Another risk factor is that men with type 2 diabetes may produce less than normal amounts of testosterone, a condition called hypogonadism. A 2007 study found that one-third of men with type 2 diabetes had low testosterone levels. Those men were also more likely to have ED, though the link may have to do with weight, not diabetes per se. Being overweight or obese is a risk factor for hypogonadism.

Olsson et al. conducted a randomised, double-blind, placebo-controlled, parallel group, and flexible dose study in 224 men with ED and one CVD, including IHD (20 %) and hypertension (80 %). This study reported that the sildenafil-treated group showed 71 % improvement in ED compared with the placebo-controlled group (24 %).64 Furthermore, no treatment-related cardiovascular adverse events were reported.65 Conti et al. showed in an early study that sildenafil is an effective treatment for ED in patients with IHD; the majority of patients reported improvement in penile erection with it.66 Another double-blind, placebo-controlled study of patients with ED and stable CAD showed statistically significant improvement with sildenafil versus placebo in both the frequency of penetration and frequency of maintained erections after penetration.67


Mancia G,  Laurent S,  Agabiti-Rosei E,  Ambrosioni E,  Burnier M,  Caulfield MJ,  Cifkova R,  Clément D,  Coca A,  Dominiczak A,  Erdine S,  Fagard R,  Farsang C,  Grassi G,  Haller H,  Heagerty A,  Kjeldsen SE,  Kiowski W,  Mallion JM,  Manolis A,  Narkiewicz K,  Nilsson P,  Olsen MH,  Rahn KH,  Redon J,  Rodicio J,  Ruilope L,  Schmieder RE,  Struijker-Boudier HA,  van Zwieten PA,  Viigimaa M,  Zanchetti A. European Society of HypertensionReappraisal of European guidelines on hypertension management: a European Society of Hypertension Task Force document, J Hypertens , 2009, vol. 27 (pg. 2121-2158)https://doi.org/10.1097/HJH.0b013e328333146d
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
Erectile dysfunction (ED), or impotence, is when a man has difficulty getting or maintaining a strong enough erection for sexual intercourse or other sexual activity. It can be caused by stress, anxiety or excessive alcohol consumption. But it can also be a symptom of an underlying condition such as atherosclerosis (narrowing of the arteries), diabetes or high blood pressure. Some medications can cause erectile dysfunction, for example beta-blockers and diuretics (commonly used to treat a variety of heart-related conditions such as high blood pressure and heart failure).
PubMed | Google ScholarSee all References A dose-related phenomenon with propranolol use was suggested by another study, which showed that patients receiving propranolol dosages exceeding 120 mg/d developed ED at a higher rate than patients who received lower dosages of the same medication.43x43Warren, SC and Warren, SG. Propranolol and sexual impotence [letter]. Ann Intern Med. 1977; 86: 112
Qigong is a form of breathing exercises commonly practised in Asia to maintain health (53). In a cross-sectional population-based comparison study in Taiwan, individuals practising Qigong demonstrate higher SF-36 scores in the domains of physical functioning, role limitations due to physical problems, bodily pain, general health and vitality (54). Techniques to concentrate the energy or qi in the pelvis or genitals are regularly practised, but the effects of Qigong on ED have not been studied.
Testosterone therapy in hypogonadism modulates metabolic components associated with CV risk. The majority of prospective clinical studies indicates that treatment achieving testosterone levels within physiological limits has beneficial or neutral effects on a lipid profile other than HDL-C, beneficial or neutral effects on inflammatory mediators, and generally beneficial effects on glycaemic state.25 The lean body mass is typically increased in hypogonadal subjects, and visceral adiposity is decreased in several studies and unchanged in the remainder. Such metabolic effects have raised interest on the potential impact on cardiovascular health. Regarding symptoms in patients with pre-existing cardiovascular conditions (angina or heart failure) TTh has been either neutral or beneficial.25 Regarding CVD risk, available clinical trial data indicate that the use of testosterone in middle-aged to elderly men does not increase cardiovascular risk25 with the exception of one study in very frail (substantial limitation of mobility and a high rate of comorbidities) elderly subjects that used an off-label high, and rapid escalation, dosing regimen.46 Prospective data from large, well-designed, long-term trials of TTh are warranted.
Crossref | PubMed | Google ScholarSee all References The risk of myocardial infarction with sexual activity has been estimated to be less than 3% in high-risk patients with prior cardiovascular disease if they can exercise to more than 7 METs without symptoms.89x89Moss, AJ and Benhorin, J. Prognosis and management after a first myocardial infarction. N Engl J Med. 1990; 322: 743–753

Dr. Eid also urges these patients to treat their diabetes in order to avoid developing ED for life. “They need to manage their diabetes and make sure they control it so the ED will not progress and will stabilize, as a result,” he said. “If the diabetes is controlled after the patient is first diagnosed, then the erections will come back. But if the patient has diabetes for many years, and suddenly decides it’s time to control it, they cannot prevent the damage that’s already been done.”
Older age. A man’s risk increases past the age of 40, as age is the variable most strongly associated with impotence. This is due to changing hormones, higher risk for heart problems and those affecting circulation, and decreased sexual desire that often occurs with increasing age. For example, based on findings from the National Health and Social Life Survey, it’s been found that “men between 50–60 years old are more than 3 times as likely to experience erection problems and to report low sexual desire compared to men aged 18 to 29 years.” (3)
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

