Medicines known as PDE5 inhibitors can help two-thirds of men with ED. These include Viagra (sildenafil), Cialis (tadalafil) and Levitra (vardenafil). You may need to take several doses over time before they work properly, and you may need to adjust the dose. National guidelines say you can be prescribed these drugs from six months after a heart attack, providing your condition is stable.
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
Erectile dysfunction (ED) is a common sexual problem affecting many men irrespective of cultures, beliefs and nationalities. While medical therapy for ED has been revolutionized by the advent of oral phosphodiesterase type 5 inhibitors and intracavernosal injection of vasoactive agents, recent technological advances such stem cell therapy, low intensity shock wave and newer generation of penile prosthesis implant offer hope to men who do not respond to conventional medical therapy. In contrast, traditional and complementary medicine (TCM) focuses on the restoration and better overall bodily regulation with the use of various herbal and animal products as well as exercises to invigorate qi (energy) in vital organs. Western medicine involves an analysis of ED symptom and underlying causes that contribute to ED, while TCM emphases the concept of holism and harmonization of body organs to achieve natural sexual life. The following article reviews our current understanding regarding the philosophical approach, and evaluates the evidence surrounding various ED therapies between mainstream Western Medicine and TCM.

The drugs come in several strengths. Most men should start with a low to moderate dose. The dose can be adjusted depending on the results. Men with potential problems should always start with the lowest dose. Every man should avoid consuming alcohol before taking these drugs. Men who do not respond to a full dose on two or three different occasions should try other treatments.

Andersson said the results came as a surprise because erectile dysfunction is associated with an increased risk of heart disease in otherwise healthy men. However, previous studies have associated the use of PDE5 inhibitors with a decreased blood pressure in the left ventricle, which reduces the amount of work required to pump blood and therefore could help explain why the drugs might benefit people with heart failure. PDE5 inhibitors were initially developed to treat angina, a type of chest pain that results from constricted arteries.


Control your blood sugar through your diet. Eating a diabetes-friendly diet will help you better control your blood sugar levels and lessen the amount of damage to your blood vessels and nerves. A proper diet geared at keeping your blood sugar levels in check can also improve your energy levels and mood, both of which can help reduce the risk of erectile dysfunction. You may consider working with a dietitian who is also a certified diabetes educator to help adjust your eating style.

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Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Phosphodiesterase type 5 is found predominantly in the smooth muscle of the corpora cavernosa but can be found in smaller quantities in platelets and other vascular smooth muscle.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
Montorsi F,  Briganti A,  Salonia A,  Rigatti P,  Margonato A,  Macchi A,  Galli S,  Ravagnani PM,  Montorsi P. Erectile dysfunction prevalence, time of onset and association with risk factors in 300 consecutive patients with acute chest pain and angiographically documented coronary artery disease, Eur Urol , 2003, vol. 44 (pg. 360-364)https://doi.org/10.1016/S0302-2838(03)00305-1
Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References However, α-blockers are a well-known cause of retrograde ejaculation secondary to a reversible relaxation of bladder neck smooth muscle.50x50Meinhardt, W, Kropman, RF, Vermeij, P, Nijeholt, AA, and Zwartendijk, J. The influence of medication on erectile function. Int J Impot Res. 1997; 9: 17–26
Gutiérrez-González, Enrique; Castelló, Adela; Fernández-Navarro, Pablo; Castaño-Vinyals, Gemma; Llorca, Javier; Salas-Trejo, Dolores; Salcedo-Bellido, Inmaculada; Aragonés, Nuria; Fernández-Tardón, Guillermo; Alguacil, Juan; Gracia-Lavedan, Esther; García-Esquinas, Esther; Gómez-Acebo, Inés; Amiano, Pilar; Romaguera, Dora; Kogevinas, Manolis; Pollán, Marina; Pérez-Gómez, Beatriz. “Dietary Zinc and Risk of Prostate Cancer in Spain: MCC-Spain Study.” Nutrients. Jan 2019, 11(1).
