There are blood pressure medications that do not cause erectile dysfunction (ED). Some older blood pressure medications, especially beta blockers and thiazide diuretics, are the most likely to cause ED as a side effect. Better options include calcium channel blockers, which lower high blood pressure through a different mechanism. Don't just go off your medications, though; high blood pressure itself is a common cause of ED, so lowering your blood pressure is an important part of your ED treatment plan. And if you stop taking your blood pressure medications 'cold turkey', your blood pressure could actually sky rocket, putting you at risk for a heart attack or a stroke. Work with your doctor on ways to lower your blood pressure without lowering your sex drive.

There are other treatment options for erectile dysfunction (ED). Alprostadil is a medication that improves blood flow to the penis and improves erections. It can be given either by injection (Caverject and other brands) at the base of the penis or by putting an alprostadil gel (brand name MUSE) directly into the urethra, using a thin tube and a little lubricant so it slides in easily. The medicine is absorbed from the lining of the urethra into the surrounding tissues. The shot is less appealing to most people, of course, but more effective.
Diabetes is one of the most common causes of ED. Men who have Diabetes are three times more likely to have Erectile Dysfunction than men who do not have Diabetes. Among men with ED, those with Diabetes are likely to have experienced the problem as much as 10 to 15 years earlier than men without Diabetes. A recent study of a clinic population revealed that 5% of the men with ED also had undiagnosed Diabetes. The risk of ED increases with the number of years you have Diabetes and the severity of your Diabetes. Even though 20% to 75% of men with Diabetes have ED, it can be successfully managed in almost all men.
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].
Men with diabetes are at a higher risk of erectile dysfunction or impotence, especially if their diabetes is not well controlled. Erectile dysfunction means you cannot have an erection that is sufficient to perform sexual intercourse. Many men experience short-term episodes of erectile dysfunction but, for about one in 10 men, the problem may continue.
Erectile dysfunction (ED) is common, affecting almost 40% of men over 40 years of age (with varying degrees of severity) and increases in frequency with age.1 Erectile dysfunction and cardiovascular disease (CVD) share common risk factors including age, hypercholesterolaemia, hypertension, insulin resistance and diabetes, smoking, obesity, metabolic syndrome, sedentary lifestyle, and depression.2 Cardiovascular disease and ED also share a common pathophysiological basis of aetiology and progression.3 Numerous studies have established that ED (i) is frequent in men with established CVD, (ii) co-exists with occult coronary artery disease (CAD) and (iii) is an independent risk factor for future cardiovascular (CV) events both in men with established CVD and in men with no known CVD.2,4,5 In the latter group, ED precedes CAD, stroke, and peripheral arterial disease by a significant period that usually ranges from 2 to 5 years (average 3 years).2 Although the ED patient can be managed by various medical specialties, and preferably a collaborative approach is most effective, this review is oriented to the cardiologist. While this review deals exclusively with sexual health of men, female sexual health and its potential relation with CVD is also an interesting, yet underexplored, field. As in men, moderating common risk factors seems to improve female sexual health and may serve as an opportunity to decrease CVD risk, with the identification of sexual dysfunction being the starting point.6
Abstract | Full Text | Full Text PDF | PubMed | Scopus (328) | Google ScholarSee all References Their mean resting systolic and diastolic blood pressure levels decreased by 6% and 11%, respectively, compared with baseline. These patients also experienced a mild decrease in mean resting right atrial pressure, pulmonary artery pressure, pulmonary artery occlusion pressure, and cardiac output. However, the hemodynamic response to exercise was preserved. Phase 2 and 3 trials showed no difference in the rate of adverse events between sildenafil and placebo in patients being treated with antihypertensive medications. The effects of sildenafil on blood pressure level were similar in patients who were taking antihypertensive medications compared with those who were not. In healthy volunteers, no consistent or significant doserelated electrocardiographic (ECG) changes were noted at 1 and 2 hours after doses of sildenafil ranging from 1.25 to 200 mg.3x3Zusman, RM, Morales, A, Glasser, DB, and Osterloh, IH. Overall cardiovascular profile of sildenafil citrate. Am J Cardiol. 1999; 83: 35C–44C
The connection between diabetes and ED is related to your circulation and nervous system. Poorly controlled blood sugar levels can damage small blood vessels and nerves. Damage to the nerves that control sexual stimulation and response can impede a man’s ability to achieve an erection firm enough to have sexual intercourse. Reduced blood flow from damaged blood vessels can also contribute to ED.
There are currently two models of the inflatable penile prosthesis (IPP), namely, the two-piece IPP vs. the three-piece IPP. The three-piece IPP consists of a pair of corporal cylinders, a scrotal pump and an abdominal reservoir filled with saline. Owing to the presence of the reservoir, the corporal cylinders can be completely deflated to give the patient the physiological flaccid state when not in use, and likewise a maximally turgid state when inflated (21). The two-piece IPP lacks an abdominal reservoir and is often offered in patients with whom placement of reservoir is challenging or not possible such as following radical cysto-prostatectomy with orthotopic ileal neobladder creation, or patients who had previous open book fracture of the pelvis with metal implants. The concept of ectopic reservoir placement has allowed many of these men the option for three-piece IPP placement (22). Technological advances have improved mechanical reliability, reduced prosthesis infection risk and offered excellent patient and partner satisfaction rate (23).

