While testosterone stimulates a man’s sex drive, it also aids in achieving and maintaining an erection. Testosterone alone doesn’t cause an erection, but it stimulates receptors in the brain to produce nitric oxide. Nitric oxide is a molecule that helps trigger a series of chemical reactions necessary for an erection to occur. When testosterone levels are too low, a man may have difficulty achieving an erection prior to sex or having spontaneous erections (for example, during sleep).
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.
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.
In order to discuss the biochemical diagnosis of hypogonadism it is necessary to outline the usual carriage of testosterone in the blood. Total serum testosterone consists of free testosterone (2%–3%), testosterone bound to sex hormone binding globulin (SHBG) (45%) and testosterone bound to other proteins (mainly albumin −50%) (Dunn et al 1981). Testosterone binds only loosely to albumin and so this testosterone as well as free testosterone is available to tissues and is termed bioavailable testosterone. Testosterone bound to SHBG is tightly bound and is biologically inactive. Bioavailable and free testosterone are known to correlate better than total testosterone with clinical sequelae of androgenization such as bone mineral density and muscle strength (Khosla et al 1998; Roy et al 2002). There is diurnal variation in serum testosterone levels with peak levels seen in the morning following sleep, which can be maintained into the seventh decade (Diver et al 2003). Samples should always be taken in the morning before 11 am to allow for standardization.

While testosterone stimulates a man’s sex drive, it also aids in achieving and maintaining an erection. Testosterone alone doesn’t cause an erection, but it stimulates receptors in the brain to produce nitric oxide. Nitric oxide is a molecule that helps trigger a series of chemical reactions necessary for an erection to occur. When testosterone levels are too low, a man may have difficulty achieving an erection prior to sex or having spontaneous erections (for example, during sleep).


There are treatments available to help you to get and maintain an erection. In addition, making healthy changes to your lifestyle could help with impotence. Switching to a healthier balanced diet, taking more exercise and cutting down on or giving up alcohol and cigarettes could help you to see an improvement in sexual function. If you think that the problem may be related to stress or anxiety, counselling can also help.
One of the first steps is to distinguish between physiological and psychological ED. Determining whether involuntary erections are present is important in eliminating the possibility of psychogenic causes for ED.[1] Obtaining full erections occasionally, such as nocturnal penile tumescence when asleep (that is, when the mind and psychological issues, if any, are less present), tends to suggest that the physical structures are functionally working.[19][20] Similarly, performance with manual stimulation, as well as any performance anxiety or acute situational ED, may indicate a psychogenic component to ED.[1]
When Solvay Pharmaceuticals, maker of market-dominating Androgel, launched its "Low T" campaign, in 2008, it claimed that 13 million American men over age 45 suffered from low testosterone, 90 percent of them undiagnosed. Its website, IsItLowT.com, showed dumpy, depressed men and their unhappy spouses remembering how it "used to be." Why settle for dumpiness and depression, the website and related TV ads suggested, when a little dab'll do you?

