Abstract | Full Text | Full Text PDF | PubMed | Scopus (207) | Google ScholarSee all References Adverse-effect profiles of headaches, flushing, rhinitis, and dyspepsia, without visual changes, mimic those of vardenafil.74x74Gresser, U and Gleiter, CH. Erectile dysfunction: comparison of efficacy and side effects of the PDE-5 inhibitors sildenafil, vardenafil and tadalafil—review of the literature. Eur J Med Res. 2002; 7: 435–446

Abstract | Full Text PDF | PubMed | Scopus (29) | Google ScholarSee all References After controlling for diabetes mellitus, tobacco use, and hyperlipidemia, hypertension was not found to be an independent predictor of vasculogenic ED in 440 impotent men as measured by the PBI.7x7Virag, R, Bouilly, P, and Frydman, D. Is impotence an arterial disorder? a study of arterial risk factors in 440 impotent men. Lancet. 1985; 1: 181–184
Despite physician’s inexperience and patient’s reluctance to disclose sexual dysfunction problems, attempts to estimate the magnitude of this clinical condition have predicted that over 150 million men worldwide experience some degree of erectile dysfunction. Several studies have demonstrated a wide range regarding the prevalence of erectile dysfunction, which is even higher in patients with essential hypertension where the relative risk is approximately two times higher than in normotensive individuals[6-11]. The etiology can be found in the structural and functional abnormalities of the penile arteries induced by high blood pressure. Smooth muscle hypertrophy, stenotic lesions due to atherosclerosis and impaired blood flow are among the prominent structural alterations whereas endothelial dysfunction and the defective nitric oxide-induced vasodilatory mechanism belong to the main functional abnormalities induced by increased blood pressure[12,13]. As a matter of fact, sexual dysfunction is encountered more frequently that it is indeed believed underlining the need for a more proper and concrete assessment.
Relation between erectile dysfunction prevalence and type of coronary syndrome (A). Time interval (months) between erectile dysfunction and coronary artery disease symptom onset in chronic coronary syndrome according to the number of vessels involved (B). ACS, acute coronary syndrome; CCS, chronic coronary syndrome, G1: ACS and 1-VD; G2: ACS and 2-,3-VD; G3: CCS. VD, vessel disease; C: the control group with normal coronary angiography. With permission from Montorsi et al.15
There are a number of herbs and supplements for use in men with ED. However, the overall quality of the studies evaluating these treatments has been low. Therefore, evidence for the effectiveness and safety of these therapies is limited. Many of these therapies have known risks, and there’s a possibility that other risks are yet to be discovered. Always use CAM therapies with caution.
De Berardis et al.6 assessed general HRQOL in 1,460 men with type 2 diabetes in Italy. Within the cohort, 615 men reported that they never experienced ED, 346 stated that they occasionally had ED, and 449 stated that they frequently had ED. They then compared general HRQOL among these three groups. In the univariate analysis, they found that degree of ED negatively correlated with general HRQOL scores in all eight domains of the Short Form 36 (SF-36) health survey questionnaire. In the multivariate analysis, ED was not independently associated with physical function, bodily pain, or role limitations due to physical problem scores but was independently associated with general HRQOL outcomes in the domains of general health (P = 0.004), role limitations due to emotional problems (P = 0.001), vitality (P = 0.001), social functioning (P = 0.01), and overall mental health (P = 0.002). Another study examining the effect of ED on quality of life in hemodialysis patients, more than half of whom had diabetes, also noted an independent, negative effect of ED on the emotional domains of general HRQOL.39
Basaria S,  Coviello AD,  Travison TG,  Storer TW,  Farwell WR,  Jette AM,  Eder R,  Tennstedt S,  Ulloor J,  Zhang A,  Choong K,  Lakshman KM,  Mazer NA,  Miciek R,  Krasnoff J,  Elmi A,  Knapp PE,  Brooks B,  Appleman E,  Aggarwal S,  Bhasin G,  Hede-Brierley L,  Bhatia A,  Collins L,  LeBrasseur N,  Fiore LD,  Bhasin S. Adverse events associated with testosterone administration, N Engl J Med , 2010, vol. 36 (pg. 109-122)https://doi.org/10.1056/NEJMoa1000485

