Although erectile dysfunction increases progressively with age, it is not an inevitable consequence of aging. Knowledge of the risk factors can guide prevention strategies. Specific antihypertensive, antidepressant, and antipsychotic drugs can be chosen to lessen the risk of erectile failure. Published lists of prescription drugs that may impair erectile functioning often are based on reports implicating a drug without systematic study. Such studies are needed to confirm the validity of these suggested associations. In the individual patient, the physician can modify the regimen in an effort to resolve the erectile problem.
While erectile dysfunction can occur at any age, the risk of developing erectile dysfunction increases with age. According to the Massachusetts Male Aging Study, the prevalence of erectile dysfunction was 52% in men 40-70 years of age. The prevalence of complete erectile dysfunction increases from 5% at 40 years of age to 15% among men 70 years of age and older.
Usually there will not be a specific treatment that will lead to the improvement of erectile dysfunction. However, there are treatments that will allow erections to happen and can be used to allow sexual activity to take place. There are three main types of treatments: non-invasive treatments such as tablet medicines and external devices (e.g. vacuum device); penile injections; or for men who have not had success with other treatments, surgery may be an option.
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.
While pills for ED are convenient, some men sustain stronger erections by injecting medication directly into the penis. Drugs approved for this purpose work by widening the blood vessels, causing the penis to become engorged with blood. Another option is inserting a medicated pellet into the urethra. The pellet can trigger an erection within 10 minutes.
Although erectile dysfunction increases progressively with age, it is not an inevitable consequence of aging. Knowledge of the risk factors can guide prevention strategies. Specific antihypertensive, antidepressant, and antipsychotic drugs can be chosen to lessen the risk of erectile failure. Published lists of prescription drugs that may impair erectile functioning often are based on reports implicating a drug without systematic study. Such studies are needed to confirm the validity of these suggested associations. In the individual patient, the physician can modify the regimen in an effort to resolve the erectile problem.
This is one of many types of constricting devices placed at the base of the penis to diminish venous outflow and improve the quality and duration of the erection. This is particularly useful in men who have a venous leak and are only able to obtain partial erections that they are unable to maintain. These constricting devices may be used in conjunction with oral agents, injection therapy, and vacuum devices.
Causes contributing to erectile dysfunction can be broadly classified into two categories: organic and psychologic. In reality, while the majority of patients with erectile dysfunction are thought to demonstrate an organic component, psychological aspects of self-confidence, anxiety, and partner communication and conflict are often important contributing factors.
Poor sleep patterns can be a contributing factor for erectile dysfunction, Mucher says. One review published in the journal Brain Research emphasized the intricate relationship between the level of sex hormones like testosterone, sexual function, and sleep, noting that testosterone levels increase with improved sleep, and lower levels are associated with sexual dysfunction. Hormone secretion is controlled by the body’s internal clock, and sleep patterns likely help the body determine when to release certain hormones. 

The lab testing obtained for the evaluation of erectile dysfunction may vary with the information obtained on the health history, physical examination, and recent lab testing. A testosterone level is not necessary in all men; however, a physician will order labs to determine a patient's testosterone level if other signs and symptoms of hypogonadism (low testosterone) such as decreased libido, loss of body hair, muscle loss, breast enlargement, osteoporosis, infertility, and decreased penile/testicular size are present.


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.
PDE5 inhibitors, the primary second-line therapy, have been the mainstay of ED treatment since the release of sildenafil (Viagra) in 1998, with the subsequent development of many others, and still more in the development stage. These medications do improve erectile quality for the majority of men, and they work by enhancing blood flow in the corpora cavernosa. These medications are generally used on demand and need to be taken about an hour before sexual intimacy. Tadalafil (Cialis) is longer acting and does come in a daily preparation potentially eliminating the ‘on-demand’ need. The daily dosing of tadalafil, 2.5–5 mg\day, has also been approved by the FDA for treatment of symptoms of BPH.41 PDE5 inhibitors are contraindicated in men taking nitrates, but otherwise PDE5 inhibitors are very safe and effective. When PDE5 inhibitors are coadministered with nitrates, pronounced systemic vasodilation and severe hypotension are possible. Many patients with ED are elderly and have the same risk factors as patients with CAD, so these drug combinations are commonly considered or encountered in clinical practice.42
*all photos are models and not actual patients.If you are interested in a prescription product, Hims will assist in setting up a visit for you with an independent physician who will evaluate whether or not you are an appropriate candidate for the prescription product and if appropriate, may write you a prescription for the product which you can fill at the pharmacy of your choice.
Vardenafil and tadalafil belong to the same group of chemical compounds as sildenafil, namely phos-phodiesterase type 5 (PDE-5) inhibitors. Some men cannot benefit from sildenafil or the two newer PDE-5 inhibitors because they have low levels of nitric oxide. British investigators reported in late 2002 that three different types of compounds are being studied as possible medications for men with low levels of nitric oxide. They are Rho-kinase inhibitors, soluble guanylate cyclase activators, and nitric oxide-releasing PDE-5 inhibitors.
The role of the endothelium in erectile function became clearer with the observation that the phosphodiesterase type 5 (PDE5) inhibitor, sildenafil, enhanced erectile function. Erection occurs with the release of nitric oxide (NO) from the vascular endothelial cells.17 The reduction in endothelial cell production of NO results in the negative impact on the smooth muscles in the corporal bodies and results in less relaxation of the smooth muscle cells with decrease in blood supply and resulting ED. A similar phenomenon is well known to impact the coronary arterial system resulting in CVD.