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 bones and the brain are two important tissues in humans where the primary effect of testosterone is by way of aromatization to estradiol. In the bones, estradiol accelerates ossification of cartilage into bone, leading to closure of the epiphyses and conclusion of growth. In the central nervous system, testosterone is aromatized to estradiol. Estradiol rather than testosterone serves as the most important feedback signal to the hypothalamus (especially affecting LH secretion).[111] In many mammals, prenatal or perinatal "masculinization" of the sexually dimorphic areas of the brain by estradiol derived from testosterone programs later male sexual behavior.[112]
Testosterone belongs to a class of male hormones called androgens, which are sometimes called steroids or anabolic steroids. In men, testosterone is produced mainly in the testes, with a small amount made in the adrenal glands. The brain's hypothalamus and pituitary gland control testosterone production. The hypothalamus instructs the pituitary gland on how much testosterone to produce, and the pituitary gland passes the message on to the testes. These communications happen through chemicals and hormones in the bloodstream.
There is increasing interest in the group of patients who fail to respond to treatment with PDE-5 inhibitors and have low serum testosterone levels. Evidence from placebo-controlled trials in this group of men shows that testosterone treatment added to PDE-5 inhibitors improves erectile function compared to PDE-5 inhibitors alone (Aversa et al 2003; Shabsigh et al 2004).
The hypogonadal-obesity-adipocytokine cycle hypothesis. Adipose tissue contains the enzyme aromatase which metabolises testosterone to oestrogen. This results in reduced testosterone levels, which increase the action of lipoprotein lipase and increase fat mass, thus increasing aromatisation of testosterone and completing the cycle. Visceral fat also promotes lower testosterone levels by reducing pituitary LH pulse amplitude via leptin and/or other factors. In vitro studies have shown that leptin also inhibits testosterone production directly at the testes. Visceral adiposity could also provide the link between testosterone and insulin resistance (Jones 2007).
Testosterone is an androgen hormone produced by the adrenal cortex, the testes (in men), and the ovaries (in women). It is often considered the primary male sex hormone. Testosterone stimulates the development of male secondary sex characteristics (like body hair and muscle growth) and is essential in the production of sperm. In women, testosterone plays a role in egg development and ovulation.
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 laboratory results should be discussed with the patient and, if possible, with his sexual partner. This educational process allows a review of the basic aspects of the anatomy and physiology of the sexual response and an explanation of the possible etiology and associated risk factors (eg, smoking and the use of various medications). Treatment options and their benefits and risks should be discussed. This type of dialogue allows the patient and physician to cooperate in developing an optimal management strategy.
Testosterone replacement therapy is currently only FDA approved for men who have been diagnosed with hypogonadism, but it’s also prescribed off-label for older men who take it in hopes that it will improve their libido. The use of testosterone therapy is increasingly common in the United States, with more than 2 million men receiving the therapy. Not every man benefits from taking testosterone supplements. Testosterone is available in different forms, including topicals such as gels, creams, and patches; injections; and pellets that are surgically placed directly beneath the skin. (7)
Organic ED involves abnormalities the penile arteries, veins, or both and is the most common cause of ED, especially in older men. When the problem is arterial, it is usually caused by arteriosclerosis, or hardening of the arteries, although trauma to the arteries may be the cause. The controllable risk factors for arteriosclerosis--being overweight, lack of exercise, high cholesterol, high blood pressure, and cigarette smoking--can cause erectile failure often before progressing to affect the heart. 

Early infancy androgen effects are the least understood. In the first weeks of life for male infants, testosterone levels rise. The levels remain in a pubertal range for a few months, but usually reach the barely detectable levels of childhood by 4–7 months of age.[15][16] The function of this rise in humans is unknown. It has been theorized that brain masculinization is occurring since no significant changes have been identified in other parts of the body.[17] The male brain is masculinized by the aromatization of testosterone into estrogen, which crosses the blood–brain barrier and enters the male brain, whereas female fetuses have α-fetoprotein, which binds the estrogen so that female brains are not affected.[18]
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.
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.
Testosterone is included in the World Health Organization's list of essential medicines, which are the most important medications needed in a basic health system.[172] It is available as a generic medication.[10] The price depends on the form of testosterone used.[173] It can be administered as a cream or transdermal patch that is applied to the skin, by injection into a muscle, as a tablet that is placed in the cheek, or by ingestion.[10]
Supplements are popular and often cheaper than prescription drugs for ED. However, supplements have not been tested to see how well they work or if they are a safe treatment for ED. Patients should know that many over-the-counter drugs have been found on drug testing to have ‘bootlegged' PDE 5 Inhibitors as their main ingredient. The amounts of Viagra, Cialis, Levitra or Stendra that may be in these supplements is not under quality control and may differ from pill to pill. The FDA has issued consumer warnings and alerts.

There are positive correlations between positive orgasm experience in women and testosterone levels where relaxation was a key perception of the experience. There is no correlation between testosterone and men's perceptions of their orgasm experience, and also no correlation between higher testosterone levels and greater sexual assertiveness in either sex.[34]
It is essential to discuss erectile dysfunction with your doctor, so any serious underlying causes can be excluded and treatment options can be discussed. Many men are embarrassed discussing this issue with their doctor, or even their partner. Open communication with your doctor, and in your relationship, is important for effectively managing this common problem.

Currently available testosterone preparations in common use include intramuscular injections, subcutaneous pellets, buccal tablets, transdermal gels and patches (see Table 2). Oral testosterone is not widely used. Unmodified testosterone taken orally is largely subject to first-pass metabolism by the liver. Oral doses 100 fold greater than physiological testosterone production can be given to achieve adequate serum levels. Methyl testosterone esters have been associated with hepatotoxicity. There has been some use of testosterone undecanoate, which is an esterified derivative of testosterone that is absorbed via the lymphatic system and bypasses the liver. Unfortunately, it produces unpredictable testosterone levels and increases testosterone levels for only a short period after each oral dose (Schurmeyer et al 1983).
It is hard to know how many men among us have TD, although data suggest that overall about 2.1% (about 2 men in every 100) may have TD. As few as 1% of younger men may have TD, while as many as 50% of men over 80 years old may have TD. People who study the condition often use different cut-off points for the numbers, so you may hear different numbers being stated.

