THIS TOOL DOES NOT PROVIDE MEDICAL ADVICE. It is intended for general informational purposes only and does not address individual circumstances. It is not a substitute for professional medical advice, diagnosis or treatment and should not be relied on to make decisions about your health. Never ignore professional medical advice in seeking treatment because of something you have read on the WebMD Site. If you think you may have a medical emergency, immediately call your doctor or dial 911. 

Erectile dysfunction (ED) is commonly called impotence. It’s a condition in which a man can’t achieve or maintain an erection during sexual performance. Symptoms may also include reduced sexual desire or libido. Your doctor is likely to diagnose you with ED if the condition lasts for more than a few weeks or months. ED affects as many as 30 million men in the United States.
ED usually has something physical behind it, particularly in older men. But psychological factors can be a factor in many cases of ED. Experts say stress, depression, poor self-esteem, and performance anxiety can short-circuit the process that leads to an erection. These factors can also make the problem worse in men whose ED stems from something physical.

Topical testosterone, specifically gels, creams and liquids, may transfer to others. Women and children are most at risk of harmful effects from contact with them. You should take care to cover the area and wash your hands well after putting on the medication. Be careful not to let the site with the topical TT touch others because that could transfer the drug.
The Organon group in the Netherlands were the first to isolate the hormone, identified in a May 1935 paper "On Crystalline Male Hormone from Testicles (Testosterone)".[177] They named the hormone testosterone, from the stems of testicle and sterol, and the suffix of ketone. The structure was worked out by Schering's Adolf Butenandt, at the Chemisches Institut of Technical University in Gdańsk.[178][179]
Studies also show a consistent negative correlation of testosterone with blood pressure (Barrett-Connor and Khaw 1988; Khaw and Barrett-Connor 1988; Svartberg, von Muhlen, Schirmer et al 2004). Data specific to the ageing male population suggests that this relationship is particularly powerful for systolic hypertension (Fogari et al 2005). Interventional trials have not found a significant effect of testosterone replacement on blood pressure (Kapoor et al 2006).
In the last few years, a lot of men and women have switched over to a pellet that goes under your skin. This is probably the best way to take testosterone now. The pellet is life-changing for both men and women (the dose for women is much lower than it is for men). Women, you won’t get bulky and grow a beard when you take testosterone to achieve normal levels, but you will probably lean out a little without losing your curves, and your energy and sex drive will be amazing. Female bodybuilders who experience weird scary side effects are taking anabolic steroids.
Treatment involves addressing the underlying causes, lifestyle modifications, and addressing psychosocial issues.[1] In many cases, a trial of pharmacological therapy with a PDE5 inhibitor, such as sildenafil, can be attempted. In some cases, treatment can involve inserting prostaglandin pellets into the urethra, injecting smooth muscle relaxants and vasodilators into the penis, a penile prosthesis, a penis pump, or vascular reconstructive surgery.[1][2] It is the most common sexual problem in men.[3]
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.
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]
THIS TOOL DOES NOT PROVIDE MEDICAL ADVICE. It is intended for general informational purposes only and does not address individual circumstances. It is not a substitute for professional medical advice, diagnosis or treatment and should not be relied on to make decisions about your health. Never ignore professional medical advice in seeking treatment because of something you have read on the WebMD Site. If you think you may have a medical emergency, immediately call your doctor or dial 911.
The brain is also affected by this sexual differentiation;[13] the enzyme aromatase converts testosterone into estradiol that is responsible for masculinization of the brain in male mice. In humans, masculinization of the fetal brain appears, by observation of gender preference in patients with congenital diseases of androgen formation or androgen receptor function, to be associated with functional androgen receptors.[95]
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]
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]
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.

