And yes, this may all seem easier said than done, when it comes to a condition that is more often than not the subject of jokes—or the cause of embarrassment. Talking to your doctor is the first step in dealing with this complication, which can wreak havoc on your quality of life. Keeping diabetes in check and enjoying a healthy lifestyle can make a huge difference in reducing ED risk, but if that isn't enough, there are successful treatments. Sex brings a range of physical and psychological benefits, whether you have diabetes or not. Preventing or reversing ED isn't just about sex—it's a step toward better health and a more satisfying life.
What young men should not do is take an ED drug like Viagra without a prescription, or mix them with other drugs. “This is a huge problem and not a safe practice,” says Penny Kaye Jensen, PhD, president of the American Academy of Nurse Practitioners. “Some young men are mixing ED drugs with mind-altering drugs, such as ecstasy or crystal methamphetamine. This is on the rise and is a potentially deadly combination.”
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.
“I’d like to say that men are regularly screened for ED, but when it comes to busy doctors taking care of patients with diabetes, sexual function tends to fall lower on the list of complications,” said Stan Honig, MD,  Director of Men’s Health, Yale School of Medicine. “I’d like to think that every doctor asks every man about sexual function, but I don’t think that’s the case.”

Excessive drinking is a common cause of erectile dysfunction, according to the Mayo Clinic. As the amount of alcohol in the blood increases, the alcohol decreases the brain’s ability to sense sexual stimulation. As a depressant, alcohol directly affects the penis by interfering with parts of the nervous system that are essential for sexual arousal and orgasm, including respiration, circulation, and sensitivity of nerve endings, according to Health Promotion at Brown University.


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.
The key to treating erectile dysfunction is to identify the underlying cause. In many cases, it takes a fair bit of trial and error. Because the majority of ED cases are caused by physiological issues, your first step should be to talk to your doctor about your concerns. After completing a physical examination and reviewing your medical history, your doctor will ask you some questions and run some tests to rule out medical causes for your ED.
In fact, one common reason many younger men visit their doctor is to get erectile dysfunction medication. Often, men with erectile dysfunction suffer with diabetes or heart disease, or may be sedentary or obese, but they don’t realize the impact of these health conditions on sexual function. Along with erectile dysfunction treatment, the doctor may recommend managing the illness, being more physically active, or losing weight.
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.
For patients who have ED related to hypertonic cavernous smooth muscle and excessive sympathetic discharge, we recommend a trial of a low-dose alpha adrenergic blocker, such as terazosin 1 mg PO at bedtime nightly. We typically increase the dosage as needed every 2–3 weeks for 3–5 months until the patient experiences improvement of the erection or we determine that treatment is ineffective. We explain the potential side effects of orthostasis, dizziness, and retrograde ejaculation in detail. We also take great care and time in explaining to the patient, and his family/partner if present, the pathophysiologic mechanism of their erectile dysfunction and the biological basis of the treatment plan. This detailed discussion helps to engage the patient in the treatment plan and provides encouragement regarding the potential for response to treatment and recovery. During these encounters, we utilize teaching tools, such as diagrams, drawings, printed handouts, and other visual aids to ensure that the discussion is patient-focused and patient-friendly. Patient education is critical to exploring treatment options and developing confidence in our ability to treat the ED, and their own ability to overcome and eventually resolve the problem of ED.
The key to treating erectile dysfunction is to identify the underlying cause. In many cases, it takes a fair bit of trial and error. Because the majority of ED cases are caused by physiological issues, your first step should be to talk to your doctor about your concerns. After completing a physical examination and reviewing your medical history, your doctor will ask you some questions and run some tests to rule out medical causes for your ED.
What happens is that the blood vessels of the penis are rather small, and a small amount of plaque in the penile arteries is going to result in erectile dysfunction. You need more plaque before the person’s actually symptomatic from a heart problem, but they’re linked. And so when anybody, any man has an erectile issue, it’s incumbent upon the physician to make certain that their cardiac status is healthy.
Low intracavernosal nitric oxide synthase levels are found in people with diabetes, smokers, and men with testosterone deficiency. Interference with oxygen delivery or nitric oxide synthesis can prevent intracavernosal blood pressure from rising to a level sufficient to impede emissary vein outflow, leading to an inability to acquire or sustain rigid erection. Examples include decreased blood flow and inadequate intracavernosal oxygen levels when atherosclerosis involves the hypogastric artery or other feeder vessels and conditions, such as diabetes, that are associated with suboptimal nitric oxide synthase activity.
The causes of ED are numerous but generally fall into two categories: organic or psychogenic. The organic causes can be subdivied into five categories: vascular, traumatic/postsurgical, neurological, endocrine-induced, and drug-induced. Examples of the psychogenic causes are depression, performance anxiety, and relationship problems. In people with diabetes, the main risk factors are neuropathy, vascular insufficiency, poor glycemic control, hypertension, low testosterone levels, and possibly a history of smoking.