Crossref | PubMed | Scopus (23) | Google ScholarSee all References In some elderly men, tadalafil could be detected in the bloodstream 6 days after oral ingestion.74x74Gresser, U and Gleiter, CH. Erectile dysfunction: comparison of efficacy and side effects of the PDE-5 inhibitors sildenafil, vardenafil and tadalafil—review of the literature. Eur J Med Res. 2002; 7: 435–446
Abstract | Full Text | Full Text PDF | PubMed | Scopus (395) | Google ScholarSee all References Sildenafil has no effect on bleeding time or prothrombin time when used either alone or in patients taking aspirin or warfarin.61x61Nehra, A, Colreavy, F, Khandheria, BK, and Chandrasekaran, K. Sildenafil citrate, a selective phosphodiesterase type 5 inhibitor: urologic and cardiovascular implications. World J Urol. 2001; 19: 40–45
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Vision changes are described most frequently as an increased perception of bright lights, a blue-green tinge to observed colors, or blurred vision. Sildenafil has no direct effect on platelet function but potentiates the inhibitory effect of sodium nitroprusside on adenosine diphosphate–induced platelet aggregation ex vivo.56x56Wallis, RM, Corbin, JD, Francis, SH, and Ellis, P. Tissue distribution of phosphodiesterase families and the effects of sildenafil on tissue cyclic nucleotides, platelet function, and the contractile responses of trabeculae carneae and aortic rings in vitro. Am J Cardiol. 1999; 83: 3C–12C
For over 25 years, Dr. Fuhrman has shown that it is possible to achieve sustainable weight loss and reverse heart disease, diabetes and many other illnesses using smart nutrition. In his medical practice, and through his books and PBS television specials, he continues to bring this life-saving message to hundreds of thousands of people around the world.

If you take a diuretic, you should stay on it until high blood pressure is under control. If erection problems persist, or blood pressure goes back up, then your doctor might switch to a drug that's less likely to cause erectile dysfunction. Or, a combination of medications might work better to control high blood pressure and lower the risk of erectile dysfunction.


Levine GN,  Steinke EE,  Bakaeen FG,  Bozkurt B,  Cheitlin MD,  Conti JB,  Foster E,  Jaarsma T,  Kloner RA,  Lange RA,  Lindau ST,  Maron BJ,  Moser DK,  Ohman EM,  Seftel AD,  Stewart WJ. Sexual activity and cardiovascular disease: a scientific statement from the American Heart Association, Circulation , 2012, vol. 125 (pg. 1058-1072)https://doi.org/10.1161/CIR.0b013e3182447787
Erectile dysfunction (ED) is defined as the inability to achieve or maintain an erection for satisfactory sexual performance. The prevalence of ED has been estimated as nearly 40% of men >40 years of age1 although these figures are contested.2 ED increases in frequency with age and is estimated to affect 15% of men aged 40–50 years, 45% of men in their 60s and 70% of men older than 70 years.3 Successful erection is a complex system involving reflex action (peripheral nerves and spinal cord), the limbic system (psychogenic stimuli) and the release of nitric oxide. Adequate levels of testosterone are required, and hence an intact hypothalamic/pituitary/testicular axis. Hence, ED can result from disease or treatment that produces hormonal deficiency, neurological impairment, problems with penile blood flow, disorders of tissue mechanics, psychological factors or any combination of these.
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
Alprostadil self-injection. With this method, you use a fine needle to inject alprostadil (Caverject Impulse, Edex) into the base or side of your penis. In some cases, medications generally used for other conditions are used for penile injections on their own or in combination. Examples include papaverine, alprostadil and phentolamine. Often these combination medications are known as bimix (if two medications are included) or trimix (if three are included).
Having your current medication checked – if you are taking medication already, it could be that your erection problems are a side effect. Have a doctor check whether this is the cause of your problems and if it is, you might be able to switch medications and then find that your erectile dysfunction goes away completely – or at least improves. Medications that can cause erection problems include:
Treatment of ED which was previously confined to invasive procedures, cavernosal injections or to rather ineffective oral medications was revolutionized in 1999 with the introduction of the orally administered PDE5 inhibitor sildenafil. Phosphodiesterase type 5 inhibitors are the first-line therapy for ED of organic aetiology unless there is a specific contraindication to their use. This class of agents is widely used because of its effectiveness and safety.38 Interactions with cardiovascular drugs have been minimal with the exception of nitrates and other nitric oxide (NO) donors (such as nicorandil), where co-administration may result in severe vasodilation and hypotension. However, nitrates are often overused in clinical practice; therefore, the option of their discontinuation should be considered. A strong body of clinical data shows that all three agents (sildenafil, tadalafil, and vardenafil) do not increase the risk of non-fatal myocardial infarction, stroke, or cardiovascular deaths. These drugs do not exacerbate ischaemia or worsen exercise tolerance in patients with known CAD who achieve levels of exercise comparable or greater than that achieved during sexual intercourse.38,39 Phosphodiesterase type 5 is expressed throughout the human body, including the pulmonary and systemic vasculature and hypertrophied myocardium. While currently their only additional indication, beyond ED, is idiopathic pulmonary hypertension (for sildenafil and tadalafil), they show potential to be of benefit in several other conditions, such as CAD and systolic heart failure.39 Mechanisms of benefit of PDE5 inhibitors include pulmonary and systemic vasodilation, increased myocardial contractility, reduced large artery stiffness and wave reflections, improved endothelial function, and reduced apoptosis, fibrosis and hypertrophy through mechanisms involving NO, cyclic guanosine monophosphate, protein kinase G and Rho kinase.39 A very important issue is whether treatment of ED per se (and not of its risk factors and comorbidities) will have an impact on cardiovascular risk. While this applies to all therapeutic modalities of ED, it is particularly pertinent for PDE5 inhibitors, since they represent the mainstay of ED therapy. Data are limited to date. Gazzaruso et al.21 showed a trend of PDE5 inhibitors to reduce cardiovascular morbidity and mortality in diabetic patients with silent CAD and ED, while Frantzen et al.40 showed that 2 years after the introduction of sildenafil, the relative risk of the incidence of CVD among men with ED compared with healthy men significantly decreased from 1.7 to 1.1.
Low testosterone levels have been observed inconsistently in STZ-induced diabetic and BB rats.18 Androgen deficiency in rats is associated with downregulation of the neuronal isoforms of nitric oxide synthase, suggesting a trophic effect of testosterone on peripheral erectile tissues. In humans, androgens play a larger role in sexual interest and motivation (libido) than in erectile capacity itself; penile erection is more resistant to androgen withdrawal than is sexual desire.19,20
In addition, when research has shown a nutrient such as zinc or niacin to improve sexual function, it's usually in people who are deficient in it. So, before you stock up on over-the-counter nutritional supplements for ED, speak with your doctor. He can test you for deficiencies and steer you toward the most effective and safest way to treat your erectile dysfunction. 

