To start with, ED is NOT in your head. You can’t simply will yourself to get an erection, no matter how much you try. Studies show over 80% of ED cases are caused by a treatable physical disorder. Diseases such as diabetes, high blood pressure, and high cholesterol are common causes. Even a perfectly healthy man can develop ED after a brain or spinal cord injury. ED can be a side effect of certain medications, too. Read more on our Causes of ED page.
Erectile dysfunction may be an unpleasant condition that no one really wants to talk about, failing to acknowledge it won’t make the problem go away. Your best defense against health problems like this is to learn everything you can about it so you can tackle the problem at the root. If you’re ready to stop living in embarrassment about your sexual function, become an advocate for yourself and your own health and talk to your doctor.
Chronic stress dumps adrenaline in your system multiple times a day. And that can lead to high blood pressure, heart disease, obesity, and diabetes. Chronic stress is like red-lining your car all day long. When you drive 100 mph all the time, something is going to break down. A high-stress environment can actually change the way your brain sends messages to your body. Dumping too much adrenaline into your bloodstream can affect blood flow and severely limit your ability to achieve and maintain an erection.
Remember those cultural messages we discussed earlier, about how men are wild sex aliens from the planet Weenus? Well, men are raised hearing those messages, too, and they can end up screwing with their sexual self-image —for instance, they can lead men to obsess over their own virility, and panic about impressing a new partner, until they've thought their boner into a corner and can't get an erection. Performance anxiety is one of the most common culprits behind lost erections, especially among younger, less experienced men.
This consensus development conference on male erectile dysfunction has provided an overview of current knowledge on the prevalence, etiology, pathophysiology, diagnosis, and management of this condition. The growing individual and societal awareness and open acknowledgment of the problem have led to increased interest and resultant explosion of knowledge in each of these areas. Research on this condition has produced many controversies, which also were expressed at this conference. Numerous questions were identified that may serve as foci for future research directions. These will depend on the development of precise agreement among investigators and clinicians in this field on the definition of what constitutes erectile dysfunction, and what factors in its multifaceted nature contribute to its expression. In addition, further investigation of these issues will require collaborative efforts of basic science investigators and clinicians from the spectrum of relevant disciplines and the rigorous application of appropriate research principles in designing studies to obtain further knowledge and to promote understanding of the various aspects of this condition.
It is important that all erectile dysfunction is reported to your doctor, as sometimes it can be an indicator of something physically wrong with you that has to be treated. Also, your doctor is in the best position to find the reason for your erectile dysfunction. Routine questions and tests will provide a guide to the cause and allow your doctor to decide what kind of treatment you might need to deal with it. This may involve referral to a specialist. Detailed information can be found at the website of the Impotence Association – www.sda.uk.net
The circulatory system plays a central role in obtaining and sustaining erections. Augmentation of blood flow to the corporal bodies depends on the intravascular pressure in the penile artery. Vascular lesions—typically atherosclerotic, but occasionally fibrotic—and systemic hypotension will limit flow to the corpora. In certain patients, blood flow at rest may be sufficient to obtain an erection but not sufficient to maintain it during intercourse, when the pelvic musculature places greater demands on a compromised blood supply.
Studies to further define vasculogenic disorders include pharmacologic duplex grey scale/color ultrasonography, pharmacologic dynamic infusion cavernosometry/ cavernosography, and pharmacologic pelvic/penile angiography. Cavernosometry, duplex ultrasonography, and angiography performed either alone or in conjunction with intracavernous pharmacologic injection of vasodilator agents rely on complete arterial and cavernosal smooth muscle relaxation to evaluate arterial and veno-occlusive function. The clinical effectiveness of these invasive studies is severely limited by several factors, including the lack of normative data, operator dependence, variable interpretation of results, and poor predictability of therapeutic outcomes of arterial and venous surgery. At the present time these studies might best be done in referral centers with specific expertise and interest in investigation of the vascular aspects of erectile dysfunction. Further clinical research is necessary to standardize methodology and interpretation, to obtain control data on normals (as stratified according to age), and to define what constitutes normality in order to assess the value of these tests in their diagnostic accuracy and in their ability to predict treatment outcome in men with erectile dysfunction.
Diabetes is a well-recognized risk factor for ED. A systematic review and meta-analysis found that the prevalence of ED was 37.5% in type 1 diabetes, 66.3% in type 2 diabetes, and 52.5% in diabetes overall—a rate approximately 3.5 times higher than that in controls.  The etiology of ED in diabetic men probably involves both vascular and neurogenic mechanisms. Evidence indicates that establishing good glycemic control can minimize this risk.
One study examined the role of testosterone supplementation in hypogonadal men with ED. These men were considered nonresponders to sildenafil, and their erections were monitored by assessing nocturnal penile tumescence (NPT). After these men were given testosterone transdermally for 6 months, the number of NPTs increased, as did the maximum rigidity with sildenafil.  This study suggests that a certain level of testosterone may be necessary for PDE5 inhibitors to function properly.
