In this study, ED proceeded CVD in almost 70% of cases. Similarly, many men with ED have been found to have pre-existing CVD. A study by Vlachopoulos et al evaluated the incidence of asymptomatic CVD in 50 men with ED.22 These authors found that 19% of men with ED had asymptomatic CVD. Similarly, Mulhall and colleagues found that 20% of men presenting with ED and vascular insufficiency on penile duplex had asymptomatic CVD.23
A variety of personal habits and lifestyle choices have been linked to ED. In some ways, this is a good thing, since habits can be broken and choices reconsidered. What's more, many of the lifestyle factors that contribute to sexual problems are ones that affect overall health and well-being, both physical and mental. Addressing these factors, therefore, can have benefits beyond improving erectile dysfunction.
Sexual dysfunction and ED become more common as men age. The percentage of complete ED increases from 5% to 15% as age increases from 40 to 70 years. But this does not mean growing older is the end of your sex life. ED can be treated at any age. Also, ED may be more common in Hispanic men and in those with a history of diabetes, obesity, smoking, and hypertension. Research shows that African-American men sought medical care for ED twice the rate of other racial groups.

MSA is a neurodegenerative disease of undetermined etiology, where ED is an early prominent sign occurring in 40% of men at the time of diagnosis (46,47). ED occurs in the majority of patients and the exact cause of it is unknown (48). Like PD, MSA likely affects the dopaminergic pathways within the brain essential for arousal (49). Orthostatic hypotension (OH) as a causal factor has been refuted by evidence that sildenafil can overcome reduced filling pressures, and the ED usually precedes the development of OH (46,49,50). Similar to other neurologic disorders that lead to ED, other disease related factors such as psychosocial stress, the burden of chronic illness, changed appearance, fatigue, decreased fine motor movement of fingers, immobility and diminished self-esteem due to loss of independence may contribute as well (51).
In some cases, however, these drugs may be unsuitable for patients with heart disease. If you are considering one of these drugs and you have heart disease, as many diabetics do, be sure to tell your doctor. In rare cases, the pills may create “priapism,” a prolonged and painful erection lasting six hours or more (although reversible with prompt medical attention).
Positron emission tomorgraphy (PET), and functional magnetic resonance imaging (fMRI) have led to a greater understanding to which center are activated during arousal. These imaging studies measure increases in cerebral blood flow or changes in cerebral activity on a real-time basis. Studies are performed when male subject are aroused by visual cues (usually sexual explicit photos or videos) and compared to images obtained during exposure to sexually neutral cues differences can be measured. Several studies have identified that the inferior frontal lobes, inferior temporal lobes and insular gyrus, and occipital lobes are involved with processing arousal cues, although each are likely to process different stimuli (20-23).
Experts often treat psychologically based impotence using techniques that decrease anxiety associated with intercourse. The patient's partner can help apply the techniques, which include gradual development of intimacy and stimulation. Such techniques also can help relieve anxiety during treatment of physical impotence. If these simple behavioral methods at home are ineffective, a doctor may refer an individual to a sex counselor.

Before taking any medication for erectile dysfunction, including over-the-counter supplements and herbal remedies, get your doctor's OK. Medications for erectile dysfunction do not work in all men and might be less effective in certain conditions, such as after prostate surgery or if you have diabetes. Some medications might also be dangerous if you:
Under normal circumstances, when a man is sexually stimulated, his brain sends a message down the spinal cord and into the nerves of the penis. The nerve endings in the penis release chemical messengers, called neurotransmitters, that signal the corpora cavernosa (the two spongy rods of tissue that span the length of the penis) to relax and fill with blood. As they expand, the corpora cavernosa close off other veins that would normally drain blood from the penis. As the penis becomes engorged with blood, it enlarges and stiffens, causing an erection. Problems with blood vessels, nerves, or tissues of the penis can interfere with an erection.

