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:
Epidemiological studies suggest that many significant clinical findings and important disease states are linked to low testosterone levels. These include osteoporosis (Campion and Maricic 2003), Alzheimer’s disease (Moffat et al 2004), frailty, obesity (Svartberg, von Muhlen, Sundsfjord et al 2004), diabetes (Barrett-Connor 1992), hypercholesterolemia (Haffner et al 1993; Van Pottelbergh et al 2003), hypertension (Phillips et al 1993), cardiac failure (Tappler and Katz 1979; Kontoleon et al 2003) and ischemic heart disease (Barrett-Connor and Khaw 1988). The extent to which testosterone deficiency is involved in the pathogenesis of these conditions, or to which testosterone supplementation could be useful in their treatment is an area of great interest with many unanswered questions.
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.
Changes in body composition are seen with aging. In general terms, aging males are prone to loss of muscle mass and a gain in fat mass, especially in the form of visceral or central fat. An epidemiological study of community dwelling men aged between 24 and 85 years has confirmed that total and free testosterone levels are inversely correlated with waist circumference and that testosterone levels are specifically related to this measure of central obesity rather than general obesity (Svartberg, von Muhlen, Sundsfjord et al 2004). Prospective studies show that testosterone levels predict future development of central obesity (Khaw and Barrett-Connor 1992; Tsai et al 2000). Reductions in free testosterone also correlate with age related declines in fat free mass (muscle mass) and muscle strength (Baumgartner et al 1999; Roy et al 2002). Studies in hypogonadal men confirm an increase in fat mass and decrease in fat free mass versus comparable eugonadal men (Katznelson et al 1998). Taken together, the epidemiological data suggest that a hypogonadal state promotes loss of muscle mass and a gain in fat mass, particularly visceral fat and therefore mimics the changes of ‘normal’ aging.

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]
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.
Mental status changes including excess aggression are a well known phenomenon in the context of anabolic steroid abuse (Perry et al 1990). An increase in self-reported aggressive behaviors have also been reported in one double blind placebo controlled trial of testosterone in young hypogonadal men (Finkelstein et al 1997), but this has not been confirmed in other studies (Skakkebaek et al 1981; O’Connor et al 2002). Aggression should therefore be monitored but in our experience is rarely a significant problem during testosterone replacement producing physiological levels.
A related issue is the potential use of testosterone as a coronary vasodilator and anti-anginal agent. Testosterone has been shown to act as a vasodilator of coronary arteries at physiological concentrations during angiography (Webb, McNeill et al 1999). Furthermore men given a testosterone injection prior to exercise testing showed improved performance, as assessed by ST changes compared to placebo (Rosano et al 1999; Webb, Adamson et al 1999). Administration of one to three months of testosterone treatment has also been shown to improve symptoms of angina and exercise test performance (Wu and Weng 1993; English et al 2000; Malkin, Pugh, Morris et al 2004). Longer term studies are underway. It is thought that testosterone improves angina due its vasodilatory action, which occurs independently of the androgen receptor, via blockade of L-type calcium channels at the cell membrane of the vascular smooth muscle in an action similar to the dihydropyridine calcium-channel blockers such as nifedipine (Hall et al 2006).
Unfortunately, some patients may have an overly simplified understanding of the role of PDE5 inhibitors in ED management. Such patients may not expect or be willing to undergo a long evaluation and testing process to obtain a better understanding of their sexual problem, and they may be less likely to involve their partner in discussing their sexual relationship with the physician. They may expect to obtain medications through a phone call to their doctor or even over the Internet, with minimal or no physician contact at all.
Men who produce more testosterone are more likely to engage in extramarital sex.[55] Testosterone levels do not rely on physical presence of a partner; testosterone levels of men engaging in same-city and long-distance relationships are similar.[54] Physical presence may be required for women who are in relationships for the testosterone–partner interaction, where same-city partnered women have lower testosterone levels than long-distance partnered women.[59]
The sexual hormone can encourage fair behavior. For the study, subjects took part in a behavioral experiment where the distribution of a real amount of money was decided. The rules allowed both fair and unfair offers. The negotiating partner could subsequently accept or decline the offer. The fairer the offer, the less probable a refusal by the negotiating partner. If no agreement was reached, neither party earned anything. Test subjects with an artificially enhanced testosterone level generally made better, fairer offers than those who received placebos, thus reducing the risk of a rejection of their offer to a minimum. Two later studies have empirically confirmed these results.[71][72][73] However men with high testosterone were significantly 27% less generous in an ultimatum game.[74] The Annual NY Academy of Sciences has also found anabolic steroid use which increase testosterone to be higher in teenagers, and this was associated with increased violence.[75] Studies have also found administered testosterone to increase verbal aggression and anger in some participants.[76]
It appears that testosterone has NOS-independent pathways as well. In one study, castrated rats were implanted with testosterone pellets and then divided into a group that received an NOS inhibitor (L-nitro-L-arginine methyl ester [L-NAME]) and a control group that received no enzyme. [24] The castrated rats that were given testosterone pellets and L-NAME still had partial erections, a result suggesting the presence of a pathway independent of NOS activity.
Dr. Fugh-Berman said these campaigns encourage men to "ask your doctor" whether their weight gain, falling asleep after dinner, reduced energy, and diminished sex drive are due to "Low T." At the same time, the companies are working other angles to influence doctors' prescribing practices through industry-sponsored continuing medical education (CME) courses and sponsored medical journal articles. They have even created a respectable-sounding journal called The Aging Male. Fugh-Berman said all these channels "are being used to persuade doctors they should be treating this."
Richard J. Wassersug, PhD, an adjunct professor of urology at the University of British Columbia, described his personal experience with androgen deprivation therapy (ADT). "If you are on ADT," he said, "and you see those Low T ads, what are you supposed to make of it? This produces a cognitive dissonance." He called the ads "hurtful" for suggesting that low testosterone makes a man less of a man.
"One of the reasons erectile dysfunction increases with age is that the diseases that lead to it also increase with age," notes Dr. Feloney. Evaluating the causes of erectile dysfunction starts with your doctor taking a good health history and giving you a physical exam. Common medical issues that can lead to erectile dysfunction include diabetes, high blood pressure, hardening of the arteries, low testosterone, and neurological disease. Talk to your doctor about better managing these health conditions.