At the same time, people with diabetes are susceptible to a type of blood vessel damage known as endothelial dysfunction. A recent study found that men with ED are at a greater risk of heart disease, which is also associated with endothelial dysfunction. If blood vessels aren't in good working order, the penis may not get enough blood for an erection.
Crossref | PubMed | Google ScholarSee all References In the general population, the estimated relative risk of experiencing a myocardial infarction within 2 hours after sexual intercourse is approximately 2.5 times higher than the baseline infarction risk of that individual, which itself is extremely low8x8Muller, JE, Mittleman, A, Maclure, M, Sherwood, JB, Tofler, GH, and Determinants of Myocardial Infarction Onset Study Investigators. Triggering myocardial infarction by sexual activity: low absolute risk and prevention by regular physical exertion. JAMA. 1996; 275: 1405–1409
The initial event for normal erectile function is sexual stimulation. Subsequent to processing in the central nervous system neural impulses are conveyed along the spinal cord, exiting through the pelvic parasympathetic preganglionic nerves. These pelvic nerves form the pelvic plexus and send their message through first messenger, acetyl choline, to the cavernosal nerves. The cavernosal nerves enter erectile bodies (corpora cavernosa) (Figure 1). Here, their nerve endings release a second messenger, nitric oxide. Nitric oxide activates the enzyme guanylyl cyclase, which lyses guanosine triphosphate (GTP) to produce a third messenger, the intracellular cyclic guanosine monophosphate (cGMP). Ultimately, the result is a decrease of intracellular calcium and an opening of potassium channels with the resultant relaxation of vascular smooth muscle in the arteries, aterioles, and sinusoids of the corpora cavernosa. The sinusoids open and rapidly fill with blood. Finally, the distended sinusoids compress their drainage pathways (venules) against the fibroelastic covering of the cavernosal bodies (tunica albuginea) and trap the blood in cavernosal bodies. The combination of an increased inflow of blood into the penis and coincident markedly diminished outflow results in rapidly increasing intracavernosal pressure that ultimately approximates systolic pressure. At this pressure the penis has sufficient axial rigidity to permit vaginal penetration.

ED is a common complication of diabetes that affects patients' quality of life. While the etiology of this complication may be multifactorial in nature, it is clear that it usually has a strong organic component. Because men with diabetes value their erectile function highly, it is important that providers encourage them to maintain good glycemic, blood pressure, and lipid control to minimize their risk of developing this complication.
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].
Penile erection is largely a vascular process, and the penile endothelium and smooth muscle tissue are very sensitive to functional and structural changes. Vasculogenic ED results from an impairment of endothelial dependent or independent smooth muscle relaxation (functional vascular ED, initial stages), occlusion of the cavernosal arteries by atherosclerosis (structural vascular ED, late stages), or a combination of these.3 Current data support a complex interplay between endothelial dysfunction, subclinical inflammation, and androgen deficiency (Figure 1). The relationship between ED and CAD at the clinical level is supported by this common pathophysiological basis. The ‘artery size’ hypothesis explains why patients with CAD frequently report ED before CAD detection.10 According to this hypothesis, for a given atherosclerotic burden, the smaller penile arteries suffer obstruction earlier than the larger coronary arteries (Figure 2). The same concept holds also true in the case of non-obstructing atherosclerosis: since the smaller penile artery have a greater endothelial surface and erection requires a large degree of vasodilation to occur when compared with arteries in other organs, the same degree of endothelial dysfunction will be symptomatic in these smaller vessels but subclinical in the larger ones (i.e. coronaries). In the same context, accelerated arterial ageing (as indicated by increased arterial stiffening that also affects large arteries of ED patients) may be a common background.11,12 Erectile dysfunction is associated with an incremental inflammatory and endothelial-pro-thrombotic activation.13 Interestingly, this activation is equal to that found in CAD patients with no ED, while when these two conditions are combined the burden is additive. Androgen deficiency may be also implicated in the common pathogenetic pathways of ED and CVD; however, this warrants further substantiation.2
“I’m hoping this study will drive that (tie) a little bit harder and faster so that physicians will routinely be including ED when they’re screening patients for cardiovascular disease,” he said. “Doctors should ask the question and consider whether hardening of the arteries is occurring, ask about family history and signs or symptoms like chest pain with exertion, and spend the requisite amount of time to find out what’s going on.”
