Following a detailed discussion about the history of erectile dysfunction and its risk factors, your doctor will examine the testicles and penis to help determine the cause of erectile dysfunction. Your doctor will check reflexes and pulses in the area to see if problems with blood vessels or nerves are contributing to the erectile dysfunction. If necessary, your doctor will order tests to help diagnose erectile dysfunction.
Several pathways have been described to explain how information travels from the hypothalamus to the sacral autonomic centers. One pathway travels from the dorsomedial hypothalamus through the dorsal and central gray matter, descends to the locus ceruleus, and projects ventrally in the mesencephalic reticular formation. Input from the brain is conveyed through the dorsal spinal columns to the thoracolumbar and sacral autonomic nuclei.
Interestingly, the Belgian company Solvay, acquired for €4.5 billion in 2010 by American pharmaceutical giant Abbott, didn't put its own or its product's name on the website. As AdWeek pointed out when the campaign launched, "One of the advantages of taking the unbranded route for Androgel is that the company does not have to warn consumers quite so prominently about Androgel's side effects."

In some cases, ED can be a warning sign of more serious disease. One study suggests ED is a strong predictor of heart attack, stroke, and death from cardiovascular disease. The researchers say all men diagnosed with ED should be evaluated for cardiovascular disease. This does not mean every man with ED will develop heart disease, or that every man with heart disease has ED, but patients should be aware of the link.
When you become aroused, your brain sends chemical messages to the blood vessels in the penis, causing them to dilate or open, allowing blood to flow into the penis. As the pressure builds, the blood becomes trapped in the corpora cavernosa, keeping the penis erect. If blood flow to the penis is insufficient or if it fails to stay inside the penis, it can lead to erectile dysfunction.
Testosterone is a steroid from the androstane class containing a keto and hydroxyl groups at the three and seventeen positions respectively. It is biosynthesized in several steps from cholesterol and is converted in the liver to inactive metabolites.[5] It exerts its action through binding to and activation of the androgen receptor.[5] In humans and most other vertebrates, testosterone is secreted primarily by the testicles of males and, to a lesser extent, the ovaries of females. On average, in adult males, levels of testosterone are about 7 to 8 times as great as in adult females.[6] As the metabolism of testosterone in males is greater, the daily production is about 20 times greater in men.[7][8] Females are also more sensitive to the hormone.[9]
The link between chronic disease and ED is most striking for diabetes. Men who have diabetes are two to three times more likely to have erectile dysfunction than men who do not have diabetes. Among men with erectile dysfunction, those with diabetes may experience the problem as much as 10 to 15 years earlier than men without diabetes. Yet evidence shows that good blood sugar control can minimize this risk. Other conditions that may cause ED include cardiovascular disease, atherosclerosis (hardening of the arteries), kidney disease, and multiple sclerosis. These illnesses can impair blood flow or nerve impulses throughout the body.
Radical prostatectomy for the treatment of prostate cancer poses a significant risk of ED. A number of factors are associated with the chance of preserving erectile function. If both nerves that course on the lateral edges of the prostate can be saved, the chance of maintaining erectile function is reasonable. The odds depend on the age of the patient. Men younger than 60 years have a 75-80% chance of preserving potency, but men older than 70 years have only a 10-15% chance.
Trials of testosterone treatment in men with type 2 diabetes have also taken place. A recent randomized controlled crossover trial assessed the effects of intramuscular testosterone replacement to achieve levels within the physiological range, compared with placebo injections in 24 men with diabetes, hypogonadism and a mean age of 64 years (Kapoor et al 2006). Ten of these men were insulin treated. Testosterone treatment led to a significant reduction in glycated hemoglobin (HbA1C) and fasting glucose compared to placebo. Testosterone also produced a significant reduction in insulin resistance, measured by the homeostatic model assessment (HOMA), in the fourteen non-insulin treated patients. It is not possible to measure insulin resistance in patients treated with insulin but five out of ten of these patients had a reduction of insulin dose during the study. Other significant changes during testosterone treatment in this trial were reduced total cholesterol, waist circumference and waist-hip ratio. Similarly, a placebo-controlled but non-blinded trial in 24 men with visceral obesity, diabetes, hypogonadism and mean age 57 years found that three months of oral testosterone treatment led to significant reductions in HbA1C, fasting glucose, post-prandial glucose, weight, fat mass and waist-hip ratio (Boyanov et al 2003). In contrast, an uncontrolled study of 150 mg intramuscular testosterone given to 10 patients, average age 64 years, with diabetes and hypogonadism found no significant change in diabetes control, fasting glucose or insulin levels (Corrales et al 2004). Another uncontrolled study showed no beneficial effect of testosterone treatment on insulin resistance, measured by HOMA and ‘minimal model’ of area under acute insulin response curves, in 11 patients with type 2 diabetes aged between 33 and 73 years (Lee et al 2005). Body mass index was within the normal range in this population and there was no change in waist-hip ratio or weight during testosterone treatment. Baseline testosterone levels were in the low-normal range and patients received a relatively small dose of 100 mg intramuscular testosterone every three weeks. A good increase in testosterone levels during the trial is described but it is not stated at which time during the three week cycle the testosterone levels were tested, so the lack of response could reflect an insufficient overall testosterone dose in the trial period.
The rise in testosterone levels during competition predicted aggression in males but not in females.[86] Subjects who interacted with hand guns and an experimental game showed rise in testosterone and aggression.[87] Natural selection might have evolved males to be more sensitive to competitive and status challenge situations and that the interacting roles of testosterone are the essential ingredient for aggressive behaviour in these situations.[88] Testosterone produces aggression by activating subcortical areas in the brain, which may also be inhibited or suppressed by social norms or familial situations while still manifesting in diverse intensities and ways through thoughts, anger, verbal aggression, competition, dominance and physical violence.[89] Testosterone mediates attraction to cruel and violent cues in men by promoting extended viewing of violent stimuli.[90] Testosterone specific structural brain characteristic can predict aggressive behaviour in individuals.[91]
Relationship problems often complicate erectile dysfunction. Improving your relationship may be part of the solution. It may be a good idea to get counseling together from a sex therapist, marriage counselor, or a medical specialist. "I almost always see couples together to discuss erectile dysfunction. It often turns out that both partners have issues regarding the sexual relationship and once they are out in the open, couples can work together on a more satisfying sexual experience," says Feloney.

