, so hormones are not the problem.
Fact
Fact: Testosterone is one hormone. Prolactin, TSH, and vitamin D are not captured by a testosterone result, and all three can contribute meaningfully to erectile dysfunction through distinct mechanisms. A normal testosterone rules out androgen deficiency — it does not rule out hypothyroidism, hyperprolactinaemia, or vitamin D deficiency.
Myth
Myth: ED tests mean scans, injections, and invasive procedures.
Fact
Fact: For most men, a proper ED assessment is a clinical history and a set of blood tests. A Doppler scan or RigiScan is indicated only in specific circumstances. Invasive testing such as cavernosometry is reserved for a very small group with highly specific indications. The assessment is considerably more accessible than most patients expect.
Myth
Myth: If my GP did not check for it, it probably is not relevant.
Fact
Fact: Sexual health is one of the most under-explored areas in primary care — not because GPs do not care, but because the consultation culture rarely creates the space, and the standard GP blood panel for ED is often minimal. The tests most commonly omitted — TSH, vitamin D, prolactin, B12 — are not exotic. They are simply not in the default order set.
If you want a simple starting point
The full landscape above is here for completeness. For most men, the clinical path is considerably shorter.
At a glance
Where does your assessment start?
Most men
History and core blood panel: testosterone (fasting, morning), glucose, lipids, TSH, and general health markers.
Some men
Extended panel: prolactin, vitamin D, vitamin B12 — when the standard workup leaves questions unanswered.
Smaller group
Penile Doppler ultrasound: when vascular characterisation will change what happens next.
Very few
Specialist testing: cavernosometry, neurophysiology, arteriography — specific indications only.
If you have had treatment that did not work, or if you have never had any blood tests done alongside your diagnosis, a structured assessment is worth having before trying again.
Frequently asked questions
A thorough assessment includes testosterone (morning, fasting), LH and FSH if testosterone is abnormal, HbA1c or fasting glucose, a full lipid profile, FBC, U&Es, and LFTs. TSH is included as standard at a specialist level. Vitamin D, prolactin, and vitamin B12 are added in selected cases — these are frequently omitted and clinically relevant more often than is generally recognised.
Yes, for several tests. Testosterone must be taken fasting and in the early morning (ideally between 07:00 and 10:00) to be valid. Fasting glucose and lipids also require an overnight fast. If you have been told your testosterone is low based on a non-fasted afternoon result, it is worth repeating under correct conditions before any clinical conclusion is drawn.
No blood test diagnoses erectile dysfunction — the diagnosis is clinical, based on history. What blood tests do is identify underlying causes and contributing factors. Erectile dysfunction is a symptom; the tests are looking for what is driving it.
A RigiScan is a device worn overnight to measure nocturnal erections. It records number, duration, and rigidity of erections during sleep and can help distinguish organic from psychogenic causes in cases of genuine diagnostic uncertainty. It is not a routine first-line test.
When the pattern suggests a vascular cause that needs characterising, when first-line treatment has failed, when Peyronie's disease is present alongside erectile dysfunction, or when escalation to more invasive treatment is being considered and a clearer vascular picture would change the approach. Not in every case.
It tells you whether testosterone deficiency is contributing. A genuinely low testosterone — confirmed on at least two properly conducted morning fasting samples — is treatable and when corrected often improves libido and can improve erectile function as part of a broader effect. A normal result is also informative: it means testosterone treatment will not help, and attention should go elsewhere.
Because severe vitamin D deficiency is associated with endothelial dysfunction and vascular impairment — the same mechanisms that underlie vasculogenic erectile dysfunction — and because it can produce fatigue and mood effects that compound sexual difficulties. It is also easily corrected. In the UK, deficiency is common. Missing it in an andrological workup is a missed opportunity.
Before you leave
If you have already been prescribed treatment for erectile dysfunction without a thorough investigation, it is worth asking what was actually checked. A full assessment takes one consultation and a set of blood tests. It does not delay treatment — it ensures that when treatment begins, it is working with your biology rather than against it.
Ready to understand what is actually happening?
A single consultation is enough to map the pattern, identify what needs investigating, and give you a clear clinical picture.
