Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Sildenafil is taken orally 1 hour before anticipated sexual intercourse and enhances the normal response to sexual stimulation; however, it has no effect on erections in the absence of stimulation.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
Excess LDL cholesterol in your blood gets deposited in arteries, the blood vessels that feed the heart and brain. These deposits can join with other substances to form plaque, a thick, hard deposit in the blood vessel that leads to atherosclerosis. Plaque can narrow the passageway inside the artery and pinch off the flow of blood to the heart muscle, and to the penis.
The mechanisms of action by which antihypertensive medications cause ED are currently unknown. Some investigators have theorized that antihypertensive medications affect erectile function by decreasing blood pressure, which reduces the perfusion pressure needed to maintain sufficient blood flow for erections through atherosclerotic penile arteries.37x37Benet, AE and Melman, A. The epidemiology of erectile dysfunction. Urol Clin North Am. 1995; 22: 699–709
If not properly controlled, both type 1 and type 2 diabetes can cause complications due to high blood sugar levels. Over time, these high levels can cause irreversible nerve damage and narrow your blood vessels. While nerve damage may affect the sensitivity of your penis, blood vessel damage can affect the blood flow to your penis and make it more difficult for you to get an erection.

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Luckily, awareness of ED as a significant and common complication of diabetes has increased in recent years, mainly because of increasing knowledge of male sexual function and the rapidly expanding armamentarium of novel treatments being developed for impotence. Studies of ED suggest that its prevalence in men with diabetes ranges from 35–75% versus 26% in general population. The onset of ED also occurs 10–15 years earlier in men with diabetes than it does in sex-matched counterparts without diabetes.
While all three forms of male sexual dysfunction can be found among diabetic men, this review will focus on the most common form, ED, because the literature is most mature in this area. Defined as the inability to achieve or maintain an erection sufficient for satisfactory sexual performance, ED is highly prevalent in diabetic men1 and is almost always organic in its etiology. Given that many patients feel that their ED is “in their heads” and that “their provider will dismiss any sexual problems they might bring up,”2 it may be a relief for patients to learn that their ED is physical, related to their diabetes, and treatable. To this end, the goal of this article is to review the epidemiology, pathophysiology, quality of life effect, and treatment of ED in men with type 2 diabetes.
Crossref | PubMed | Scopus (23) | Google ScholarSee all References Only 1 published study has investigated the effect of vardenafil on cardiac function.75x75Thadani, U, Smith, W, Nash, S et al. The effect of vardenafil, a potent and highly selective phosphodiesterase-5 inhibitor for the treatment of erectile dysfunction, on the cardiovascular response to exercise in patients with coronary artery disease. J Am Coll Cardiol. 2002; 40: 2006–2012
Some commonly prescribed cardiovascular drugs (beta-blockers, diuretics, angiotensin-converting enzyme inhibitors, etc.) contribute to ED.18 Previous studies have shown a strong association between ED and diuretics in patients treated with hydrochlorothiazide or chlorthalidone.19,20 It has also been shown that patients treated with first-generation non-selective beta-blockers, such as propranolol, had more frequent ED than those treated with a placebo.21
As ED has become more prevalent among the U.S. population, entrepreneurs have set out to serve this patient population by introducing a variety of non-invasive devices to help correct the condition. There’s the penis pump, which includes a plastic tube that fits over the penis and a hand or battery-powered pump attached to the tube, and a band that circles the base of the penis when it becomes erect.
It’s crucial that any underlying medical condition, such as angina or diabetes, is detected. So if you’re experiencing problems with ED, book an appointment with your doctor. He or she will assess and examine you to try to establish the cause of the problem, and may refer you for tests. Don’t take any medicine for ED without first discussing it with your doctor.
Since their introduction in the therapeutic field, more than a decade ago, PDE-5 inhibitors have revolutionized the treatment of sexual dysfunction. By blocking the activity of PDE-5 isoenzyme, localized throughout the smooth muscle cells of the vasculature (genital vessels included), PDE-5 inhibitors increase the levels of cyclic guanosine monophosphate thus exerting vasodilating properties and facilitating penile erection[40-42]. Due to these properties, sildenafil was the first drug of its class to receive wide acceptance. Its short half-life, food interactions and the associated visual disturbances however, paved the way for the development of newer PDE-5 inhibitors. As such vardenafil with its more rapid onset of action, and tadalafil with its longer half-life and the lack of food interactions or side effects, have offered significant alternatives to sildenafil[43-50].

