Abstract | Full Text | Full Text PDF | PubMed | Scopus (58) | Google ScholarSee all References Theoretically, the risk of a cardiac event during sexual activity should be increased. Sexual activity is associated with an elevated heart rate, blood pressure level, and myocardial oxygen demand, and this increase in hemodynamic stress may result in myocardial ischemia.79x79Kimmel, SE. Sex and myocardial infarction: an epidemiologic perspective. Am J Cardiol. 2000; 86: 10F–13F
The second way relates to the risk associated with the sexual activity in a patient with either overt or occult CVD. In this case, the diagnosis of ED should prompt an initial cardiovascular assessment based on the history and clinical examination in order to define the baseline risk according to (i) the likelihood of silent CAD18,31 (especially since ED patients have a high probability to have silent CAD) or to the stage of clinically evident CAD, (ii) other cardiovascular conditions either unrelated, or related to ED (e.g. heart failure, peripheral arterial disease).
Ginkgo biloba. Known primarily as a treatment for cognitive decline, ginkgo has also been used to treat erectile dysfunction -- especially cases caused by the use of certain antidepressant medications. But the evidence isn't very convincing. One 1998 study published in the Journal of Sex & Marital Therapy found that it did work. But a more rigorous study, published in Human Pharmacology in 2002, failed to replicate this finding. "Ginkgo has come out of fashion in the past few years," says Ronald Tamler, MD, assistant professor of medicine and codirector of the men's health program at Mount Sinai Medical Center in New York City. "That's because it doesn't do much. I can say that in my practice, I have not seen ginkgo work -- ever."
Like all diabetic complications, ED can occur even when you have followed your doctor’s advice and carefully managed your diabetes. Also like all diabetes complications, ED is less likely to occur with good blood sugar control. Poorly controlled diabetes and high cholesterol increase the chances of vascular complications, which may lead to ED or other circulatory problems. In addition, regular smoking and alcohol use can contribute to ED.
Three FDA-approved oral medications, sildenafil, tadalafil, and vardenafil are available. These drugs are phosphodiesterase type 5 (PDE-5) inhibitors that can prolong levels of cGMP in tissue allowing improved smooth muscle relaxation, thus facilitating an erection. PDE-5 inhibitor drugs are effective in 56-63% of diabetic men with ED. More stringent glycemic control can improve these results. Men with testosterone deficiency may benefit from a combination of oral ED medication and testosterone supplementation.

And yes, this may all seem easier said than done, when it comes to a condition that is more often than not the subject of jokes—or the cause of embarrassment. Talking to your doctor is the first step in dealing with this complication, which can wreak havoc on your quality of life. Keeping diabetes in check and enjoying a healthy lifestyle can make a huge difference in reducing ED risk, but if that isn't enough, there are successful treatments. Sex brings a range of physical and psychological benefits, whether you have diabetes or not. Preventing or reversing ED isn't just about sex—it's a step toward better health and a more satisfying life.
Surgery for erectile dysfunction is usually considered only after all other options have failed. The two surgical options include the insertion of a semi-rigid rod or the implantation of a three-piece inflatable prosthesis. Penile prosthesis implantation has low infection, complication, and malfunction rates. However, since placement of an implant requires permanent injury to the erectile tissue of the penis, implant treatment is considered irreversible.
Vasculogenic sexual dysfunction is the main cause of sexual dysfunction in untreated hypertensive patients. However, due to the complex etiologic and pathophysiologic nature of sexual dysfunction, exclusion of concomitant diseases and drugs should be the initial step when approaching a hypertensive patient with this clinical condition that is not receiving any antihypertensive medication. Consequently, a significant amount of neurological, psychiatric, urologic and endocrine disorders should be ruled out before vasculogenic sexual dysfunction is diagnosed.

The use of shock wave therapy has revolutionized the treatment of many aspects of medicine. High intensity extracorporeal shockwave therapy has been used for the treatment of nephro-urolithiasis while medium intensity shockwave therapy is used by orthopaedic surgeons to treat joint pain as well as tendinitis. Low intensity shockwaves therapy was first noted to improve ischaemia-induced myocardial dysfunction in animal studies when low intensity shockwaves were applied to porcine myocardium (13). Shockwaves induces a localized stress on cell membranes in the same way that shear stress affects endothelial cell membranes (14) and this triggers the release of angiogenic factors, such as increased NO production through increased activity of endothelial NO synthase (eNOS) and neuronal NO synthase (nNOS), platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) (15). These shockwaves also cause membrane hyperpolarization (16), activation of the Ras signaling pathway, non-enzymatic synthesis of NO and induction of stress fibers and intercellular gaps (17).
Conversely, and of significant clinical importance, is how often patients with ED as their first and sole clinical manifestation suffer from subclinical CAD.17 Previous studies reported a rate of inducible ischaemia by exercise stress testing (EST) in 22% (with a wide range of 5–56%) of ED patients reflecting differences in patient population, risk factors and criteria used for ED and CAD diagnosis. Interestingly, those patients further assessed with coronary angiography had obstructive atherosclerosis in >90% of cases.4,18 In a prospective angiographic study, we documented that 19% of ED patients suffer from clinically silent obstructive CAD.18
In a study by Segal et al. (11), 4 out of 5 healthy individuals were able to achieve tumescence beyond 60% maximum rigidity when subjected to PVS using the Viberect® alone, with no other external visual sexual stimulation. In a randomized controlled study by Fode et al. (12) involving 68 men who underwent nerve-sparing radical prostatectomy, 30 men who received PVS to the frenulum daily for 6 weeks, using the Ferticare® vibrator, showed a trend towards better erections. After 1 year, 53% in the PVS group had an IIEF score ≥18 compared with 32% in the control group, although no statistical achievement was achieved. The role of PVS in penile rehabilitation is based on the postulation that PVS provides early activation of the parasympathetic erectile spinal centres at S2–S4 level, which result in early recovery of the neuropraxic cavernosal nerves.