Nehra A,  Jackson G,  Miner M,  Billups KL,  Burnett AL,  Buvat J,  Carson CC,  Cunningham GR,  Ganz P,  Goldstein I,  Guay AT,  Hackett G,  Kloner RA,  Kostis J,  Montorsi P,  Ramsey M,  Rosen R,  Sadovsky R,  Seftel AD,  Shabsigh R,  Vlachopoulos C,  Wu FC. The Princeton III Consensus recommendations for the management of erectile dysfunction and cardiovascular disease, Mayo Clin Proc , 2012, vol. 87 (pg. 766-778)https://doi.org/10.1016/j.mayocp.2012.06.015

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
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.
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.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (24) | Google ScholarSee all References Withdrawal of sexual stimulation causes a return of sympathetic tone and degradation of cGMP, predominantly by phosphodiesterase type 5 (PDE-5) within the trabecular smooth muscle.11x11Nehra, A. Intracavernosal therapy: when oral agents fail. Curr Urol Rep. 2001; 2: 468–472
Erectile dysfunction supplements and other natural remedies have long been used in Chinese, African and other cultures. But unlike prescription medications for erectile dysfunction, such as sildenafil (Viagra), vardenafil (Levitra, Staxyn), tadalafil (Cialis, Adcirca) and avanafil (Stendra), erectile dysfunction herbs and supplements haven't been well-studied or tested. Some can cause side effects or interact with other medications. And the amount of the active ingredient can vary greatly from product to product.
The pathophysiological basis for the predictive ability of ED has been discussed above. It should be emphasized, however, that ED should not only be viewed as a manifestation of obstructive CAD that could be identified by ischaemia revealing tests. Owing to the inflammatory and pro-thrombotic activation of the disease,13 it should also be regarded as an early warning sign of an imminent acute event (mainly acute myocardial infarction)22 due to the rupture of a subclinical plaque, and thus identification of the risk should ideally include plaque vulnerability tests. Finally, an issue that has important clinical implications is by how long the clinical manifestation of ED precedes the clinical manifestation of CAD. According to studies, men with ED and no cardiac symptoms have an increased incidence of experiencing a cardiac event, both acute and chronic, in the ensuing 2–5 years, thus providing a ‘window of opportunity’ for risk reduction management in these patients.2
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.

Clinical practice in TCM has been an exemplary case of customized treatment with holism epitomizes the essence of TCM. TCM encompasses these aspects, taking a holistic approach to patient’s problem and these methods combine body, mind and spirit, and healings are achieved via the concept of energy rather than matter, as in modern medicine. Compared to the complexity of modern science, which is the basis of Western medicine, this concept is easily understood and comprehended, and is readily accepted because of its holistic approach.


Cardiovascular disease and erectile dysfunction (ED) are closely interrelated disease processes. Erectile dysfunction reportedly affects 10 million to 20 million men in the United States and more than 100 million men worldwide. Each year, about 500,000 persons in the United States survive a myocardial infarction, and an estimated 11 million have existing cardiovascular disease, making the issue of sexual function and cardiac disease relevant to many patients. We explore the relationship between ED and the presence of cardiovascular disease in the general population. We also review the prevalence and pathophysiological associations of ED and cardiovascular disease. The risks of sexual activity for patients with cardiovascular disease are discussed, as are prevention and treatment strategies for ED in this patient population.

Heart disease and erectile dysfunction can be related. In fact, ED and heart disease are considered two signs of the same disease process. The smaller arteries in the penis are affected by atherosclerosis sooner, perhaps three or more years before they cause heart disease symptoms.11 A large international study found that men with ED were more likely to die from heart causes; have a heart attack, stroke or be admitted to the hospital with heart failure than men with no or mild ED.12
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.
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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
PubMed | Google ScholarSee all References As with sildenafil, use of nitrate or NO-donor medications is contraindicated while taking tadalafil because of the potential for marked hypotensive interactions.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

The body’s source for nitric oxide production is the amino acid L-arginine, which is naturally found in many foods. The average American ingests about 3,000–5,000 mg of L-arginine per day, as it is an amino acid naturally contained in many foods. Meats of all varieties, nuts, and dairy products are rich in L-arginine, so the body is accustomed to intake levels of several thousand milligrams every day.