If you have a neurological disorder or spinal cord injury and other erectile dysfunction treatments aren’t effective, two types of surgical implants could offer solutions to your ED. “An implantable pump can be used to manually create an erection by pumping fluid into cylinders placed inside the penis,” explains Feloney. “The other option is a malleable prosthesis that works like a gooseneck lamp to direct the penis into position for intercourse." Risks for these ED treatments include infection and mechanical breakdown.


Pay attention to your vascular health. High blood pressure, high blood sugar, high cholesterol, and high triglycerides can all damage arteries in the heart (causing heart attack), in the brain (causing stroke), and leading to the penis (causing ED). An expanding waistline also contributes. Check with your doctor to find out whether your vascular system — and thus your heart, brain, and penis — is in good shape or needs a tune-up through lifestyle changes and, if necessary, medications.
The somatosensory pathways for erections originate in the penile skin, glans and urethra. Glans afferent sensory free nerve endings are 10-fold more than their corpuscular receptors, and are derived from Aδ and unmyelinated C fibers. The nerve endings coalesce to form the dorsal penile nerve along with other sensory nerve fibers. Through the pudendal nerve they enter the S2-4 nerve roots to terminate on spinal neurons and interneurons. The dorsal nerve is not purely somatic, however. Nerve bundles within the dorsal nerve contain nitric oxide (NO) synthase, found typically in autonomic nerves, and stimulation of the sympathetic chain can leak to evoked potentials from the dorsal nerve and vice versa (10-12).
Q. I started to suffer from erectile dysfunction? Why is this happening and what can I do to treat it? I am a healthy 52 year old. I have hypertension but i take pills to treat it and my levels are around 130/80. except that I am at great shape. In the last few months I feel that a problem in my sex life. I want to have sex but i can't due to erectile dysfunction. What can be the reason for this? and more important what can I do?
All devices that are currently approved by the FDA are considered safe for use in magnetic resonance imaging environments. However, 2 previously approved devices–the OmniPhase and the DuraPhase penile prostheses–are not considered safe in this environment. Other surgical procedures–including venous ligation to limit penile venous outflow and penile revascularization procedures–are rarely successful and are not recommended.19 These surgeries are only indicated when a patient demonstrates recent-onset ED and an occlusive lesion seen on angiogram or magnetic resonance angiography and should be performed only in centers of excellence for ED.
Side effects include lightheadedness, fainting, priapism, urethral bleeding (intraurethral), dyspareunia in the partner (intraurethral), hematoma (intracavernosal) or penile curvature secondary to scar (intracavernosal). Efficacy of intraurethral alprostadil has been demonstrated to be around 50% ("able to have intercourse") in randomized controlled trials.31,32 For intracorporeal injection, typically alprostadil is tried alone, or compounded with papaverine (nonspecific phosphodiesterase inhibitor that increases intracellular cyclic adenosine monophosphate and cGMP) and/or phentolamine (competitive, non-selective alpha1- and alpha2-adrenoreceptor blocker). Pinsky et al33 reported an extensive review of the benefits and drawbacks of the combinations of these drugs.
Instead of the hesitation with which he had accosted the cardinal a quarter of an hour before, there might be read in the eyes of the young king that will against which a struggle might be maintained, and which might be crushed by its own impotence, but which, at least, would preserve, like a wound in the depth of the heart, the remembrance of its defeat.
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For many of the 30 million Americans affected by erectile dysfunction, Viagra, Levitra, and Cialis are the first line of ED treatment — and they’re successful for about 80 percent of men. These drugs, called phosphodiesterase-5 inhibitors, are approved by the U.S. Food and Drug Administration (FDA) and work by increasing blood flow to an erection. Common side effects include nasal congestion and headache. Note: If you take nitroglycerin pills for heart disease, you won’t be able to take ED pills, as they can cause a dangerous drop in blood pressure.