A thorough history (including cardiovascular symptoms, age, presence of risk factors and comorbid conditions such as obesity, hypertension, dyslipidaemia, pre-diabetes, CAD, peripheral artery disease, symptoms suggestive of sleep apnoea, family history of premature atherothrombotic CVD and lifestyle factors), assessment of ED severity (according to SHIM) and duration, and physical examination (for both heart and peripheral circulation pathology) are mandatory first-line elements of investigation. A resting electrocardiogram, measurement of fasting plasma glucose, and estimation of glomerular filtration rate are desirable tests that may be used to further characterize cardiovascular status and risk and to identify men who require additional cardiologic workup. Owing to the accumulating evidence supporting the link with CVD, the measurement of testosterone is recommended in all men with a diagnosis of organic ED, especially in those for whom phosphodiesterase type 5 (PDE5) inhibitor therapy failed.
Causes of ED may be of primary developmental origin or secondary. Lack of sex hormone in the early developmental stage of male children is the major cause of primary ED. The secondary cause of ED involves arteriosclerosis, diabetes or psychogenic disturbances. Other secondary factors may include hypertension, hyperlipidaemia, obesity and tobacco use. The primary causes of ED are beyond the scope of this review; we will not be discussing the neurovascular mechanisms pertaining to ED and will focus on the relationship between IHD and ED.
Third, men with Diabetes need to control their blood sugar levels. When your blood sugar is not under control, your body does not produce enough Nitric Oxide (NO) and vascular tissues don’t respond as effectively to NO. When enough blood flows into the penis, penile veins close off and block the blood from flowing out. This process results in an erection. If your body does not produce enough NO or if your penile tissues do not respond to NO, the pressure of the blood flowing into your penis is not sufficient to trap the blood, you penis will not get hard.
Intraurethral alprostadil (Muse) provides a less invasive alternative to intrapenile injection. It is a pellet that is inserted 5–10 min before intercourse, and its effects last for 1 h. The response rate is ∼50–60%. It can be used twice daily but is not recommended for use with pregnant partners. Complications of priapism and penile fibrosis are less common than after alprostadil given by penile injection. The cost is ∼$18–24 per treatment.

The views expressed in this article intend to highlight alternative studies and induce conversation. They are the views of the author and do not necessarily represent the views of hims, and are for informational purposes only, even if and to the extent that this article features the advice of physicians and medical practitioners. This article is not, nor is it intended to be, a substitute for professional medical advice, diagnosis, or treatment, and should never be relied upon for specific medical advice.


A substantial body of literature documents the prevalence of ED in men with diabetes. Unfortunately, the majority of these studies do not distinguish between type 1 and type 2 disease, and, therefore, it is difficult to determine if prevalence rates between the two forms of diabetes differ significantly. Acknowledging this limitation in the literature, prevalence estimates of ED in cross-sectional studies of diabetic populations range from 20 to 71% (Table 1). Most of these studies did not control for severity of disease, duration of disease, or control of hyperglycemia.
PubMed | Google ScholarSee all References Diabetes was found to play a major role in vasculogenic impotence in a study of 265 patients with ED who underwent color duplex ultrasonography of the cavernosal arteries after intracavernosal injection of prostaglandin E1.13x13Chung, WS, Shim, BS, and Park, YY. Hemodynamic insult by vascular risk factors and pharmacologic erection in men with erectile dysfunction: Doppler sonography study. World J Urol. 2000; 18: 427–430

If you have symptoms of ED, it’s important to check with your doctor before trying any treatments on your own. This is because ED can be a sign of other health problems. For instance, heart disease or high cholesterol could cause ED symptoms. With a diagnosis, your doctor could recommend a number of steps that would likely improve both your heart health and your ED. These steps include lowering your cholesterol, reducing your weight, or taking medications to unclog your blood vessels.

On any matter relating to your health or well-being, please check with an appropriate health professional. No statement herein is to be construed as a diagnosis, treatment, preventative, or cure for any disease, disorder or abnormal physical state. The statements herein have not been evaluated by the Foods and Drugs Administration or Health Canada. Dr. Marchione and the doctors on the Bel Marra Health Editorial Team are compensated by Bel Marra Health for their work in creating content, consulting along with formulating and endorsing products.


The diagnosis of ED in a patient may affect its management in two ways.30 The first relates to the fact that the ED patient, irrespective of whether he has or has not established CVD, is ‘reclassified’ into a higher risk category for future CV events. Management in this case is altered in the sense that more aggressive treatment of risk factors, as well as a close follow-up, is warranted. Implementation of biomarkers in this setting is desirable.

Men with diabetes tend to develop erectile dysfunction 10 to 15 years earlier than men without diabetes. As men with diabetes age, erectile dysfunction becomes even more common. Above the age of 50, the likelihood of having difficulty with an erection occurs in approximately 50% to 60% of men with diabetes. Above age 70, there is about a 95% likelihood of having some difficulty with erectile dysfunction.
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