Stress is your body responding to your environment. And it’s a good thing—in limited doses. When you get stressed out your body makes chemicals like adrenaline that make you stronger, faster, fitter, and even able to think more clearly. Most people call this reaction the “fight-or-flight” response, and it’s a life-saver in dangerous situations. In a very real sense, adrenaline makes you a part-time superhero. The problems happen when your body deals with constant stress.
A common and important cause of ED is vasculogenic. Many men with ED have comorbid conditions such as hyperlipidemia, hypercholesterolemia, tobacco abuse, diabetes mellitus, or coronary artery disease (CAD). [6] The Princeton III Consensus recommends screening men who present with ED for cardiovascular risk factors; ED may be the earliest presentation of atherosclerosis and vascular disease. [7]

A vacuum erection device helps draw blood into the penis by applying negative pressure. This type of device is sometimes referred to as penis pump and may be used just prior to sexual intercourse. Several types of FDA approved vacuum therapy devices are available under prescription. When pharmacological methods fail, a purpose-designed external vacuum pump can be used to attain erection, with a separate compression ring fitted to the base of the penis to maintain it. These pumps should be distinguished from other penis pumps (supplied without compression rings) which, rather than being used for temporary treatment of impotence, are claimed to increase penis length if used frequently, or vibrate as an aid to masturbation. More drastically, inflatable or rigid penile implants may be fitted surgically.
Hormone deficiency or hypogonadism, whether primary or secondary, has been thought to impact erectile function. Approximately a third of men in the European Male Aging Study demonstrated low testosterone, suggesting that hypogonadism is overrepresented among men with ED.11 Hormone deficiency, however, is less frequently the cause of ED than diabetes or vascular disease. Many entities with a strong relationship to ED also diminish bioavailable testosterone, including obesity, diabetes, and opioid use. Other hormones involved in testosterone metabolism or availability, like thyroid stimulating hormone and gonadotropins, also may impact erectile quality, presumably through regulating bioavailable testosterone. Understanding the relationship between testosterone and ED has been impaired by a lack of standardized measurement of this hormone and the cyclic nature of its release and consumption.
Lifestyle choices that impair blood circulation can contribute to ED. Smoking, excessive drinking, and drug abuse may damage the blood vessels and reduce blood flow to the penis. Smoking makes men with atherosclerosis particularly vulnerable to ED. Being overweight and getting too little exercise also contribute to ED.  Studies indicate that men who exercise regularly have a lower risk of ED.
These oral medications reversibly inhibit penile-specific PDE5 and enhance the nitric oxide–cGMP pathways of cavernous smooth muscle relaxation; that is, all prevent the breakdown of cGMP by PDE5. It is important to emphasize to patients that these drugs augment the body’s natural erectile mechanisms, therefore the neural and psychoemotional stimuli typically needed for arousal still need to be activated for the drugs to be efficacious.

Given the high risk of priapism during escalation of therapy for intracorporeal injection, it is recommended that the drugs be administered in a supervised office visit initially and that the patient be given a well-articulated plan for treatment of priapism if it occurs. Escalation guidelines for alprostadil alone vary, but a general guideline is to start at 2.5 mcg and increase by 2.5 mcg to a dose of 5 mcg and then in increments of 5 mcg to 10 mcg until an erection sufficient for penetration, not lasting more than 1 hour, is achieved. If there is no response to the initial 2.5-mcg dose, escalation dosing can be slightly more liberal.34 A European prospective trial of PGE1 alone found 91% of the 54 patients completing the 4 years of the study reported good or better tolerability and satisfaction with therapy.35


A physical cause can be identified in about 80% of cases.[2] These include cardiovascular disease, diabetes mellitus, neurological problems such as following prostatectomy, hypogonadism, and drug side effects. Psychological impotence is where erection or penetration fails due to thoughts or feelings; this is somewhat less frequent, in the order of about 10% of cases.[2] In psychological impotence, there is a strong response to placebo treatment.

