Other factors leading to erectile dysfunction are diabetes mellitus, which is a well-known cause of neuropathy).[1] ED is also related to generally poor physical health, poor dietary habits, obesity, and most specifically cardiovascular disease, such as coronary artery disease and peripheral vascular disease.[1] Screening for cardiovascular risk factors, such as smoking, dyslipidemia, hypertension, and alcoholism is helpful.[1]
A larger national study, the National Health and Social Life Survey, looked at sexual function in men and women.4 This study surveyed 1,410 men aged 18 to 59 and also documented an increase in ED with age. Additionally, the study found a decrease in sexual desire with increasing age. Men in the oldest cohort (50 to 59) were more than 3 times as likely to experience erection problems and to report low sexual desire compared with men 18 to 29. Experience of sexual dysfunction was more likely among men in poor physical and emotional health. The study also concluded that sexual dysfunction is an important public health concern and that emotional issues are likely to contribute to the experience sexual dysfunction.

The participants were seen every 4 weeks. Blood was taken to measure hormone levels, and questionnaires were given to assess physical function, health status, vitality, and sexual function. Body fat and muscle measurements were also taken at the beginning and end of the 16 weeks. The study was funded in part by NIH’s National Institute on Aging (NIA) and National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Results appeared in the September 12, 2013, issue of the New England Journal of Medicine.

ICI Alprostadil may be used as a mixture with two other drugs to treat ED. This combination therapy called "bimix or trimix" is stronger than alprostadil alone and has become standard treatment for ED. Only the Alprostadil ingredient is FDA approved for ED. The amount of each drug used can be changed based on the severity of your ED, by an experienced health professional. You will be trained by your health professional on how to inject, how much to inject and how to safely raise the drug's dosage if necessary.
They also don't make clear how risky exposure to testosterone gel is for others—female partners, children, even pets. The gel is actually notorious for transferring to others. It can cause excess hair to grow on women's faces and arms, deepen their voices, interrupt menstruation, and make them anxious and irritable. In children, exposure to testosterone gels and creams can cause premature puberty and aggression. And in pets, it can cause aggressive behavior and enlargement of the genitalia.
What you need to know about delayed ejaculation Delayed ejaculation is a sexual disorder that can be distressing for a man and his partner and may disrupt a relationship. There are many reasons why delayed ejaculation occurs, including tissue damage, age, drugs, and the side effects of medication. They may be physiological or psychological. Find out how to get help. Read now
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.
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.
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Both ED and low testosterone (hypogonadism) increase with age. The incidence of the latter is 40% in men aged 45 years and older. [15] Testosterone is known to be important in mood, cognition, vitality, bone health, and muscle and fat composition. It also plays a key role in sexual dysfunction (eg, low libido, poor erection quality, ejaculatory or orgasmic dysfunction, reduced spontaneous erections, or reduced sexual activity). [16]

Of particularly concern are antihypertensive medications for CVD (eg, digoxin, disopyramide [Norpace], gemfibrozil [Lopid]), anxiety, depression (eg, lithium, monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, tricyclic antidepressants), or psychosis (eg, chlorpromazine, haloperidol, pimozide [Orap], thioridazine, thiothixene). Antihypertensive drugs, such as diuretics (eg, spironolactone, thiazides) and beta blockers, may be associated with ED. Discontinuation or switching to alternative drugs, such as angiotensin-converting enzyme inhibitors or calcium channel blockers (eg, diltiazem, nifedipine, amlodipine), may reduce ED. The newer angiotensin II receptor antagonists may be less problematic with respect to ED, but long-term data is needed to evaluate this.


Erectile dysfunction is defined as the persistent inability to achieve or maintain penile erection sufficient for satisfactory sexual performance. The Massachusetts Male Aging Study surveyed 1,709 men aged 40–70 years between 1987 and 1989 and found there was a total prevalence of erectile dysfunction of 52 percent. It was estimated that, in 1995, over 152 million men worldwide experienced ED. For 2025, the prevalence of ED is predicted to be approximately 322 million worldwide.