Testosterone is most commonly associated with sex drive in men. It also affects mental health, bone and muscle mass, fat storage, and red blood cell production. Abnormally low or high levels can affect a man’s mental and physical health. Your doctor can check your testosterone levels with a simple blood test. Testosterone therapy is available to treat men with low levels of testosterone. If you have low T, ask your doctor if this type of therapy might benefit you.
If PDE-5 inhibitors are not suitable or don’t work, other therapies include injections into the base of the penis, which cause flow of blood into the penis and a fairly immediate erection that lasts around an hour. The drugs injected are alprostadil (Caverject and Erectile dysfunctionex) and Invicorp (VIP and phentolamine). Alprostadil may also be inserted as a gel into the opening of the penis. This is not suitable if your partner is pregnant.
This penile tumescence monitor is placed at the base and near the corona of the penis. It is connected to a monitor that records a continuous graph depicting the force and duration of erections that occur during sleep. The monitor is strapped to the leg. The nocturnal penile tumescence test is conducted on several nights to obtain an accurate indication of erections that normally occur during the alpha phase of sleep.
Professional-athlete-turned-biohacker Maximilian Gotzler gave a speech about boosting testosterone at the 2015 Bulletproof Conference. He started by leading the room through the Haka, a Maori war dance that New Zealand’s pro rugby team has made popular. The Pasadena Conference Center trembled as over 100 people shouted and stomped in unison. It was awesome.
The sex hormone testosterone is far more than just the stuff of the alpha male's swagger. Though it plays a more significant role in the life of the biological male, it is actually present in both sexes to some degree. Despite popular perceptions that testosterone primarily controls aggression and sex drive—although it does play a role in both of those things—research has shown that individual levels of testosterone are also correlated with our language skills and cognitive abilities. Testosterone occurs in the body naturally, but can be administered as a medication, too: its most common uses are in the treatment of hypogonadism and breast cancer, as well as in hormone therapy for transgender men.
It is normal for a man to have five to six erections during sleep, especially during rapid eye movement (REM). Their absence may indicate a problem with nerve function or blood supply in the penis. There are two methods for measuring changes in penile rigidity and circumference during nocturnal erection: snap gauge and strain gauge. A significant proportion of men who have no sexual dysfunction nonetheless do not have regular nocturnal erections.
It may also become a treatment for anemia, bone density and strength problems. In a 2017 study published in the journal of the American Medical Association (JAMA), testosterone treatments corrected anemia in older men with low testosterone levels better than a placebo. Another 2017 study published in JAMA found that older men with low testosterone had increased bone strength and density after treatment when compared with a placebo. 

