Although not proven, it is likely that erectile dysfunction can be prevented by good general health, paying particular attention to body weight, exercise, and cigarette smoking. For example, heart disease and diabetes are problems that can cause erectile dysfunction, and both are preventable through lifestyle changes such as sensible eating and regular exercise. Furthermore, early diagnosis and treatment of associated conditions like diabetes, hypertension and high cholesterol may prevent or delay erectile dysfunction, or stop the erectile dysfunction from getting more serious. 

Growth of spermatogenic tissue in testicles, male fertility, penis or clitoris enlargement, increased libido and frequency of erection or clitoral engorgement. Growth of jaw, brow, chin, nose, and remodeling of facial bone contours, in conjunction with human growth hormone.[21] Completion of bone maturation and termination of growth. This occurs indirectly via estradiol metabolites and hence more gradually in men than women. Increased muscle strength and mass, shoulders become broader and rib cage expands, deepening of voice, growth of the Adam's apple. Enlargement of sebaceous glands. This might cause acne, subcutaneous fat in face decreases. Pubic hair extends to thighs and up toward umbilicus, development of facial hair (sideburns, beard, moustache), loss of scalp hair (androgenetic alopecia), increase in chest hair, periareolar hair, perianal hair, leg hair, armpit hair.
With an inflatable implant, fluid-filled cylinders are placed lengthwise in the penis. Tubing joins these cylinders to a pump placed inside the scrotum (between the testicles). When the pump is engaged, pressure in the cylinders inflate the penis and makes it stiff. Inflatable implants make a normal looking erection and are natural feeling for your partner. Your surgeon may suggest a lubricant for your partner. With the implant, men can control firmness and, sometimes, the size of the erection. Implants allows a couple to be spontaneously intimate. There is generally no change to a man's feeling or orgasm.