But there are also medical devices like the Elator, which is approved by the Food and Drug Administration (FDA) and is custom-made with medical-grade silicone based on a patient’s girth and shaft. The technology, which has no known risk factors, has two thin bars that glide along the bottom of the penis, and hold the organ partially or fully erect with a soft, flexible loop, a sliding latch and a base lock and base ring.
Crossref | PubMed | Scopus (174) | Google ScholarSee all References All these men had ED and twice underwent symptom-limited supine bicycle exercise echocardiography 1 hour after taking either sildenafil (50 mg or 100 mg) or placebo. This study found no significant changes in resting heart rate, diastolic blood pressure level, or wall motion score index, and the exercise capacity of the 2 groups was similar. Both groups had similar numbers of patients who experienced dyspnea and/or chest pain, had a positive exercise echocardiographic test, and had exercise-induced wall motion abnormalities. Sildenafil caused a mean decrease of 7 mm Hg in the resting systolic blood pressure level compared with the placebo group. In conclusion, this study showed that in patients with stable coronary artery disease, sildenafil caused no change in symptoms, exercise endurance, or presence/extent of exercise-induced ischemia as measured by exercise echocardiography.
Crossref | Google ScholarSee all References A 1985 study found that ED accounted for 400,000 outpatient visits and 30,000 hospital admissions per year in the United States, with a direct total cost of $146 million.4x4Feldman, HA, Goldstein, I, Hatzichristou, DG, Krane, RJ, and McKinlay, JB. Impotence and its medical and psychosocial correlates: results of the Massachusetts Male Aging Study. J Urol. 1994; 151: 54–61
Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References However, some researchers have questioned whether the strain of sexual activity can be compared accurately with standard types of physical activity and whether sexual activity is more closely related to episodes of anger or fear.85x85DeBusk, RF. Evaluating the cardiovascular tolerance for sex. Am J Cardiol. 2000; 86: 51F–56F
Diaclina (also known as Panzer’s Darkling Beetle), Korean bug are used as aphrodisiacs in China, Korea and Southeast Asia. These are consumed either whole or as compounds within capsules. It is felt that the aphrodisiac properties come by stimulating the urogenital structures. Flies have been studied for their aphrodisiac effects, including Spanish fly, Chinese cantharide, and Eastern-Indian cantharide (32). The active compound found in the dried and mashed up bodies of these flies is cantharidin, which is a pheromone produced in the accessory glands of the male flies’ genitals. Cantharidin, stimulates the urogenital tract, causing pelvic hyperemia and possibly erections. As cantharidin is toxic and its safety dose not well determined, its use cannot be recommended. Cantharidin is lethal at high doses and exposure can lead to gastrointestinal and urogenital hemorrhage as well as acute renal failure.
Overall, sildenafil appears to be relatively safe and effective for treatment of ED in men with stable cardiovascular disease who are not taking NO-donor medications. In a study of 105 men with ED and known or likely coronary artery disease, patients underwent symptom-limited supine bicycle echocardiography 2 times after receiving either sildenafil or placebo.63x63Arruda-Olson, AM, Mahoney, DW, Nehra, A, Leckel, M, and Pellikka, PA. Cardiovascular effects of sildenafil during exercise in men with known or probable coronary artery disease: a randomized crossover trial. JAMA. 2002; 287: 719–725

In the vessels that supply the heart, healthy arteries enlarge in diameter up to 50% during exercise when sufficient nitric oxide is present. Because of its brief half-life, a continual supply of nitric oxide is required for optimal effect. If the supply of nitric oxide is inadequate, endothelial dysfunction—a core factor in heart disease—is made worse. Endothelial dysfunction can trigger the growth of coronary plaque.8
Admitting to your doctor that you are having trouble achieving an erection can be difficult, but take comfort in the fact that they are not judging you and are there to improve your health and well-being. If you are just beginning a blood pressure treatment regimen and are beginning to experience erectile dysfunction, tell your doctor as soon as you can—they can solve the problem by simply changing the prescription.