The obvious risks are the same that accompany any surgery: infection, pain, bleeding, and scarring. If for some reason the prosthesis or parts become damaged or dislocated, surgical removal may be necessary. With a general success rate of about 90 percent, any of the devices will restore erections, but they will not affect sexual desire, ejaculation, or orgasm.
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
Gene therapy has the potential to become a future management option for patients with CAD and ED. Animal studies have been conducted to evaluate the effects of gene therapy. A rat model was studied by Bivalacqua et al. to evaluate the effect of the combination of eNOS gene therapy and sildenafil. This research suggested that erectile response was greater in male rats with diabetes treated with combination eNOS gene therapy and sildenafil, compared with male rats with diabetes treated with eNOS gene therapy or sildenafil alone.76–78
bike seats erectile dysfunction boston medical group BP Cholesterol depression Diabetes diet discussion doctor ed ED Best Treatment BMG erectile dysfunction erectile dysfunction and prostate cancer fish oil men Heart Diseas Heart Disease High Blood Pressure Hypertension medications Men's Health Obesity prostate cancer scrotal temperature SDB sexual desire sexual dysfunction sexual foods sexual function sexual health Sleep apnea sleep disordered breathing Tips Treatment vegetables yoga
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
Abstract | Full Text | Full Text PDF | PubMed | Scopus (58) | Google ScholarSee all References Avoiding sexual activity between 6 AM and noon may be recommended to higher-risk patients because this is the time of peak incidence of most arrhythmias, myocardial ischemia, sudden cardiac death, and cerebrovascular accidents.1x1Muller, JE. Sexual activity as a trigger for cardiovascular events: what is the risk?. Am J Cardiol. 1999; 84: 2N–5N
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
Other effective Diabetic Erectile Dysfunction Treatment therapies available include (a) an intraurethral suppository of the vasodilator drug alprostadil (prostaglandin E1), (b) intracavernosal self injection (penile self injection) of the non-specific PDE drug papaverine, the non-selective alpha-adrenergic antagonist phentolamine, and the vasodilator prostaglandin E1, used alone or in combination, or (c) penile prostheses (penile implants).
With great interest we have read the recently published review by Vlachopoulos et al, a very detailed and extensive overview of erectile dysfunction in the cardiovascular patients. Guidelines for the management of erectile dysfunction with heart failure were noted, as well as advice about dealing with erectile dysfunction (ED) in patients with cardiovascular disease (CVD). However, many others have written similar reviews and guideline concerning the care for ED as well as (female) sexual dysfunction in CAD in the past years (1-4), cardiologists should be familiar with this matter by now. The problem is the actual translation of this knowledge into actions in cardiologists' daily clinical practice. Our research group performed a survey among Dutch cardiologists, aiming to evaluate their inquiry about erectile function in day-to-day practice, to detect their attitude towards this discussion and their perceived barriers for addressing sexual activity. Results from this survey indicated that cardiologists (n=414) did not routinely discuss erectile dysfunction: 48.7% indicated to discuss sexual function 'sometimes' and only 16.9% said to discuss the subject regularly. Of respondents, 41.5% marked that care for patients' sexual quality of life is not their responsibility. Nevertheless, 42% indicated that they would benefit from training to obtain knowledge about treatment of erectile and sexual dysfunction in cardiologic patients. Barriers not to inquire about sexual activity included 'the patient does not ask about it' (53.7%), 'I do not have an angle or motive to start about it'(45.9%), as well as time constraints (42.9%) and lack of training in dealing with sexual dysfunction (35.2%). The more experienced the cardiologist was the less he/she stated the need for training or for a referral directory(5). Since all cardiologists should, meanwhile, know that ED is part of their responsibility, as it is a sentinel marker of CVD(6). It is now case to pay attention to the implementation of the care for erectile and other sexual dysfunction in the cardiology practice. Our study suggests that physicians' experience in the field plays an important role in discussing sexual activity and that sexual healthcare can be improved with more education about the subject. Furthermore a directory of the available healthcare professionals for the referral of patients with sexual dysfunction was indicated as mandatory. We suggest that attention of cardiologists should not only be focused on writing about ED and CVD, attention should be diverted to the actual implementation of care for patients with ED as well, in order to improve patient-centered healthcare in cardiology.