Recently, a panel with cooperation from international andrology and urology societies, published specific recommendations with regard to the diagnosis of Late-onset Hypogonadism (Nieschlag et al 2005). These are summarized in the following text. It is advised that at least two serum testosterone measurements, taken before 11 am on different mornings, are necessary to confirm the diagnosis. The second sample should also include measurement of gonadotrophin and prolactin levels, which may indicate the need for further investigations for pituitary disease. Patients with serum total testosterone consistently below 8 nmol/l invariably demonstrate the clinical syndrome of hypogonadism and are likely to benefit from treatment. Patients with serum total testosterone in the range 8–12 nmol/l often have symptoms attributable to hypogonadism and it may be decided to offer either a clinical trial of testosterone treatment or to make further efforts to define serum bioavailable or free testosterone and then reconsider treatment. Patients with serum total testosterone persistently above 12 nmol/l do not have hypogonadism and symptoms are likely to be due to other disease states or ageing per se so testosterone treatment is not indicated.
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.
Testosterone may prove to be an effective treatment in female sexual arousal disorders,[52] and is available as a dermal patch. There is no FDA approved androgen preparation for the treatment of androgen insufficiency; however, it has been used off-label to treat low libido and sexual dysfunction in older women. Testosterone may be a treatment for postmenopausal women as long as they are effectively estrogenized.[52]
The aim of treatment for hypogonadism is to normalize serum testosterone levels and abolish symptoms or pathological states that are due to low testosterone levels. The exact target testosterone level is a matter of debate, but current recommendations advocate levels in the mid-lower normal adult range (Nieschlag et al 2005). Truly physiological testosterone replacement would require replication of the diurnal rhythm of serum testosterone levels, but there is no current evidence that this is beneficial (Nieschlag et al 2005).
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.
The partial synthesis in the 1930s of abundant, potent testosterone esters permitted the characterization of the hormone's effects, so that Kochakian and Murlin (1936) were able to show that testosterone raised nitrogen retention (a mechanism central to anabolism) in the dog, after which Allan Kenyon's group[183] was able to demonstrate both anabolic and androgenic effects of testosterone propionate in eunuchoidal men, boys, and women. The period of the early 1930s to the 1950s has been called "The Golden Age of Steroid Chemistry",[184] and work during this period progressed quickly. Research in this golden age proved that this newly synthesized compound—testosterone—or rather family of compounds (for many derivatives were developed from 1940 to 1960), was a potent multiplier of muscle, strength, and well-being.[185]
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.
The main surgical treatment of ED involves insertion of a penile implant (also called penile prostheses). Because penile vascular surgery is not recommended for aging males who have failed oral PDE5 inhibitors, ICI or IU therapies, implants are the next step for these patients. Although placement of a penile implant is a surgery which carries risks, they have the highest rates of success and satisfaction among ED treatment options.

Her remark was entirely destructive of poetry, since it was to the effect that poetry had nothing whatever to do with her; all her friends spent their lives in making up phrases, she said; all his feeling was an illusion, and next moment, as if to taunt him with his impotence, she had sunk into one of those dreamy states which took no account whatever of his existence.
Modern drug therapy for ED made a significant advance in 1983, when British physiologist Giles Brindley dropped his trousers and demonstrated to a shocked Urodynamics Society audience his papaverine-induced erection.[35] The drug Brindley injected into his penis was a non-specific vasodilator, an alpha-blocking agent, and the mechanism of action was clearly corporal smooth muscle relaxation. The effect that Brindley discovered established the fundamentals for the later development of specific, safe, and orally effective drug therapies.[36][better source needed][37][better source needed]
Now, there are lots of ways that you can reduce stress and anxiety in your life. One of those things you can do is exercising daily. Now, it doesn’t mean getting into a gym all the time, but it can just be doing sit-ups at home, long walks at the grocery store, bicycling, and if you can afford the gym, getting there maybe two to three days a week. But don’t forget, a healthy body equals a healthy mind. Meditation, yoga, breathing exercises– now, here’s where you can take a few moments to be centered and communicate with your inner self, peace. Healthy eating– now, taking control of the intake of what goes into your body makes you to start feeling better and looking better. That wellness is the opposite of anxiety. And treating issues and tackling things that are weighing you down, taking that very first step is liberating.