Alteration of NO levels is the focus of several approaches to the treatment of ED. Inhibitors of phosphodiesterase, which primarily hydrolyze cGMP type 5, provided the basis for the development of the PDE5 inhibitors. Chen et al administered oral L-arginine and reported subjective improvement in 50 men with ED. [14] These supplements are readily available commercially. Reported adverse effects include nausea, diarrhea, headache, flushing, numbness, and hypotension.
Replacement therapy may produce desired results, such as greater muscle mass and a stronger sex drive. However, the treatment does carry some side effects. Oily skin and fluid retention are common. The testicles may also shrink, and sperm production could decrease significantly. Some studies have found no greater risk of prostate cancer with testosterone replacement therapy, but it continues to be a topic of ongoing research.

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 changes in average serum testosterone levels with aging mean that the proportion of men fulfilling a biochemically defined diagnosis of hypogonadism increases with aging. Twenty percent of men aged over 60 have total testosterone levels below the normal range and the figure rises to 50% in those aged over 80. The figures concerning free testosterone are even higher as would be expected in view of the concurrent decrease in SHBG levels (Harman et al 2001).

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.
In order to discuss the biochemical diagnosis of hypogonadism it is necessary to outline the usual carriage of testosterone in the blood. Total serum testosterone consists of free testosterone (2%–3%), testosterone bound to sex hormone binding globulin (SHBG) (45%) and testosterone bound to other proteins (mainly albumin −50%) (Dunn et al 1981). Testosterone binds only loosely to albumin and so this testosterone as well as free testosterone is available to tissues and is termed bioavailable testosterone. Testosterone bound to SHBG is tightly bound and is biologically inactive. Bioavailable and free testosterone are known to correlate better than total testosterone with clinical sequelae of androgenization such as bone mineral density and muscle strength (Khosla et al 1998; Roy et al 2002). There is diurnal variation in serum testosterone levels with peak levels seen in the morning following sleep, which can be maintained into the seventh decade (Diver et al 2003). Samples should always be taken in the morning before 11 am to allow for standardization.
Sexual dysfunction and ED become more common as men age. The percentage of complete ED increases from 5% to 15% as age increases from 40 to 70 years. But this does not mean growing older is the end of your sex life. ED can be treated at any age. Also, ED may be more common in Hispanic men and in those with a history of diabetes, obesity, smoking, and hypertension. Research shows that African-American men sought medical care for ED twice the rate of other racial groups.
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.
A physical exam checks your total health. Examination focusing on your genitals (penis and testicles) is often done to check for ED. Based on your age and risk factors, the exam may also focus on your heart and blood system: heart, peripheral pulses and blood pressure. Based on your age and family history your doctor may do a rectal exam to check the prostate. These tests are not painful. Most patients do not need a lot of testing before starting treatment.
In order to discuss the biochemical diagnosis of hypogonadism it is necessary to outline the usual carriage of testosterone in the blood. Total serum testosterone consists of free testosterone (2%–3%), testosterone bound to sex hormone binding globulin (SHBG) (45%) and testosterone bound to other proteins (mainly albumin −50%) (Dunn et al 1981). Testosterone binds only loosely to albumin and so this testosterone as well as free testosterone is available to tissues and is termed bioavailable testosterone. Testosterone bound to SHBG is tightly bound and is biologically inactive. Bioavailable and free testosterone are known to correlate better than total testosterone with clinical sequelae of androgenization such as bone mineral density and muscle strength (Khosla et al 1998; Roy et al 2002). There is diurnal variation in serum testosterone levels with peak levels seen in the morning following sleep, which can be maintained into the seventh decade (Diver et al 2003). Samples should always be taken in the morning before 11 am to allow for standardization.
If you have unstable heart disease of any kind, heart failure or unstable, what we call angina, contraindication to using the medications. All right? So if you’re in an unstable medical state, these medications are not a good idea. Now, there are relative issues. If you may be taking a blood pressure medicine or a medicine for your prostate which dilates your blood vessel a little bit– you know, the typical ones are what we call the alpha blockers– you may have an additive effect from the medication. But for the most part, the medicines are incredibly safe.