Towards this direction, several sufficiently powered studies have demonstrated a higher incidence of erectile dysfunction in patients with coronary artery disease, either asymptomatic or overt. At the same time, patients with erectile dysfunction are more prone to have established coronary artery stenosis of more than 50% and consequently evident CV disease[75]. This is in conformity with the “artery size hypothesis” according to which smaller arteries (e.g., penile arteries) are the first to undergo a vascular lesion prior to the larger ones (e.g., coronary arteries). Moreover, in such patients erectile dysfunction is connected to the number of occluded vessels and more interestingly occurs over three years before coronary artery disease becomes apparent[76-80].

Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.

This content is strictly the opinion of Dr. Josh Axe and is for informational and educational purposes only. It is not intended to provide medical advice or to take the place of medical advice or treatment from a personal physician. All readers/viewers of this content are advised to consult their doctors or qualified health professionals regarding specific health questions. Neither Dr. Axe nor the publisher of this content takes responsibility for possible health consequences of any person or persons reading or following the information in this educational content. All viewers of this content, especially those taking prescription or over-the-counter medications, should consult their physicians before beginning any nutrition, supplement or lifestyle program.
However, sildenafil should be used carefully with nitrates because their combination can result in severe hypotension and death.68 Both short- and long-acting nitrates are commonly prescribed to treat angina, but they have no prognostic benefit. In addition, there are numerous alternatives to treat angina, such as ranolazine and ivabradine, which do not interact with PDE5 inhibitors. As a result, patients with ED wishing to take PDE5 inhibitors can safely discontinue their nitrates and replace this treatment with the other anti-anginal agents.68
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.

In the past 6 years, the FDA has approved three oral agents for the treatment of ED: sildenafil, vardenafil, and tadalafil. All three are phosphodiesterase type 5 (PDE-5) inhibitors and work by potentiating the effect of nitric oxide in the penis. In particular, they block the hydrolysis of cyclic guanosine monophosphate to guanosine 5'-monophosphate, thus enhancing nitric oxide–mediated smooth muscle relaxation, increasing blood flow to the penis and facilitating erection.
Crossref | PubMed | Google ScholarSee all References In study patients taking these medications compared with controls, significant decreases in total cholesterol and low-density lipoprotein cholesterol levels were found, as well as significant increases in length of maximal tumescence per nocturnal penile tumescence testing at 2 weeks. Hypoglycemia secondary to the use of insulin or hypoglycemic agents may result in ED or orgasmic dysfunction.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
Alcohol consumption, bad nutrition, a sedentary lifestyle, excessive stress, psychological issues, relationship issues, use of illegal drugs and overuse of prescribed drugs, poor sleep habits and excessive physical activity are all contributing factors to ED. Ailments like diabetes, as well as low and high blood pressure, in addition to prostate cancer, may also result in ED.
Nebivolol seems to have an advantage over other beta-blockers when used to treat men with hypertension and ED. It has additional vasodilating effects because it stimulates endothelial release of nitric oxide (NO), resulting in relaxation of smooth muscle in the corpus cavernosum, allowing penile erection.25 Despite limited studies, nebivolol does not seem to worsen erectile function and some studies have demonstrated significant improvement in erectile function with nebivolol compared with second-generation cardioselective beta-blockers.23,26–28
Cardiovascular disease and ED represent 2 common disease processes that are often intimately associated with one another. These common pathophysiological links necessitate a solid scientific and clinical understanding of these 2 disorders and a team effort between the cardiologist and urologist to provide effective management strategies for these patients.

