All the above subjects were assessed for the prevalence of one or more sexual dysfunction experienced over the past 12 months using a sexual dysfunction checklist (Appendix A) by a trained psychiatrist (BSA). The checklist contains items corresponding to 12 areas of sexual dysfunction described in the Diagnostic Criteria for Research, ICD-10 Classification of Mental and Behavioural Disorders.[15] This was necessary as the SCAN does not contain a detailed assessment for the ICD-10 section on Sexual dysfunction not caused by organic disorder or disease (F52). The disorders specifically tapped by the checklist were aversion towards sex, low sexual desire, difficulty in achieving and in maintaining erection, premature ejaculation, inhibited or delayed ejaculation orgasm with flaccid penis, anorgasmia, pain at the time of coitus, dissatisfaction with frequency of intercourse per week (in the last year and in a representative week 5 years earlier), partner and, own sexual function.
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.
The penis is composed of three cylinders: two on the top, the corpora cavernosa and one on the bottom, the corpus spongiosum. All of these are involved in the process of an erection. The corpora cavernosa are composed of potential spaces that can distend with blood, causing rigidity of the penile shaft. The corpus spongiosum is important for rigidity of the glans of the penis. When aroused, stimulated chemicals are released from the nervous system (nitric oxide is one) that stimulate the arteries to the penis to relax and increase blood flow into the penis. These potential spaces, like a sponge, can expand when more blood flow comes in the penis. Each corpora cavernosa is surrounded by an outer coating the tunica albuginea. When the penis fills with blood, these potential spaces, the sinusoids, compress the veins in the corpora against the side of the tunica albuginea, thus preventing blood from leaving the penis. It is this compression of the veins that allows for the erection to become fully rigid.
These are not currently approved by the FDA for ED management, but they may be offered through research studies (clinical trials). Patients who are interested should discuss the risks and benefits (informed consent) of each, as well as costs before starting any clinical trials. Most therapies not approved by the FDA are not covered by government or private insurance benefits.

In the evaluation of physical causes of ED, the health care provider is assessing for conditions that may affect the nerves, arteries, veins, and functional anatomy of the penis (for example, the tunica albuginea, the tissue surround the corpora). In determining a physical (or organic) cause, your health care provider will first rule out certain medical conditions, such as high blood pressure, high cholesterol, heart and vascular disease, low male hormone level, prostate cancer, and diabetes, which are associated with erectile dysfunction. Medical/surgical treatment of these conditions may also cause ED. In addition to these health conditions, certain systemic digestive (gastrointestinal) and respiratory diseases are known to result in erectile dysfunction:


