This form of therapy has a response rate of well over 70%. The sympathetic nervous system normally maintains the penis in a flaccid or non-erect state. All of the vasoactive drugs, when injected into the corpora cavernosae, inhibit or override sympathetic inhibition to encourage relaxation of the smooth muscle trabeculae. The rush of blood engorges the penile corpora cavernosae sinusoidal spaces and creates an erection.
In the short term, alcohol relaxes muscles in the penis, letting blood to flow in (which is a good thing). However, alcohol also prevents other blood vessels from closing and trapping all the extra blood. Erections depend on trapping increased blood flow in the erectile tissue of the penis. If you don’t trap that extra blood, you don’t get an erection. In the long run, excessive alcohol consumption can cause liver scarring, high blood pressure, and can damage your blood vessels resulting in erectile dysfunction.
Condom troubles. Can the simple act of putting on a condom cause so much stress that it actually leads to erectile dysfunction? Sure it can — in fact, one recent survey of 234 young men conducted by the Children's Memorial Hospital in Chicago found that 25 percent had lost an erection while putting on a condom. “Putting on a condom requires a break from stimulation, and when it is on, it can reduce sensation,” says Dr. Montague.
As blood flows into the penis, the corpora cavernosa swell, and this swelling compresses the veins (blood vessels that drain the blood out of the penis) against the tunica albuginea. Compression of the veins prevents blood from leaving the penis. This creates a hard erection. When the amount of cGMP decreases by the action of a chemical called phosphodiesterase type 5 (PDE5), the muscles in the penis tighten, and the blood flow into the penis decreases. With less blood coming into the penis, the veins are not compressed, allowing blood to drain out of the penis, and the erection goes down.
Other hormone levels: Measurement of other hormones beside testosterone (luteinizing hormone [LH], prolactin level, and cortisol level) may provide clues to other underlying causes of testosterone deficiency and erectile problems, such as pituitary disease or adrenal gland abnormalities. Doctors may check thyroid levels in some individuals as both hypothyroidism (low thyroid function) and hyperthyroidism (overactive thyroid function) can contribute to erectile dysfunction.
Chlamydia and erectile dysfunction: What's the link? Some people who have chlamydia also experience erectile dysfunction (ED), which involves problems getting or maintaining an erection. Chlamydia can infect the prostate gland, leading to prostatitis, pain, and ED. In this article, learn more about the link between this common infection and ED, and treatments for both. Read now

For most men, improving erectile dysfunction means improving blood flow to the penis. Immediate relief often requires medications that increases nitric oxide (NO) in the blood vessels of the penis. NO causes the smooth muscle cells in the blood vessels of the penis to stretch, which increases the flow of blood. NO also keeps the smooth muscle cells younger and helps prevent and even reverse hardening and narrowing of the blood vessels over time. Proper diet (see more below) and regular exercise are key because both can boost NO.
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.

Currently, there are no therapies that cure erectile dysfunction. However, a number of effective therapies are available that allow an individual to have an erection when desired. Depending on the cause of the erectile dysfunction, certain therapies may be more effective than others. Although there is limited data on lifestyle modification, intuitively, decreasing risk factors for erectile dysfunction may help prevent progression of disease.
Chronic and persistent alcohol use is known to induce sexual dysfunction, which leads to marked distress and interpersonal difficulty. This, in turn, is known to worsen the alcohol abuse. Sexual dysfunction in the alcoholic may be due to the depressant effect of alcohol itself, alcohol-related disease or due to a multitude of psychological forces related to the alcohol use.[1] The spectrum of sexual dysfunction encompasses:
In many of these cases, a discussion between the physician, the man with erectile dysfunction, and possibly his partner can help to resolve the issues leading to treatment failure. For men who experience severe side effects, can’t take the drugs for other reasons (such as taking medicines such as nitroglycerin), or don’t respond in spite of further education on the correct use of the drugs, there are other treatment options that can help most men remain sexually active.
The article, "Inactivation of phosphorylated endothelial nitric oxide synthase (Ser-1177) by O-GlcNAc in diabetes-associated erectile dysfunction," appears in the Aug. 16 issue of the Proceedings of the National Academy of Sciences and was published online Aug. 5.  Melissa F. Kramer and Robyn E. Becker, also of the Brady Urological Institute, collaborated on this study.
Getting (and maintaining) an erection requires a surprising amount of things to go right. You have to get aroused, then pass that signal from your brain, through your nerves and hormones, to your blood vessels and muscles before an erection can even happen. If one thing goes wrong in that complicated exchange between your cardiovascular, and nerve system, and your hormone levels, blood vessels, and even your mood the result is usually erectile dysfunction. In other words, getting an erection is hard.