If your doctor says it's OK, you may be able to stop taking blood pressure medications temporarily to see if your sex life improves. To make sure your blood pressure remains within a safe range, you may need frequent blood pressure readings while you're not taking the blood pressure lowering medication that may be causing your sexual difficulties. This can be done with a home blood pressure monitoring device for convenience.
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.
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 (95) | Google ScholarSee all References When used in combination with NO-donor medications such as nitroglycerin, the modest blood pressure effects of sildenafil are potentiated, resulting in a significant decrease in systolic (21-55 mm Hg) and diastolic (up to 26 mm Hg) blood pressure levels, as well as vasodilatory symptoms such as headache, light-headedness, and nausea.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N

The drugs you take to lower your blood pressure may earn you lower marks in the bedroom, by leading to a bout of erectile dysfunction (ED), or the inability to get or maintain an erection during sex. High blood pressure medications such as beta blockers and diuretics do their life-saving job by lessening blood flow to your vital organs—and that includes down under. Less blood flow means no erection. The good news for guys is that not all high blood pressure medication cause ED. Talk with your doctor about switching to the ones that don't.


The treatment of ED using TCM ties in with the treatment of late-onset hypogonadism (LOH). LOH occurs due to the breakdown in coordination between the heart and the kidneys, deficiencies of the spleen and kidney (yang), deficiencies of the liver and kidney (yin) and deficiencies of the kidney (yin and yang). The endocrine function of the pituitary and gonads becomes disordered with age due to a depression of overall function. This results in accumulation of free radicals and other toxins that cannot be relieved solely with male hormone supplementation. Warm yang can energize kidneys to benefit the body, remove toxins, invigorate qi and promote blood circulation. Free radicals are removed, blood fat regulated, cardio-cerebral blood flow improved and again the key here is to improve the function of the digestive, respiratory and endocrine systems, hence regulating the body in every aspect holistically (28).
Crossref | PubMed | Scopus (53) | Google ScholarSee all References This study found that, although hypertensive patients had more coronary artery disease, no direct evidence supported an association between hypertension and arteriogenic impotence, as measured by the PBI, peak systolic velocity, and resistive index, in patients with mild to moderate hypertension.
PubMed | Google ScholarSee all References The risk of ED was 1.83 times higher in men with a total cholesterol level greater than 240 mg/dL as opposed to less than 180 mg/dL. Also, an HDL cholesterol level greater than 60 mg/dL was found to be protective against the development of ED. In the MMAS, HDL cholesterol levels were noted to have an inverse relationship with the presence of ED.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
After adjusting for cardiovascular risk factors including diabetes, heart failure and stroke, those taking PDE5 inhibitors were found to be markedly less likely to die than those taking alprostadil or no erectile dysfunction drugs. Filling more prescriptions for PDE5 inhibitors appeared to be associated with a greater benefit, although Andersson said that trend should be interpreted with caution because the study was not large enough for a definitive dose-response analysis.
An Anti-Inflammatory Diet PlanDiabetes Smart TipsLiving Well with Rheumatoid ArthritisLiving Well with Colitis or Crohn'sManage Your Child's ADHDMood, Stress and Mental HealthTalking to Your Doctor About Hepatitis CTalking to Your Doctor About PsoriasisTalking to Your Doctor About Rheumatoid ArthritisYour Guide to Diabetes ManagementYour Guide to Headache and Migraine PainYour Guide to Managing DepressionSee All

Sexual dysfunction has been evaluated in ancient literature of TCM in terms of subjective sensation and the actual sexual performance (3). In TCM, methods and matters related to direct sexual activity is described in terms of “ten motions”, “seven impairments” and “eight benefits”, which asserted that the ideal intensity and frequency of sexual activity should be moderate. TCM is all about balance, to achieve better overall regulation of the yin and the yang. The aim of treatment of ED using TCM is not for the end point of a penile erection but rather for a natural and harmonious sex life. TCM aims to achieve regulation in terms of the man’s anxiety, fatigability, changing hormonal levels, insomnia and gastroparesis. Medicine to invigorate qi can enhance physical fitness, and medicine to warm the kidneys can regulate sex hormones, increase libido, invigorate the spleen, regulate the stomach and improve general well-being (3). Medications used to treat a “stagnated liver” provide tranquilization and helps to stabilize the mind, hence improving mental processes and emotional wellness. As a result, the patient’s overall condition and quality of life is improved.
Crossref | PubMed | Scopus (539) | Google ScholarSee all References The MMAS found the total prevalence of minimal to severe ED to be 52% and estimated that more than 617,000 new cases were expected to occur annually in the United States.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
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.