DHEA is a hormone made by the human body. It’s a building block for testosterone. According to a study published in Urology, this supplement may be able to help men whose ED is related to having low testosterone. However, there’s no definitive evidence of this benefit. It’s clear that DHEA can cause various side effects, including liver damage and acne. Long-term use of DHEA can also cause hormonal imbalances.
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Overall, sildenafil appears to be relatively safe and effective for treatment of ED in men with stable cardiovascular disease who are not taking NO-donor medications. In a study of 105 men with ED and known or likely coronary artery disease, patients underwent symptom-limited supine bicycle echocardiography 2 times after receiving either sildenafil or placebo.63x63Arruda-Olson, AM, Mahoney, DW, Nehra, A, Leckel, M, and Pellikka, PA. Cardiovascular effects of sildenafil during exercise in men with known or probable coronary artery disease: a randomized crossover trial. JAMA. 2002; 287: 719–725
When it comes to combating heart disease, most information sources promote drugs and surgery as the only viable options, with lip service to dietary advice that simply does not work. As a result, the demand for high-tech, expensive, but largely ineffective medical care is soaring, causing medical costs and insurance rates to skyrocket. This chase for "cures" is both financially devastating and futile. Morbidity and premature mortality from heart disease continue to rise, with no sign of abating.
Since their introduction in the therapeutic field, more than a decade ago, PDE-5 inhibitors have revolutionized the treatment of sexual dysfunction. By blocking the activity of PDE-5 isoenzyme, localized throughout the smooth muscle cells of the vasculature (genital vessels included), PDE-5 inhibitors increase the levels of cyclic guanosine monophosphate thus exerting vasodilating properties and facilitating penile erection[40-42]. Due to these properties, sildenafil was the first drug of its class to receive wide acceptance. Its short half-life, food interactions and the associated visual disturbances however, paved the way for the development of newer PDE-5 inhibitors. As such vardenafil with its more rapid onset of action, and tadalafil with its longer half-life and the lack of food interactions or side effects, have offered significant alternatives to sildenafil[43-50].
DHEA is a hormone made by the human body. It’s a building block for testosterone. According to a study published in Urology, this supplement may be able to help men whose ED is related to having low testosterone. However, there’s no definitive evidence of this benefit. It’s clear that DHEA can cause various side effects, including liver damage and acne. Long-term use of DHEA can also cause hormonal imbalances.
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).
Crossref | PubMed | Scopus (443) | Google ScholarSee all References Nitroglycerin and other NO donors work through the same NO-cGMP pathway that sildenafil affects, thereby decreasing vascular resistance and blood pressure level.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
Tribulus terrestris is a dicotyledonous herbal plant of the Zygophyllaceae family, used to increase serum testosterone levels, which has only been shown in animal studies (40). A prospective, randomized, double blind study of 30 men showed that Tribulus terrestris was not more effective than placebo on improving IIEF scores or serum total testosterone (41). Two accounts of hepato-nephrotoxicity have been reported in young men who ingested high doses of this herbal medication (42,43).
Artery size also explains the onset of ED before occurrence of CAD. Coronary arteries are 3–4 mm in diameter, while the penile artery is 1–2 mm in diameter.17 Endothelial dysfunction and plaque burden in the small arteries may cause symptoms of ED before they affect blood flow in large arteries. Also, an asymptomatic lipid-rich plaque in the coronary arteries carries the risk of rupture that leads to acute coronary syndrome or death, so ED may be predictive of these serious events without warning cardiac symptoms.17
airdone/ShutterstockErectile dysfunction (ED) is a serious issue for men, which helps explain all the prescription drugs, over-the-counter treatments, and herbal concoctions that claim to cure ED. (In fact, it’s one of the top nine health risks men need to watch out for.) But before any guy decides to take matters into his own hands, he should talk to his doctor about a heart checkup: A new study published in the journal Vascular Medicine suggests ED can signal cardiovascular concerns.
Perk J,  De Backer G,  Gohlke H,  Graham I,  Reiner Z,  Verschuren WM,  Albus C,  Benlian P,  Boysen G,  Cifkova R,  Deaton C,  Ebrahim S,  Fisher M,  Germano G,  Hobbs R,  Hoes A,  Karadeniz S,  Mezzani A,  Prescott E,  Ryden L,  Scherer M,  Syvänne M,  Scholte Op Reimer WJ,  Vrints C,  Wood D,  Zamorano JL,  Zannad F. European Guidelines on cardiovascular disease prevention in clinical practice (version 2012). The Fifth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by representatives of nine societies and by invited experts). Developed with the special contribution of the European Association for Cardiovascular Prevention & Rehabilitation (EACPR), Eur Heart J , 2012, vol. 33 (pg. 1635-1701)https://doi.org/10.1093/eurheartj/ehs092

Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Phase 2 and 3 trials reported minimal associated cardiac adverse effects, which occurred in 3% of patients taking sildenafil and in 3.5% of patients receiving placebos.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N


DHEA is a hormone made by the human body. It’s a building block for testosterone. According to a study published in Urology, this supplement may be able to help men whose ED is related to having low testosterone. However, there’s no definitive evidence of this benefit. It’s clear that DHEA can cause various side effects, including liver damage and acne. Long-term use of DHEA can also cause hormonal imbalances.


The Massachusetts Male Aging Study of 1,290 men, aged 40–70 years, has documented the extraordinarily high prevalence of erectile dysfunction among aging men: 50% of men at 50 years of age, and 70% by age 70 have erectile dysfunction.2 Furthermore, a recent Italian study of men with severe heart disease has uncovered an astounding 93% with erectile dysfunction 24 months before their heart attack or onset of heart disease symptoms.3
A study conducted by Prince Henry’s Institute in Melbourne Australia published in the Medical Journal of Australia found that men over 20 years of age with erectile dysfunction (ED) have twice the risk of cardiovascular incidents than those of men with normal sexual health. It was also found out that 2% of men aged 55 and older experienced major stroke and cardiac arrest after the initial episode of ED, within a year; 11% experienced something within five years.  Experts from Prince Henry’s Institute warned men with these failures to seek advice on erectile dysfunction and high blood pressure. This may indicate a missing vital warning sign of impending heart disease. Why is this happening? Do men with ED predispose themselves to have cardiovascular diseases and strokes or just the other way around?
Uses and risks of viagra Viagra treats erectile dysfunction and pulmonary arterial hypertension. For sexual purposes, it helps someone with erectile dysfunction achieve and maintain an erection. However, Viagra can have unpleasant side effects, and an overdose can be serious. We cover everything you need to know about Viagra in this article. Read now
The choice is yours. You do not have to die of a heart attack, and you do not have to have erectile dysfunction. Both are the result of dietary choices, and you can make a choice right now to protect your life. Do you want to die of a heart attack or don’t you? If you don’t, then are you willing to do what it takes to reduce your risk almost 100 percent? I don’t know about you, but for me, just dropping my risk 20 to 40 percent with medical care is not enough. I want maximum protection.
The pilot study by Vardi et al. (18) showed that LIESWT was effective in treating men with ED, suggesting a physiologic impact of LIESWT on cavernosal hemodynamics. The LIESWT is an effective penile rehabilitation tool that improves erectile function and potentially reverses underlying ED. Recent meta-analysis (19) of 14 studies showed that LiESWT could significantly improve the International Index of Erectile Function (IIEF) [mean difference: 2.00; 95% confidence interval (CI), 0.99–3.00; P<0.0001] and Erection Hardness Score (EHS) (risk difference: 0.16; 95% CI, 0.04–0.29; P=0.01). In addition, the therapeutic efficacy was noted to last for at least 3 months. LiESWT has been cited to a potential cure for ED, unlike other well established non-surgical methods of treatment (i.e., PDE5i, ICI and VED) being on demand treatments.
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).
The truth is medication or psychosexual counselling are the first treatments a doctor will suggest because they’ve been proven to work. If a doctor has approved a medication for you then it’s safe. If you would still like to see if herbal supplements work for you, then there is a list below of supplements thought to work for erectile dysfunction. Just before you invest your money in them, remember they aren’t proven to work:

Following the breakthrough in ED treatment using PDE5-inhibitors, Western medicine has now moved on to a new frontier of regenerative medicine, with stem cell and gene therapy leading the way (25). There is a practical need for novel therapy as a significant portion of diabetic or post-prostatectomy ED patients do not respond to oral pharmacotherapy. To date, stem cells derived from different sites including adipose tissue-derived stem cells, bone marrow mesenchymal stem cells and muscle-derived stem cells have been investigated using animal models for ED, to study their effects on neural, vascular, endothelial or smooth muscle regeneration (25,26).

