PubMed | Google ScholarSee all References In comparison, a study of 132 patients evaluated by penile duplex ultrasonography after intracorporeal papaverine injection found that hypertension alone was not an independent risk factor for vasculogenic ED.34x34Shabsigh, R, Fishman, IJ, Schum, C, and Dunn, JK. Cigarette smoking and other vascular risk factors in vasculogenic impotence. Urology. 1991; 38: 227–231
Because ED has several causes, sorting out exactly what is causing your problem may take some time. First, make sure your doctor knows about all the medicines you are using, including over-the-counter or herbal products. Drugs frequently used to treat high blood pressure, anxiety, depression, and peptic ulcers can all cause ED. But don’t stop taking any of your medications without first talking to your doctor.
Acupuncture. Though acupuncture has been used to treat male sexual problems for centuries, the scientific evidence to support its use for erectile dysfunction is equivocal at best. In 2009, South Korean scientists conducted a systematic review of studies on acupuncture for ED. They found major design flaws in all of the studies, concluding that "the evidence is insufficient to suggest that acupuncture is an effective intervention for treating ED."
While Western medicine emphases the link between cardiovascular function and ED, TCM places importance on liver and kidney ailments as causative factor for development of ED. Western medicine involves a step-wise approach by targeting the relevant organ systems to treat various clinical symptoms; but TCM focuses on restoring the balance between various organs to achieve harmony and holistic approach to inner sense (4). 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 (see Table 1).

Erections are extremely complicated and surprisingly fragile. Erections involve chemical signals, nerve impulses, complicated blood pressure changes, and overall fitness in systems ranging from your heart and hormones to your mood. When medication changes how one of these factors works—like blood pressure drops or depression medication—ED is a common side effect. The problem with these completely predictable medically induced side effects is how people react.

People sometimes refer to ED as "impotence," although the two aren't really the same condition. ED is the physical inability to develop or maintain an erection that is rigid enough for sex. Impotence is a broader term. While one cause of it is ED, impotence may also involve a lack of sexual desire, an inability to ejaculate, or problems with orgasm.

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

Diabetes is known to sabotage two body parts that provide essential components of an erection: nerves and blood vessels. Studies suggest that diabetic nerve damage (neuropathy) is the most important risk factor for ED in people with diabetes. If pelvic nerves that trigger penis muscles to relax are impaired, there may be a break in the chain between brain and penis, disrupting erection. Some researchers suspect that an inadequate supply of oxygen to the nerves causes this damage.
Before a man concludes that oral drugs don’t work for him, he should have his testosterone levels checked to rule out hormone deficiency as the cause of (or as a contributor to) his sexual dysfunction. Other symptoms of low testosterone include a low sex drive and infertility. Checking testosterone levels requires a blood test. If a man’s levels of testosterone are decreased or at the lower end of normal, his doctor may prescribe supplemental testosterone therapy, either as testosterone injections or testosterone gel, which is applied daily to the skin. In some cases, testosterone therapy alone can resolve sexual dysfunction, or it can be combined with the use of oral erectile dysfunction drugs.

To understand what happens in ED, it's helpful to know some anatomical basics. When aroused by either sensory or mental stimuli, the brain sends a signal through the nerves to the penis, causing the muscles there to relax. This opens up space for blood to flow in and engorge the penis. A membrane within the penis traps blood inside to help maintain the erection, which subsides when the penile muscles contract, forcing blood back into the rest of the body. Any number of things can go wrong in this process, leading to erectile dysfunction.

While a widely held perception is that CVD drugs cause ED, data attest towards the contrary and some agents may be even beneficial.41 Only thiazide diuretics lead clearly to ED, while some older beta-blockers also do so, but the side-effect of ED was very low (∼3%) when the patient was blinded for the drug administration.42 In fact, the vasodilating nebivolol may even improve erectile function.35,43 ACE-inhibitors, angiotensin-receptor blockers, and calcium-channel blockers are reported to have neutral or even a positive effect on erectile function35,41,43 but more evidence is needed. Regarding statins, the largest body of evidence point towards a beneficial effect.44 A negative effect has been reported in high statin doses, possibly related to a potential reduction in serum testosterone levels, but this dose dependency warrants further investigation. In terms of patient management, when ED onset and therapy initiation are linked and a cause-and-effect association is presumed, a short period of drug withdrawal with monitoring for ED resolution for verification may be an option. In patients who developed ED long after the initiation of CV drug treatment, sexual dysfunction is less likely to be drug associated and PDE5 inhibition therapy may be initiated.