Diabetes, high blood pressure (hypertension), elevations in blood lipids or cholesterol are considered blood vessel problems and have all been associated with Erectile Dysfunction. The blood vessel abnormalities caused by these diseases affect vessels throughout the body and often produce other symptoms of vascular diseases. Diabetics and patients with hypertension frequently have heart disease. These conditions typically interfere with the ability of the penile vessels to work properly and ultimately cause ED.
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

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


The views expressed in this article intend to highlight alternative studies and induce conversation. They are the views of the author and do not necessarily represent the views of hims, and are for informational purposes only, even if and to the extent that this article features the advice of physicians and medical practitioners. This article is not, nor is it intended to be, a substitute for professional medical advice, diagnosis, or treatment, and should never be relied upon for specific medical advice.
Nebivolol seems to have an advantage over other beta-blockers when used to treat men with hypertension and ED. It has additional vasodilating effects because it stimulates endothelial release of nitric oxide (NO), resulting in relaxation of smooth muscle in the corpus cavernosum, allowing penile erection.25 Despite limited studies, nebivolol does not seem to worsen erectile function and some studies have demonstrated significant improvement in erectile function with nebivolol compared with second-generation cardioselective beta-blockers.23,26–28
Penile vibratory stimulator is a battery operated device with oscillating discs that can provide excitation of afferent penile nerves at various regulated frequency and amplitudes. PVS has been utilised to activate the ejaculatory reflex for patients with spinal cord injury above T10 seeking to collect retrogradely ejaculated semen in fertility treatment (10). The Viberect is a vibratory stimulation handheld device approved by FDA for treatment of ED. It is clamp-shaped with two oscillating discs facing each other near the tips, and the glans penis is placed between the two oscillating discs to receive concurrent dorsal and ventral stimulation at adjustable frequencies and amplitudes.
When it comes to boosting sexual performance, many men will walk all over God’s green earth looking for ways to maintain a good sex life. Luckily men, all you have to do is walk — not run — 2 miles a day. This, along with other healthier lifestyle interventions can help obese men reduce their risk of ED, or even “reverse” current impotence, according to a 2005 study. This comes of importance, since maintaining a trim waistline is a good defense for ED, as men with a 42-inch waist are 50 percent more likely to have ED than those with a 32-inch waist. Getting to a healthy weight and maintaining it is a good strategy for preventing and treating ED.
The 12-week study of 164 men, all with hypertension, was divided into 2 groups of 82, one group with sexual dysfunction, the other group reported normal sexual functioning. Both groups took losartan in dosages of 50 to 100 milligrams daily for the 12 weeks of the study. In the group of men with sexual dysfunction, 88 percent reported improvement in at least one area of sexual function and 73.7% reported an improved quality of life.
Nebivolol seems to have an advantage over other beta-blockers when used to treat men with hypertension and ED. It has additional vasodilating effects because it stimulates endothelial release of nitric oxide (NO), resulting in relaxation of smooth muscle in the corpus cavernosum, allowing penile erection.25 Despite limited studies, nebivolol does not seem to worsen erectile function and some studies have demonstrated significant improvement in erectile function with nebivolol compared with second-generation cardioselective beta-blockers.23,26–28
I have cared for hundreds of men with erectile dysfunction that have reversed their condition with a Nutritarian diet and the judicious use of dietary supplements. I have cared for hundreds of heart patients with angina and advanced heart disease, who have turned their backs on invasive cardiac procedures, recovered from angina and opened up the closed blood vessels in their diseased hearts. Out of thousands of men with advanced heart and erectile problems who have followed my nutritional advice, I have never had a patient suffer a heart attack or cardiac related death.
Abstract | Full Text PDF | PubMed | Scopus (19) | Google ScholarSee all References However, there has been disagreement regarding the effects of diuretics on erectile function; many studies found that only rarely have these medications been implicated convincingly as the cause of a patient's ED.36x36Wein, AJ and Van Arsdalen, KN. Drug-induced male sexual dysfunction. Urol Clin North Am. 1988; 15: 23–31

Faced with concern about ED pills and the heart, the FDA has urged caution in patients who have suffered heart attacks, strokes, or serious disturbances of the heart's pumping rhythm in the previous six months, in men with a history of congestive heart failure or unstable angina, and in men with low blood pressure or uncontrolled high blood pressure (above 170/110 mm Hg). Because certain medications can boost the blood levels of these drugs, men taking erythromycin or certain antifungal or anti-HIV medications should use only low-dose PDE-5 inhibitors. Reduced dosage is also important for men with advanced age and for those with significant kidney or liver disease.