Exercise and lifestyle modifications may improve erectile function. Weight loss may help by decreasing inflammation, increasing testosterone, and improving self-esteem. Patients should be educated to increase activity, reduce weight, and stop smoking, as these efforts can improve or restore erectile function in men without comorbidities. Precise glycemic control in diabetic patients and pharmacologic treatment of hypertension may be important in preventing or reducing sexual dysfunction. [49]
The use of injection therapy requires being taught how to properly inject the medication, determination of the best dose, and monitoring for side effects. It is recommended that one inject on the side of the penis at the base and to alternate sides. Injection therapy should be used no more frequently than once every 24 hours. Individuals on blood thinners must be careful with use of injection therapy.

A vacuum erection device helps draw blood into the penis by applying negative pressure. This type of device is sometimes referred to as penis pump and may be used just prior to sexual intercourse. Several types of FDA approved vacuum therapy devices are available under prescription. When pharmacological methods fail, a purpose-designed external vacuum pump can be used to attain erection, with a separate compression ring fitted to the base of the penis to maintain it. These pumps should be distinguished from other penis pumps (supplied without compression rings) which, rather than being used for temporary treatment of impotence, are claimed to increase penis length if used frequently, or vibrate as an aid to masturbation. More drastically, inflatable or rigid penile implants may be fitted surgically.


When stimulated by the nerves, the spongy tissue arranges itself in such a way that more blood can be stored in the penis. The veins running through the outer sheath of the penis then compress which stops the blood from leaving the penis. As the blood is stopped from flowing out, the penis fills with blood and stretches within the outer casing, giving an erection.

Meditation is known to lower the heart rate and regulate blood flow around the body, which bodes well for ED sufferers, as what's an erection if not a big gathering of blood? Meditation has also been shown to reduce anxiety and change negative thought associations. Sara Lazar, a neuroscientist at Harvard, was one of the first people to scan meditators' brains and discovered that the amygdala, the part of the brain where anxiety calls home, was smaller for meditators than the control group.
Many factors can contribute to sexual dysfunction in older men, including physical and psychological conditions, comorbidities and the medications used to treat them. Aspects of an ageing man’s lifestyle and behaviour and androgen deficiency, most often decreasing testosterone levels, may affect sexual function as well. A study of men between the ages of 30 and 79 years showed that 24% had testosterone levels below 300 ng/dL and 5.6% had symptomatic androgen deficiency.2
In many cases, diagnosing erectile dysfunction requires little more than a physical exam and a review of your symptoms. If your doctor suspects that an underlying health problem may be at play, however, he may request additional testing. Once you’ve determined the cause for your ED, you and your doctor can decide on a form of treatment – here are some of the options:
Iatrogenic hypotension can occur in men in neurodegenerative disease using sildenafil (49). Hussain et al. placed men with PD and MSA on sildenafil and recorded blood pressure before and after. Half of the 12 MSA patients developed postural hypotension, while none of the twelve PD patients did. Since MSA can be difficult to distinguished diagnostically from PD, baseline blood pressure measurements prior to prescribing the medication and seeking medical assistance if symptomatic hypotension occurred was recommended for all patients with PD, and MSA. Of note, none of the men with MSA who developed hypotension discontinued sildenafil use due to its effectiveness at improving their erections.

Physical causes may include the narrowing of the blood vessels caused by hypertension (high blood pressure), nutritional deficiencies, certain prescription treatments and medications for enlarged prostate or prostate cancer, excess drinking, obesity, heavy smoking, kidney issues, thyroid problems, hormonal changes due to aging, injury, or surgery, diabetes, and high cholesterol levels.


Much of the emphasis on erectile pathophysiology has been placed on penile smooth muscle function and cavernosal hemodynamics. The neuroanatomy and neurophysiology of erection can be characterized but its full extent is poorly understood. Neurologic disease does not always reproducibly affect erections in a uniform manner compared to other types of sexual dysfunction (SD). This offers many obstacles to understanding the role the nervous systems plays in SD and consequently obscures what treatment options readily optimize erections specific to the neurologic insult.