ED is often the result of atherosclerosis, and as a result, men with ED frequently have cardiovascular disease. Sexual activity is associated with increased physical exertion, which in some men may increase the risk of having a heart attack (myocardial infarction or MI). The major risk factors associated with cardiovascular disease are age, hypertension, diabetes mellitus, obesity, smoking, abnormal lipid/cholesterol levels in the blood, and lack of exercise. Individuals with three or more of these risk factors are at increased risk for a heart attack during sexual activity. The Princeton Consensus Panel developed guidelines for treating ED in men with cardiovascular disease. Thus, if you have ED and cardiovascular disease (for example, angina or prior heart attack), you should discuss whether or not treatment of ED and sexual activity are appropriate for you.
Parasympathetic input allows erection by relaxation of trabecular smooth muscle and dilation of the helicine arteries of the penis. This leads to expansion of the lacunar spaces and entrapment of blood by compressing venules against the tunica albuginea, a process referred to as the corporal veno-occlusive mechanism. The tunica albuginea must have sufficient stiffness to compress the venules penetrating it so that venous outflow is blocked and sufficient tumescence and rigidity can occur.
The first line and by far the most common treatment today is with the prescription drug sildenafil citrate, sold under the brand name Viagra. An estimated 20 million prescriptions for the pill have been filled since it was approved by the FDA in March 1998. It is also the most effective treatment with a success rate of more than 60%. The drug boosts levels of a substance called cyclic GMP, which is responsible for widening the blood vessels of the penis. In clinical studies, Viagra produced headaches in 16% of men who took it, and other side effects included flushing, indigestion, and stuffy nose.
Erectile dysfunction is clearly a symptom of many conditions, and certain risk factors have been identified, some of which may be amenable to prevention strategies. Diabetes mellitus, hypogonadism in association with a number of endocrinologic conditions, hypertension, vascular disease, high levels of blood cholesterol, low levels of high density lipoprotein, drugs, neurogenic disorders, Peyronie's disease, priapism, depression, alcohol ingestion, lack of sexual knowledge, poor sexual techniques, inadequate interpersonal relationships or their deterioration, and many chronic diseases, especially renal failure and dialysis, have been demonstrated as risk factors. Vascular surgery is also often a risk factor. Age appears to be a strong indirect risk factor in that it is associated with an increased likelihood of direct risk factors. Other factors require more extensive study. Smoking has an adverse effect on erectile function by accentuating the effects of other risk factors such as vascular disease or hypertension. To date, vasectomy has not been associated with an increased risk of erectile dysfunction other than causing an occasional psychological reaction that could then have a psychogenic influence. Accurate risk factor identification and characterization are essential for concerted efforts at prevention of erectile dysfunction.
You're right that this should be a last resort, but Paduch also agrees that sometimes a little confidence can help you get back on track. The thing is, you should only take an ED medicine if it's prescribed by your doctor (otherwise you'll miss out on the important medical info you should know before you take it). Another option is an l-arginine supplement, which can increase nitric oxide and blood flow.
In addition, a man affected by lower testosterone may feel less sexually inclined, less interested in viewing sexual material, and less interested in physical activities. To add to this, a man dealing with less testosterone may also become less assertive, more inclined to stay in, and more likely to seek out medical help for his erectile dysfunction.
In other cases, men who habitually use alcohol or other drugs may experience similar results. Alcohol is a depressant to the central nervous system. This means that a little bit might be able to lighten the mood, but too much can basically shut down all communication between the brain and the penis. When this happens, no amount of will or stimulation will result in an erection. Other drugs can also affect the body’s ability to achieve an erection, including heroin and MDMA, otherwise known as ecstasy.
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.
Not to give your already stressed-out dude one more thing to worry about, but stress is the cause of 20 percent of all erectile problems, from one-off boner blunders to a lingering inability to get and maintain an erection. Of course, sex difficulties are just the tip of the stress-induced health problem iceberg — sustained stress can also lead to insomnia, stomach troubles, chest pains, anxiety, and more severe health issues in the long term.
Acetylcholine released by the parasympathetic nerves is thought to act primarily on endothelial cells to release a second nonadrenergic-noncholinergic carrier of the signal that relaxes the trabecular smooth muscle. Nitric oxide released by the endothelial cells, and possibly also of neural origin, is currently thought to be the leading of several candidates as this nonadrenergic-noncholinergic transmitter; but this has not yet been conclusively demonstrated to the exclusion of other potentially important substances (e.g., vasoactive intestinal polypeptide). The relaxing effect of nitric oxide on the trabecular smooth muscle may be mediated through its stimulation of guanylate cyclase and the production of cyclic guanosine monophosphate (cGMP), which would then function as a second messenger in this system.
Unfortunately, some patients may have an overly simplified understanding of the role of PDE5 inhibitors in ED management. Such patients may not expect or be willing to undergo a long evaluation and testing process to obtain a better understanding of their sexual problem, and they may be less likely to involve their partner in discussing their sexual relationship with the physician. They may expect to obtain medications through a phone call to their doctor or even over the Internet, with minimal or no physician contact at all.