After getting a diagnosis of ED, most patients can begin treatment right away, but treatment may be delayed for some patients until the health of the heart is more fully assessed or improved. The most common treatment for ED is a pill (phosphodiesterase-5 inhibitor; PDE5-I): Viagra (sildenafil), Cialis (tadalafil), or Levitra (vardenafil). Each of these pills improves erections when taken before sexual activity; alternatively, a low dose of Cialis can be taken once a day. These medicines work by allowing the blood vessels that supply blood to the penis to dilate better during sexual stimulation. The PDE5-Is decrease blood pressure a little bit, but they are safe with most other medications and with other blood pressure pills. The PDE5-Is are not safe with nitrate medications like nitroglycerin, Nitrostat, Nitro Paste, Imdur, isosorbide mononitrate, and Isordil. Mixing a PDE5-I with a nitrate medication could result in severely low blood pressure and even death. Inform all medical professionals (including the ambulance or emergency department) about your most recent ED pill ingestion so that nitrates can be avoided. If you have high blood pressure or benign prostatic hypertrophy (enlarged prostate) and take medicines called α-blockers, your doctor may need to start you on the lowest dose of the PDE5-I.

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.
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

Although DM patients often correctly assume that their ED is of organic origin, a psychogenic component should be considered, especially in the younger patient. If this is the case, the patient may benefit from psychosocial therapy that includes anxiety reduction and desensitization, cognitivebehavioral intervention, sexual stimulation techniques, and interpersonal assertiveness with couples communication training.6 Not all healthcare providers offer these options. Freudian-based psychotherapy for EDDM has not been proved to be efficacious.
RESPeRATE is the only non-drug, FDA-Cleared device for lowering blood pressure naturally. It is clinically proven, doctor recommended and has no side effects.   RESPeRATE lowers blood pressure by relaxing constricted blood vessels which cause high blood pressure. RESPeRATE does so by harnessing the therapeutic power of slow paced breathing with prolonged exhalation in a way that is virtually impossible to achieve on your own. All you have to do is breathe along with RESPeRATE’s guiding tones.   Learn More…

Crossref | PubMed | Scopus (1) | Google ScholarSee all References Angiotensin-converting enzyme inhibitors also have low rates of secondary ED associated with their use in both animal and human studies.45x45Srilatha, B, Adaikan, PG, Arulkumaran, S, and Ng, SC. Sexual dysfunction related to antihypertensive agents: results from the animal model. Int J Impot Res. 1999; 11: 107–113
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
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.

Abstract | Full Text | Full Text PDF | PubMed | Scopus (395) | Google ScholarSee all References Phosphodiesterase type 5 is primarily responsible for the breakdown of cGMP in cavernosal tissues. The inhibition of PDE-5 by sildenafil therefore causes continued activation of the NO-cGMP pathway in the cavernosal tissue, thereby improving erectile function.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
Table 3Metabolic Equivalent (MET) Values for Various Physical Activities56x56Wallis, 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
"If you have an active sex life after a heart attack, it is probably safe to use PDE5 inhibitors," said Daniel Peter Andersson, MD, PhD, a postdoctoral researcher at Karolinska Institutet in Stockholm and the study's lead author. "This type of erectile dysfunction treatment is beneficial in terms of prognosis, and having an active sex life seems to be a marker for a decreased risk of death."
Relaxation of erectile tissue requires nitric oxide from nonadrenergic-noncholinergic neurons and the endothelium.21 Penile tissue from diabetic men with ED demonstrates impaired neurogenic and endothelium-mediated relaxation of smooth muscle,22 increased accumulation of advanced glycation end products (AGEs),23 and upregulation arginase, a competitor with nitric oxide synthase for its substrate L-arginine.24 Normal responses to direct smooth muscle relaxants in most of these studies implies that the impairments are due to decreased synthesis, release, or activity of nitric oxide. The fundamental mechanisms mediating these changes are thought to be the same as for other diabetic complications: increased polyol pathway flux, intracellular accumulation of AGEs, activation of protein kinase C, and increased flux through the hexosamine pathway.25
×