Low testosterone represents another link between erectile dysfunction and heart disease. A man’s testosterone levels gradually diminish beginning at age 30. By the time he reaches his 70s, testosterone levels may have dropped to a tenth of youthful levels. Diminishing testosterone levels contribute to loss of muscle, increased body fat, and reduced libido. Fatigue is common, as is depression. Low testosterone levels can also result in reduced concentration, irritability, passivity, loss of interest in activities, and even hypochondria.

There are two kinds of penis implants. One kind is a rigid but flexible rod implanted in the penis. You bend it up for sex or down for daily living. The other kind is an inflatable implant. The device stores fluid in a reservoir under the skin of your abdomen or scrotum. You press on the reservoir to pump fluid into cylinders in the penis. That creates an erection. A valve drains the fluid out of the penis when you're done.


If you have several atherosclerotic risk factors or symptoms of heart disease, your doctor might do additional tests to look for atherosclerosis in the coronary arteries. A stress test involves monitoring the heart with an electrocardiogram or images before and after exercise. An angiogram, or cardiac catheterization, involves entering a blood vessel in the leg or wrist to pass instruments into the heart to directly visualize the coronary arteries. During this procedure, atherosclerosis can be treated by inflating a balloon or placing a metal stent in the coronary blood vessel to keep it open. If you and your doctor begin a treatment plan to prevent atherosclerosis at the first sign of ED, then you may significantly delay or prevent the need for these more invasive procedures.

A number of drugs are known to cause ED in patients with DM (Table 1). For example, many EDDM patients are on antihypertensive medications. Replacement of thiazides or beta-blockers with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers may be sufficient to regain erectile ability.5 Furthermore, discontinuation of selective serotonin reuptake inhibitors, if these drugs are not essential for patient well-being, may be therapeutic. Careful monitoring following drug discontinuation will help to determine if ED is due to the medication or other underlying disorders. The benefits of continued drug therapy with these drugs should always be weighed against the likelihood of causing ED and impacting on the patient's QOL.


The information provided on this site is for informational purposes only and is not intended as a substitute for advice from your physician or other health care professional or any information contained on or in any product label or packaging. You should not use the information on this site for diagnosis or treatment of any health problem or for prescription of any medication or other treatment. You should consult with a healthcare professional before starting any diet, exercise or supplementation program, before taking any medication, or if you have or suspect you might have a health problem. You should not stop taking any medication without first consulting your physician.