An analysis of 14 studies involving more than 90,000 patients with ED confirmed the relation between ED and an increased risk of cardiovascular events and mortality. [56] Compared with patients without ED, those with ED had a 44% increased risk of cardiovascular events, a 25% increased risk of all-cause mortality, a 62% increased risk of MI, and a 39% increased risk of cerebrovascular events. Treatment of ED, either through lifestyle interventions or by pharmacologic means, may improve prognosis and reduce risk.
The information shared on our websites is information developed solely from internal experts on the subject matter, including medical advisory boards, who have developed guidelines for our patient content. This material does not constitute medical advice. It is intended for informational purposes only. No one associated with the National Kidney Foundation will answer medical questions via e-mail. Please consult a physician for specific treatment recommendations.
Soler et al. compared sildenafil to vardenafil and tadalafil (69). Sildenafil was effective in 85% of SCI patients, 74% of the patients on vardenafil and 72% of the patients on tadalafil. Sildenafil was associated with more rigid and longer lasting erections. Additionally, 50 mg of sildenafil was effective in 55% of patients compared to more than 70% of the patients on vardenafil and tadalafil requiring 20 mg for a similar response. Men who used tadalafil were able to achieve erections 24 hours after administration, improving overall satisfaction related to the possible spontaneity of sexual encounters. Del Popolo also evaluated the time/duration effectiveness of PDE5i sildenafil 50 mg versus tadalafil 10 mg (64). Tadalafil 10 mg significantly increased the percentage of successful intercourse attempts at 12–24 hours compared with sildenafil. One can suspect that vardenafil, which has a longer half-life than sildenafil, could offer a similar benefit but a study investigating this occurrence has yet to be performed.
Prior to the introduction of PDE5i in 1998, intracavernosal vasoactive medications and penile implant surgery were the mainstays of treatment. Penile implant surgery involves placement of inflatable or malleable rods within the corpora cavernosa to provide rigidity for intercourse. Choice of which implant to place usually depends upon manual dexterity and function of the patient, patient anatomy, physician preference and surgical approach.
The dorsal artery provides for engorgement of the glans during erection, whereas the bulbourethral artery supplies the bulb and the corpus spongiosum. The cavernous artery effects tumescence of the corpus cavernosum and thus is principally responsible for erection. The cavernous artery gives off many helicine arteries, which supply the trabecular erectile tissue and the sinusoids. These helicine arteries are contracted and tortuous in the flaccid state and become dilated and straight during erection. [9]
Thinking about sex creates a burst of dopamine, which is a brain chemical that’s linked to excitement, motivation and pleasure. It also plays a crucial role in helping you to get an erection! In a man who is bored with or indifferent about sex, thinking about the act is unlikely to be accompanied by that dopamine burst, making it likely that the man will experience erectile dysfunction.

The severity of ED has been correlated with the extent of CVD. Banks et al reported that the risk of future CV events increased progressively according to ED severity.28 This was shown in both men with and without known CVD at baseline and after controlling for confounders. Solomon and colleagues found an inverse correlation between international index of erectile function (IIEF) scores and plaque burden seen on coronary angiography.29 In addition, Yaman et al demonstrated a significant correlation between ED severity on IIEF questionnaires and coronary artery calcification.30