Additionally, the physiologic processes involving erections begin at the genetic level. Certain genes become activated at critical times to produce proteins vital to sustaining this pathway. Some researchers have focused on identifying particular genes that place men at risk for ED. At present, these studies are limited to animal models, and little success has been reported to date. [4] Nevertheless, this research has given rise to many new treatment targets and a better understanding of the entire process.

Men who produce more testosterone are more likely to engage in extramarital sex.[55] Testosterone levels do not rely on physical presence of a partner; testosterone levels of men engaging in same-city and long-distance relationships are similar.[54] Physical presence may be required for women who are in relationships for the testosterone–partner interaction, where same-city partnered women have lower testosterone levels than long-distance partnered women.[59]
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.
"Some say it's just a part of aging, but that's a misconception," says Jason Hedges, MD, PhD, a urologist at Oregon Health and Science University in Portland. A gradual decline in testosterone can't explain a near-total lack of interest in sex, for example. And for Hedges' patients who are in their 20s, 30s, and early 40s and having erectile problems, other health problems may be a bigger issue than aging.

Testosterone is significantly correlated with aggression and competitive behaviour and is directly facilitated by the latter. There are two theories on the role of testosterone in aggression and competition.[77] The first one is the challenge hypothesis which states that testosterone would increase during puberty thus facilitating reproductive and competitive behaviour which would include aggression.[77] Thus it is the challenge of competition among males of the species that facilitates aggression and violence.[77] Studies conducted have found direct correlation between testosterone and dominance especially among the most violent criminals in prison who had the highest testosterone levels.[77] The same research also found fathers (those outside competitive environments) had the lowest testosterone levels compared to other males.[77]

Once a complete sexual and medical history has been completed, appropriate laboratory studies should be conducted. In the initial evaluation of ED, sophisticated laboratory testing is rarely necessary. For example, serum testosterone (and sometimes prolactin) is typically only useful when the patient demonstrates hypogonadal features or testicular atrophy, or when clinical history is suggestive. Additional hormonal evaluation may include thyroid stimulating hormone in those with a clinical suspicion of hypothyroidism or appropriate diabetes screening in those presenting with a concern for impaired glucose metabolism. If the patient has not been evaluated with a lipid panel and hyperlipidemia is suspected, measurement and appropriate referral to internal medicine or cardiology is recommended. In most cases, a tentative diagnosis can be established with a complete sexual and medical history, physical examination, and limited or no laboratory testing.
Although her male patients may or may not get the low testosterone diagnosis they believe Dr. Wyne should give them, they will get a comprehensive examination. Besides their testosterone level, she will look at their triglycerides, glucose (blood sugar) tolerance, liver enzymes, and other counts as well as the condition of their testicles. "I need to know if they're normal going into it," she explained.

