The Penile Artery Is the Canary in the Coronary

Opening Scene

He was forty-three years old, and he came to see me about his breathing.

“I get winded on stairs,” he said. “Three flights and I’m breathing hard. That did not used to happen.” He paused. “And I just turned 43. I don’t understand it.”

He was a former college athlete. Recreational soccer player into his late thirties. Currently inactive, which he described with the guilt of a man who knows he should be doing something about it. His blood pressure at check-in was 141/90. His resting heart rate was 78. His BMI was 28.

I asked the question I ask when the symptom presentation and the age and the resting heart rate tell me a specific clinical story.

“Any changes in your erections?”

He looked at the wall. Men do this when the answer is yes and they have not said it out loud yet. There is always a moment of calculation.

“About eight months ago, yeah. I stopped having morning erections. That was the first thing. Then it started affecting things with my wife. I thought it was stress. I thought it was work. I thought I was just tired.” He looked back at me. “I’ve been taking sildenafil when it matters. My GP prescribed it.”

His GP had done the right thing in one sense. He had not done the right thing in the sense that matters.

I ordered an ApoB, hs-CRP, fasting insulin, fasting lipids, and a coronary calcium score. His ApoB came back at 134 mg/dL. His hs-CRP was 2.2 mg/L. His fasting insulin was 19.8 mIU/L. His CAC score was 88.

He was forty-three years old with a CAC score of 88, and he had come in to talk about getting winded on stairs.

The staircase and the bedroom were the same story. They always are. He just didn’t know the language yet.

What I told him next took about thirty minutes and is the substance of everything that follows.

What Most Men Hide About Stamina

Stamina is a word men use to discuss two separate concerns that they almost never connect in the same conversation: cardiovascular endurance and sexual function. The men who are experiencing both forms of decline are usually addressing neither with clinical seriousness.

The reason is structural. Sexual function in men over 40 carries an enormous weight of identity, shame, and perceived inadequacy that makes honest self-disclosure exceptionally difficult, even in a clinical setting. Cardiovascular fitness decline is discussed more openly but typically minimized, attributed to age or busy schedules or the natural consequence of reduced training. Together, they constitute a pattern that men who most need medical attention most reliably dismiss.

Here is what that dismissal sounds like in their own words:

“I’ve been experiencing erectile dysfunction for the last eight months. I no longer experience morning erections. My wife has been patient but I can see the concern in her face. I keep telling myself it’s stress.” (r/sex)

“I just turned 43 and I used to run ten miles without thinking about it. Now I run three and I’m winded. I’ve also noticed a significant drop in sexual stamina. I assumed these were unrelated. Are they?” (r/AskDocs)

“How do you handle the sadness of realizing that spontaneous intimacy might be a thing of the past? I’m 46 and I can’t figure out if this is a physical problem or a head problem.” (r/over40)

What these men are not saying, because they do not have the framework to say it, is that both stamina problems share a single upstream biology. The endothelium. Nitric oxide. The capacity of blood vessels to dilate, fill, and sustain flow under demand.

The cardiovascular and sexual stamina stories in a man over 40 are not parallel narratives. They are the same narrative, told in two different organ systems, measurable by the same biomarkers, reversible through the same interventions, and predictive of the same endpoints.

That framework is what I want to give you here.

The Mechanism, In Plain English

The core concept is one that I return to in clinic more often than almost any other: the penile artery is the canary in the coronary.

The penile arteries are small, approximately 1 to 2 millimeters in diameter. The coronary arteries that supply the heart muscle are larger, approximately 3 to 4 millimeters. The same process of endothelial dysfunction and atherosclerotic plaque development that eventually occludes a coronary artery begins in the smaller penile arteries first, because flow limitations become symptomatic at a smaller degree of luminal narrowing in a smaller vessel.

Erectile dysfunction in men under 60 precedes a major cardiovascular event by an average of 3 to 5 years, because the penile arteries (1–2 mm in diameter) are smaller than coronary arteries (3–4 mm), so the same process of endothelial dysfunction and atherosclerotic plaque becomes symptomatic in the penile vasculature first. Men with new-onset erectile dysfunction under age 60 should receive a complete cardiovascular risk assessment including ApoB, hs-CRP, fasting insulin, and blood pressure measurement, not only a PDE5 inhibitor prescription (Montorsi et al., European Urology, 2003).

This is the clinical principle that explains why a prescribing approach that treats the erectile dysfunction without evaluating the cardiovascular substrate is missing the most important information the symptom is offering.

The mechanism in both organ systems is the same: nitric oxide bioavailability.