Smoking.   Smoking and erectile dysfunction are related as smoking leads to plaque build up in the arteries called cardiovascular disease, which restricts blood flow through the veins.  Arterial sclerosis from smoking restricts blood flow, and thus can prevent the massive amount of blood required for you to achieve an eretion, resulting in erectile dysfunction.

If the patient reports a history of trauma to the genitals that preceded his erectile dysfunction, further evaluation with pharmacologic injection and penile color duplex ultrasound (PCDU) would be indicated to assess for arterial insufficiency or venous occlusive dysfunction (19). Prior to PCDU, however, you might give him a trial of oral PDE5 inhibitors. If those medications are effective, you have effectively ruled out significant arterial insufficiency or venous leakage disease as an etiology. Regardless of outcome of PCDU, no surgical intervention would likely be offered to this man who responds well to oral agents.


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.
A medical history focused on risk factors, such as cigarette smoking, hypertension, alcoholism, drug abuse, trauma, and endocrine problems including hypothyroidism, low testosterone levels, and hyperprolactinemia, is very important. Commonly used drugs that disrupt male sexual function are spironolactone (Aldactone), sympathetic blockers such as clonidine (Catapres), guanethidine (Islemin), methyldopa (Aldomet), thiazide diuretics, most antidepressants, ketoconazole (Nizoral), cimetidine (Tagamet), alcohol, methadone, heroin, and cocaine. Finally, assessment of psychiatric history will help identify emotional issues such as interpersonal conflict, performance anxiety, depression, or anxiety.
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:
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.
It's not easy to get in the mood when you're overwhelmed by responsibilities at work and home. Stress can take its toll on many different parts of your body, including your penis. Deal with stress by making lifestyle changes that promote well-being and relaxation, such as exercising regularly, getting enough sleep, and seeking professional help when appropriate.
Unconventional CV risk factors, such as impaired erections during masturbation and reduced flaccid acceleration, are interesting parameters to implement in Sexual Medicine context, because they can help fill the gap of information on CV risk, left by the conventional risk factors (the so-called residual risk) (38). However, it should be recognized that not all the healthcare professionals who deal with the complaint of ED (i.e., general practitioners, diabetologists, cardiologists, sport physicians, nurses, etc.) have the facilities or competence for the specific assessment of these parameters. In contexts different than Sexual Medicine and Andrology, the assessment of conventional risk factors is certainly more convenient. Metabolic syndrome (MetS) represents a cluster of metabolic derangements easily and commonly evaluated in several different medical contexts. In a population of more than 600 subjects attending the Sexual Medicine and Andrology Unit of the University of Florence for ED, the presence of MetS was associated with an increased incidence of MACE during 4.3 years of follow-up in younger (first tertile of age: 18–52 years) (Figure 3, Panel A and B) but not in middle aged and older men (second and third tertiles of age: 53–60 and 61–88 years, respectively) (Figure 3, Panel B). Similar to MetS, the algorithms for estimating the risk of developing MACE are easily computed and they take into account factors largely available in a clinical setting. In Europe, the most commonly used algorithm is the SCORE, which takes into account age, smoking habits, systolic blood pressure and total cholesterol (26). These parameters are introduced in a calculation tool that returns the 10-year risk of developing the first MACE. The same estimated risk rate can obviously be derived from different combinations and extent of the single risk factors and, as aforementioned, age has a heavy weight in the amount of risk, even when the other parameters are normal. For overcoming this overestimation, the concept