The diagnosis of late-onset hypogonadism requires the combination of low serum testosterone levels with symptoms of hypogonadism. Questionnaires are available which check for the symptoms of hypogonadism. These have been validated for the assessment of aging patients with hypogonadism (Morley et al 2000; Moore et al 2004) but have a low specificity. In view of the overlap in symptoms between hypogonadism, aging and other medical conditions it is wise to use a formal method of symptom assessment which can be used to monitor the effects of testosterone replacement.


There are two keys to incorporating fat in your diet: getting enough fat, and getting the right kinds of it. A study from 1984 (done, no doubt, with Big Brother watching) looked at 30 healthy men who switched from eating 40% fat (much of it saturated) to 25% fat (much of it unsaturated), with more protein and carbs to make up the difference in calories. After 6 weeks, their average serum testosterone, free testosterone, and 4-androstenedione (an important hormone for testosterone synthesis) all dropped significantly [6]. I think getting 40% of your calories from fat is too little – I recommend 50-70% of calories from fat, or even more in some cases.

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.
Erectile dysfunction - (ED) or impotence is sexual dysfunction characterized by the inability to develop or maintain an erection of the penis during sexual activity. A penile erection is the hydraulic effect of blood entering and being retained in sponge-like bodies within the penis. The process is most often initiated as a result of sexual arousal, when signals are transmitted from the brain to nerves in the penis.
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.

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]
ICI Alprostadil may be used as a mixture with two other drugs to treat ED. This combination therapy called "bimix or trimix" is stronger than alprostadil alone and has become standard treatment for ED. Only the Alprostadil ingredient is FDA approved for ED. The amount of each drug used can be changed based on the severity of your ED, by an experienced health professional. You will be trained by your health professional on how to inject, how much to inject and how to safely raise the drug's dosage if necessary.
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]
"Smoking is a short- and long-term cause of erectile dysfunction," warns Feloney. "In the short-term nicotine constricts the blood vessels that you need to get an erection, and in the long-term nicotine contributes to hardening of the arteries that can cause erectile dysfunction." Some approaches for quitting include making a clean break, avoiding the triggers of smoking, trying a nicotine patch or gum, and joining a smoke cessation program.
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]
Capogrosso, P., Colicchia, M., Ventimiglia, E., Castagna, G., Clementi, M. C., Suardi, N., ... Salonia, A. (2013, July). One patient out of four with newly diagnosed erectile dysfunction is a young man — worrisome picture from the everyday clinical practice. The journal of sexual medicine. 10(7), 1833–1841. Retrieved from https://onlinelibrary.wiley.com/doi/full/10.1111/jsm.12179
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