If you have several atherosclerotic risk factors or symptoms of heart disease, your doctor might do additional tests to look for atherosclerosis in the coronary arteries. A stress test involves monitoring the heart with an electrocardiogram or images before and after exercise. An angiogram, or cardiac catheterization, involves entering a blood vessel in the leg or wrist to pass instruments into the heart to directly visualize the coronary arteries. During this procedure, atherosclerosis can be treated by inflating a balloon or placing a metal stent in the coronary blood vessel to keep it open. If you and your doctor begin a treatment plan to prevent atherosclerosis at the first sign of ED, then you may significantly delay or prevent the need for these more invasive procedures.
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Previous studies reported that there is a strong chance of future cardiac events when ED occurs in younger men compared with older men.11 Another study suggested that there is consistent association across age groups.12 A study of men with diabetes found that ED acts as an indicator of cardiovascular events after adjusting for other illnesses, psychological aspects and the usual cardiovascular risk factors.13 Another large-scale study comprising 25,650 men with pre-existing ED suggested that these men had a 75 % increased risk of peripheral vascular disease.14 Moreover, some studies demonstrated a relationship between ED score and number of diseased coronary arteries and plaque burden in coronary arteries.2,15
Other factors that “stress” the body can also increase your risk for ED. These include: substance abuse, using marijuana, smoking cigarettes, depression, anxiety and low self esteem. Cigarette smoking — or using nicotine — leads to constricted blood vessels, which has negative effects for sexual health. Other mental/emotional obstacles can cause less desire for sex and decrease testosterone. Several ways to help manage stress include:

A deficiency of L-arginine, however, does not generally disrupt nitric oxide synthesis because L-arginine availability is not the rate-limiting step in this process. In fact, research over the past five years has identified an endogenous (occurs in the body naturally) inhibitor called “asymmetric dimethylarginine” or ADMA, an amino acid which blocks the production of nitric oxide. By acting as an L-arginine mimic, this damaging look-alike effectively elbows out L-arginine and pushes it off to the side in the biochemical pathway leading to the synthesis of nitric oxide. ADMA is relatively elevated in patients with hypertension, high levels of cholesterol, triglycerides, homocysteine and low-density lipoprotein (LDL), and low levels of high-density lipoprotein (HDL), as well as with aging itself. This inhibitor of nitric oxide synthesis may very well be the common factor shared by all of these abnormal conditions. Increased levels of this detrimental inhibitor (ADMA) block nitric oxide production, leading to endothelial dysfunction.

The Massachusetts Male Aging Study of 1,290 men, aged 40–70 years, has documented the extraordinarily high prevalence of erectile dysfunction among aging men: 50% of men at 50 years of age, and 70% by age 70 have erectile dysfunction.2 Furthermore, a recent Italian study of men with severe heart disease has uncovered an astounding 93% with erectile dysfunction 24 months before their heart attack or onset of heart disease symptoms.3


Crucial to the understanding of the relationship between ED and CVD and the management of ED patients within the context of the (potential) CVD were the consecutive Princeton Consensus Recommendations (I: 2000, II: 2005, and III: 2012). The reader is strongly encouraged to refer to the most recent, third (2012) Princeton Consensus.30 Key notions in the assessment and management of the patient with organic ED are that (i) he should be considered at increased CVD risk until recommended checks suggest otherwise, and (ii) ED identifies increased CVD risk in the presence or absence of CVD symptoms or history.
Finally, prevalence rates will be affected by whether the study population is accrued from a single hospital/clinic setting or from a more general population of men with diabetes. For example, Siu et al.4 studied 500 Chinese diabetic men (of which 97% had type 2 disease) seen at a single medical clinic in Hong Kong during 1999 and found the overall prevalence of ED to be 63.6%. Contrast this to Fedele et al.,5 who studied 9,756 diabetic men accrued from 178 diabetes centers in Italy. Among the 8,373 men with type 2 diabetes, only 37% reported ED, considerably less than in the Chinese study.
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