Although some men believe that taking testosterone medications may help them feel younger and more vigorous as they age, few rigorous studies have examined testosterone therapy in men who have healthy testosterone levels. And some small studies have revealed mixed results. For example, in one study healthy men who took testosterone medications increased muscle mass but didn't gain strength.
Vacuum devices for ED, also called pumps, offer an alternative to medication. The penis is placed inside a cylinder. A pump draws air out of the cylinder, creating a partial vacuum around the penis. This causes it to fill with blood, leading to an erection. An elastic band worn around the base of the penis maintains the erection during intercourse.
Recognized risk factors for ED include cardiovascular disease (CVD) (hypertension, atherosclerosis, and hyperlipidemia), diabetes, depression, alcohol use, smoking, pelvic/perineal surgery or trauma, neurologic disease, obesity, pelvic radiation, and Peyronie’s disease. One study suggested that the relationship between arterial disease and ED is very strong, with 49% (147 of 300) of patients with coronary artery disease noted on cardiac catheterization reporting significant erectile dysfunction.6 Endothelial dysfunction has been indicated as the pathophysiologic mechanism responsible for both CVD and ED.7 The Boston Area Community Health survey demonstrated a dose-response between smoking and incidence of erectile dysfunction.8 Animal studies have demonstrated both smooth-muscle disruption and decreased production of neural nitric oxide synthase in cigarette-exposed animals.9
Epidemiological studies have also assessed links between serum testosterone and non-coronary atherosclerosis. A study of over 1000 people aged 55 years and over found an inverse correlation between serum total and bioavailable testosterone and the amount of aortic atherosclerosis in men, as assessed by radiological methods (Hak et al 2002). Increased intima-media thickness (IMT) is an early sign of atherosclerosis and has also been shown to predict cardiovascular mortality (Murakami et al 2005). Cross-sectional studies have found that testosterone levels are negatively correlated with carotid IMT in independently living men aged 74–93 years (van den Beld et al 2003), diabetic men (Fukui et al 2003) and young obese men (De Pergola et al 2003). A 4-year follow up study of the latter population showed that free testosterone was also inversely correlated with the rate of increase of IMT (Muller et al 2004).
Richard J. Wassersug, PhD, an adjunct professor of urology at the University of British Columbia, described his personal experience with androgen deprivation therapy (ADT). "If you are on ADT," he said, "and you see those Low T ads, what are you supposed to make of it? This produces a cognitive dissonance." He called the ads "hurtful" for suggesting that low testosterone makes a man less of a man.
^ Mehta PH, Jones AC, Josephs RA (Jun 2008). "The social endocrinology of dominance: basal testosterone predicts cortisol changes and behavior following victory and defeat" (PDF). Journal of Personality and Social Psychology. 94 (6): 1078–93. CiteSeerX 10.1.1.336.2502. doi:10.1037/0022-3514.94.6.1078. PMID 18505319. Archived from the original (PDF) on April 19, 2009.
Many experts believe that atrophy, a partial or complete wasting away of tissue, and fibrosis, the growth of excess tissue, of the smooth muscle tissue in the body of the penis (cavernous smooth muscle) triggers problems with being able to maintain a firm erection. Poor ability to maintain an erection is often an early symptom of erectile dysfunction. Although the condition is called venous leak, the real problem is not with the veins but malfunction of the smooth muscle that surrounds the veins. The end result is difficulty with maintain a firm erection (losing an erection too quickly) that is now believe to be an early manifestation of atherosclerosis and vascular disease.
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.

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.
Think of erectile dysfunction as your body’s “check engine light.” The blood vessels in the penis are smaller than other parts of the body, so underlying conditions like blocked arteries, heart disease, or high blood pressure usually show up as ED before something more serious like a heart attack or stroke. ED is your body’s way of saying, “Something is wrong.” And the list of things that cause erectile dysfunction can include:
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.
Erectile dysfunction may be an unpleasant condition that no one really wants to talk about, failing to acknowledge it won’t make the problem go away. Your best defense against health problems like this is to learn everything you can about it so you can tackle the problem at the root. If you’re ready to stop living in embarrassment about your sexual function, become an advocate for yourself and your own health and talk to your doctor.
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.

In addition to its role as a natural hormone, testosterone is used as a medication, for instance in the treatment of low testosterone levels in men and breast cancer in women.[10] Since testosterone levels decrease as men age, testosterone is sometimes used in older men to counteract this deficiency. It is also used illicitly to enhance physique and performance, for instance in athletes.
For obvious reasons, ED can be a sensitive subject, one that until relatively recently men were more likely to try to hide than to deal with. Fortunately, a deeper understanding of the variety of causes of erectile dysfunction has led to medications, therapies, and other treatments that can be more individualized and more likely to be effective—and more open discussion about addressing the concern.
When females have a higher baseline level of testosterone, they have higher increases in sexual arousal levels but smaller increases in testosterone, indicating a ceiling effect on testosterone levels in females. Sexual thoughts also change the level of testosterone but not level of cortisol in the female body, and hormonal contraceptives may affect the variation in testosterone response to sexual thoughts.[51]
Testosterone is only one of many factors that influence aggression and the effects of previous experience and environmental stimuli have been found to correlate more strongly. A few studies indicate that the testosterone derivative estradiol (one form of estrogen) might play an important role in male aggression.[66][67][68][69] Studies have also found that testosterone facilitates aggression by modulating vasopressin receptors in the hypothalamus.[70]
Testosterone is the principle sex hormone responsible for the development of reproductive function in male vertebrates. Testosterone is one of the hormones referred to as androgens, which are also known of as anabolic steroids. As a steroid hormone, testosterone is derived from cholesterol and the structure of this hormone is similar across all mammals, reptiles, birds and fish.
Best of all? It's easy. "Low T Center is set up so men can walk in, take a simple blood test, and know within 30 minutes whether or not they are a candidate for testosterone replacement therapy, or TRT. Men who qualify get their first injection on the spot, and will continue to come in three times per month to receive a quick testosterone injection."
Diabetes is a well-recognized risk factor for ED. A systematic review and meta-analysis found that the prevalence of ED was 37.5% in type 1 diabetes, 66.3% in type 2 diabetes, and 52.5% in diabetes overall—a rate approximately 3.5 times higher than that in controls. [39]  The etiology of ED in diabetic men probably involves both vascular and neurogenic mechanisms. Evidence indicates that establishing good glycemic control can minimize this risk.