Sexuality and erection are controlled by multiple areas of the human brain including the hypothalamus, the limbic system, and the cerebral cortex. Stimulatory or inhibitory messages are relayed to the spinal erection centers to facilitate or inhibit erection (5). Two mechanisms have been proposed to explain the inhibition of erection in psychogenic dysfunction: direct inhibition of the spinal erection center by the brain as an exaggeration of the normal suprasacral inhibition and excessive sympathetic outflow or elevated peripheral catecholamine levels, which may increase penile smooth muscle tone and prevent the relaxation necessary for erection (8). Animal studies demonstrate that the stimulation of sympathetic nerves or systemic infusion of epinephrine causes detumescence of the erect penis (6,7). Clinically, higher levels of serum norepinephrine have been reported in patients with psychogenic ED than in normal controls or patients with vasculogenic ED (9).
Another common reason for failures of oral therapy is the absence of sexual or genital stimulation prior to attempting sexual intercourse. These medicines facilitate an erection by increasing blood flow to the penis, but they do not act as an aphrodisiac or as an initiator of the erection. A man who is not “in the mood” or does not have adequate physical stimulation will not respond with an erection.
Occasional ED is common in all men, including young and healthy men. But if you have a persistent or recurrent problem with initiating or maintaining an erection and it's causing you or your partner distress, talk to your doctor. “Lack of nighttime erections is another cause for concern, said Wang. These occurrences serve to nourish the penis with oxygen and keeping the blood supply healthy, he explained. "Young men should get four or five of these a night. If you are not getting these and you are having frequent problems with ED, you need to check in with your doctor,” he recommended.
When we say it’s a barometer of men’s health, it’s a signal. It’s an indicator that things may be right or not. And so when a man develops an erectile problem– and we’re talking about something that is occurring over time. It’s not something that just occurred overnight. When it occurs overnight, it’s more often than not a psychogenic, an anxiety reaction.
Since the decrease in T levels is often a consequence of obesity or weight gain (51), the milestone of treating testosterone deficiency in obese men is encouraging substantial lifestyle changes, including physical activity and weight loss. In fact, it is universally recognized that a low calorie diet or bariatric surgery can induce a significant increase in T plasma levels, reaching 10 nmol/L with the most invasive surgical procedures (62). Weight loss-induced T rise is more evident in young individuals (62), and, therefore, it must be strongly recommended in this age band.
The recommended starting dose of tadalafil for use as needed for most patients is 10 mg taken orally approximately one hour before sexual activity. A doctor may adjust the dose higher to 20 mg or lower to 5 mg depending on efficacy and side effects. Doctors recommended that patients take tadalafil no more frequently than once per day. Some patients can take tadalafil less frequently since the improvement in erectile function may last 36 hours. Patients may take tadalafil with or without food. Tadalafil is currently the only PDE5 inhibitor that is FDA-approved for daily use for erectile dysfunction and is available in 2.5 mg or 5 mg dosages for daily use.
Ageing is one of the most important unmodifiable risk factors for the development of metabolic disorders and CV diseases. Accordingly, the common algorithms for the estimation of risk of forthcoming diabetes or CV events include age as a factor of the equations (24-29). The weight attributed to age for estimating the risk in these equations is often so significant that younger men are automatically considered at low risk, irrespective of the other possible risk factors. However, even in younger subjects, overlooking the contribution of cardio-metabolic factors to pathogenesis of ED is a mistake that can lead to the loss of the opportunity of early recognition of patients who deserve a change in life-style or a pharmacological correction of risk factors. ED, besides being considered one of the clinical manifestations of metabolic and cardiovascular diseases (CVD), is regarded as an early marker of CV events (17). In fact, according to Montorsi’s hypothesis (30), impairment of penile artery blood flow occurs before that of coronary or carotid arteries, whose diameter is greater and needs longer time to acquire a clinically relevant damage. The clinical consequence of this pathological event is that ED often manifests earlier than myocardial infarction or stroke. In particular, it has been demonstrated that ED occurs on average three years before the first major adverse CV event (MACE) (31). Quite surprisingly, although CV risk increases with ageing, the role of ED as a harbinger of forthcoming MACE becomes progressively less evident. Data derived from almost 2,500 community-dwelling men aged 40–79 years, involved in the Olmsted County study show that ED is associated with an almost 50-fold higher risk of incident heart diseases in men aged 40–49 years, whereas the difference in risk between ED and non-ED men progressively declines in older men (32). The different CV risk associated with ED in different age bands has been confirmed by the meta-analysis of the available longitudinal studies (33). These observations suggest that, in younger men, the role of ED as a marker of CV risk is even