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.
If a trial of oral therapy and withdrawal of offending medications do not restore erectile function or if a patient has medical or financial contraindications to pharmacologic therapy, most primary care practitioners should consider referring the patient to a specialist for additional evaluation and discussion of alternative treatment options. However, some primary care practitioners may recommend vacuum constriction devices.
A number of epidemiological studies have found that bone mineral density in the aging male population is positively associated with endogenous androgen levels (Murphy et al 1993; Ongphiphadhanakul et al 1995; Rucker et al 2004). Testosterone levels in young men have been shown to correlate with bone size, indicating a role in determination of peak bone mass and protection from future osteoporosis (Lorentzon et al 2005). Male hypogonadism has been shown to be a risk factor for hip fracture (Jackson et al 1992) and a recent study showed a high prevalence of hypogonadism in a group of male patients with average age 75 years presenting with minimal trauma fractures compared to stroke victims who acted as controls (Leifke et al 2005). Estrogen is a well known determinant of bone density in women and some investigators have found serum estrogen to be a strong determinant of male bone density (Khosla et al 1998; Khosla et al 2001). Serum estrogen was also found to correlate better than testosterone with peak bone mass (Khosla et al 2001) but this is in contradiction of a more recent study showing a negative correlation of estrogen with peak bone size (Lorentzon et al 2005). Men with aromatase deficiency (Carani et al 1997) or defunctioning estrogen receptor mutations (Smith et al 1994) have been found to have abnormally low bone density despite normal or high testosterone levels which further emphasizes the important influence of estrogen on male bone density.
A large number of trials have demonstrated a positive effect of testosterone treatment on bone mineral density (Katznelson et al 1996; Behre et al 1997; Leifke et al 1998; Snyder et al 2000; Zacharin et al 2003; Wang, Cunningham et al 2004; Aminorroaya et al 2005; Benito et al 2005) and bone architecture (Benito et al 2005). These effects are often more impressive in longer trials, which have shown that adequate replacement will lead to near normal bone density but that the full effects may take two years or more (Snyder et al 2000; Wang, Cunningham et al 2004; Aminorroaya et al 2005). Three randomized placebo-controlled trials of testosterone treatment in aging males have been conducted (Snyder et al 1999; Kenny et al 2001; Amory et al 2004). One of these studies concerned men with a mean age of 71 years with two serum testosterone levels less than 12.1nmol/l. After 36 months of intramuscular testosterone treatment or placebo, there were significant increases in vertebral and hip bone mineral density. In this study, there was also a significant decrease in the bone resorption marker urinary deoxypyridinoline with testosterone treatment (Amory et al 2004). The second study contained men with low bioavailable testosterone levels and an average age of 76 years. Testosterone treatment in the form of transdermal patches was given for 1 year. During this trial there was a significant preservation of hip bone mineral density with testosterone treatment but testosterone had no effect on bone mineral density at other sites including the vertebrae. There were no significant alterations in bone turnover markers during testosterone treatment (Kenny et al 2001). The remaining study contained men of average age 73 years. Men were eligible for the study if their serum total testosterone levels were less than 16.5 nmol/L, meaning that the study contained men who would usually be considered eugonadal. The beneficial effects of testosterone on bone density were confined to the men who had lower serum testosterone levels at baseline and were seen only in the vertebrae. There were no significant changes in bone turnover markers. Testosterone in the trial was given via scrotal patches for a 36 month duration (Snyder et al 1999). A recent meta-analysis of the effects on bone density of testosterone treatment in men included data from these studies and two other randomized controlled trials. The findings were that testosterone produces a significant increase of 2.7% in the bone mineral density at the lumber spine but no overall change at the hip (Isidori et al 2005). These results from randomized controlled trials in aging men show much smaller benefits of testosterone treatment on bone density than have been seen in other trials. This could be due to the trials including patients who are not hypogonadal and being too short to allow for the maximal effects of testosterone. The meta-analysis also assessed the data concerning changes of bone formation and resorption markers during testosterone treatment. There was a significant decrease in bone resorption markers but no change in markers of bone formation suggesting that reduction of bone resorption may be the primary mode of action of testosterone in improving bone density (Isidori et al 2005).
In a prospective study from the Prostate Cancer Prevention Trial database, Thompson et al reported that men presenting with ED had a significantly higher chance of developing a cardiovascular event over a 7-year follow-up period. [55] The hazard ratio was 1.45, which is in the range of risk associated with current smoking or a family history of MI.
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.
Talk with your doctor before trying supplements for ED. They can contain 10 or more ingredients and may complicate other health conditions. Asian ginseng and ginkgo biloba (seen here) are popular, but there isn't a lot of good research on their effectiveness. Some men find that taking a DHEA supplement improves their ability to have an erection. Unfortunately, the long-term safety of DHEA supplements is unknown. Most doctors do not recommend using it.
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]
If testosterone deficiency occurs during fetal development, then male characteristics may not completely develop. If testosterone deficiency occurs during puberty, a boy’s growth may slow and no growth spurt will be seen. The child may have reduced development of pubic hair, growth of the penis and testes, and deepening of the voice. Around the time of puberty, boys with too little testosterone may also have less than normal strength and endurance, and their arms and legs may continue to grow out of proportion with the rest of their body.
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However, a review of a United Kingdom medical record database found no evidence that the use of 5-alpha reductase inhibitors independently increase the risk for ED. In 71,849 men with benign prostatic hyperplasia (BPH), the risk of ED was not increased with the use of finasteride or dutasteride only (odds ratio [OR] 0.94), or a 5-alpha reductase inhibitor plus an alpha blocker (OR 0.92) compared with an alpha blocker only. In addition, the risk of ED was not increase in 12 346 men prescribed finasteride 1 mg for alopecia, compared with unexposed men with alopecia (OR 0.95). The risk of ED did increase with longer duration of BPH, regardless of drug exposure. [48]
Conditions that may be associated with ED include diabetes, [25, 26, 27] hypertension, [28] , and CAD, as well as neurologic disorders, endocrinopathies, benign prostatic hyperplasia, [29] , sleep apnea [30] , COPD, [31] and depression (see Table 1 below). [32, 33, 34, 35] In fact, almost any disease may affect erectile function by altering the nervous, vascular, or hormonal systems. Various diseases may produce changes in the smooth muscle tissue of the corpora cavernosa or influence the patient’s psychological mood and behavior.