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

Erectile dysfunction is the persistent inability to maintain an erection that is not firm enough or lasts long enough to have sexual intercourse. This is a common problem and at least 40 % of men suffer from erectile dysfunction at least occasionally. Manipal Fertility has been instrumental in bringing Men’s Health as an independent area of focus not only for fertility but also erectile dysfunction. We are the pioneers in introducing Non Invasive Shockwave therapy for Erectile Dysfunction.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Since then, several other oral PDE-5 inhibitors have been developed, including vardenafil and tadalafil, which generated considerable interest in both the scientific and lay communities. There was also much concern about their safety, especially in men with cardiovascular disease. Compared with the 2 newer PDE-5 inhibitors vardenafil and tadalafil, sildenafil has been available for a much longer time; therefore, the vast majority of published cardiovascular safety studies have been performed on this medication. Recommended starting and maximum doses of oral PDE-5 inhibitors are shown in Table 1.
High blood pressure and erectile dysfunction (ED) often go hand in hand. While having high blood pressure (hypertension) itself may not initially cause any symptoms, it will damage your arteries over time, leading them to become less flexible and progressively more narrow. This not only increases the risk of heart attacks and stroke, but has the potential to compromise blood flow to many organs in the body, including the penis, if left untreated.
ED is generally associated with significant changes in established cardiovascular risk factors. Atherosclerosis is the main cause of ED development in both the general population and patients with diabetes. However, the prevalence of ED is greater in patients with diabetes than in the general population.8 ED has been shown to occur at rates as high as 50 % in patients with CAD.9 A meta-analysis of 12 prospective cohort studies has provided evidence that ED is a predictor of IHD associated with an increased risk of CVD, stroke and all-cause mortality.10

Both erectile dysfunction and heart disease have been linked with impaired activity of nitric oxide, the body’s most powerful vasodilator. An endogenous (produced by the body) compound called asymmetric dimethylarginine is an L-arginine analog, which interferes with the production of nitric oxide and may increase the risk for erectile dysfunction and heart disease.

The first step in the process is always to reevaluate if the medication that’s causing the problem is even necessary in the first place. Do you still need the medication(s) that you’re taking? When you’re experiencing medically induced ED, this has to be your starting point. Obviously you shouldn’t make this decision on your own. However, reevaluating your need for medication can be a simple conversation with your doctor. Remind your healthcare provider of the medications you’re taking, and explain any symptoms or side effects—like ED. Going off of medication might sound like an extreme step, but I’ve seen many examples of this in practice.
Yohimbe A number of clinical trials have shown that the primary component of this bark from an African tree can improve sexual dysfunction associated with selective-serotonin reuptake inhibitors (SSRIs) used to treat depression. This herb has been linked to a number of side effects, including increased blood pressure, fast or irregular heartbeat, and anxiety. Yohimbe shouldn't be used without a doctor's supervision.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (53) | Google ScholarSee all References Erectile dysfunction is a common physiological disorder. According to estimates from the National Institutes of Health, ED affects 10 million to 20 million men in the United States; another 10 million men are affected by partial ED, defined as present but diminished erectile function.2x2NIH Consensus Development Panel on Impotence. NIH Consensus Conference: impotence. JAMA. 1993; 270: 83–90
According to Harvard Special Health Report Erectile Dysfunction, one study in the European Heart Journal looked at men newly diagnosed with heart disease, but without ED, who started treatment with the beta-blocker atenolol (Tenormin). Some of the study participants were told about the sexual side effect of the blood pressure drug, and ED was reported by almost one-third of the participants. In contrast, among those who were not told the drug's name or its side effects, only 3% said they experienced ED.
The following products are considered to be alternative treatments or natural remedies for Erectile Dysfunction. Their efficacy may not have been scientifically tested to the same degree as the drugs listed in the table above. However there may be historical, cultural or anecdotal evidence linking their use to the treatment of Erectile Dysfunction.

Although ED is a common complication of diabetes, its effect on quality of life is not well understood. Recent work for the Exploratory Comprehensive Evaluation of Erectile Dysfunction (ExCEED) database demonstrates that in the general population of patients presenting to their urologist, ED negatively affects both general and disease-specific health-related quality of life (HRQOL).35 While this study provides insight into the detrimental affect of ED on quality of life, the cohort is somewhat selected, in that all of the patients were seen in sexual dysfunction clinics and therefore may have been more likely to be bothered by their condition and to report worse quality of life.


Quassinoids isolated from Tongkat Ali have been reputed to be anti-tumor, anti-malarial, anti-amoebic and anti-inflammatory. Its leaves are used for washing itches, its fruits for the treatment of dysentery, its bark used as a vermifuge, the taproots used for treatment of hypertension and the root bark for treatment of diarrhea and fever. The roots extracts are used for sexual dysfunction, aging, malaria, cancer, diabetes, anxiety, aches, constipation, exercise recovery, fever, increased energy, increased strength, leukemia, osteoporosis, stress and syphilis. Animal studies done on middle age sex rats showed enhancement of the sexual qualities in terms of hesitation time among middle aged rats (46).

For oral erectile dysfunction medicines to work as desired, they must be used properly in the first place. This means taking the medicine 30–45 minutes before engaging in sexual intimacy; taking the drug on an empty stomach or at least avoiding a heavy or high-fat meal before taking the drug (this is especially important when using sildenafil); and engaging in adequate genital stimulation before attempting intercourse. Drinking small amounts of alcohol (one to two drinks) should not compromise the effectiveness of erectile dysfunction medicines, but larger amounts of alcohol can diminish a man’s ability to have an erection.
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