of vascular age, based on the predicted CV risk, has been introduced. Vascular age of a subjects with a specific CV risk profile corresponds to the chronological age of a subjects who has the same estimated risk but only due to chronological age, because of the absence of the other modifiable risk factors (i.e., a non-smoker, normotensive and normocholesterolemic subject) (39,40). Vascular age carries the advantage of easily and directly communicating the concept of high relative risk to patients, in particular to younger ones, who are by definition at low absolute risk (“Your CV risk is the same of a man that is 15 years older than you”). Based on this interesting and useful concept of vascular age, we recently studied the clinical consequences of having a high discrepancy between the estimated vascular and the actual chronological age in our population of men consulting for ED. In our sample, a greater difference between vascular and chronological age was associated with higher glucose and triglyceride levels as well as with impaired penile colour Doppler ultrasound parameters, suggesting a CV impairment (41). When evaluating the subset of men for whom information on incident MACE during a mean follow-up of 4.3 years was available, a greater difference between vascular and chronological age was associated with the incidence of MACE in younger, but not in older men (42).
The connection between diabetes and ED is related to your circulation and nervous system. Poorly controlled blood sugar levels can damage small blood vessels and nerves. Damage to the nerves that control sexual stimulation and response can impede a man’s ability to achieve an erection firm enough to have sexual intercourse. Reduced blood flow from damaged blood vessels can also contribute to ED.
The first goal in treating ED is to manage your diabetes. This includes keeping your blood sugar and blood pressure under control. If ED persists, treatments are available. While oral medications are a common first therapy, they don’t work for all men with diabetes. The penile implant may be an option. The implant is concealed inside the body. It offers support for an erection whenever and wherever desired.
Erectile function can be impaired in several endocrine disorders and treating these conditions can improve ED (43). This is the case of adrenal insufficiency, whose treatment with glucocorticoid and mineralocorticoid replacement is able to improve erectile function (44). Similarly, an adequate control of thyroid function in hyper- and hypothyroid patients is associated with an improvement in ED (45,46). However, although ED is a common complaint in subjects with Addison’s disease, hypo- and even more hyperthyroidism (45-48), the prevalence of these disorders is subjects with ED is not so high for recommending the routine screening of adrenal and thyroid hormone in these men (49). In contrast with the low prevalence of adrenal or thyroid disturbances in ED subjects, testosterone (T) deficiency is frequently found in subjects with ED (49,50) and, in turn, low T is frequently associated with the occurrence of sexual dysfunctions, including ED, even in general population (51). Accordingly, the Fourth ICSM recommends the routine assessment of T levels in patients with ED (43). The assessment of prolactin (PRL) in ED patients is controversial because an actual pathological increase in PRL levels (severe hyperprolactinemia: prolactin ≥735 mU/L or 35 ng/mL) is rarely found in ED men (52). Furthermore, the role of PRL in inducing ED is still not clarified. Hyperprolactinemia has been consistently associated with loss of sexual desire (43,53) and development of hypogonadotropic hypogonadism, both conditions that can in turn induce ED. However, a direct role of high PRL levels in inducing an impairment of erectile function is not consistently proven (52,54) and, conversely, more recent evidence suggests that lower, rather than higher, PRL levels are associated with impaired erectile function (55-57). For these reasons, at present, the assessment of PRL levels in subjects with ED is not routinely recommended (43) and it could be advisable only in men with hypogonadotropic hypogonadism, as a possible cause of this condition.

