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ED is not just a sexual issue — it is a cardiovascular warning signal. This panel investigates both the hormones and the vessels.
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A dual-focus panel covering both hormonal markers (testosterone, SHBG, oestradiol, prolactin) and vascular risk markers (lipid profile, HbA1c.
Erectile dysfunction (ED) is a common condition that affects approximately 52 percent of men between 40 and 70 years old to some degree. It is not simply a sexual inconvenience — it is now recognised as an independent risk marker for cardiovascular disease, because the small penile arteries show atherosclerotic changes approximately three to five years before the larger coronary arteries. This panel therefore serves a dual purpose: investigating the hormonal contributors to ED (testosterone, SHBG, oestradiol, prolactin) and simultaneously screening for the cardiovascular and metabolic risk factors (lipid profile, HbA1c, fasting glucose) that underlie vascular ED. Men who present with ED and are found to have cardiovascular risk factors should be viewed as cardiovascular patients first. All results are reviewed by a GMC-registered physician with clear guidance on both sexual health and cardiovascular risk reduction.
Understand what each marker measures, why it matters, and what the science says — not just a list of numbers.
This panel is designed for adults who want a comprehensive, evidence-based picture of their metabolic health — not a GP referral panel.
Men aged 40 and over with new or progressive erectile difficulties
Men whose ED has not responded to PDE5 inhibitors (e.g. sildenafil), suggesting non-vascular or hormonal causes
Men with known risk factors for cardiovascular disease wanting to assess the vascular ED connection
Men with diabetes who have developed sexual dysfunction
Men wanting a comprehensive investigation before discussing ED with their GP
Blood testing provides a biochemical assessment of ED risk factors but cannot directly measure penile blood flow or endothelial function, which require specialist investigations such as penile Doppler ultrasound, nocturnal penile tumescence testing, or dynamic infusion cavernosometry. ED has both physiological and psychological components and a blood panel alone is insufficient to determine the primary aetiology. Testosterone must be collected between 7 and 9 am in a fasted, rested state; values collected in the afternoon underestimate the true morning peak by 20 to 30 percent. HbA1c is a three-month average and may not reflect very recent glycaemic deterioration. This panel does not include blood pressure measurement, which is an essential component of the cardiovascular assessment of ED.
From order to physician-reviewed report in as little as three working days.
Venous draw recommended for this combined hormonal and lipid panel.
10-hour fast; collect between 7 and 9 am for accurate testosterone and lipids.
Priority processing within 24 hours of receipt.
Hormonal and cardiovascular commentary from a GMC physician in 3 to 5 working days.
Three options designed to fit your schedule, location, and preference — all producing a laboratory-standard sample.
Adults 18+ in mainland UK. Not suitable if you have had a transfusion in the last 3 months.
Order anytime; kit dispatched within 24 hours Mon–Fri.
Allow 24–48 hours for sample transit on top of lab processing time.
Adults 18+ within 20 miles of a serviced city centre.
Mon–Sun, 06:00–20:00. Next-day booking typical.
Sample reaches the lab within 24 hours of collection.
Adults 16+ with photo ID. Paediatric draws by appointment at selected sites.
Mon–Fri, with Saturday hours at most metropolitan locations.
Samples processed same-day at the receiving clinic.
Every test is processed in a UKAS ISO 15189-accredited laboratory, overseen by GMC-registered physicians, and governed by UK GDPR. No overseas processing, no offshore data.
Follow these guidelines to ensure accurate, reproducible results. Most markers are sensitive to recent food, exercise, and sleep.
Can't find your answer? Our clinical support team is available Monday to Friday, 9am–5pm.
Contact supportThe penile arteries have a lumen diameter of approximately 1 to 2 millimetres, compared with 3 to 4 millimetres in coronary arteries. Atherosclerosis affects smaller arteries first, meaning penile artery endothelial dysfunction and plaque formation occur approximately 3 to 5 years before the equivalent changes in the larger coronary arteries. ED in a man with no other obvious cause — particularly in his 40s or 50s — is therefore an early indicator of systemic vascular disease. Studies have shown that men presenting with ED and no known cardiovascular disease have a two to three-fold higher risk of subsequent cardiac events than age-matched controls without ED.
Testosterone supports erectile function through both central and peripheral mechanisms. Centrally, it drives libido and sexual motivation. Peripherally, testosterone upregulates nitric oxide synthase (NOS) in penile smooth muscle — nitric oxide is the primary molecule causing smooth muscle relaxation and arterial dilation required for an erection. Testosterone also maintains the structural integrity of penile smooth muscle and cavernous tissue. Men with hypogonadism often have reduced responsiveness to PDE5 inhibitors precisely because the peripheral nitric oxide pathway is undertreated; restoring testosterone can improve PDE5 inhibitor efficacy.
Yes, often substantially. The Mediterranean dietary pattern, regular aerobic exercise, weight loss (particularly reduction of visceral fat), smoking cessation, and moderation of alcohol have all been shown in clinical trials to improve erectile function independent of medication. A meta-analysis in the Journal of Sexual Medicine found that lifestyle interventions improved IIEF (International Index of Erectile Function) scores by an average of 2 to 3 points — equivalent to the effect of low-dose PDE5 inhibitors. The mechanism is primarily improved endothelial function and nitric oxide bioavailability from reduced vascular inflammation and oxidative stress.
Either approach works. Many men find it easier to discuss ED when they have objective data in hand — it shifts the conversation from subjective complaint to evidence-based assessment and makes the consultation more productive. However, if you have co-existing symptoms such as chest pain, shortness of breath, significant urinary symptoms, or lump in the testicle, see your GP immediately rather than testing first. Your physician commentary will include guidance on what to bring to a GP appointment based on your results.
No. PDE5 inhibitors (sildenafil, tadalafil, vardenafil) enhance the nitric oxide-cGMP pathway that mediates erection, but they do not address the underlying hormonal or vascular pathology. They are symptomatic treatments, not disease-modifying. This is why identifying and correcting underlying causes — low testosterone, dyslipidaemia, hyperglycaemia — is clinically important alongside symptom management. Men who do not respond to PDE5 inhibitors typically have more severe vascular disease, significant hypogonadism, or a primary neurological cause, which blood testing helps to differentiate.