Basaria S,  Coviello AD,  Travison TG,  Storer TW,  Farwell WR,  Jette AM,  Eder R,  Tennstedt S,  Ulloor J,  Zhang A,  Choong K,  Lakshman KM,  Mazer NA,  Miciek R,  Krasnoff J,  Elmi A,  Knapp PE,  Brooks B,  Appleman E,  Aggarwal S,  Bhasin G,  Hede-Brierley L,  Bhatia A,  Collins L,  LeBrasseur N,  Fiore LD,  Bhasin S. Adverse events associated with testosterone administration, N Engl J Med , 2010, vol. 36 (pg. 109-122)https://doi.org/10.1056/NEJMoa1000485
Abstract | Full Text | Full Text PDF | PubMed | Scopus (25) | Google ScholarSee all References The Framingham Heart Study found a baseline risk of myocardial infarction in a healthy 50-year-old nonsmoking man to be approximately 1% per year, or 1 chance per million per hour.87x87Anderson, KM, Odell, PM, Wilson, PW, and Kannel, WB. Cardiovascular disease risk profiles. Am Heart J. 1991; 121: 293–298
The discovery in 1992 of the second messenger of cavernosal smooth muscle relaxation was the critical step that led to the era of nonhormonal oral drug therapy for ED. In 1998, the multicenter trial of sildenafil in the treatment of ED was published in the New England Journal of Medicine, and the era of the phosphodiesterase type 5 (PDE-5) inhibitor began.1 For 5 years, sildenafil was the primary therapy for men with EDDM. Recently, 2 new PDE-5 inhibitors, vardenafil and tadalafil, were introduced.
Erection is a neurovascular event that involves spinal and supra spinal pathways. The final common pathway involves the release of nitric oxide (NO) from both endothelial cells and neurons, which acts as a vasodilator causing penile engorgement and erection. NO is degraded by the enzyme phosphodiesterase (PDE) type 5 in the penis. Erectile dysfunction (ED), defined as the persistent inability to achieve and/or maintain an erection sufficient for satisfactory sexual performance, results when the neurovascular pathway is interrupted by medical conditions or drugs. A 15-item self-administered questionnaire, the International Index of Erectile Function (IIEF), is one of the most useful tools to evaluate erectile function (EF) in clinical trials, although of much less use in routine clinical practice. The MMAS (Massachusetts Male Aging Study) was the first major epidemiological investigation to study the prevalence of ED. The study found that ED was three times more common in patients with diabetes mellitus. The aetiopathogenesis of ED in diabetes is multifactorial, with vascular and neural factors being equally implicated. Hyperglycaemia is believed to give rise to biochemical perturbations that lead to these microvascular changes. In the MMAS, ED in diabetes was strongly correlated with glycaemic control, duration of disease and diabetic complications. The incidence increased with increasing age, duration of diabetes and deteriorating metabolic control, and was higher in individuals with type 2 diabetes than those with type 1.ED in men with diabetes often affects their quality of life and, as patients are often reluctant to come forward with their symptoms, a carefully taken history is one of the most useful approaches in identifying affected individuals. The PDE inhibitors have revolutionised the management of ED and oral drug therapy is currently first-line therapy for the condition. These agents act by potentiating the action of intracavernosal NO, thereby leading to a more sustained erection. Sildenafil was the first PDE5 inhibitor to undergo evaluation and has been studied extensively. More recently two other agents, vardenafil and tadalafil, have been introduced. All the drugs have been shown to be effective across a wide range of aetiologies of ED, including diabetes. The drugs have been shown to improve EF domain scores, penetration and maintenance of erection, resulting in more successful intercourse. Their effects are greater at higher doses. Sildenafil and vardenafil are shorter-acting agents, while tadalafil has a longer half-life allowing the user more flexibility in sexual activity. Common adverse effects include headache, nasal congestion and dyspepsia, all actions related to inhibition of PDE5. The drugs are generally well tolerated and withdrawal from the clinical studies as a result of drug-related adverse effects were rare. The use of PDE5 inhibitors in the presence of oral nitrates is absolutely contraindicated. The clinical studies to date have not evaluated the use of one drug in the case of treatment failure with another agent. Sublingual apomorphine, which stimulates central neurogenic pathways, is a new agent and may be a suitable alternative in those patients in whom PDE5 inhibitors are ineffective or contraindicated. In clinical trials, all IIEF domains except sexual desire were found to have improved after apomorphine. The median times to erection in these studies were 18.9 and 18.8 minutes for the 2 and 3mg doses, respectively. Intraurethral and intracavernosal alprostadil may be a useful alternative when oral drug therapy is ineffective or contraindicated. The management of ED in the diabetic patient may often involve a multidisciplinary approach where psychosexual counselling and specialist urologist advice is required in addition to the skills and expertise of the diabetologist. Finally, the introduction of the new oral agents have completely revolutionised the management of ED and allowed more individuals to come forward for treatment.
Apart from their beneficial effect in erectile dysfunction and their safe profile in antihypertensive medication, PDE-5 inhibitors have even more advantages to demonstrate. Several lines of evidence has proven that patients receiving PDE-5 inhibitors are more likely to initiate an antihypertensive regime and more willing to add a new agent to their existing treatment, a fact that raises significantly patient’s adherence and as a matter of fact control of high blood pressure and quality of life[63,64]. Moreover, a handful of clinical data has demonstrated the considerable vasodilating and anti-proliferative properties of PDE-5 inhibitors in the pulmonary vasculature, establishing them as a first-line treatment in patients with pulmonary arterial hypertension[65,66]. The same properties have been considered as potentially responsible for improving microcirculation in patients with secondary Raynaud phenomenon and ameliorating cardiopulmonary exercise performance in patients with heart failure[67,68]. In addition, the therapeutic implementation of PDE-5 inhibitors has expanded in the field of benign prostate hyperplasia-lower urinary tract symptoms (BPH-LUTS). The common pathophysiologic substrate between erectile dysfunction and BPH-LUTS has rendered PDE-5 inhibitors an effective treatment which significantly improves measures of both conditions while at the same time exhibits high efficacy and safety. The beneficial effect is much more pronounced when taking into consideration the fact that a-blockers, the mainstay of therapy for benign prostate hyperplasia frequently provoke sexual side effects, erectile dysfunction included[69].
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.
Vacuum therapy devices have a few disadvantages. One must interrupt foreplay to use them. You must use the correct-size tension ring and remove it, to prevent penile bruising, after sustaining the erection for 30 minutes. Initial use may produce some soreness. Such devices may be unsuitable for men with certain bleeding disorders. In general, vacuum constriction devices are successful in management of long-term ED.
If impotence affects you or someone you love, don’t lose hope. You may be suffering from a medical or emotional issue that is causing low libido or impotence — possibly interfering with both your confidence and relationship — but the good news is there are effective natural remedies for impotence that can help reverse this problem in most men. Around 70 percent of ED cases are resolved with natural impotence remedies that can help restore your sexual health.