Nitric oxide (NO) is produced by the endothelium through the enzyme endothelial nitric oxide synthase (eNOS). NO diffuses into the smooth muscle layer of arteries and causes relaxation, vasodilation, and increased blood flow. In the penis, NO is the primary signaling molecule for the smooth muscle relaxation that permits the engorgement and rigidity of erection. In the coronary arteries, NO governs the moment-to-moment regulation of blood flow during physical activity. When eNOS function declines, endothelial-dependent vasodilation declines, and what a man notices in his body is: reduced exercise capacity on stairs and a reduced erectile response in the bedroom.

Erectile function and cardiovascular fitness share the same upstream driver: nitric oxide bioavailability and endothelial integrity. This is why the same intervention, aerobic exercise at 150 or more minutes per week (specifically zone 2 training), simultaneously improves erectile function scores, reduces cardiovascular mortality risk, and lowers blood pressure through a single mechanism: increased eNOS activity and improved endothelial responsiveness (Gokce et al., Journal of the American College of Cardiology, 2003).

A 2011 meta-analysis published in the Journal of Sexual Medicine found that aerobic exercise equivalent to 160 minutes per week was associated with improvement in erectile function scores equivalent to mild-to-moderate PDE5 inhibitor therapy in men with vasculogenic erectile dysfunction (Gerbild et al., Sexual Medicine, 2018). This is not a minor finding. It means that a man who exercises regularly, not intensely, not athletically, just consistently at an aerobic intensity, is producing a therapeutic benefit in erectile function through the same mechanism that a $40-per-month sildenafil prescription addresses pharmacologically, and he is simultaneously reducing his cardiovascular mortality risk.

The pharmacological approach is not wrong. PDE5 inhibitors work by inhibiting the enzyme that degrades cyclic GMP, prolonging the signal downstream of NO. They are effective, safe, and underused given the burden of vasculogenic ED. But they do not address the endothelial dysfunction upstream. They work around it. A man who takes sildenafil without addressing the endothelial substrate is treating the symptom while the underlying cardiovascular process continues unchecked.

There is also a third component in the stamina story that cardiovascular endurance and erectile function both share: the autonomic nervous system. The capacity to achieve and maintain both exercise performance and erectile response depends on parasympathetic nervous system tone. When chronic sympathetic activation, from stress, poor sleep, or elevated cortisol, suppresses parasympathetic function, both capacities degrade. The man who is chronically activated, never fully resting, never in a low-threat state, will notice this in both the gym and the bedroom before he ever receives a cardiovascular diagnosis.

The decline in physical stamina and erectile function that men over 40 experience together is not coincidental aging. It is the predictable consequence of three converging processes: reduced eNOS activity and endothelial NO production, elevated sympathetic tone suppressing parasympathetic function, and early atherosclerotic narrowing affecting smaller-diameter vessels first. All three processes are measurable, partially reversible, and clinically significant years before a coronary event (Chiurlia et al., American Journal of Cardiology, 2005).

The urgency of this framing is not meant to produce alarm. It is meant to produce action. A man who understands that his staircase difficulty and his bedroom difficulty share a common upstream driver, and that both are responsive to the same interventions, has much more reason to act than a man who has been told one is a normal part of aging and the other can be managed with a blue pill.

The Honesty Scale

SDE rates every claim: Solid (1), Promising (2), Early/Theoretical (3–4), Unsupported (5).

• Erectile dysfunction as independent cardiovascular risk factor and predictor of future cardiac events: Solid (1), Multiple large prospective cohort studies confirm ED as an independent predictor of cardiovascular events, with hazard ratios of 1.4 to 1.8 over 5 to 10 years, even after controlling for age, hypertension, and cholesterol (Montorsi et al., European Urology, 2003).

• Aerobic exercise (150+ min/week) improving erectile function in vasculogenic ED: Solid (1), Meta-analytic evidence is consistent. Effect size is equivalent to mild-to-moderate PDE5 inhibitor therapy in men with cardiovascular risk-associated ED (Gerbild et al., Sexual Medicine, 2018).

• PDE5 inhibitors (sildenafil, tadalafil) improving erectile function: Solid (1), Extensive RCT evidence. Their cardiovascular effect is generally neutral to mildly beneficial, with transient blood pressure reduction; contraindicated with nitrate medications.

• ED as the first manifestation of coronary artery disease in men under 60: Promising (2), The “artery size hypothesis” is well-supported mechanistically and in multiple observational studies; head-to-head prospective trials with imaging endpoints are still accumulating.

• Zone 2 cardio (moderate intensity aerobic exercise) as cardiovascular mortality reduction strategy: Solid (1), Dose-response relationship well-established; 150+ minutes moderate intensity or 75+ minutes vigorous intensity per week reduces all-cause cardiovascular mortality (Physical Activity Guidelines Advisory Committee, USDHHS, 2018).