The sexual hormone can encourage fair behavior. For the study, subjects took part in a behavioral experiment where the distribution of a real amount of money was decided. The rules allowed both fair and unfair offers. The negotiating partner could subsequently accept or decline the offer. The fairer the offer, the less probable a refusal by the negotiating partner. If no agreement was reached, neither party earned anything. Test subjects with an artificially enhanced testosterone level generally made better, fairer offers than those who received placebos, thus reducing the risk of a rejection of their offer to a minimum. Two later studies have empirically confirmed these results.[71][72][73] However men with high testosterone were significantly 27% less generous in an ultimatum game.[74] The Annual NY Academy of Sciences has also found anabolic steroid use which increase testosterone to be higher in teenagers, and this was associated with increased violence.[75] Studies have also found administered testosterone to increase verbal aggression and anger in some participants.[76]

In rare cases, the drug Viagra ® can cause blue-green shading to vision that lasts for a short time. In rare cases, the drug Cialis® can cause or increase back pain or aching muscles in the back. In most cases, the side effects are linked to PDE5 inhibitor effects on other tissues in the body, meaning they are working to increase blood flow to your penis and at the same time impacting other vascular tissues in your body. These are not ‘allergic reactions'.
Dr. Ronald Swerdloff, chief of the endocrinology division at the Harbor-UCLA Medical Center and a professor of medicine at UCLA's David Geffen School of Medicine, served on the panel of experts who developed the Endocrine Society's guidelines. He is also the principal investigator for one of the 12 sites of The Testosterone Trial in Older Men, a nationwide study funded mainly by the National Institute on Aging. The study of 800 men over age 65 with low testosterone is looking at whether men using AndroGel for one year, compared to placebo, will show improvements in walking speed, sexual activity, vitality, memory, and anemia. The study will be completed in June 2015.
The other interesting thing about the study: men’s testosterone levels were lowest in March (at the end of winter) and highest in August (at the end of summer). Sunlight affects your vitamin D production, so you have seasonal dips and peaks. Get a blood test to check your levels, and if you’re low, take a high-quality vitamin D3 supplement. If you’re going to take D3, take vitamin K2 and vitamin A with it. The three work in sync, so you want them all to be balanced. Here are my dosage recommendations.
The Massachusetts Male Aging Study (MMAS) documented an inverse correlation between ED risk and high-density lipoprotein (HDL) cholesterol levels but did not identify any effect from elevated total cholesterol levels. [15] Another study involving male subjects aged 45-54 years found a correlation with abnormal HDL cholesterol levels but also found a correlation with elevated total cholesterol levels. The MMAS included a preponderance of older men.
Research has even found possible links to frequent ejaculation and a lower risk of prostate cancer. In one study of 32,000 men published in 2016 in the journal European Urology, for example, men who ejaculated at least 21 times per month while in their 20s were less likely to be diagnosed with prostate cancer than those who ejaculated four to seven times per month. And men who ejaculated more often in their 40s were 22 percent less likely to get a prostate cancer diagnosis.
Side effects include lightheadedness, fainting, priapism, urethral bleeding (intraurethral), dyspareunia in the partner (intraurethral), hematoma (intracavernosal) or penile curvature secondary to scar (intracavernosal). Efficacy of intraurethral alprostadil has been demonstrated to be around 50% ("able to have intercourse") in randomized controlled trials.31,32 For intracorporeal injection, typically alprostadil is tried alone, or compounded with papaverine (nonspecific phosphodiesterase inhibitor that increases intracellular cyclic adenosine monophosphate and cGMP) and/or phentolamine (competitive, non-selective alpha1- and alpha2-adrenoreceptor blocker). Pinsky et al33 reported an extensive review of the benefits and drawbacks of the combinations of these drugs.
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?
When I first started TRT, my physician prescribed a cream that you rub into your skin. The cream version of TRT is not too convenient, because if someone touches you while you have the cream on, the testosterone can rub off on him/her. This can be really bad around kids or pregnant women. If you’re sleeping next to someone, the cream can get on the sheets and transfer over that way, too. The cream can be annoying, but it works. There’s also a gel version called AndroGel; I skipped it because it doesn’t absorb as well as the cream does.
Dr. Shiel received a Bachelor of Science degree with honors from the University of Notre Dame. There he was involved in research in radiation biology and received the Huisking Scholarship. After graduating from St. Louis University School of Medicine, he completed his Internal Medicine residency and Rheumatology fellowship at the University of California, Irvine. He is board-certified in Internal Medicine and Rheumatology.

If you’re experiencing psychological ED, you may benefit from talk therapy. Therapy can help you manage your mental health. You’ll likely work with your therapist over several sessions, and your therapist will address things like major stress or anxiety factors, feelings around sex, or subconscious conflicts that could be affecting your sexual well-being.