Impotence, also known as erectile dysfunction or ED, is a condition in which a man is unable to get or hold an erection long enough to have a satisfactory sex life. Impotence is a common problem, affecting up to half of Australian men between the ages of 40 and 70 years. The risk of developing erectile dysfunction increases as you get older.In the past, doctors considered impotence to be a mainly psychological problem, caused by performance anxiety or stress. Now, doctors know that many cases of impotence have a physical cause, which usually can be treated. Often, a combination of physical and psychological factors contributes to erectile dysfunction.Physical causes of impotencePhysical causes of impotence can include:problems with blood to flow into and out of the penis;damage to the nerves that send signals from the body’s central nervous system to the penis; and, more rarely,a deficiency in testosterone or other hormones.Some medicines can contribute to impotence, as can some types of surgery and radiotherapy treatments.Blocked blood vessels to the penisA very common cause of impotence is when blood flow into the penis is reduced. This can be due to atherosclerosis, also known as hardening of the arteries. In atherosclerosis, the arteries are clogged and narrowed, resulting in reduced blood flow.Risk factors for atherosclerosis include:high cholesterol;high blood pressure;obesity;sleep apnoea;diabetes; andsmoking.If your erection problems are caused by atherosclerosis, there is a chance that the arteries in other parts of your body (e.g. the coronary arteries that supply your heart) are also affected by atherosclerosis. In fact, erection problems may be the first sign that you are at risk of coronary heart disease.Because the arteries to the penis are narrower than those to the heart, you may develop symptoms of erectile dysfunction before you experience any symptoms of heart disease, such as angina. So seeing your doctor about erection problems may be important for your overall physical health.Impotence can also be caused by a blood clot that prevents enough blood from flowing into the penis to cause an erection.Venous leakageIn some men, blood can flow in to the penis easily, but the problem is that it leaks out again, so an erection cannot be sustained. This is called venous leakage. Doctors aren’t certain of the cause of venous leakage, but they can perform surgery to help repair it.Medicines that can cause impotenceMany medicines can cause erection problems as a side effect, including:diuretics (sometimes known as ‘water tablets’ - often used for high blood pressure);high blood pressure medications;cholesterol-lowering medicines (including statins);some types of antipsychotics;antidepressants;cancer treatments;some medicines used to treat heartburn and stomach ulcers;antihistamines;some pain medicines; andcertain epilepsy medications.If you experience impotence after starting a new medication, tell your doctor, who may be able to prescribe a different medicine for you. Don’t stop taking a medicine without first consulting your doctor. You should also tell your doctor about any over-the-counter medicines or complementary remedies you may be taking.The following table contains a list of specific medicines that may cause or contribute to erectile dysfunction. This list may not cover all types of medicines that can cause erectile dysfunction, so always ask your doctor if you are in doubt. Also, for some of these medicines ED is a very rare side effect. Most men taking these medicines do not experience erectile dysfunction.Medicines that may cause erectile dysfunctionType of medicineExamplesACE inhibitorscaptopril (Capoten), enalapril (Renitec), perindopril (Perindo), ramipril (Tritace), and othersAntidepressantsamitriptyline (Endep), clomipramine (Anafranil), desvenlafaxine (Pristiq), fluoxetine (Prozac), paroxetine (Aropax), sertraline (Zoloft), venlafaxine (Altven, Efexor), and othersAnti-epilepticsclonazepam (Rivotril), pregabalin (Lyrica)Antifungalsitraconazole (Sporanox)Anti-ulcer drugscimetidine (Magicul), nizatidine (Tazac), ranitidine (Zantac), and othersBeta-blockerspropranolol (Inderal), metoprolol (Betaloc, Lopresor), and othersOther blood pressure-lowering medicinesclonidine (Catapres), lercanidipine/enalapril (Zan-Extra), losartan (Cozaar), perindopril/amlodipine (Coveram), olmesartan/amlodipine (Sevikar), telmisartan/amlodipine (Twynsta), valsartan/hydrochlorothiazide (Co-Diovan)Calcium-channel blockersdiltiazem (Cardizem), felodipine (Plendil), nifedipine (Adalat)Cholesterol-lowering drugsatorvastatin (Lipitor), ezetimibe/simvastatin (Vytorin), fluvastatin (Lescol, Vastin), gemfibrozil (Ausgem), pravastatin (Pravachol), simvastatin (APO-simvastatin, Lipex, Zocor), and othersDiuretics ('water tablets')bumetanide (Burinex), chlorthalidone (Hygroton), spironolactone (Aldactone), and othersSchizophrenia drugsamisulpride (Solian, Sulprix), haloperidol (Haldol, Serenace), olanzapine (Lanzek, Ozin, Zypine, Zyprexa), paliperidone (Invega), risperidone (Rispa, Risperdal), ziprasidone (Zeldox)Combination cholesterol-lowering and anti-hypertensiveamlodipine/atorvastatin (Caduet, Cadatin)Pain medicinesfentanyl (Denpax, Durogesic), hydromorphone (Jurnista), morphine (Momex SR, MS Contin), oxycodone (OxyContin, OxyNorm, Targin), tramadolMiscellaneousoestrogens, antiandrogens, anticancer drugs and some chemotherapy treatments, baclofen (Clofen, Lioresal); cyproterone (Androcur, Cyprohexal, Cyprostat), degarelix (Firmagon), etoricoxib (Arcoxia), finasteride (Proscar and Propecia), flutamide (Flutamin), rotigotine (Neupro), triptorelin (Diphereline)*The names in brackets are just some examples of the trade names each specific medicine is marketed under in Australia. The medicine may also be known by other trade names.Diabetes and erectile dysfunctionMen who have diabetes have a higher risk of developing impotence than other men. Diabetes contributes to impotence because it can damage blood vessels and cause a type of nerve damage known as peripheral neuropathy.Hormones and impotenceLow levels of the male hormone, testosterone, are more commonly linked to a lowered sex drive, rather than impotence