Testosterone is used as a medication for the treatment of males with too little or no natural testosterone production, certain forms of breast cancer,[10] and gender dysphoria in transgender men. This is known as hormone replacement therapy (HRT) or testosterone replacement therapy (TRT), which maintains serum testosterone levels in the normal range. Decline of testosterone production with age has led to interest in androgen replacement therapy.[170] It is unclear if the use of testosterone for low levels due to aging is beneficial or harmful.[171]
Cavernosography measurement of the vascular pressure in the corpus cavernosum. Saline is infused under pressure into the corpus cavernosum with a butterfly needle, and the flow rate needed to maintain an erection indicates the degree of venous leakage. The leaking veins responsible may be visualized by infusing a mixture of saline and x-ray contrast medium and performing a cavernosogram.[21] In Digital Subtraction Angiography (DSA), the images are acquired digitally.
"Bring back the younger inner you," says the Low T Center. According to its website, its president, Mr. (notably not "Dr.") Mike Sisk, "created these centers out of a need." They promise their testosterone injections "do not just help boost a low sex drive but can also boost energy, decrease body fat, irritability, and depression." They go so far as to claim that "research finds testosterone replacement can solve long-term health issues like Alzheimer's and heart disease."

At the present time, it is suggested that androgen replacement should take the form of natural testosterone. Some of the effects of testosterone are mediated after conversion to estrogen or dihydrotestosterone by the enzymes aromatase and 5a-reductase enzymes respectively. Other effects occur independently of the traditional action of testosterone via the classical androgen receptor- for example, its action as a vasodilator via a cell membrane action as described previously. It is therefore important that the androgen used to treat hypogonadism is amenable to the action of these metabolizing enzymes and can also mediate the non-androgen receptor actions of testosterone. Use of natural testosterone ensures this and reduces the chance of non-testosterone mediated adverse effects. There are now a number of testosterone preparations which can meet these recommendations and the main factor in deciding between them is patient choice.
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. 
Testosterone begins with cholesterol. In fact, every single sex hormone you make you synthesize from cholesterol – that’s one reason a “heart healthy” low-fat, low-cholesterol diet limits your performance. Fat and cholesterol don’t make you fat. They give your body the building blocks to create abundant testosterone and other sex hormones, which actually makes you lose weight and build muscle, especially if your current testosterone levels are low [1].
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:
But when a premenopausal woman’s testosterone levels are too high, it can lead to polycystic ovary syndrome (PCOS), a condition that increases the risk of irregular or absent menstrual cycles, infertility, excess hair growth, skin problems, and miscarriage. High levels of testosterone in women, whether caused by PCOS or by another condition, can cause serious health conditions such as insulin resistance, diabetes, high cholesterol, high blood pressure, and heart disease. (12)
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).
Erectile dysfunction can cause strain on a couple. Many times, men will avoid sexual situations due to the emotional pain associated with ED, causing their partner to feel rejected or inadequate. It is important to communicate openly with your partner. Some couples consider seeking treatment for ED together, while other men prefer to seek treatment without their partner's knowledge. A lack of communication is the primary barrier for seeking treatment and can prolong the suffering. The loss of erectile capacity can have a profound effect on a man. The good news is that ED can usually be treated safely and effectively.

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.

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]

However, testosterone is only one of many factors that aid in adequate erections. Research is inconclusive regarding the role of testosterone replacement in the treatment of erectile dysfunction. In a review of studies that looked at the benefit of testosterone in men with erection difficulties, nearly half showed no improvement with testosterone treatment. Many times, other health problems play a role in erectile difficulties. These can include:

One study examined the role of testosterone supplementation in hypogonadal men with ED. These men were considered nonresponders to sildenafil, and their erections were monitored by assessing nocturnal penile tumescence (NPT). After these men were given testosterone transdermally for 6 months, the number of NPTs increased, as did the maximum rigidity with sildenafil. [18] This study suggests that a certain level of testosterone may be necessary for PDE5 inhibitors to function properly.
An occasional problem achieving an erection is nothing to worry about. But failure to do so more than 50% of the time at any age may indicate a condition that needs treatment. About 40% of men in their 40s report at least occasional problems getting and maintaining erections. So do more than half (52%) of men aged 40 to 70, and about 70% of men in their 70s.
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.

In Australia, where it is illegal for drug makers to advertise directly to consumers—as it is everywhere except the United States and New Zealand— Dr. Vitry told me via e-mail that the country's FDA-like regulatory body, Medicines Australia, fined Bayer a minuscule, but symbolic, 10,000 Australian dollars for breaching MA's code of conduct in its TRT disease-awareness campaign. Although Bayer implied that low testosterone was the most prevalent cause of the symptoms described, and that there was a high incidence of low T, Vitry said Medicines Australia didn't nail Bayer for illegal direct-to-consumer advertising because its campaign "did not encourage patients to seek a prescription for a specific testosterone product."


Another study compared the response of surgically and medically castrated rabbits to vardenafil with that of control rabbits. [22] Castrated rabbits did not respond to vardenafil, whereas noncastrated rabbits did respond appropriately. This result suggests that a minimum amount of testosterone is necessary for PDE5 inhibitors to produce an erection.
In the hepatic 17-ketosteroid pathway of testosterone metabolism, testosterone is converted in the liver by 5α-reductase and 5β-reductase into 5α-DHT and the inactive 5β-DHT, respectively.[1][147] Then, 5α-DHT and 5β-DHT are converted by 3α-HSD into 3α-androstanediol and 3α-etiocholanediol, respectively.[1][147] Subsequently, 3α-androstanediol and 3α-etiocholanediol are converted by 17β-HSD into androsterone and etiocholanolone, which is followed by their conjugation and excretion.[1][147] 3β-Androstanediol and 3β-etiocholanediol can also be formed in this pathway when 5α-DHT and 5β-DHT are acted upon by 3β-HSD instead of 3α-HSD, respectively, and they can then be transformed into epiandrosterone and epietiocholanolone, respectively.[149][150] A small portion of approximately 3% of testosterone is reversibly converted in the liver into androstenedione by 17β-HSD.[148]
Androgens may modulate the physiology of vaginal tissue and contribute to female genital sexual arousal.[48] Women's level of testosterone is higher when measured pre-intercourse vs pre-cuddling, as well as post-intercourse vs post-cuddling.[49] There is a time lag effect when testosterone is administered, on genital arousal in women. In addition, a continuous increase in vaginal sexual arousal may result in higher genital sensations and sexual appetitive behaviors.[50]

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