The great majority of ED cases in diabetic men have a physical cause, such as neuropathy or circulatory problems. In some cases, however, the cause of ED is psychological, including depression, guilt, or anxiety. With a thorough exam, the doctor should be able to determine whether the ED is psychological or physical in nature. If the cause is psychological, your doctor may refer you to a psychiatrist, psychologist, sex therapist, or marital counselor. Do not view such a diagnosis as an insult. Most psychologically-based ED is easily and successfully treated.
Sure, this condition might be common – but isn’t erectile dysfunction a problem that only middle and senior-aged men get? It is true that erectile problems are common in older men. It often happens due to lower levels of testosterone and reduced blood flow to the penis. But this study showed that a quarter of all men under the age of 40 experience erectile dysfunction of some kind!
Of the drugs used for depression, tricyclic antidepressants may be associated with erectile problems and other drugs may be substituted to prevent this complication. Currently available substitutes include bupropion, nefazodone, and trazodone. The selective serotonin reuptake inhibitors (eg, fluoxetine, sertraline, paroxetine, citalopram) can also cause difficulties with ED, but they might also have other significant sexual side effects, including decreased libido and anorgasmia.
Physical causes may include the narrowing of the blood vessels caused by hypertension (high blood pressure), nutritional deficiencies, certain prescription treatments and medications for enlarged prostate or prostate cancer, excess drinking, obesity, heavy smoking, kidney issues, thyroid problems, hormonal changes due to aging, injury, or surgery, diabetes, and high cholesterol levels.
Erectile dysfunction or disorder (ED) is the inability to develop and maintain an erection for satisfactory sexual intercourse or activity. Erectile dysfunction or erectile disorder are the preferred terms as opposed to impotence. There are no uniform criteria defining how consistent the problem has to be and for what duration it must be present to considered ED. The Diagnostic and Statistical Manual of Mental Disorder-5 specifies a duration of at least 6 months in its definition of ED.1
Your doctor will ask you questions about your symptoms and health history. They may do tests to determine if your symptoms are caused by an underlying condition. You should expect a physical exam where your doctor will listen to your heart and lungs, check your blood pressure, and examine your testicles and penis. They may also recommend a rectal exam to check your prostate. Additionally, you may need blood or urine tests to rule out other conditions.
Erectile dysfunction can occur as a side effect of medication taken for another health condition. Common culprits are high blood pressure meds, antidepressants, some diuretics, beta-blockers, heart medication, cholesterol meds, antipsychotic drugs, hormone drugs, corticosteroids, chemotherapy, and medication for male pattern baldness, among others.
Inside the cell, NOS catalyzes the oxidation of L-arginine to NO and L-citrulline. Endogenous blockers of this pathway have been identified. The gaseous NO that is produced acts as a neurotransmitter or paracrine messenger. Its biologic half-life is only 5 seconds. NO may act within the cell or diffuse and interact with nearby target cells. In the corpora cavernosa, NO activates guanylate cyclase, which in turn increases cyclic guanosine monophosphate (cGMP). Relaxation of vascular smooth muscles by cGMP leads to vasodilation and increased blood flow.
It happens when they're drunk or when they've taken coke or when the invoice they submitted three months ago still hasn't been paid yet. Usually, they get sober, they get their money, and it passes. But not for all of them—according to 2013 data from the Journal of Sexual Medicine, one out of every four new erectile dysfunction diagnoses is in someone under the age of 40.
Alprostadil (also known as prostaglandin E1 [PGE1]) is the prominent known smooth-muscle dilator of the corpus cavernosum. Its mechanism of action is believed to be the promotion of intracellular accumulation of cyclic adenosine monophosphate, thereby causing decreased intracellular accumulation of calcium and resulting smooth muscle relaxation. Alprostadil can be delivered to the erectile tissue either via an intraurethral suppository that is massaged and then absorbed across the corpus spongiosum of the urethra to the corpora cavernosa, or directly injected into the corpora cavernosa. When administered urethrally, doses are substantially higher than when directly injected (typical dosing is 500 mcg to 1 mg intraurethral compared with 2.5 mcg to 20 mcg intracavernosal).