But recently Brandon had some troubles keeping it up. At first, Kayla just thought it was her and that he needed some kind of a change to what they usually did, but later Brandon admitted that as of late, he just couldn’t seem to maintain an erection, and that it took way too much effort to go long. It wasn’t that he wasn’t aroused; his body just wasn’t keeping up.


In men without cardiovascular disease, erectile dysfunction (ED) pills are very safe. The three rivals -- Viagra, Cialis, and Levitra -- have similar side effects, including headache, facial flushing, nasal congestion, diarrhea, backache, and, in a few Viagra or Levitra users, temporary impaired color vision (men with retinitis pigmentosa, a rare eye disease, should check with their ophthalmologists before using these medications).
The mechanisms of action by which antihypertensive medications cause ED are currently unknown. Some investigators have theorized that antihypertensive medications affect erectile function by decreasing blood pressure, which reduces the perfusion pressure needed to maintain sufficient blood flow for erections through atherosclerotic penile arteries.37x37Benet, AE and Melman, A. The epidemiology of erectile dysfunction. Urol Clin North Am. 1995; 22: 699–709
Hypertension can affect endothelial function in many ways. It can reduce endothelium-dependent vasodilatation by increasing the vasoconstrictor tone as a result of increased peripheral sympathetic activity.41–43 Another mechanism is hypertension-induced increase in cyclooxygenase activity that leads to an increase in reactive oxygen species; these in turn damage endothelial cells and disrupt their function.44–46 In some cases, endothelial NO synthase (eNOS) gene variations may relate to hypertension-associated endothelial dysfunction.6
Penile implants - are generally used if physical damage (like an accident) makes the anatomical parts needed for an erection not work. These are inserted by surgery and can provide a permanent treatment choice if others fail to work. The implants can be semi-rigid or inflatable. They can be pretty expensive and are not usually available on the NHS.

To reduce the risk of side effects from these medications, including sexual problems, take medications exactly as prescribed. If you still have side effects, talk to your doctor about other possible medications that may have fewer side effects. On the other hand, you should not take any medication that promotes and erection while on medication to lower blood pressure.


27. Haahr MK, Jensen CH, Toyserkani NM, et al. Safety and Potential Effect of a Single Intracavernous Injection of Autologous Adipose-Derived Regenerative Cells in Patients with Erectile Dysfunction Following Radical Prostatectomy: An Open-Label Phase I Clinical Trial. EBioMedicine 2016;5:204-10. 10.1016/j.ebiom.2016.01.024 [PMC free article] [PubMed] [CrossRef]
Diabetes occurs when you have too much sugar circulating in your bloodstream. There are two main types of diabetes: type 1 diabetes, which affects less than 10 percent of those who have diabetes, and type 2 diabetes, which accounts for over 90 percent of diabetes cases. Type 2 diabetes often develops as a result of being overweight or inactive. Approximately 30 million Americans have diabetes, and about half of them are men.
Diabetes doubles or even triples the chance that you’ll have erectile dysfunction (ED) and that you could develop it a decade earlier than other men. In fact, the two conditions are so closely linked that some experts believe that for men younger than 45, impotence, or ED, could be an early warning sign of diabetes. The good news is that diabetes treatment, especially if you identify type 2 diabetes early, can also ease ED.
Does drinking water improve erectile dysfunction? Erectile dysfunction or ED is a common concern for men. Everyday factors, such as hydration levels, may affect a person's ability to get or maintain an erection. Drinking water may, therefore, help some men with ED. In this article, learn about the link between hydration and ED, and other factors that can cause ED. Read now
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