Erection is a vascular event. The penis becomes rigid when blood flow to the corpora cavernosa increases sixfold and venous outflow is physiologically impeded. Penile perfusion is governed by three organ systems—the neurologic, circulatory, and endocrinologic systems—each necessary for potency. The neurologic system accounts for vasodilation and venoconstriction of the corporal blood vessels so that blood is shunted to the erectile tissues; the circulatory system provides adequate blood flow to the hypogastric-cavernous bed, a distal branch off the internal iliac vessels; and the endocrine system, mediated by testosterone, plays a permissive role through mechanisms that have yet to be elucidated.
Whenever I am prescribing a medication to a patient, I’m always asking myself, what can the patient do before requiring the medication? What changes do they have to make in order to reduce the amount of medication or preclude their even needing it? So a good candidate is somebody who has an understanding of a healthy lifestyle, about physical activity, about sleep, about nutrition, alcohol, smoking. So patients, individuals, have to do their share before they’re a candidate for anything. All right?
Erectile dysfunction affects millions of men. Although for some men erectile function may not be the best or most important measure of sexual satisfaction, for many men erectile dysfunction creates mental stress that affects their interactions with family and associates. Many advances have occurred in both diagnosis and treatment of erectile dysfunction. However, its various aspects remain poorly understood by the general population and by most health care professionals. Lack of a simple definition, failure to delineate precisely the problem being assessed, and the absence of guidelines and parameters to determine assessment and treatment outcome and long-term results, have contributed to this state of affairs by producing misunderstanding, confusion, and ongoing concern. That results have not been communicated effectively to the public has compounded this situation.
The most important organic causes of impotence are cardiovascular disease and diabetes, neurological problems (for example, trauma from prostatectomy surgery), hormonal insufficiencies (hypogonadism) and drug side effects. Psychological impotence is where erection or penetration fails due to thoughts or feelings (psychological reasons) rather than physical impossibility; this is somewhat less frequent but can often be helped. In psychological impotence, there is a strong response to placebo treatment.
PDE 5 inhibitors are broken down primarily by enzyme, cytochrome P450enzyme CYP3A4. Medications that decrease or increase the activity of CYP3A4 may affect levels and effectiveness of PDE 5 inhibitors. Such drugs include medications for the treatment of HIV (protease inhibitors) and the antifungal medications ketoconazole and itraconazole. Thus caution is recommended.
There are hundreds of medications that have the side effect of ED and/or decreased libido. Examples of drugs implicated as a cause of ED include hydrochlorothiazides and beta-blocking agents. Medications used to treat depression, particularly the SSRIs such as citalopram (Celexa), escitalopram (Lexapro), fluoxetine (Prozac, Prozac Weekly, Sarafem), fluvoxamine (Luvox, Luvox CR), paroxetine (Paxil, Paxil CR, Pexeva) and sertraline (Zoloft), may also contribute to ED.9 Bupropion (Wellbutrin) which has a predominant effect on blocking the reuptake of dopamine is an antidepressant with lower incidence of ED.10 The side effects of 5ARIs occurring in fewer than 5% of patients can include gynaecomastia, ED, loss of libido and ejaculatory dysfunction.11

ED usually has a multifactorial etiology. Organic, physiologic, endocrine, and psychogenic factors are involved in the ability to obtain and maintain erections. In general, ED is divided into 2 broad categories, organic and psychogenic. Although most ED was once attributed to psychological factors, pure psychogenic ED is in fact uncommon; however, many men with organic etiologies may also have an associated psychogenic component.