more dramatic than in older ones and as a consequence, investigating the presence of metabolic or CV conditions in younger ED patients is pivotal for identifying men in whom an early life-style modification may avoid serious CV consequences. Even more than erection during sexual intercourse, erection during masturbation is considered a physiologic function that mirrors metabolic and CV health. In fact, erections during masturbation are far less affected by relational and psychological components than sex-related ones (34). In a population of subjects attending the Sexual Medicine and Andrology Unit of the University of Florence for sexual dysfunction, more than 2,500 men reported autoeroticism in the previous 3 months. Among these men, the impairment of erection during masturbation was associated with family and personal history of CVD (35), as well as with impaired response to the test with the intracavernous injection (ICI) of prostaglandin E1, which suggests an arteriogenic damage of penile arteries and predicts forthcoming MACE (36). For a subset of these men (n=862), information on the occurrence of MACE during a mean follow-up of 4.3 years was available and those who reported impaired erections during masturbation had a significantly higher incidence of MACE (35). However, when considering separately younger and older men, this association was confirmed only in younger ones, and it was still significant after excluding men reporting severe ED during masturbation (35). This suggests that the impairment of erection during masturbation is a symptom not completely overlapping with sex-related ED and that it can provide different and supplementary information, in particular when assessed in younger and apparently healthy men. Similarly to what is observed for erection during masturbation, acceleration of blood in penile arteries, as measured by the colour Doppler ultrasound in flaccid conditions, is associated with an adverse CV profile in men consulting for ED. A reduction in flaccid acceleration, which can be used by clinicians to objectively verify the arteriogenic origin of ED and to characterize the extent of a self-reported symptom, has been also associated with a future risk of CV events, with the association being significant in younger but not in older men (37).
It would be convenient if a fairy dickmother flew from the sky and told you this would be the drink that renders you flaccid, but when it comes to figuring out your limit, you’re on your own. There’s no hard and fast rule as to how much will actually affect you, either; Dr Mills notes that some men may be able to drink a lot and get erections, as everybody’s threshold is different.
Erectile dysfunction is when a man either can’t have an erection or can’t keep an erection long enough to have sex. For only 20% of men with ED, the cause is due to a psychological problem or disorder.2 When the cause of your ED is due to a physical condition, your ED is not a reflection on you or your sexual partner, since lack of arousal isn’t the problem.
In many of these cases, a discussion between the physician, the man with erectile dysfunction, and possibly his partner can help to resolve the issues leading to treatment failure. For men who experience severe side effects, can’t take the drugs for other reasons (such as taking medicines such as nitroglycerin), or don’t respond in spite of further education on the correct use of the drugs, there are other treatment options that can help most men remain sexually active.

Supplements are popular and often cheaper than prescription drugs for ED. However, supplements have not been tested to see how well they work or if they are a safe treatment for ED. Patients should know that many over-the-counter drugs have been found on drug testing to have ‘bootlegged' PDE 5 Inhibitors as their main ingredient. The amounts of Viagra, Cialis, Levitra or Stendra that may be in these supplements is not under quality control and may differ from pill to pill. The FDA has issued consumer warnings and alerts.
Dr. Niket Sonpal is the Associate Program Director of the Internal Medicine Residency at Brookdale Hospital Medical Center in Brooklyn and an Associate Professor at Touro College of Osteopathic Medicine. He’s a practicing Gastroenterologist and Hepatologist with a focus on Men’s and Women’s Health, and a regular contributor to Women’s health, Shape and Prevention Magazine.
"The good news is, our study also found that a large proportion of men were naturally overcoming erectile dysfunction issues. The remission rate of those with erectile dysfunction was 29%, which is very high. This shows that many of these factors affecting men are modifiable, offering them an opportunity to do something about their condition," Professor Wittert says.
THIS TOOL DOES NOT PROVIDE MEDICAL ADVICE. It is intended for general informational purposes only and does not address individual circumstances. It is not a substitute for professional medical advice, diagnosis or treatment and should not be relied on to make decisions about your health. Never ignore professional medical advice in seeking treatment because of something you have read on the WebMD Site. If you think you may have a medical emergency, immediately call your doctor or dial 911.
You may find that using a vacuum device requires some practice or adjustment. Using the device may make your penis feel cold or numb and have a purple color. You also may have bruising on your penis. However, the bruises are most often painless and disappear in a few days. Vacuum devices may weaken ejaculation but, in most cases, the devices do not affect the pleasure of climax, or orgasm.