"Medications that create blood flow to the penis can't help when an erection is blocked by the fear or anxiety of the fight-or-flight response,” says Feloney. “This type of erectile dysfunction probably has a lot to do with evolution — men didn't need an erection when a dinosaur was chasing them." The best way to treat erectile dysfunction caused by performance anxiety, depression, a poor relationship, or stress may be with a combination of ED drug treatment and sex therapy, individual therapy, or couples therapy from sexual health professionals.
Medical conditions, such as hypertension, diabetes mellitus, and cardiovascular disease (CVD), and psychological conditions, such as depression and anxiety, also contribute to sexual dysfunction in middle-aged or elderly men. CVD and hypertension cause a narrowing and hardening of the arteries, leading to reduced blood flow to the corporal bodies, which is essential for achieving an erection. Diabetes is a common aetiology of sexual dysfunction, because it can affect both the blood vessels and the nerves that supply the penis. Men with diabetes are four times more likely to experience ED, and on average, experience ED 15 years earlier than men without diabetes.7 Obesity is also correlated to the development of several types of dysfunction, including a decrease in sex drive and an increase in episodes of ED.8
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. 
5. Medline Plus. US National Library of Medicine. NIH National Institutes of Health. Drugs that may cause impotence (updated 21 Jan 2015). http://www.nlm.nih.gov/medlineplus/ency/article/004024.htm (accessed Nov 2016). myDr myDr provides comprehensive Australian health and medical information, images and tools covering symptoms, diseases, tests, medicines and treatments, and nutrition and fitness.Related ArticlesImpotence treatmentsIf you have impotence (erectile dysfunction), the treatment your doctor recommends will depend on thErectile dysfunction: visiting your doctorFind out what questions a doctor may ask when discussing erectile dysfunction (ED, or impotenceGum disease linked to erectile dysfunctionAdvanced gum disease (periodontitis) has been linked to an increased risk of erectile dysfunction, wPeyronie's diseasePeyronie’s disease is condition where a band of scar tissue forms in the penis, causing aAdvertisement
Clearly, PDE5i have revolutionized the treatment of ED in general and the neurogenic ED population is no exception. They remain safe and effective in most men with neurogenic ED; however, care must be taken in prescribing PDE5i to men high spinal cord lesions, MSA or possibly PD. VEDs are minimally-invasive and can be as effective as other modalities at leading to erection. However, high discontinuation rates are associated with VED use related to pain, difficulty using the device or cold penis. Intracavernosal therapy has been a mainstay of treatment for neurogenic ED and remains extremely successful in the SCI population. Trial of intracavernosal therapy for other causes of neurogenic ED can be considered second-line therapy, but there is a relative paucity of data for clinical outcomes related to its use outside of SCI men. Surgical therapy via penile implantation remains another second line approach and may also be utilized to assist men with bladder management. Higher complication rates of infections, and perforation have been reported compared to neurologically intact men. Many other compounds are currently being evaluated for the treatment of neurogenic ED as well as gene and stem cell therapy, but still should be considered investigational until substantiated by randomized controlled trials.
The device consists of an acrylic cylinder placed over the penis that uses a lubricant to achieve a good seal between the penile body and cylinder. An erection is then achieved by creating a vacuum inside the cylinder with a pump connected to the cylinder. Once an erection is achieved, a constriction band is applied to the base of the penis to maintain the erection. The cylinder can then be removed and the patient can engage in intercourse with the constriction band at the base of the penis maintaining the erection. The band can remain on for approximately 30 minutes and then must be removed. The erection produced by the device differs from a normal erection likely because of venous occlusion from the constriction band resulting in generalized swelling of the entire penis, with probable preservation of arterial inflow.
So here’s something that’s really fascinating. Healthy eating is a way to reduce anxiety and stress. Now how, you may be asking, right? Well, think about it. We live in a world where there are so many variables and where we don’t have control over our lives. But now, with healthy eating, we have control over what goes into our body. And now having that control empowers us to be even healthier, to be more directive in what we do. And certainly, that begins then to reduce the anxiety and the stress. So all in one, you have a healthier body, but certainly a healthier mind.
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