Everything you need to know about chlamydia Chlamydia is the most common STI in the United States, yet most people do not experience obvious symptoms. Chlamydia affects men and women and can harm the reproductive systems, sometimes permanently. Find out about the causes and symptoms of chlamydia, as well as what the best treatments are and how to get screened. Read now
Testosterone is observed in most vertebrates. Testosterone and the classical nuclear androgen receptor first appeared in gnathostomes (jawed vertebrates).[186] Agnathans (jawless vertebrates) such as lampreys do not produce testosterone but instead use androstenedione as a male sex hormone.[187] Fish make a slightly different form called 11-ketotestosterone.[188] Its counterpart in insects is ecdysone.[189] The presence of these ubiquitous steroids in a wide range of animals suggest that sex hormones have an ancient evolutionary history.[190]
There are risks to prosthetic surgery and patients are counselled before the procedure. If there is a post-operative infection, the implant will likely be removed. The devices are reliable, but in the case of mechanical malfunction, the device or a part of the device will need to be replaced surgically. If a penile prosthesis is removed, other non-surgical treatments may no longer work.

Fatherhood decreases testosterone levels in men, suggesting that the emotions and behavior tied to decreased testosterone promote paternal care. In humans and other species that utilize allomaternal care, paternal investment in offspring is beneficial to said offspring's survival because it allows the parental dyad to raise multiple children simultaneously. This increases the reproductive fitness of the parents, because their offspring are more likely to survive and reproduce. Paternal care increases offspring survival due to increased access to higher quality food and reduced physical and immunological threats.[60] This is particularly beneficial for humans since offspring are dependent on parents for extended periods of time and mothers have relatively short inter-birth intervals,[61] While extent of paternal care varies between cultures, higher investment in direct child care has been seen to be correlated with lower average testosterone levels[62] as well as temporary fluctuations. For instance, fluctuation in testosterone levels when a child is in distress has been found to be indicative of fathering styles. If a father's testosterone levels decrease in response to hearing their baby cry, it is an indication of empathizing with the baby. This is associated with increased nurturing behavior and better outcomes for the infant[63].


Associated morbidity may include various other male sexual dysfunctions, such as premature (early) ejaculation and male hypoactive sexual desire disorder. The NHSLS found that 28.5% of men aged 18-59 years reported premature ejaculation, and 15.8% lacked sexual interest during the past year. An additional 17% reported anxiety about sexual performance, and 8.1% had a lack of pleasure in sex. [51]
Implantation of penile prosthesis remains an important option for men with ED if medical treatment fails or is inappropriate. Prostheses are available as a saline-filled silicone device or a malleable device. The benefit of the former is a more natural appearance in the deflated state, closely approximating the appearance of a flaccid penis. The trade-off is a higher mechanical failure rate and higher cost. Satisfaction rates for patients who underwent penile prosthesis surgery have been reported to be near 90%.36 However, in the majority of patients who receive this treatment, less invasive alternatives have failed and therefore satisfaction with this treatment would be expected to be higher in this subset of patients. Risks of these devices include surgical and anesthetic risk, device infection, and device malfunction. Mechanical failure rates depend on the specific device being investigated. Overall, the percentage of devices that are free from mechanical failure at 5 years ranges from 84% to 94%.19 Infection rates in the era of coated devices and improved techniques are reported to be less than 1%.37

Both testosterone and 5α-DHT are metabolized mainly in the liver.[1][147] Approximately 50% of testosterone is metabolized via conjugation into testosterone glucuronide and to a lesser extent testosterone sulfate by glucuronosyltransferases and sulfotransferases, respectively.[1] An additional 40% of testosterone is metabolized in equal proportions into the 17-ketosteroids androsterone and etiocholanolone via the combined actions of 5α- and 5β-reductases, 3α-hydroxysteroid dehydrogenase, and 17β-HSD, in that order.[1][147][148] Androsterone and etiocholanolone are then glucuronidated and to a lesser extent sulfated similarly to testosterone.[1][147] The conjugates of testosterone and its hepatic metabolites are released from the liver into circulation and excreted in the urine and bile.[1][147][148] Only a small fraction (2%) of testosterone is excreted unchanged in the urine.[147]
In one study, 9.6% reported ‘occasional’ erectile dysfunction, 8.9% reported erectile dysfunction occurring ‘often’, and 18.6% reported erectile dysfunction occurring ‘all the time’. Of these, only 11.6% had received treatment.In another study, only 14.1% of men reported that they had received treatment, despite experiencing erectile dysfunction for longer than 12 months.
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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