The common associations between cardiovascular disease and ED have led some researchers to explore whether onset of ED can be an effective predictor of the presence of cardiovascular disease. A study of 40 patients with cardiac disease found an association between sexual dysfunction and the presence of cardiovascular disease, as well as a correlation between the severity of ED and the number of coronary arteries with extensive atherosclerosis.16x16Greenstein, A, Chen, J, Miller, H, Matzkin, H, Villa, Y, and Braf, Z. Does severity of ischemic coronary disease correlate with erectile function?. Int J Impot Res. 1997; 9: 123–126
Now that we better appreciate the complex sequence of events necessary for erections to occur, it’s no surprise that testosterone alone yields less than perfect results. Erectile dysfunction represents more than just low testosterone, which is just one facet of the spectrum of dysfunctional phenomena that cause sexual dysfunction. Nonetheless, when testosterone is combined with popular drugs like Viagra®, success is enhanced to an even greater degree—orgasmic function improves, along with erectile capacity and libido.20 Testosterone also activates penile nitric oxide; ultrasound studies have demonstrated a 27% increase in arterial blood flow into the penis with testosterone supplementation.23
Testosterone therapy (TTh) should be reserved for patients who (i) are symptomatic (ED or reduced libido) of testosterone deficiency45 and (ii) they have biochemical evidence of low testosterone (TT <8 nmol/L or 2.3 ng/mL). In men with borderline TT (8–12 nmol/L or 2.3–3.5 ng/mL), a TTh trial (for 3–6 months and continuation if effective) may be envisaged. While adding a PDE5 inhibitor can be considered in men who have not improved with TTh, the usual clinical scenario is to add TTh in patients who have not responded to PDE5 inhibitors. Improvement is dependent on the testosterone levels with better results being obtained at lower levels of TT.45 Despite evidence of benefit in patients with pre-existing cardiovascular conditions (angina or heart failure), it should be emphasized that TTh is not a medication with cardiovascular indications.
The bad news: Men with diabetes are three times more likely to report having problems with sex than non-diabetic men. The most common sexual problem is Erectile Dysfunction, or ED, sometimes called impotence. Even worse, because ED is such a private issue, many men feel embarrassed to discuss the problem with their doctor, or even their partner, so the problem is never addressed.
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