Some may use alcohol as a way to get into the mood and overcome some of the nerves associated with having sex, but too much of a good thing can actually backfire. In fact, having a long history of alcohol abuse may lead to long-term erectile dysfunction. As many as 70 percent of men with chronic erectile dysfunction also have a history of alcohol abuse.
On the horizon is gene therapy that would deliver genes that produce products or proteins that may not be functioning properly in the penile tissue of men with ED. Replacement of these proteins may result in improvement in erectile function. Experimental animal models have demonstrated improvement in erectile function with gene therapy. Human studies may also demonstrate success with this therapy. Gene therapy may take a long time for regulatory approval and public acceptance.
Prostate cancer isn’t considered a cause of ED on its own, but radiation treatments, hormone therapy, and surgery to remove the entire prostate gland can lead to difficulty in getting or keeping an erection. Sometimes erectile dysfunction related to prostate cancer treatment is only temporary, but many guys experience ongoing difficulties that need to be addressed by other means.
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.
Your like a lot of posters in forums. You make crazy statement's and weather you know it or not, your totaly wrong. Im 56 and my wife is 37. We have a good sex life and are always going at it when we can. I pity peeps like you and fig your kind of logic helps you deal with your inadequate performance. Get help or live alone and leave the keyboard alone.
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.
A useful and simple way to distinguish between physiological and psychological impotence is to determine whether the patient ever has an erection. If never, the problem is likely to be physiological; if sometimes (however rarely), it could be physiological or psychological. The current diagnostic and statistical manual of mental diseases (DSM-IV) has included a listing for impotence.

Measurement of the penile vibration perception threshold provides an inexpensive, reproducible, and painless screening test with acceptable sensitivity for detecting neuropathy. Abnormalities at the level of the sacral cord can be documented by sacral latency testing, while upper motor neuron impotence can be demonstrated with genital-cerebral evoked response testing. These latter procedures are not indicated in unselected patients with impotence.
This may be the oldest excuse in the book as a reason not to have safe sex, but research has confirmed that condoms may interfere with some men’s ability to have and hold an erection. For example, a 2006 study found that, over a three-month period, about 37 percent of men lost at least one erection when putting on a condom, or during sex with a condom, SexualHealth.com reported.
Defined as experiencing difficulty having an erection at least 50 percent of the time, about 30 million men in the U.S. suffer from erectile dysfunction (ED), according to the National Institutes of Health. So, if odds are pretty good you’ll experience a failure to launch at some point in your life, take solace in this finding from the University of Adelaide: You can reverse ED by focusing on lifestyle factors, not just popping a blue pill.

Alteration of NO levels is the focus of several approaches to the treatment of ED. Inhibitors of phosphodiesterase, which primarily hydrolyze cGMP type 5, provided the basis for the development of the PDE5 inhibitors. Chen et al administered oral L-arginine and reported subjective improvement in 50 men with ED. [14] These supplements are readily available commercially. Reported adverse effects include nausea, diarrhea, headache, flushing, numbness, and hypotension.
Heart disease isn't the only risk. ED is also a predictor of stroke, because when the arteries are narrowed there is more chance of a blood clot, which can spread to the brain. It is also a common complication of diabetes. But embarrassment stops people seeking help, says Jackson. "We need to encourage men to talk to their spouses about this problem, instead of making an excuse to avoid sex.
The FDA does not recommend alternative therapies to treat sexual dysfunction.[24] Many products are advertised as "herbal viagra" or "natural" sexual enhancement products, but no clinical trials or scientific studies support the effectiveness of these products for the treatment of erectile dysfunction, and synthetic chemical compounds similar to sildenafil have been found as adulterants in many of these products.[25][26][27][28][29] The United States Food and Drug Administration has warned consumers that any sexual enhancement product that claims to work as well as prescription products is likely to contain such a contaminant.[30]
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.
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.
The lab testing obtained for the evaluation of erectile dysfunction may vary with the information obtained on the health history, physical examination, and recent lab testing. A testosterone level is not necessary in all men; however, a physician will order labs to determine a patient's testosterone level if other signs and symptoms of hypogonadism (low testosterone) such as decreased libido, loss of body hair, muscle loss, breast enlargement, osteoporosis, infertility, and decreased penile/testicular size are present.
If you have symptoms of ED, it’s important to check with your doctor before trying any treatments on your own. This is because ED can be a sign of other health problems. For instance, heart disease or high cholesterol could cause ED symptoms. With a diagnosis, your doctor could recommend a number of steps that would likely improve both your heart health and your ED. These steps include lowering your cholesterol, reducing your weight, or taking medications to unclog your blood vessels.
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