Injury to the nerves and arteries near the penis can lead to erectile dysfunction. According to the National Institutes of Diabetes and Digestive and Kidney Diseases, surgeries for prostate and bladder cancer can injure penile nerves and arteries, although it doesn’t always happen. Spinal cord injuries can affect the ability to achieve and maintain an erection, as can injuries to the penis, prostate, bladder and pelvis.
Although ED and diabetes are two separate conditions, they tend to go hand in hand. Half of men with diabetes will experience ED within 10 years of their diagnosis.8 For some men, ED may be the first symptom of diabetes even if they have not yet been diagnosed, particularly in men younger than 45.6 Left untreated, ED can damage self-confidence and relationships.
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.
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.
Describing the epidemiology of ED in young men requires, first of all, defining what it is meant by youth. While the definition of old age is matter of discussion and a precise threshold does not exist, the most shared definition in Western Countries is age above 65 years (http://www.who.int/healthinfo/survey/ageingdefnolder/en/). Considering that most of the epidemiological studies on general populations aimed at studying health changes with age, enrol men more than 40 years, it seems reasonable to define young age as below 40 years. Epidemiological studies on erectile function, which considered the prevalence of ED according to age bands, consistently find a significant increase with ageing. Advancing age remains one of the most important unmodifiable risk factors for ED (1). Studies on ED mostly involve middle-aged and older men, with younger aged men often overlooked. In a multi-centre worldwide study, involving more than 27,000 men from eight countries, Rosen et al. (2) showed an ED prevalence of 8% among men aged 20–29 years and 11% among those aged 30–39 years. Most of the studies involving younger men and conducting age-stratified analyses have been performed in Europe, where the prevalence of ED in men younger than 40 years ranges between 1% to 10% (3-10). The prevalence reported in these studies is highly variable due to different methodologies used in defining ED, population accrual, acquisition of data and choice of tools for investigating erectile function. A smaller number of studies on this topic have been conducted outside Europe. Both in Australia (11,12) and in America (13-15), the available information suggests a similar range of prevalence of ED among young subjects, with the same extent of variability among studies. According to these data, ED in younger men, although still not extensively studied and largely overlooked by the scientific community, is a quite common condition. In a recent study conducted in a Urology Clinic, it has been observed that one out of four men seeking medical care for ED was younger than 40 years (16). In our Sexual Medicine and Andrology Unit, established in an Endocrinology setting at the University of Florence, medical consultations for younger men are infrequent, with a prevalence of men aged less than 40 years at only 14.1% of more than 3,000 men complaining of ED. However, when considering the new referrals to our Unit during the last 6 years, we can notice a progressive increase in prevalence of men below 40 years seeking medical care for ED (Figure 1). According to these data, ED is becoming a common concern even among young men, and the clinical practitioner in sexual medicine must become aware of how to manage the problem and avoid underestimating a symptom. The identification of ED in a young man may potentially provide a great deal of useful information that can help improve their quality and even length of life.
This patient has thoroughly researched erectile dysfunction on the internet and has a powerful knowledge base from which he draws reference. He is also emotionally labile. The most urgent recommendation for this patient is that he seek appropriate psychiatric treatment to help in management of his psychiatric conditions and suicidal ideation. It was also recommended that he seek care with a sexual therapist to work through additional issues related to his “addiction” to masturbation. During his urologic visit we performed both cold and hot perception testing and biothesiometer, which were normal. He was displeased with these findings as they were incongruent with his chief complaints; normal results caused him to become tearful. A penile ultrasound was performed without injection of a pharmacologic agent to assess the appearance of his cavernous tissue and cavernous arteries, which had normal appearance and measurement, respectively, on ultrasound. (This quick bedside procedure has the potential to be both diagnostic and therapeutic for the patient; the importance of this cannot be underestimated).
ED may occur with or without other sexual dysfunction, including decreased libido (decreased interest in sexual activity), orgasmic dysfunction (troubles achieving an orgasm/climax), and ejaculatory dysfunction (problems with the fluid released during sex, including lack of ejaculation [anejaculation], small volume ejaculate, ejaculation that occurs too quickly [premature ejaculation], ejaculate that goes backward into the bladder [retrograde ejaculation] and pain with ejaculation).
The medications are extremely effective, which is very good. And the medications are, for the most part, extremely well-tolerated. But there are, like with any medications, a potential downside. The one absolute downside to the use of any of these erection what we call PDE5 medications is if a patient is using a nitroglycerin medication. And nitroglycerins are used for heart disease and for angina, for the most part, although there are some recreational uses of nitrites. And that’s important because your blood vessels will dilate and your blood pressure will drop. And that is an absolute contraindication.
Though psychological causes of erectile dysfunction may be more complex than medical causes, they are still treatable. You should know, however, that resolving psychological impotence may not be quite as simple as taking Viagra (sildenafil citrate). ED drugs are designed to sidestep the physiological causes for ED such as low blood pressure or vascular damage – they won’t help you with issues of anxiety, stress, or low self-esteem. The best treatment for psychological ED will address the problem at its root.
As recently as two decades ago, doctors tended to blame erectile dysfunction on psychological problems or, with older men, on the normal aging process. Today, the pendulum of medical opinion has swung away from both notions. While arousal takes longer as a man ages, chronic erectile dysfunction warrants medical attention. Moreover, the difficulty is often not psychological in origin. Today, urologists believe that physical factors underlie the majority of cases of persistent erectile dysfunction in men over age 50.