• Testosterone replacement therapy as treatment for stamina and ED in men with documented hypogonadism: Promising (2), The TRAVERSE trial (2023) showed TRT did not significantly increase cardiovascular events in men with hypogonadism; TRT can improve sexual function and energy; benefit is specific to men with confirmed low testosterone, not for symptomatic men with normal levels (Lincoff et al., NEJM, 2023).

• L-citrulline/arginine supplementation for endothelial NO production and ED: Early (3), Small RCTs suggest modest benefit on erectile function scores; effect size is modest compared to aerobic exercise; mechanistically plausible.

What the Other Voices Get Wrong

Paul Saladino’s carnivore content creates a specific blind spot on this topic that has measurable consequence. Men who follow his framework for metabolic health, including his consistent argument that elevated LDL does not drive cardiovascular risk, may tolerate rising ApoB levels with a sense of metabolic confidence that the evidence does not support. For men with new-onset ED and an ApoB above 110, the carnivore endorsement of LDL permissiveness is not a neutral lifestyle choice. It is a frame that delays the clinical evaluation that would reveal an atherosclerotic process already underway (Saladino, YouTube). The ACC/AHA cholesterol guidelines, based on the cumulative evidence of multiple statin trials, remain the relevant clinical standard for cardiovascular risk reduction (Grundy et al., Circulation, 2019).

The direct-to-consumer telehealth ED model, represented by companies like Hims and Roman, addresses the erectile function complaint without the cardiovascular evaluation. Prescribing sildenafil to a forty-three-year-old with new-onset ED, elevated blood pressure, and elevated ApoB, which is the pattern in my opening scene, solves the presenting problem while missing the clinical signal. This is not unique to those companies. It reflects a broader systemic gap in how ED is treated in primary care. The problem is not that sildenafil is prescribed. The problem is that the complete cardiovascular workup, ApoB, hs-CRP, fasting insulin, CAC consideration, is not routinely performed at the time of the first ED prescription. A man receiving sildenafil through a telehealth app has no idea whether his ED is a symptom of correctable vascular disease.

Andrew Huberman’s nitric oxide content is mechanistically accurate and genuinely useful: his explanations of how L-citrulline affects arginine availability, how resistance training stimulates NO production, and how sleep affects erectile function are correct. The gap is framing. His content treats the mechanism as interesting biology. What is missing is the clinical urgency that the mechanism justifies: new-onset ED in a man under 60 is a reason to see a cardiologist, not just a reason to add a supplement stack. Mechanism without clinical consequence framing produces informed men who are not appropriately concerned (Huberman Lab, hubermanlab.com).

Cardiologist’s Note

I want to address something men consistently ask me that I do not address fully in the mechanism section.

If erectile dysfunction is a cardiovascular signal, does treating the cardiovascular disease restore erectile function?

The honest answer is: partially, sometimes, and dependent on how far the atherosclerotic process has progressed.

Men with ED driven primarily by endothelial dysfunction, elevated ApoB, insulin resistance, hypertension, and low physical activity who make the relevant behavioral and pharmacological changes frequently report meaningful improvement in erectile function. This is consistent with the biology: improving endothelial health improves NO bioavailability, which is the upstream driver of erectile response.

Men with ED driven by established atherosclerotic plaque in the penile vasculature will have a more limited response to lifestyle change alone. PDE5 inhibitors remain useful in this group, and they are not a concession to cardiovascular failure. They are appropriate therapy.

What I want men to understand is the sequencing: treat the root cause with the full clinical evaluation and appropriate cardiovascular risk reduction, not just the downstream symptom with a single prescription. Doing both simultaneously is entirely reasonable. Doing only the downstream treatment is a missed clinical opportunity.

What to Do This Week

These are sequenced from highest evidence to lowest barrier. Do not do all seven at once. Pick the first three and do those well.

1. Get a complete cardiovascular risk panel at your next blood draw. The panel that matters for the man with stamina concerns: ApoB (target below 80 mg/dL for low risk, below 70 for elevated risk), hs-CRP, fasting insulin, fasting lipids (full panel), and blood pressure measured twice sitting after five minutes of rest. This combination, not total cholesterol alone, tells the vascular story.

2. Start 150 minutes per week of zone 2 aerobic exercise. This week. Zone 2 is an intensity at which you can hold a conversation but not comfortably sing. Brisk walking qualifies. Cycling qualifies. This is not an invitation to run hard or purchase gym equipment. One hundred fifty minutes per week, across four or five sessions, is the minimum effective dose for endothelial benefit. Begin this week. Not when the weather changes.

3. If you have had new-onset ED for more than six months and are under 60, ask your physician for a cardiovascular risk assessment, not just a PDE5 inhibitor prescription. The specific ask: “I want to know my ApoB, my hs-CRP, and whether I should have a coronary calcium score given my age and this symptom.” Most physicians will engage with this framing. Some will not. If yours does not, it is worth seeking a second opinion from a cardiologist.

