When you come to see me about your erections, they become my second priority. My first is making sure you will be around long enough to enjoy them — for a long time.
Erectile dysfunction is a symptom. It has causes. Most of those causes are findable — and most are treatable. But there is something more important than finding a treatment: accepting ED as a normal part of ageing is not just wrong. It can be dangerous. The same vascular disease that causes erection problems can be silently affecting your heart and arteries years before any cardiac symptoms appear. If you dismiss it, you may be closing a window on a diagnosis that, caught early, could prevent a cardiac event. This page maps the territory. The spoke pages go deeper on each topic.
What I am actually looking for
I have been doing this long enough to see the full range of what people bring into the consulting room. Three conversations have stayed with me.
The man who had decided he was done
He was 40. He had enjoyed a satisfying sex life, and he had made a calm, considered decision that that chapter was behind him. He wanted a health check, not a rescue. I respected that entirely. His erections were not the clinical question. His cardiovascular picture was — and we addressed that.
The man who could only manage once a day
He was 86. He was distressed because he felt his sexual function was declining — he could only achieve an erection once a day, where previously he had managed more. I respected his expectation too. I also gently helped him understand what is realistic at different stages of life. We talked about what his body was telling him, and what it was not.
The couple who had lost count
They came together, and there was real fear in the room. He had noticed that his ejaculatory frequency had dropped from six or seven times in a row to three. They had interpreted this as a sign that something was seriously wrong. It was not. We talked about what normal variation looks like across a relationship, and what would genuinely need investigating.
I respect every baseline. But respecting your expectations is not the same as accepting all of them as realistic — and more importantly, it is not the same as deciding that nothing needs looking at.
My question is never: is this normal for your age? My question is: is this telling me something I should not miss? Those are two completely different conversations. The first one is about your preferences. The second one might be about your heart.
Something I notice consistently in clinic: patients tell me things they have never told their GP. Not because they were hiding it — when I ask whether I can share the full picture with their GP, the answer is almost always yes. The problem was not that they did not want their GP to know. The problem was that nobody asked. Sexual health sits in a particular silence in primary care — not from malice, but because the system rarely creates the space. I ask. Directly. And people answer.
Sex is one of the most intimate things a person can share with a clinician. I consider it a privilege to be trusted with it. Whether it involves one person or several, in one configuration or many — my questions are clinical, not moral. I have never sat in judgement of a patient's sexuality. Not because I am trying to be open-minded. Because it genuinely does not occur to me.
If something here does not reflect your experience, or you feel the information could be better — I would welcome that feedback. This page is reviewed regularly and improved with patient input.
What is actually happening
An erection is a vascular event. Sexual arousal triggers nerve signals that release nitric oxide in the erectile tissue of the penis. This relaxes smooth muscle, increases arterial inflow, and as the erectile chambers fill with blood, they compress the outflow veins — trapping blood inside at high pressure. The result is rigidity.
When that process fails, it usually fails at one of two points: the inflow (arterial insufficiency) or the trapping mechanism (venous leak). But the mechanism that triggers it — and the mechanism that can override it — is neurological and psychological. Adrenaline, released in response to stress or anxiety, directly constricts the penile arteries and prevents the process from starting.
This is why the old question — is it physical or is it in your head? — is the wrong question. For most people, it is both. Mixed aetiology is the clinical norm, not the exception.
Vascular and structural. Atherosclerosis, high blood pressure, diabetes, and smoking all damage the endothelial lining of blood vessels, reducing nitric oxide production and restricting arterial inflow. Venous leak — where blood drains out of the penis too quickly — is a separate but related structural problem. These causes tend to develop gradually and affect erections in all contexts.
Neurological. Nerve damage from diabetes, pelvic surgery, spinal cord injury, or neurological conditions can interrupt the signals required to initiate an erection. Medications — particularly antidepressants, antihypertensives, and opioids — can affect the same pathways.
Psychogenic and relational. Stress, performance anxiety, depression, and relationship dynamics can activate the sympathetic nervous system — the adrenaline response — which physically prevents erection regardless of physical capacity. This mechanism is real, measurable, and often the dominant driver in younger men.
How do I know what is causing mine
The pattern of your symptoms tells me most of what I need to know before any test is ordered. I am looking for variability — and where that variability falls.
A brief self-assessment can help calibrate how significant the difficulty is and give us a shared starting point for our conversation.