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.
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.
If a trial of oral therapy and withdrawal of offending medications do not restore erectile function or if a patient has medical or financial contraindications to pharmacologic therapy, most primary care practitioners should consider referring the patient to a specialist for additional evaluation and discussion of alternative treatment options. However, some primary care practitioners may recommend vacuum constriction devices.
Dr. Adriane Fugh-Berman, associate professor of pharmacology and director of the industry watchdog group PharmedOut.org at Georgetown University School of Medicine, calls this kind of direct-to-consumer pharmaceutical advertising "evil." She likened the efforts to sell TRT to earlier campaigns to push hormone replacement therapy for post-menopausal women. "They stole the playbook," she said. "This hormone is being thrown around like sugar water."
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.
Autopsy studies have found histological prostate cancer to be very common, with one series showing a prevalence of greater than fifty percent in men over age sixty (Holund 1980). The majority of histological cancers go undetected so that the clinical incidence of the disease is much lower, but it is still the most prevalent non-skin cancer in men (Jemal et al 2003). Prostate cancer is also unusual in comparison to other adult cancers in that the majority of those with the disease will die of other causes. Treatment of prostate cancer with androgen deprivation is known to be successful and is widely practiced, indicating an important role for testosterone in modifying the behavior of prostate cancer. In view of this, testosterone treatment is absolutely contraindicated in any case of known or suspected prostate cancer. The question of whether testosterone treatment could cause new cases of prostate cancer, or more likely cause progression of undiagnosed histological prostate cancer that would otherwise have remained occult, is an important consideration when treating ageing males with testosterone.
I think that a very powerful argument to young men who want to perform at the highest level is to point out the destructive nature of what they’re doing. If they’re having 18 drinks per week, if they’re having three, four, five drinks at any one time, they’re going to guarantee that their erections are not going to be at the highest level. I can’t tell you the number of men who come in saying, they went out, they had a date, they had a big dinner– which, by the way, is also not a great thing for erections, because all the blood is now going to your gut instead of to the genital area. And how important lifestyle changes are to improving your performance, as well, if not better, than the medications. So make certain that you exercise modestly, not excessively. Make certain that you have a smaller meal on an evening or a day that you want to have a sexual encounter, because you want the blood to go, once again, to the penile area and not to your gut. And really, the whole idea of stress– if you’re stressed out, if you’re worried about a lot of things, if you’re distracted, you can’t initiate that psychic stimulus to your spinal cord and then ultimately to your penis. So stress management is incredibly important.
There is a polymorphic CAG repeat sequence in the androgen receptor gene, which codes for a variable number of glutamine amino acids in the part of the receptor affecting gene transcription. A receptor with a short CAG sequence produces greater activity when androgens attach, and men with shorter CAG polymorphisms exhibit androgenic traits, such as preserved bone density (Zitzmann et al 2001) and prostate growth during testosterone treatment (Zitzmann et al 2003). Indirect evidence of the importance of androgens in the development of prostate cancer is provided by case control study findings of a shorter, more active CAG repeat sequence in the androgen receptor gene of patients with prostate cancer compared with controls (Hsing et al 2000, 2002).
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]
Vascular damage may result from radiation therapy to the pelvis and prostate in the treatment of prostate cancer. [36] Both the blood vessels and the nerves to the penis may be affected. Radiation damage to the crura of the penis, which are highly susceptible to radiation damage, can induce ED. Data indicate that 50% of men undergoing radiation therapy lose erectile function within 5 years after completing therapy; fortunately, some respond to one of the PDE5 inhibitors.

“Although having sex at 70 is not the same as having sex at 20, erectile dysfunction is not a normal part of aging,” according to Michael Feloney, MD, urologic surgeon and expert on sexual dysfunction issues at the Nebraska Medical Center in Omaha. “You should still be able to have a satisfying sex life as you age." If you are experiencing erectile dysfunction, these 10 dos and don'ts may help.


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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