Two of the immediate metabolites of testosterone, 5α-DHT and estradiol, are biologically important and can be formed both in the liver and in extrahepatic tissues.[147] Approximately 5 to 7% of testosterone is converted by 5α-reductase into 5α-DHT, with circulating levels of 5α-DHT about 10% of those of testosterone, and approximately 0.3% of testosterone is converted into estradiol by aromatase.[2][147][153][154] 5α-Reductase is highly expressed in the male reproductive organs (including the prostate gland, seminal vesicles, and epididymides),[155] skin, hair follicles, and brain[156] and aromatase is highly expressed in adipose tissue, bone, and the brain.[157][158] As much as 90% of testosterone is converted into 5α-DHT in so-called androgenic tissues with high 5α-reductase expression,[148] and due to the several-fold greater potency of 5α-DHT as an AR agonist relative to testosterone,[159] it has been estimated that the effects of testosterone are potentiated 2- to 3-fold in such tissues.[160]
Qaseem, A., Snow, V., Denberg, T. D., Casey, D. E., Forciea, M. A., Owens, D. K., & Shekelle, P. (2009). Hormonal testing and pharmacologic treatment of erectile dysfunction: A clinical practice guideline from the American College of Physicians. Annals of internal medicine, 151(9), 639-649. Retrieved from http://annals.org/aim/article/745155/hormonal-testing-pharmacologic-treatment-erectile-dysfunction-clinical-practice-guideline-from
The participants were seen every 4 weeks. Blood was taken to measure hormone levels, and questionnaires were given to assess physical function, health status, vitality, and sexual function. Body fat and muscle measurements were also taken at the beginning and end of the 16 weeks. The study was funded in part by NIH’s National Institute on Aging (NIA) and National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Results appeared in the September 12, 2013, issue of the New England Journal of Medicine.
An international consensus document was recently published and provides guidance on the diagnosis, treatment and monitoring of late-onset hypogonadism (LOH) in men. The diagnosis of LOH requires biochemical and clinical components. Controversy in defining the clinical syndrome continues due to the high prevalence of hypogonadal symptoms in the aging male population and the non-specific nature of these symptoms. Further controversy surrounds setting a lower limit of normal testosterone, the limitations of the commonly available total testosterone result in assessing some patients and the unavailability of reliable measures of bioavailable or free testosterone for general clinical use. As with any clinical intervention testosterone treatment should be judged on a balance of risk versus benefit. The traditional benefits of testosterone on sexual function, mood, strength and quality of life remain the primary goals of treatment but possible beneficial effects on other parameters such as bone density, obesity, insulin resistance and angina are emerging and will be reviewed. Potential concerns regarding the effects of testosterone on prostate disease, aggression and polycythaemia will also be addressed. The options available for treatment have increased in recent years with the availability of a number of testosterone preparations which can reliably produce physiological serum concentrations. 