Association between severity of erectile dysfunction and SIEDY Scale 1, Scale 2 and Scale 3 (organic, relational and intrapsychic pathogenetic components of erectile dysfunction, respectively). Data are derived from a population of 1,873 men aged 18–44 years, representing the first tertile of age in a population of patients consulting the Sexual Medicine and Andrology Unit of the University of Florence for erectile dysfunction. Data are adjusted for age, smoking habits, alcohol intake and education. Erectile dysfunction is defined according to a previously validated definition (21) using the sum of the scores obtained from question 1A (Do you have full erection sufficient for penetration? Rating 0= always, 1= often, 2= quite often and 3= sometimes) and question 2 (Does it occur to have a normal erection which you are not able to maintain? Rating 0= sometimes, 1= quite often, 2= often, and 3= always) of SIEDY, which reproduce the definition of erectile dysfunction as “The persistent inability to achieve and/or maintain an erection adequate for satisfactory sexual activity” (1). SIEDY, Structured Interview on Erectile Dysfunction.
In most young men with ED, additional testing to assess for the origin of ED is unnecessary as the history gives you the information that you need. With this said, it may be therapeutic for the patient to know his laboratory assessments are normal, in which case additional testing does add significant value to the assessment. From the history alone, we find that most of these men will have situational erectile dysfunction that responds well to low dose oral PDE-5 inhibitors. If the patient does respond well to these medications, the diagnosis of neurogenic erectile dysfunction, clinically significant arterial insufficiency, or venous-occlusive dysfunction can efficiently be ruled out. If the patient responds inconsistently or does not respond to the oral medications, additional workup should be considered, dependent on the additional history provided.
Given the different questions and response options used here, I’d be cautious about concluding that the NSSHB is necessarily registering a rise in ED among young men compared to the aforementioned US study from the 90s. Given that the NSSHB response options allowed for different degrees of severity, it’s likely that this study is detecting more guys who occasionally have mild erectile issues (issues that may not even be significant enough to prompt distress or clinical attention). Also, the NSSHB was bound to produce different figures given that participants only had to think about the most recent time they had sex, as opposed to recalling all sexual experiences over the last year (indeed, thinking only about a single, recent event could make it easier to remember a mild problem that would otherwise be forgotten). For these reasons, the NSSHB data just aren’t directly comparable to the 90s data.
A 25-year-old male presents with a past medical history of mild traumatic brain injury, remote bilateral orchitis, depression, anxiety, and PTSD from childhood bullying. He presents with his mother. His chief complaint is ED that began at 19 years old. He reports that it is "hard to obtain an erection, takes a lot of work to get almost nothing out of it" and “extreme loss of sensation in specific areas” on his penis. He feels that this might be related to “over masturbation without lubricant” 1–3 times per day and reports that he is “addicted to masturbation”, using it as a coping mechanism to manage his PTSD. He reports strong, sustainable erections with tadalafil 5 mg and recovery of sensation when he uses marijuana. He has read extensively on the internet and self-treats with topical vitamin creams, self-administered laser treatment to the penis, pulsed electromagnetic therapy, and hyperbaric oxygen treatment for ED for the past 6 months. He reports no change with any of these treatments. He reports reduced libido and has recently started treatment with HCG and testosterone gel for testosterone of 198 without any change in his symptoms with T of 450. His free T is normal. He lives at home, is unemployed, and is sedentary. He takes Wellbutrin. His physical examination is normal. His CBC, CMP, pituitary, and thyroid functions are normal. Prior to the visit, his mother called the clinic to inform personnel that her son was very sensitive, potentially suicidal, and emotionally disturbed by this problem. He has seen two other urologists already for his erectile dysfunction and been displeased with the outcome of his visits.
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Alcohol consumption is a common behavior in social circumstances worldwide. Epidemiological studies have suggested that moderate alcohol consumption reduces cardiovascular morbidity and mortality. The cardiovascular protective effects of alcohol may be attributed to its antioxidant, vasorelaxant, and antithrombotic properties, elevation of high-density lipoprotein or increase of nitric oxide production. Erectile dysfunction (ED) is a harbinger of cardiovascular diseases. Most epidemiological studies have also found that alcohol consumption, like its relationship with coronary artery disease, is related to ED in a J-shaped manner, with moderate consumption conferring the highest protection and higher consumption less benefits. In epidemio-logical studies, it is difficult to distinguish the ethanol effects from those of associated confounding factors. Meanwhile, long-term alcohol users, especially in those with alcohol liver disease, are highly associated with ED. More research is needed to investigate the true effects of alcohol consumption on cardiovascular diseases or ED.
These are among the most challenging patients seen in urology practice today: a young, healthy man with neither systemic disease nor a history of trauma, who has complaints of ED (Table 2). These men often have co-morbid diagnoses, such as anxiety, depression, or mood disorders, which make the issue of ED more complex for both the patient and the urologist (12). The psychological burden of ED in these young men is more pronounced than it might be in older men as this is the phase of life during which many men expect to be highly sexually active (4). These young men are usually technologically savvy and may have scrutinized much of the readily available information on the internet regarding ED. Often they arrive to clinic armed with an understanding of the diagnostic evaluation that may be offered to further investigate the etiology of their concerns. This makes the evaluation and treatment of these men more challenging since additional diagnostic testing is often not indicated after a thorough history and physical examination. In many cases, they may have self-diagnosed and self-treated based on the information that they obtained prior to seeing a physician. Many of these men will see multiple urologists on their quest to find a pathophysiology that they can accept, and many have unrealistic expectations of a rapid cure or a surgical cure.
Circulatory problems: An erection occurs when the penis fills with blood and a valve at the base of the penis traps it. Diabetes, high blood pressure, cholesterol, clots, and atherosclerosis (hardening of the arteries) can all interfere with this process. Such circulatory problems are the number one cause of erectile dysfunction. Frequently, erectile dysfunction is the first noticeable symptom of cardiovascular disease.

Instead of injecting a medicine, some men insert a suppository of alprostadil into the urethra. A suppository is a solid piece of medicine that you insert into your body where it dissolves. A health care professional will prescribe a prefilled applicator for you to insert the pellet about an inch into your urethra. An erection will begin within 8 to 10 minutes and may last 30 to 60 minutes.
To avoid the dreaded whiskey d---, you don’t necessarily have to stop drinking alcohol. Just drink in moderation. The National Institute on Alcohol Abuse and Alcoholism defines moderate drinking as no more than two drinks a day for men, and one drink a day for women. The liver can only process 1 ounce of liquor or one standard drink in one hour. Consuming more than this will lead the system to become saturated, where extra alcohol will increase in the blood and body tissues, until the liver is ready to metabolize it again. Until then, high blood alcohol concentration will last for several hours and affect you physiologically.

The physical exam should focus on femoral and peripheral pulses, femoral bruits (vascular abnormalities), visual field defects (prolactinoma or pituitary mass), breast exam (hyperprolactinemia), penile strictures (Peyronie’s disease), testicle atrophy (testosterone deficiency), and asymmetry or masses (hypogonadism). A rectal exam allows for assessment of both the prostate and sphincter tone, abnormalities that are associated with autonomic dysfunction. Sacral and perineal neurological exam will help in assessing autonomic function.
It can be embarrassing to talk to your doctor about your sex life, but it's the best way to get treated and get back to being intimate with your partner. Your doctor can pinpoint the source of the problem and may recommend lifestyle interventions like quitting smoking or losing weight. Other treatment options may include ED drugs, hormone treatments, a suction device that helps create an erection, or counseling.
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.
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).
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.
Once observed that the organic component of ED is the most important one in younger patients (Figure 2), the summarized evidence underlines that metabolic and CV risk must not be underestimated in younger men even when they are apparently healthy. In fact, it is particularly in these men that recognizing the presence of risk factors can help in changing life-style, thus really changing the natural history of metabolic and CV diseases. In older men the damage is often already established and the identification of further risk factors usually does not add information to the estimation of CV risk. ED is a symptom that can provide a chance for both the patients and physicians to unearth the presence of CV risk factors and improve both the quality and length of life of these men.
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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