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
Montorsi F,  Briganti A,  Salonia A,  Rigatti P,  Margonato A,  Macchi A,  Galli S,  Ravagnani PM,  Montorsi P. Erectile dysfunction prevalence, time of onset and association with risk factors in 300 consecutive patients with acute chest pain and angiographically documented coronary artery disease, Eur Urol , 2003, vol. 44 (pg. 360-364)https://doi.org/10.1016/S0302-2838(03)00305-1
The art of acupuncture has become the new treatment for everything from back pain, depression, and even ED. Impotence could be more of a state of mind, and acupuncture may help. Through this alternative therapy, fine needles are placed in various parts of the body to relieve pain or stress. Although there are many mixed studies for acupuncture and ED, many tend to confirm positive results. A 1999 study found acupuncture improved the quality of erection and even restored sexual activity in 39 percent of participants.
When antihypertensive medication comes to the fore, certain issues need to be carefully addressed. This is due to the fact that medically induced erectile dysfunction is one of the major reasons for non-adherence and treatment discontinuation, a reality that could have deleterious consequences on patient’s cardiovascular profile and health quality in the long term[38,39].
Getting frequent exercise and maintaining a healthy weight are, of course, also important. Plus, avoiding or minimizing risky dietary factors such as salt, alcohol, caffeine, and too much animal products is crucial. Animal protein elevates insulin-like growth factor 1 (IGF-1) in the blood, a growth-promoting hormone that is associated with increased risk of several cancers and cardiovascular disease.19, 20
Organic nitrates are drugs that widen arteries by increasing their supply of nitric oxide; that's how they open the partially blocked coronary arteries in patients with angina. But because nitrates and ED pills both act on nitric oxide, the drugs don't mix; healthy volunteers given Viagra followed an hour later by nitroglycerin see their blood pressures drop by 25–51 mm Hg, a potentially dangerous amount. All experts agree that men who are taking nitrates cannot use ED pills; this includes all preparations of nitroglycerin (short-acting, under-the-tongue tablets or sprays), long-acting nitrates (isosorbide dinitrate or Isordil, Sorbitrate, and others, and isosorbide mononitrate, Imdur, ISMO, and others), nitroglycerin patches and pastes, and amyl nitrite or amyl nitrate (so-called poppers, which some men use for sexual stimulation).
The safety of PDE5 inhibitors in patients with IHD has been shown in multiple trials. Arruda-Olson et al. investigated the safety of sildenafil during exercise stress tests in patients with IHD to ascertain whether the drug induces or exacerbates myocardial ischaemia. This was a prospective, randomised crossover study that demonstrated safety of sildenafil when given 1 hour before an exercise stress test.69 Another study that investigated 120 trials of sildenafil revealed that the rates of MI and cardiovascular death with sildenafil are as low as with placebo.70
And diabetes affects more than the blood system. “Diabetes also results in nerve dysfunction and, in the penile shaft, [eventually] the muscle starts to atrophy and is replaced by scar tissue or collagen rather than smooth muscle. That’s the ultimate end result in men,” explains urologist Ajay Nehra, MD, professor of urology at the Mayo Clinic in Rochester, Minn. That scenario — damage to all the tissues that support your penis — is what could happen if you do not get and keep your diabetes under control.