Medications for erectile dysfunction don't work for everyone and may cause side effects that make a particular drug hard to take. "Work with your doctor to find the right treatment. There are still options for people who fail at medical treatment," advises Feloney. Alternatives to erectile dysfunction drugs include vacuum pump devices, medications injected into the penis, testosterone replacement if needed, and a surgical penile implant.
Acupuncture may help treat psychological ED, though studies are limited and inconclusive. You’ll likely need several appointments before you begin to notice any improvements. When choosing an acupuncturist, look for a certified practitioner who uses disposable needles and follows U.S. Food and Drug Administration guidelines for needle disposal and sterilization.
Findings that improvements in serum glucose, serum insulin, insulin resistance or glycemic control, in men treated with testosterone are accompanied by reduced measures of central obesity, are in line with other studies showing a specific effect of testosterone in reducing central or visceral obesity (Rebuffe-Scrive et al 1991; Marin, Holmang et al 1992). Furthermore, studies that have shown neutral effects of testosterone on glucose metabolism have not measured (Corrales et al 2004), or shown neutral effects (Lee et al 2005) (Tripathy et al 1998; Bhasin et al 2005) on central obesity. Given the known association of visceral obesity with insulin resistance, it is possible that testosterone treatment of hypogonadal men acts to improve insulin resistance and diabetes through an effect in reducing central obesity. This effect can be explained by the action of testosterone in inhibiting lipoprotein lipase and thereby reducing triglyceride uptake into adipocytes (Sorva et al 1988), an action which seems to occur preferentially in visceral fat (Marin et al 1995; Marin et al 1996). Visceral fat is thought to be more responsive to hormonal changes due to a greater concentration of androgen receptors and increased vascularity compared with subcutaneous fat (Bjorntorp 1996). Further explanation of the links between hypogonadism and obesity is offered by the hypogonadal-obesity-adipocytokine cycle hypothesis (see Figure 1). In this model, increases in body fat lead to increases in aromatase levels, in addition to insulin resistance, adverse lipid profiles and increased leptin levels. Increased action of aromatase in metabolizing testosterone to estrogen, reduces testosterone levels which induces further accumulation of visceral fat. Higher leptin levels and possibly other factors, act at the pituitary to suppress gonadotrophin release and exacerbate hypogonadism (Cohen 1999; Kapoor et al 2005). Leptin has also been shown to reduce testosterone secretion from rodent testes in vitro (Tena-Sempere et al 1999). A full review of the relationship between testosterone, insulin resistance and diabetes can be found elsewhere (Kapoor et al 2005; Jones 2007).
Cross-sectional studies have not shown raised testosterone levels at the time of diagnosis of prostate cancer, and in fact, low testosterone at the time of diagnosis has been linked with more locally aggressive and malignant tumors (Massengill et al 2003; Imamoto et al 2005; Isom-Batz et al 2005). This may reflect loss of hormone related control of the tumor or the effect of a more aggressive tumor in decreasing testosterone levels. One study found that 14% of hypogonadal men, with normal digital rectal examination and PSA levels, had histological prostate cancer on biopsy. It is possible that low androgen levels masked the usual evidence of prostate cancer in this population (Morgentaler et al 1996). Most longitudinal studies have not shown a correlation between testosterone levels and the future development of prostate cancer (Carter et al 1995; Heikkila et al 1999; Stattin et al 2004) but a recent study did find a positive association (Parsons et al 2005). Interpretation of such data requires care, as the presentation of prostate cancer could be altered or delayed in patients with lower testosterone levels.
Cardiovascular disease, and its underlying pathological process atherosclerosis, is an important cause of morbidity and mortality in the developed and developing world. Coronary heart disease in particular is the commonest cause of death worldwide (AHA 2002; MacKay and Mensah 2004). As well as increasing with age, this disease is more common in the male versus female population internationally, which has led to interest in the potential role of sex hormones in modulating risk of development of atherosclerosis. Concerns about the potential adverse effects of testosterone treatment on cardiovascular disease have previously contributed to caution in prescribing testosterone to those who have, or who are at risk of, cardiovascular disease. Contrary to fears of the potential adverse effects of testosterone on cardiovascular disease, there are over forty epidemiological studies which have examined the relationship of testosterone levels to the presence or development of coronary heart disease, and none have shown a positive correlation. Many of these studies have found the presence of coronary heart disease to be associated with low testosterone levels (Reviews: Jones, Jones et al 2003; Jones et al 2005).
Effective treatment for erectile dysfunction is available, and for most men will allow the return to a fulfilling sex life. The side effects of the treatment for erectile dysfunction vary depending on the treatment that is used. Some may interrupt the spontaneity of sexual activity. For example, PDE-5 inhibitors typically need to be taken one hour before sex. Side effects may include headaches, indigestion, vasodilation, diarrhoea and blue tinge to vision. Other treatments such as penile injections may cause pain at the injection site, or an erection that will not go down. Treatment options need to be carefully discussed with your doctor to determine which one is best suited to you.
Acupuncture may help treat psychological ED, though studies are limited and inconclusive. You’ll likely need several appointments before you begin to notice any improvements. When choosing an acupuncturist, look for a certified practitioner who uses disposable needles and follows U.S. Food and Drug Administration guidelines for needle disposal and sterilization.
Can erectile dysfunction be reversed? Erectile dysfunction (ED) is a very common issue, and it can usually be reversed with lifestyle changes, counseling, medications, or surgery. While short-term treatments are available, addressing the underlying cause will usually resolve the condition. Learn about causes and effective methods of reversing ED here. Read now

Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5α-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5α-reductase. DHT binds to the same androgen receptor even more strongly than testosterone, so that its androgenic potency is about 5 times that of T.[110] The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.
Longitudinal studies in male aging studies have shown that serum testosterone levels decline with age (Harman et al 2001; Feldman et al 2002). Total testosterone levels fall at an average of 1.6% per year whilst free and bioavailable levels fall by 2%–3% per year. The reduction in free and bioavailable testosterone levels is larger because aging is also associated with increases in SHBG levels (Feldman et al 2002). Cross-sectional data supports these trends but has usually shown smaller reductions in testosterone levels with aging (Feldman et al 2002). This is likely to reflect strict entry criteria to cross-sectional studies so that young healthy men are compared to older healthy men. During the course of longitudinal studies some men may develop pathologies which accentuate decreases in testosterone levels.

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.
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