4. Address sleep duration as a priority this week. Testosterone peaks during REM sleep. Erectile function is tightly coupled to REM sleep quality, which is why the loss of morning erections is one of the first signs of poor sleep architecture in men. Anything below seven hours or anything that significantly fragments sleep is degrading this system.

5. Audit your alcohol intake specifically. Alcohol at three or more drinks per day acutely impairs NO synthesis, raises blood pressure, disrupts sleep architecture, and reduces testosterone. Many men with stamina concerns who examine their intake honestly discover it is higher than they report to their physicians. Alcohol is the most common unexamined variable in this clinical pattern.

6. If you are taking sildenafil or tadalafil, continue. Add the cardiovascular evaluation, not instead of the medication. PDE5 inhibitors are safe, effective, and do not prevent the cardiovascular investigation from happening. Do both in parallel.

7. Do not start testosterone replacement therapy for stamina concerns without a full hormonal and cardiovascular workup first. Testosterone at supraphysiologic levels drives erythrocytosis, sleep apnea, and potentially worsens some cardiovascular parameters. The TRAVERSE trial cleared TRT of the headline cardiovascular risk concern for men with documented hypogonadism, but the indication is specific: confirmed low testosterone with symptoms, not symptom assumption without measurement (Lincoff et al., NEJM, 2023).

The Featured Snippet Block

Does exercise improve erectile function in men?

Yes. Aerobic exercise at 150–200 minutes per week improves erectile function scores in men with vasculogenic erectile dysfunction at a magnitude comparable to mild-to-moderate PDE5 inhibitor therapy. The mechanism is increased endothelial nitric oxide synthase (eNOS) activity and improved endothelial responsiveness, which restores the NO-mediated smooth muscle relaxation that underlies erectile response. Exercise is the upstream intervention. PDE5 inhibitors address the same system downstream.

What is the connection between cardiovascular health and sexual performance in men?

Erectile dysfunction and cardiovascular fitness share the same upstream mechanism: endothelial nitric oxide bioavailability. The penile arteries (1–2 mm diameter) are smaller than coronary arteries (3–4 mm), so the same endothelial dysfunction and atherosclerotic process affects them first. New-onset erectile dysfunction in men under 60 precedes a major cardiovascular event by an average of 3–5 years. It is a cardiovascular symptom and should prompt cardiovascular evaluation, not only a PDE5 inhibitor prescription.

When to Call Your Cardiologist

The conversation about erectile dysfunction belongs in a cardiologist’s office, not only in a telehealth inbox.

Call your cardiologist specifically if any of the following apply:

New-onset ED combined with exertional shortness of breath, chest tightness, or left arm discomfort. Any of these combinations means the symptom complex should be evaluated the same week, not at a routine follow-up.

New-onset ED in a man under 55 with no obvious lifestyle explanation (not obese, not inactive, not diabetic, not hypertensive on medication). This is a higher clinical priority than the same symptom in a man with multiple known risk factors, because the absence of obvious cause heightens the probability of a cardiac driver.

ED in a man currently taking nitrate medications for chest pain. PDE5 inhibitors are contraindicated with nitrates and the combination can cause severe hypotension. Do not take sildenafil without disclosing nitrate use to your prescribing physician.

New-onset exertional symptoms (breathlessness on one flight of stairs, lightheadedness with mild exertion) in combination with any of the above. Exercise stress testing and coronary evaluation is the appropriate next step.

The conversation does not have to begin with alarm. It can begin exactly the way it did in my office with the man in my opening scene: “I’ve been getting winded more easily, and I wanted to ask about some changes in my sexual function.”

That sentence, spoken out loud to a physician who is listening, is how a man who is heading toward a cardiovascular event at fifty-three gets to be sixty-three instead.

Close

The man from my opening scene came back six months later with an ApoB of 91 (from 134), following statin therapy and dietary changes. His CAC was not going backward, but its trajectory had flattened. His blood pressure was 124/78. He had been walking forty minutes every morning for five months.

“The other thing has also improved,” he said, in the tone men use when they are pleased but still a little surprised.

I told him it was the same thing. He had improved both by addressing the one upstream driver they shared.

He nodded slowly.

“I thought they were completely separate problems.”

Most men do. That is what this piece is for.

If your stamina, cardiovascular or otherwise, has been telling you something you have not yet taken to a physician, the SDE Vascular Clock Starter Kit is the assessment that tells you which biomarkers to ask for and what the numbers mean in clinical context. It is the briefing document I wish every man over 40 had before their first cardiology visit.

The Stop Dying Early newsletter is where I continue this clinical conversation weekly.

IMOKA: the Ekegusii word for the moment when a thing that was obscure becomes perfectly clear. Not a revelation exactly. More like the removal of a veil that had always been there.

The two stamina problems were the same problem. The veil is gone.

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