Some blood pressure medicines can also cause erectile dysfunction. Thiazide diuretics and beta-blockers are most likely to cause problems, but this is not a common effect of these medicines and will not happen to everyone. If you are taking either of these medicines and are worried about erectile dysfunction, your GP may be able to change your medicines.
Sexual dysfunction is a common, underappreciated complication of diabetes. Male sexual dysfunction among diabetic patients can include disorders of libido, ejaculatory problems, and erectile dysfunction (ED). All three forms of male dysfunction can cause significant bother for diabetic patients and can affect their quality of life. Despite this, health care providers often do not specifically ask their male diabetic patients about sexual function. This results in considerable underdiagnosis because patients are often reluctant or embarrassed to initiate discussion of these issues themselves. By not recognizing sexual dysfunction as a common organic sequel-lae of diabetes that should be addressed and treated, providers are missing an important opportunity to improve their patients' daily existence and quality of life.
After the initiation of TTh patients should be evaluated at 3 and 6 months, and annually thereafter to assess response to treatment and monitor adverse effects. Assessment should include physical examination with particular attention to the prostate. At these intervals testosterone levels should also be monitored, as well as PSA, haematocrit, and HDL.45
Penile erection is largely a vascular process, and the penile endothelium and smooth muscle tissue are very sensitive to functional and structural changes. Vasculogenic ED results from an impairment of endothelial dependent or independent smooth muscle relaxation (functional vascular ED, initial stages), occlusion of the cavernosal arteries by atherosclerosis (structural vascular ED, late stages), or a combination of these.3 Current data support a complex interplay between endothelial dysfunction, subclinical inflammation, and androgen deficiency (Figure 1). The relationship between ED and CAD at the clinical level is supported by this common pathophysiological basis. The ‘artery size’ hypothesis explains why patients with CAD frequently report ED before CAD detection.10 According to this hypothesis, for a given atherosclerotic burden, the smaller penile arteries suffer obstruction earlier than the larger coronary arteries (Figure 2). The same concept holds also true in the case of non-obstructing atherosclerosis: since the smaller penile artery have a greater endothelial surface and erection requires a large degree of vasodilation to occur when compared with arteries in other organs, the same degree of endothelial dysfunction will be symptomatic in these smaller vessels but subclinical in the larger ones (i.e. coronaries). In the same context, accelerated arterial ageing (as indicated by increased arterial stiffening that also affects large arteries of ED patients) may be a common background.11,12 Erectile dysfunction is associated with an incremental inflammatory and endothelial-pro-thrombotic activation.13 Interestingly, this activation is equal to that found in CAD patients with no ED, while when these two conditions are combined the burden is additive. Androgen deficiency may be also implicated in the common pathogenetic pathways of ED and CVD; however, this warrants further substantiation.2
For centuries, men have tried all sorts of natural remedies for erectile dysfunction (ED) -- the repeated inability to get or maintain an erection firm enough for sexual intercourse. But do they really work? It is simply not scientifically known at this point. Furthermore, you take these remedies at your own risk, because their safety profiles have not been established. What follows are commentaries by experts and reviews in the field of alternative treatments that are available over the counter for erectile dysfunction and impotence.
Guidelines recommend that phosphodiesterase type 5 (PDE5) inhibitors are the first-line drug for the treatment of ED (Table 1). Sildenafil citrate was the first oral drug approved for ED in the US.59 The newer PDE5 inhibitors include vardenafil, tadalafil and avanafil. The inhibition of PDE5 enhances cyclic guanosine monophosphate (cGMP)-NO-mediated vasodilatation by preventing PDE5 catabolism of cGMP and so delaying detumescence. PDE5 inhibitors increase the number and duration of erections, as well as the percentage of successful sexual intercourse.60
A considerable number of patients with ED can have psychogenic factors as the only cause, or in combination with organic causes of ED. Depression, low self-esteem and social stresses are among the psychogenic factors that can lead to ED. Depression is an independent risk factor for both ED and IHD; these three disease conditions are interlinked.51 Psychogenic ED can be managed by multiple psychological interventions such as cognitive behavioural therapy, couples counselling and guided sexual stimulation techniques.52
According to the Mayo Clinic, oral medications are usually the first-line treatment for ED. Those medications include Sildenafil (Viagra), vardenafil (Levitra, Staxyn), tadalafil (Cialis) and avanafil (Stendra). They operate by helping relax muscles in the penis by strengthening the effects of nitric oxide, a naturally occurring chemical in the body. The drugs increase blood flow to allow patients to get an erection.