Medications: Many common medicines produce erectile dysfunction as a side effect. Medicines that can cause erectile dysfunction include many used to treat high blood pressure, antihistamines, antidepressants, tranquilizers, and appetite suppressants. Examples of common medicines that can cause erectile dysfunction include propranolol (Inderal) or other beta-blockers, hydrochlorothiazide, digoxin (Lanoxin), amitriptyline (Elavil), famotidine (Pepcid), cimetidine (Tagamet), metoclopramide (Reglan), naproxen, indomethacin (Indocin), lithium (Eskalith, Lithobid), verapamil (Calan, Verelan, Isoptin), phenytoin (Dilantin), gemfibrozil (Lopid), amphetamine/dextroamphetamine (Adderall), and phentermine. Prostate cancer medications that lower testosterone levels such as leuprolide (Lupron) may affect erectile function. Some chemotherapies such as cyclophosphamide (Cytoxan) may affect erectile function.

ED has been for long time considered a problem mainly related to psychological conditions and distress. Accordingly, until phosphodiesterase type 5 inhibitors (PDE5i) were introduced, psychoanalysis and cognitive-behavioural therapy were the only option for ED. In the last few decades, ED has been recognized as a clinical consequence of several different organic diseases and the importance of vascular health in erectile function has been so emphasized that ED is now considered not only the result of vascular impairment, but also a harbinger of forthcoming cardiovascular (CV) events (17). Despite the increasing attention of research towards organic mechanisms and conditions leading to ED, it is now known that considering this symptom as entirely due to organic disorders, is as imprecise as considering it only secondary to psychological conditions. In fact, this pathogenetic dichotomy is now obsolete (1,18,19), because it is now known that ED is a multidimensional disorder deriving from the interaction of different components related to organic conditions, relational context and psychological status (20,21). Even when only one of these components is involved in the initial development of erectile impairment, eventually the other ones will appear, thus further worsening ED (21-23). The multidimensional nature of ED is still not fully accepted by health care professionals when dealing with young patients. In fact, complaints of ED in young men is often underestimated and attributed to transient and self-limiting psychological conditions, such as performance anxiety. Young patients are often reassured without any further medical investigations, including physical exam. However, organic disorders, as well as relational and psychological or psychiatric conditions, can be meaningful in determining ED in younger men. In a population of subjects seeking medical care at the Sexual Medicine and Andrology Unit of the University of Florence for sexual dysfunction, the first tertile of age (n=1,873 subjects) represents younger subjects (18–44 years). Pathogenetic components of ED in our sample are investigated by the Structured Interview on Erectile Dysfunction (SIEDY), a structured interview including 13 questions, whose answers, organized in a Likert scale, provide three scales, one for the organic subdomain [(SIEDY Scale 1); (22)], one for the relational subdomain [(SIEDY Scale 2); (23)] and one for the intrapsychic subdomain [(SIEDY Scale 3); (21)]. According to these scale scores, organic, relational and intrapsychic conditions are all significant risk factors for ED in younger patients of our population (Figure 2).
Sexual dysfunction is common in patients with diabetes mellitus. Vascular, neurological and hormonal alterations are involved in this complication. Many studies showed altered endothelium-dependent and neurogenic relaxations in corpus cavernosum from diabetic patients with erectile dysfunction (ED). This finding has been associated with a lack of nitric oxyde (NO) production and a significant increase in NO synthase (NOS) binding sites in penile tissues, induced by diabetes. Advanced glycation endproducts (AGEs) concur to diabetic vascular complications by quenching NO activity and by increasing the expression of mediators of vascular damage such as vascular endothelial growth factor (VEGF), possessing permeabilizing and neoangiogenic effects, and endothelin-1 (ET-1), with vaso-constricting and mitogenic action. Moreover, the differential gene expression for various growth factors in penile tissues may be involved in the pathophysiology of ED associated with diabetes. Neuropathy is also likely to be an important cause of diabetic ED: morphological alterations of autonomic nerve fibers in cavernosal tissue of patients with diabetic ED have been demonstrated. Finally, androgens enhance nNOS gene expression in the penile corpus cavernosum of rats, suggesting that they play a role in maintaining NOS activity. However, sexual dysfunctions in women with diabetes has received less attention in clinical research. Several studies suggest an increased prevalence of deficient vaginal lubrication, making sexual intercourse unpleasant. Sexual dysfunction is associated with lower overall quality of marital relation and more depressive symptoms in diabetic women.
"Erectile dysfunction can be a very serious issue because it's a marker of underlying cardiovascular disease, and it often occurs before heart conditions become apparent. Therefore, men should consider improving their weight and overall nutrition, exercise more, drink less alcohol and have a better night's sleep, as well as address risk factors such as diabetes, high blood pressure and cholesterol.

ED is easily and successfully treated! If your sex drive is unaffected, but you experience problems achieving or sustaining erection for a period of four to five weeks, you may have ED. Talk to your doctor immediately. Don’t delay—erectile dysfunction doesn’t “just go away!” Additionally, ED could be a sign of a serious, even life-threatening complication, such as congestive heart failure or kidney disease. Ignoring your ED because it’s embarrassing could jeopardize your health.
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