itself. Only a small percentage of cases of impotence are caused by hormone deficiency.Low testosterone levels may be the result of a condition called hypogonadism, in which the testicles don’t produce enough testosterone. More rarely, low testosterone can be caused by the pituitary (a small gland at the base of the brain) not secreting sufficient hormones to stimulate the testes to produce testosterone. The pituitary is also sometimes affected by small benign (non-cancerous) tumours that secrete prolactin, another hormone that can cause impotence.Mildly decreased levels of testosterone are often not due to specific testicular or pituitary problems, but rather stress or depression. In this situation, testosterone replacement is rarely of any benefit.Other hormone problems, including thyroid disease, can also cause impotence.Prostate cancer and erectile dysfunctionThe advanced stages of prostate cancer can affect the nerves and arteries that are vital for an erection.Radiation treatment for prostate cancer can harm the erectile tissues of the penis, and prostate cancer surgery can cause nerve or artery damage to the penis.Treatment for advanced prostate cancer often includes medicines that counteract testosterone, and commonly cause erectile dysfunction as well as loss of sexual interest.Peyronie’s diseasePeyronie’s disease is an uncommon condition that affects a man’s sex life because his penis curves abnormally and causes pain when he has an erection. He might also be unable to have a hard erection. The curvature of the penis is caused by a scar, called a plaque, that forms in the penis.Other physical causes of impotenceSeveral other factors and conditions can contribute to erectile dysfunction, including the following.Depression. Many men find that when they’re suffering from depression, they lose interest in sex and can’t get or keep an erection. Asking your doctor for treatments for depression may help alleviate your erection problems as well.Smoking contributes to vascular disease (disease of the blood vessels), so it can contribute to erectile dysfunction by affecting blood flow to the penis. Giving up smoking often has a beneficial effect on erectile function.Excessive alcohol use. Alcoholism can cause permanent nerve damage, resulting in impotence. This nerve damage is called peripheral neuropathy. Long-term alcohol use can impair the liver’s ability to function, resulting in a hormone imbalance in which a man has too much of the female sex hormone, oestrogen. On a day-to-day level, alcohol dulls the central nervous system, adversely affecting sexual response.Illicit drug use. Illicit drugs such as marijuana, cocaine, heroin, barbiturates, and amphetamines act on the central nervous system, impairing the body’s ability to respond sexually.Certain exercises. Nerve and artery damage can be caused by prolonged cycling, rodeo riding, or use of a rowing machine, resulting in the inability to get an erection. Often, minimising the use of hard bicycle seats and exercise machine seats, as well as correct positioning of the seat, will help restore sexual function.Surgery to organs near the nerve pathways of the penis, such as the bladder, rectum and prostate, can cause nerve or artery damage to the penis, resulting in the inability to have an erection.Injuries. Impotence can be caused by spinal cord injury; injury to your sex organs; or a pelvic fracture, which can cause damage to the nerves of the penis, or damage the blood vessels, resulting in reduced blood flow to the penis.Conditions affecting the nervous system. Multiple sclerosis (MS) and other degenerative diseases of the nervous system, such as Parkinson’s disease, can damage the nerves involved in erections.Psychological causes of impotenceMost cases of impotence have physical causes, but, in some men, psychological factors are the main contributors to impotence.Impotence that’s triggered by psychological factors is more common in men who are sexually inexperienced. Psychological erectile dysfunction may only occur when you’re with just one particular person. You’re also more likely to have morning erections, and be able to have an erection when you masturbate, than men whose impotence has a physical cause.Here are some psychological factors that can have an impact on your erections.Stress and anxietyWhen you’re stressed and focusing on other issues apart from sex, you might find that you don’t want to have sex as often and there might be a drop in your ability to perform when you do try. You might find that tackling the source of your stress can have benefits in the bedroom as well.Fear of failureAnxiety about your sexual prowess (commonly called performance anxiety) can, in itself, contribute to failure. By putting pressure on yourself, you become too anxious to get an adequate erection.Most men experience isolated episodes of erectile failure. Even when the transient physical cause has passed, anxiety that it may recur is sufficient to prevent erection. Anxiety, whether about something specifically sexual or part of a wider anxiety syndrome, is never helpful to good sexual function.Problems with your relationship and impotenceImpotence may be a manifestation of a poor relationship, or a problematic time in a relationship. Sexual boredom, tension or anger among partners, and lack of intimacy and communication are all possible triggers of erectile dysfunction. In these cases, seeing a counsellor may help.It’s worth remembering that impotence is a complex medical condition, which may have more than one cause. For example, if impotence is the result of a side effect of medicine or an underlying disease, the anxiety caused by lack of performance may perpetuate the erectile dysfunction even after the physical cause has been dealt with.Almost any chronic (ongoing) physical or mental health disorder, including those with no direct effect on penile nerves or blood supply, can have a powerful effect on sexuality, sexual self-image and erectile function.If you’re worried about your sexual response or the quality of your erections, don’t be afraid to talk to your doctor, who has access to treatments that can help. Last Reviewed: 16 December 2016