The user should stop using the vacuum pump if pain occurs... Use of a vacuum pump may bruise or rupture the blood vessels either immediately below the surface of the skin or within the deep structures of the penis or scrotum, resulting in hemorrhage and/or the formation of a hematoma. There is now sufficient information available regarding the risks, benefits, and use of vacuum pumps.
Although not indicated for routine use, nocturnal penile tumescence (NPT) testing may be useful in the patient who reports a complete absence of erections (exclusive of nocturnal "sleep" erections) or when a primary psychogenic etiology is suspected. Such testing should be performed by those with expertise and knowledge of its interpretation, pitfalls, and usefulness. Various methods and devices are available for the evaluation of nocturnal penile tumescence, but their clinical usefulness is restricted by limitations of diagnostic accuracy and availability of normative data. Further study regarding standardization of NPT testing and its general applicability is indicated.
Psychological processes such as depression, anxiety, and relationship problems can impair erectile functioning by reducing erotic focus or otherwise reducing awareness of sensory experience. This may lead to inability to initiate or maintain an erection. Etiologic factors for erectile disorders may be categorized as neurogenic, vasculogenic, or psychogenic, but they most commonly appear to derive from problems in all three areas acting in concert.
The association between low testosterone and ED is not entirely clear. Although these 2 processes certainly overlap in some instances, they are distinct entities. Some 2-21% of men have both hypogonadism and ED; however, it is unclear to what degree treating the former will improve erectile function.  About 35-40% of men with low testosterone see an improvement in their erections with testosterone replacement; however, almost 65% of these men see no improvement. 
It can also help to tell your partner (either before you start or when it happens) that hey, sometimes it takes your penis a while to warm up or sometimes it comes and goes as it pleases — and that they shouldn't take it personally and you won't let it ruin the moment. When it happens, take a few deep breaths, focus on your partner, and go back to doing whatever was feeling good before. "If they approach that with authentic confidence, the partner is usually like 'OK, cool,'" says Skyler. "Remember, you're more than just your penis."
Is your erectile dysfunction due to psychological (stress, relationship problems, etc.) or physical factors? Your doctor may ask if you note erections at night or in the early morning. Men have involuntary erections in the early morning and during REM sleep (a stage in the sleep cycle with rapid eye movements). Men with psychogenic erectile dysfunction (erectile dysfunction due to psychological factors such as stress and anxiety rather than physical factors) usually maintain these involuntary erections. Men with physical causes of erectile dysfunction (for example, atherosclerosis, smoking, and diabetes) usually do not have these involuntary erections. Men with psychogenic erectile dysfunction may relate the onset of problems to a "stressor," such as failed relationship. Your doctor may suggest a test to determine if you have erections during sleep, which may suggest that there may be a psychological cause of the erectile dysfunction.
Medical conditions, such as hypertension, diabetes mellitus, and cardiovascular disease (CVD), and psychological conditions, such as depression and anxiety, also contribute to sexual dysfunction in middle-aged or elderly men. CVD and hypertension cause a narrowing and hardening of the arteries, leading to reduced blood flow to the corporal bodies, which is essential for achieving an erection. Diabetes is a common aetiology of sexual dysfunction, because it can affect both the blood vessels and the nerves that supply the penis. Men with diabetes are four times more likely to experience ED, and on average, experience ED 15 years earlier than men without diabetes.7 Obesity is also correlated to the development of several types of dysfunction, including a decrease in sex drive and an increase in episodes of ED.8
Constriction of the trabecular smooth muscle and helicine arteries induced by sympathetic innervation makes the penis flaccid, with blood pressure in the cavernosal sinuses of the penis near venous pressure. Acetylcholine is thought to decrease sympathetic tone. This may be important in a permissive sense for adequate trabecular smooth muscle relaxation and consequent effective action of other mediators in achieving sufficient inflow of blood into the lacunar spaces. When the trabecular smooth muscle relaxes and helicine arteries dilate in response to parasympathetic stimulation and decreased sympathetic tone, increased blood flow fills the cavernous spaces, increasing the pressure within these spaces so that the penis becomes erect. As the venules are compressed against the tunica albuginea, penile pressure approaches arterial pressure, causing rigidity. Once this state is achieved, arterial inflow is reduced to a level that matches venous outflow.
If you just got off solo, you might have to wait before you can hop into bed with your partner, says Dr. Brahmbhatt. It might have something to do with a spike in the hormone prolactin after you orgasm, according to a study published in the International Journal of Impotence Research. This hormone has been linked to difficulties maintaining an erection or even ejaculating.
Lifestyle choices that impair blood circulation can contribute to ED. Smoking, excessive drinking, and drug abuse may damage the blood vessels and reduce blood flow to the penis. Smoking makes men with atherosclerosis particularly vulnerable to ED. Being overweight and getting too little exercise also contribute to ED. Studies indicate that men who exercise regularly have a lower risk of ED.