The term “heart disease” is often used interchangeably with the term “cardiovascular disease.” Cardiovascular disease generally refers to conditions that involve narrowed or blocked blood vessels that can lead to a heart attack, chest pain (angina) or stroke. Other heart conditions, such as those that affect your heart’s muscle, valves or rhythm, also are considered forms of heart disease.
Abnormalities in the vascular, neural, endocrine, muscular, or psychiatric systems can result in ED.2,3 EDDM is due to multisystemic disease. Atrophy or apoptosis of cavernosal smooth muscle can occur due to loss of Bcl-2 expression in cavernosal smooth muscle and lead to ED. Abnormal amounts of advanced glycation end products is a common occurrence. These chemicals may have an effect on potassium channels that facilitate intracellular calcium release and subsequent cavernosal smooth muscle relaxation. Connective tissue synthesis is increased due to transforming growth factor-beta. The decrease in smooth muscle and the increase in collagen decreases the compliance of the erectile tissue. Neuropathic damage to both the somatic and autonomic nerves has been clearly defined in DM. Partial occlusion of the pelvic or intracavernosal arteries, hypogonadotropic hypogonadism, and depression associated with a chronic illness (DM) can all play a primary or secondary role in the development of EDDM. On a molecular level, studies have demonstrated decreased levels of endothelial and neuronal nitric acid synthase (NS) and decreased cavernosal artery and sinusoidal response to nitric oxide. Abnormalities in nitric oxide rapidly render the functional syncytium of the corpora cavernosa unable to synchronously relax. As the patient with diabetes ages, the concentration of constrictors, including endothelin, prostanoids, and possibly angiotensin, increases as the production of the relaxants, including nitric oxide, vasointestinal peptide, and prostacyclin, decreases.
Experimental in vivo studies have implicated central and peripheral neuropathy, impaired neurotransmission, and endothelial dysfunction in the pathogenesis of diabetic ED.26,27 Copulatory behavior and penile reflexes are uniformly impaired 4–12 months after the onset of diabetes in the BB rat.26,27 McVary et al.26 found that peripheral neuropathy accounts for only part of the dysfunctional findings, and that spinal sexual reflexes were also severely impaired.
Crossref | PubMed | Scopus (72) | Google ScholarSee all References This study found that the mean PSV was a better predictor of the presence of cardiovascular disease than stratification by standard cardiac risk factors such as diabetes mellitus, hypertension, obesity, and smoking. The researchers recommended that persons with no history of prior perineal trauma and with a PSV lower than 35 mL/s should undergo exercise testing before receiving treatment of ED because these patients had a 42% risk of having ischemic heart disease. However, other investigators questioned the utility of using penile arterial flow to predict the presence of ischemic heart disease.18x18Chiu, AW, Chen, KK, Chen, MT, Chang, LS, and Chang, MS. Penile brachial index in impotent patients with coronary artery disease. Eur Urol. 1991; 19: 213–216
Oral medicines: The best known ED medications are the Big Three: Viagra (sildenafil citrate, made by Pfizer, Inc.), Levitra (vardenafil HCl, made by Bayer and GlaxoSmithKline), and Cialis (tadalafil, made by Eli Lilly). The three are chemically very similar, and all have proven very effective. Because they are effective, convenient, and relatively inexpensive (about nine dollars per pill), these medicines have become the treatment of choice for most men experiencing ED.
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