In comparison, 37% of men who had received external radiotherapy as their primary therapy reported the ability to attain functional erections suitable for intercourse, along with 43% of men who had received brachytherapy as primary treatment. Pretreatment sexual health-related quality of life score, age, serum prostate-specific antigen (PSA) level, race or ethnicity, body mass index, and intended treatment details were associated with functional erections 2 years after treatment. [45]
The FDA recommends that men follow general precautions before taking a medication for ED. Men who are taking medications that contain nitrates, such as nitroglycerin, should NOT use these medications. Taking nitrates with one of these medications can lower blood pressure too much. In addition, men who take tadalafil or vardenfil should use alpha blockers with care and only as instructed by their physician, as they could result in hypotension (abnormally low blood pressure). Experts recommend that men have a complete medical history and physical examination to determine the cause of ED. Men should tell their doctor about all the medications they are taking, including over-the-counter medications.

Dr. Wyne, in Houston, said, "When I hear a catchy little phrase, or someone is trying to get us to use a drug that is not based on clinical data, the cynical part of me asks where did it come from." She added, "There is a very important role for testosterone replacement therapy. It's wonderful that we have all these options, but we need to be using them appropriately, in a safe and efficacious manner."


early 15c., "physical weakness," also "poverty," from Middle French impotence "weakness," from Latin impotentia "lack of control or power," from impotentem (nominative impotens); see impotent. In reference to a want of (male) sexual potency, from c.1500. The figurative senses of the word in Latin were "violence, fury, unbridled passion." Related: Impotency.


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:
In accordance with sperm competition theory, testosterone levels are shown to increase as a response to previously neutral stimuli when conditioned to become sexual in male rats.[40] This reaction engages penile reflexes (such as erection and ejaculation) that aid in sperm competition when more than one male is present in mating encounters, allowing for more production of successful sperm and a higher chance of reproduction.
You should talk to your doctor about possible treatments. You may want to talk to other patients who have had the treatment planned for you. You also may want to seek a second doctor's opinion about surgery before making your decision. You may find it difficult to talk to your doctor about impotence. You will want to find a doctor who treats this condition and will help you feel comfortable talking about the problem and choosing the best treatment. You can also get more information by contacting your local National Kidney Foundation affiliate.