Is this telling me something about my heart
The penile arteries are 1 to 2 millimetres in diameter. The coronary arteries that supply the heart are 3 to 4 millimetres. Atherosclerosis — the narrowing and hardening of arteries — affects the smaller vessels first. This means that erectile dysfunction caused by vascular disease typically appears two to five years before cardiac symptoms develop.
An erection is a vascular event. And vascular events do not happen in isolation.
The basic workup every new ED presentation should trigger
Before any treatment decision, a proper first assessment includes: blood pressure measurement, fasting blood glucose or HbA1c, a lipid profile, and a morning testosterone level. If your GP has not offered this, it is reasonable to ask. If you are coming to see me directly, I will organise it from the start.
The Princeton IV Consensus (2024) formally designates erectile dysfunction as a cardiovascular risk-enhancing factor — comparable in significance to a family history of premature heart disease. This is not a reason to panic. It is a reason to look at your cardiovascular picture properly, and not as an afterthought.
It works alone but not with a partner
This is the most common pattern I see in clinic. The erection works reliably when you are alone, fails with someone who matters. The nervous system responds to how much the moment matters — and the more someone matters, the higher the stakes feel.
There is an entire spoke page on this, because it deserves more than a paragraph.
What are the treatment options
Treatment depends on the cause — which is why a proper assessment comes first. The options below follow the standard clinical hierarchy, from least to most invasive.
PDE5 inhibitors. These work by enhancing the nitric oxide pathway, making it easier to achieve and maintain an erection when you are aroused. They do not cause erections without stimulation. One failed attempt is not a reliable test — it typically takes four to eight properly-conducted attempts to determine whether a medication is working for you. They are not harmful to the heart for most men; the contraindication with nitrate medications is a pharmacological interaction, not evidence of cardiac toxicity. A patient leaflet explaining how to use them is available below.
Injection therapy (ICI). The needle is fine, the technique is straightforward, and I teach it in clinic with a supervised first injection. Most men who start ICI continue it long-term. A complete guide is available below.
Shockwave therapy. I offer this for selected patients with vasculogenic ED as part of a broader treatment plan. I am transparent about the evidence base: the EAU 2026 guidelines support it for mild to moderate cases; the AUA is more cautious. I would not recommend it as a standalone treatment for significant vascular disease.
Venous surgery. Surgical repair of venous leak is not recommended by current EAU or AUA guidelines due to poor long-term outcomes. If you have been told you need venous surgery, I would encourage a second opinion.
Penile implant. This is a considered decision, not a rushed one. It is the right answer for a specific group of men — those who have tried other options, or who have structural disease severe enough that other options will not work. When it is appropriate, it resolves the problem definitively.
Treatment resources
Patient leaflets for PDE5 inhibitors and injection therapy are available to download. They cover how each treatment works, how to use it correctly, and what to watch for.
What about testosterone
Testosterone deficiency rarely acts alone as the cause of erectile dysfunction. Its primary role is in sexual desire — and it does contribute to the health of erectile tissue and the NO pathway, so low levels are worth correcting when present. But if your testosterone is normal, replacing it will not fix your erection.
The important caveat is that testosterone deficiency frequently coexists with ED from other causes. In men with diabetes, metabolic syndrome, or significant weight gain, testosterone may be suppressed, and addressing it is part of a complete cardiometabolic picture.
Testosterone varies significantly across the day and is affected by acute illness, sleep deprivation, and stress. A reliable sample requires a fasting morning blood test, taken between 07:00 and 11:00. A single low result is not sufficient for a diagnosis — it needs to be confirmed on a second occasion, at least four weeks later. If you have had your testosterone checked at a random time of day and told it is low, the result may need repeating under proper conditions before any treatment is considered.
What you may have been told — and what the evidence shows
Myth vs Fact
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. Most of my patients have never been asked about their erections by their GP. The conversation did not happen because nobody started it. That does not mean nothing was worth discussing.
Fact
Fact: Erectile dysfunction is not an inevitable consequence of ageing. It has causes — most of them findable. More importantly, the vascular disease that causes ED often precedes cardiac symptoms by two to five years. Dismissing it as normal ageing does not just delay treatment for ED. It may delay a diagnosis that could prevent a heart attack.