The study, led by the University of Exeter and the University of Oxford, looked at data on more than 220,000 men across three cohorts, 6,000 of whom experienced erectile dysfunction. The research echoed recent findings that erectile dysfunction has a genetic cause, and goes further by opening the possibility that living a healthier lifestyle may help reduce risk.


Surprisingly, one of the main causes of erectile dysfunction (ED) or impotence may be in that icy mug of beer you are enjoying right now! A common cause of difficulty with erection is overuse of alcohol. Small amounts of alcohol can help us relax and help remove inhibitions, which can help the sexual mood and actually increase sexual activity. Nevertheless, as the amount of alcohol in the blood increases, the alcohol only serves to depress the brain’s ability to sense sexual stimulation.


The brain is an often-overlooked erogenous zone. Sexual excitement starts in your head and works its way down. Depression can dampen your desire and can lead to erectile dysfunction. Ironically, many of the drugs used to treat depression can also suppress your sex drive and make it harder to get an erection, and they can cause a delay in your orgasm.
This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. The NIDDK translates and disseminates research findings through its clearinghouses and education programs to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by the NIDDK is carefully reviewed by NIDDK scientists and other experts.
When blood sugar levels are out of control, nerve and blood vessel damage occurs throughout your body. Nerve damage breaks down the ability to turn sexual stimulation into an erection.6 Poor blood circulation reduces blood flow to the penis. Together they impact your ability to get an erection that is rigid and lasts long enough for sexual satisfaction.
Currently, placement of a penile prosthesis is the most common surgical procedure performed for erectile dysfunction. Penile prosthesis placement is typically reserved for men who have tried and failed (either from efficacy or tolerability) or have contraindications to other forms of therapy including PDE5 inhibitors, intraurethral alprostadil, and injection therapy.

Erectile Dysfunction is typically caused by a problem with blood flow in the penis due to the hardening and narrowing of the blood vessels of the penis. This occurs most commonly due to aging itself, which causes the smooth muscle cells that line the blood vessels to become stiffer and less able to stretch. This prevents the flow of blood that the penis requires to become erect.
Patients should continue testosterone therapy only if there is improvement in the symptoms of hypogonadism and should be monitored regularly. You will need periodic blood tests for testosterone levels and blood tests to monitor your blood count and PSA. Testosterone therapy has health risks, and thus doctors should closely monitor its use. Testosterone therapy can worsen sleep apnea and congestive heart failure.
Combination therapy has proven effective for some men who don’t respond adequately to oral medicines. The idea is to use two drugs with different mechanisms of action for better results. Commonly, sildenafil is used in combination with pellets of alprostadil (synthetic prostaglandin E1) that are inserted into the urethra (the tube in the penis that carries urine from the bladder to the outside of the body). Alprostadil also increases the blood supply to the penis, but by different means.
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