Many clinical studies have looked at the effect of testosterone treatment on body composition in hypogonadal men or men with borderline low testosterone levels. Some of these studies specifically examine these changes in older men (Tenover 1992; Morley et al 1993; Urban et al 1995; Sih et al 1997; Snyder et al 1999; Kenny et al 2001; Ferrando et al 2002; Steidle et al 2003; Page et al 2005). The data from studies, on patients from all age groups, are consistent in showing an increase in fat free mass and decrease in fat mass or visceral adiposity with testosterone treatment. A recent meta-analysis of 16 randomized controlled trials of testosterone treatment effects on body composition confirms this pattern (Isidori et al 2005). There have been less consistent results with regard to the effects of testosterone treatment of muscle strength. Some studies have shown an increase in muscle strength (Ferrando et al 2002; Page et al 2005) with testosterone whilst others have not (Snyder et al 1999). Within the same trial some muscle group strengths may improve whilst others do not (Ly et al 2001). It is likely that the differences are partly due to the methodological variations in assessing strength, but it also possible that testosterone has different effects on the various muscle groups. The meta-analysis found trends toward significant improvements in dominant knee and hand grip strength only (Isidori et al 2005).
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.

Before assessing the evidence of testosterone’s action in the aging male it is important to note certain methodological considerations which are common to the interpretation of any clinical trial of testosterone replacement. Many interventional trials of the effects of testosterone on human health and disease have been conducted. There is considerable heterogenicity in terms of study design and these differences have a potential to significantly affect the results seen in various studies. Gonadal status at baseline and the testosterone level produced by testosterone treatment in the study are of particular importance because the effects of altering testosterone from subphysiological to physiological levels may be different from those of altering physiological levels to supraphysiological. Another important factor is the length of treatment. Randomised controlled trials of testosterone have ranged from one to thirty-six months in duration (Isidori et al 2005) although some uncontrolled studies have lasted up to 42 months. Many effects of testosterone are thought to fully develop in the first few months of treatment but effects on bone, for example, have been shown to continue over two years or more (Snyder et al 2000; Wang, Cunningham et al 2004). 

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
Although vardenafil does not seem to produce significant clinical QT prolongation, it has been suggested that it be avoided in patients who have congenital QT prolongation abnormalities and in patients using class I antiarrhythmic drugs, such as quinidine and procainamide. It is also best to avoid the use of vardenafil with class III antiarrhythmic drugs, such as amiodarone or sotalol.

"Stress and anxiety can adversely affect sexual performance and are common causes of erectile dysfunction,” warns Feloney. “Feelings of stress and anxiety can also lead to depression and a loss of interest in sex." It's important to get these feelings out in the open where you can deal with them. Issues that can lead to erectile dysfunction include fear from previous bad experiences with sex, family or work related stress, poor communication with your partner, and unrealistic goals and expectations.
Hacking your testosterone influences everything from body composition to energy levels to mood. It’s easy to eat more butter; it’s hard to visit a doctor and get tested, but that’s what I recommend: know your levels. If you’re 25, you’ll know what your target is when you’re 35. By the time you’ve noticed symptoms of low testosterone, it’s too late to get your “normal” measurements!
Several studies accessed the prevalence of ED. The Massachusetts Male Aging Study reported a prevalence of 52%.2 The study demonstrated that ED is increasingly prevalent with age: approximately 40% of men are affected at age 40 and nearly 70% of men are affected at age 70. The prevalence of complete ED increased from 5% at age 40 to 15% at age 70.2 Age was the variable most strongly associated with ED.
Commercials do mention other potential side-effects for the male user, calling them "rare," including swollen and painful breasts, blood clots in the legs, increased risk for prostate cancer, problems breathing during sleep (sleep apnea), change in the size and shape of the testicles, and a low sperm count. But you're not supposed to focus on the details. Instead, just think of the energy you'll have. The great sex you'll have. And the muscles. It will be a veritable second adolescence as your aging body bursts into new bloom.
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.
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).
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."
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.
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
Abnormally high levels of testosterone could be the result of an adrenal gland disorder, or even cancer of the testes. High levels may also occur in less serious conditions. Congenital adrenal hyperplasia, which can affect males and females, is a rare but natural cause for elevated testosterone production. Your doctor may order other tests if your levels are exceedingly high.
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