Fact
Fact: Any new presentation of erectile dysfunction warrants a basic workup: history, examination, HbA1c, lipid profile, morning testosterone. Anxiety as a diagnosis does not rule out vascular, hormonal, or medication-related contributors. It is not a reason to skip the investigation — it is a reason to look at all the drivers together.
Fact
Fact: PDE5 inhibitors enhance the physiological response to arousal — they do not repair vascular disease, correct a hormone deficiency, or resolve a relationship dynamic that is not working. They are a useful tool in the right context. They are not a substitute for understanding what is actually happening.
Fact
Fact: Morning erections suggest that your neurovascular pathways are at least partially intact. They do not exclude mixed aetiology, organic contributors, or the need for a proper assessment. They are one data point, not a complete picture.
How severe is your difficulty — a quick self-assessment
In men over 40, vascular disease is the most common underlying contributor — atherosclerosis reducing arterial inflow, or veno-occlusive dysfunction affecting the trapping mechanism. In younger men, psychogenic factors and performance anxiety are more frequently the primary driver, though physical contributors including medication side effects, diabetes, and testosterone deficiency should always be excluded. Mixed aetiology — where both physical and psychological factors are present — is the norm rather than the exception at any age.
Yes — and this is one of the most important things to understand about ED. The penile arteries are significantly smaller than the coronary arteries, which means they tend to show the effects of vascular disease earlier. Studies consistently find that ED precedes major cardiac events by two to five years on average. The Princeton IV Consensus (2024) formally classifies ED as a cardiovascular risk-enhancing factor. This is not a reason for alarm — it is a reason to use an ED presentation as an opportunity to review cardiovascular risk properly, including blood pressure, glucose, and lipids.
It depends on the cause. Psychogenic ED, medication-induced ED, and ED driven by reversible lifestyle factors — obesity, alcohol, sedentary behaviour — often improves significantly or resolves with appropriate intervention. Vascular disease is not reversible in the structural sense, but its progression can be slowed and its effects managed effectively. For men with significant structural vascular damage, treatment options including injection therapy and penile implants provide reliable solutions even when the underlying physiology cannot be fully restored.
Both are PDE5 inhibitors and work by the same mechanism. The main practical difference is duration: sildenafil (Viagra) is active for approximately four to five hours and should be taken 30 to 60 minutes before activity, ideally not with a heavy meal. Tadalafil (Cialis) remains active for up to 36 hours, which removes the need to time the dose precisely, and is also available as a low daily dose (2.5 to 5 mg) for a continuous background effect. Neither drug causes erections without sexual stimulation. The choice between them usually comes down to lifestyle preference and individual response.
Losing an erection during penetration or shortly after is one of the most common presentations. The causes range from vascular — where inflow is adequate but the trapping mechanism is insufficient, allowing blood to drain out too quickly — to psychological, where the activation of the sympathetic nervous system (the adrenaline response) interrupts the process at the point of highest pressure. Distinguishing between these requires a proper history and, in some cases, a penile Doppler ultrasound. A common and treatable pattern.
If your GP has offered a thorough assessment — full history, basic blood tests including testosterone, glucose and lipids, blood pressure, and a clear management plan — a specialist may not be immediately necessary. If you have been told "it's stress" or given a prescription without any investigation, it is reasonable to want a more structured assessment. A specialist consultation is also appropriate if first-line treatment has not worked, if there is a specific concern about the vascular picture, or if you want a penile Doppler to characterise the blood flow pattern properly. You do not need a GP referral to see me — self-referral is straightforward.
An enlarged prostate (BPH) does not directly cause ED through mechanical means. However, the two conditions share common risk factors and often coexist — particularly in men over 50. More relevant is the effect of BPH treatments: certain medications (particularly 5-alpha-reductase inhibitors such as finasteride and dutasteride) can affect libido and erections in a minority of men. If your ED started or worsened after starting treatment for prostate symptoms, that connection is worth discussing.
Before anything else — a piece of advice
Sex is not a performance. It is an interaction — and at its most fundamental, a form of communication between two people. The moment it becomes a test with measurable outcomes, it stops being either of those things.
Before any investigation, any medication, any referral — the single most useful thing is usually a conversation with your partner. Not in bed. Not in a moment of crisis. A calm conversation, at a point when neither of you is under pressure, about what you are each experiencing and what you each need.
There is no formula for this, because you are not a formula. What I can tell you is that every couple I see who navigates this well has found a way to talk about it. Not necessarily easily. But honestly.