Treatment depends on the underlying cause. In general, exercise, particularly of the aerobic type, is effective for preventing ED during midlife. Exercise as a treatment is under investigation.[22]:6, 18–19 For tobacco smokers, cessation often results in a significant improvement.[23] Oral pharmacotherapy and vacuum erection devices are first-line treatments,[22]:20, 24 followed by injections of drugs into the penis, as well as penile implants.[22]:25–26 Vascular reconstructive surgeries are beneficial in certain groups.[24]
Metabolism (breakdown) of vardenafil can be slowed by aging, liver disease, and concurrent use of certain medications (such as erythromycin [an antibiotic], ketoconazole [Nizoral, a medication for fungal/yeast infections], and protease inhibitors [medications used to treat AIDS]). Slowed breakdown allows vardenafil to accumulate in the body and potentially increase the risk for side effects. Therefore, in men over 65 years of age with liver disease, or who are also taking medication(s) that can slow the breakdown of vardenafil, the doctor will initiate vardenafil at low doses to avoid its accumulation. For example,
Certain types of blood pressure medications, antiulcer drugs, antihistamines, tranquilizers (especially before intercourse), antifungals (hetoconazole), antipsychotics, antianxiety drugs, and antidepressants, known as selective serotonin reuptake inhibitors (SSRIs, including Prozac and Paxil), can interfere with erectile function. Smoking, excessive alcohol consumption, and illicit drug use may also contribute. In rare cases, low levels of the male hormone testosterone may contribute to erectile failure. Finally, psychological factors, such as stress, guilt, or anxiety, may also play a role, even when the impotence is primarily due to organic causes.
Trauma to the pelvic blood vessels or nerves can also lead result in ED. Bicycle riding for long periods has been implicated as an etiologic factor; direct compression of the perineum by the bicycle seat may cause vascular and nerve injury. [37] On the other hand, bicycling for less than 3 hours per week may be somewhat protective against ED. [37] Some of the newer bicycle seats have been designed to diminish pressure on the perineum. [37, 38]
Then you have to be able to make the right diagnosis. What is the basis for their erectile dysfunction? Is it psychogenic? Is it some sort of neurological or blood vessel or hormonal issue? So you have to make a diagnosis. You have to be able to make an assessment. And then only after those things are done, then you start to think about medications.
Obesity and metabolic syndrome can cause changes in blood pressure, body composition, and cholesterol which may lead to ED. Other conditions that may contribute to erectile dysfunction include Parkinson’s, multiple sclerosis, Peyronie’s disease, sleep disorders, alcoholism, and drug abuse. Taking certain medications can also increase your risk for ED.
The neurovascular events that ultimately occur result in the inhibition of adrenergic tone and the release of the nonadrenergic, noncholinergic neurotransmitter, nitric oxide. Nitric oxide is believed to be released from nonadrenergic, noncholinergic nerves and endothelial cells. It subsequently stimulates the guanylate cyclase enzyme system in penile smooth muscle. This results in increased levels of cyclic guanosine monophosphate (cGMP) and ultimately in smooth muscle relaxation, enhancement of arterial inflow, and veno-occlusion, producing adequate firmness for sexual activity.
Oral therapies via the PDE5i sildenafil, vardenafil, and tadalafil have been proven to be generally safe and effective in select NED populations. The majority of the treatment effectiveness data has been generated in the SCI population. Data regarding the use of PDE5i outside of the SCI population is lacking (58). Furthermore, the ED that exists in the population with neurologic disorders is often multifactorial and may be caused by psychogenic, psychosocial, hormonal, medication-related and disability-related factors. A careful evaluation of each patient must be performed to isolate these factors prior to initiating vasoactive therapy.

In some cases, ED can be a warning sign of more serious disease. One study suggests ED is a strong predictor of heart attack, stroke, and death from cardiovascular disease. The researchers say all men diagnosed with ED should be evaluated for cardiovascular disease. This does not mean every man with ED will develop heart disease, or that every man with heart disease has ED, but patients should be aware of the link.
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