About half of men between 40 and 70 have some degree of erectile dysfunction.1 Most treat it as a private embarrassment or an inevitable part of ageing. It is neither. It is a circulation signal, and it tends to arrive early.
An erection is a nitric oxide event
In 1992, researchers showed that nitric oxide is the physiological mediator of erection.2 Nerve endings and the vessel lining release nitric oxide; it relaxes the smooth muscle of the penile arteries and the erectile tissue; blood flows in. The drugs that treat erectile dysfunction, the PDE5 inhibitors, don't create this signal. They protect it, by slowing the breakdown of the messenger molecule nitric oxide produces. No nitric oxide, nothing to protect.
That matters because the arteries involved are small, about one to two millimetres across, compared with three to four in the heart. When the endothelium starts making less nitric oxide, or inflammation starts damaging it, the smallest arteries show it first.
Three years ahead
In a study of 300 men with coronary artery disease confirmed by angiography, nearly half had erectile dysfunction, and in almost all of them it had appeared before the heart symptoms, by an average of about three years.3 In the Prostate Cancer Prevention Trial, men who developed erectile dysfunction had a significantly higher risk of a subsequent cardiovascular event, a risk comparable to that from smoking or a family history of heart attack.4 A meta-analysis of cohort studies covering more than 90,000 men found erectile dysfunction associated with a roughly 44 percent higher risk of cardiovascular events and 25 percent higher all-cause mortality.5
The small arteries fail first. For many men, erectile dysfunction is the earliest reading they will ever get on their cardiovascular system.
The mechanism is shared: endothelial dysfunction and reduced nitric oxide, the same process behind rising blood pressure and, further down the road, plaque.6 Which is why the first response to erectile dysfunction should not be a prescription from a website. It should be a blood pressure reading and a conversation with a physician.
What the human studies show about restoring the signal
- Lifestyle changes work. In a randomised trial of obese men with erectile dysfunction, two years of diet and exercise improved erectile function scores significantly, and about a third of the men in the intervention group regained normal function.7 A review of intervention studies found that around 40 minutes of moderate-to-vigorous aerobic exercise, four times a week, improved erectile function in men whose ED had vascular causes.8
- Feeding the nitric oxide pathway helps. In a trial of men with mild erectile dysfunction, 1.5 grams of L-citrulline a day for a month improved erection hardness in half of them, compared with 8 percent on placebo.9 A meta-analysis of arginine supplementation trials found significant improvements in erectile function scores at doses of 1.5 to 5 grams a day.10 Citrulline is the more efficient way to deliver arginine to the blood, as we explain elsewhere in the Journal.
- Blood pressure and ED travel together. The levers that lower pressure protect the same endothelium: movement, sleep, less alcohol, no smoking, nitrate-rich food, slow breathing.
What to do, in order
- Treat it as information. Measure your blood pressure properly for a week; the Blueprint shows how.
- See your physician, and say the word. Erectile dysfunction is a reason to look at your cardiovascular risk, and the earlier the better.
- Work the levers. The two best-evidenced are exercise and diet, and they are also the two that lower blood pressure most.
- Support the pathway. Nitrate, citrulline and the antioxidants that protect nitric oxide, at the doses the studies used.
None of this is a treatment for erectile dysfunction, and none of it replaces your physician. It is a reason to take the signal seriously while it is still just a signal.