Interestingly, the Belgian company Solvay, acquired for €4.5 billion in 2010 by American pharmaceutical giant Abbott, didn't put its own or its product's name on the website. As AdWeek pointed out when the campaign launched, "One of the advantages of taking the unbranded route for Androgel is that the company does not have to warn consumers quite so prominently about Androgel's side effects."
When testosterone and endorphins in ejaculated semen meet the cervical wall after sexual intercourse, females receive a spike in testosterone, endorphin, and oxytocin levels, and males after orgasm during copulation experience an increase in endorphins and a marked increase in oxytocin levels. This adds to the hospitable physiological environment in the female internal reproductive tract for conceiving, and later for nurturing the conceptus in the pre-embryonic stages, and stimulates feelings of love, desire, and paternal care in the male (this is the only time male oxytocin levels rival a female's).[citation needed]
Trials of testosterone treatment in men with type 2 diabetes have also taken place. A recent randomized controlled crossover trial assessed the effects of intramuscular testosterone replacement to achieve levels within the physiological range, compared with placebo injections in 24 men with diabetes, hypogonadism and a mean age of 64 years (Kapoor et al 2006). Ten of these men were insulin treated. Testosterone treatment led to a significant reduction in glycated hemoglobin (HbA1C) and fasting glucose compared to placebo. Testosterone also produced a significant reduction in insulin resistance, measured by the homeostatic model assessment (HOMA), in the fourteen non-insulin treated patients. It is not possible to measure insulin resistance in patients treated with insulin but five out of ten of these patients had a reduction of insulin dose during the study. Other significant changes during testosterone treatment in this trial were reduced total cholesterol, waist circumference and waist-hip ratio. Similarly, a placebo-controlled but non-blinded trial in 24 men with visceral obesity, diabetes, hypogonadism and mean age 57 years found that three months of oral testosterone treatment led to significant reductions in HbA1C, fasting glucose, post-prandial glucose, weight, fat mass and waist-hip ratio (Boyanov et al 2003). In contrast, an uncontrolled study of 150 mg intramuscular testosterone given to 10 patients, average age 64 years, with diabetes and hypogonadism found no significant change in diabetes control, fasting glucose or insulin levels (Corrales et al 2004). Another uncontrolled study showed no beneficial effect of testosterone treatment on insulin resistance, measured by HOMA and ‘minimal model’ of area under acute insulin response curves, in 11 patients with type 2 diabetes aged between 33 and 73 years (Lee et al 2005). Body mass index was within the normal range in this population and there was no change in waist-hip ratio or weight during testosterone treatment. Baseline testosterone levels were in the low-normal range and patients received a relatively small dose of 100 mg intramuscular testosterone every three weeks. A good increase in testosterone levels during the trial is described but it is not stated at which time during the three week cycle the testosterone levels were tested, so the lack of response could reflect an insufficient overall testosterone dose in the trial period.
Remember that each person is unique, and each body responds differently to treatment. TT may help erectile function, low sex drive, bone marrow density, anemia, lean body mass, and/or symptoms of depression. However, there is no strong evidence that TT will help memory recall, measures of diabetes, energy, tiredness, lipid profiles, or quality of life.
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