Testosterone was first used as a clinical drug as early as 1937, but with little understanding of its mechanisms. The hormone is now widely prescribed to men whose bodies naturally produce low levels. But the levels at which testosterone deficiency become medically relevant still aren’t well understood. Normal testosterone production varies widely in men, so it’s difficult to know what levels have medical significance. The hormone’s mechanisms of action are also unclear.
Alcohol is a depressant, not an aphrodisiac or a libido enhancer. Excessive consumption can interfere with the ability to achieve an erection at any age, and even occasional drinking can make erectile dysfunction worse in older men. Feloney advises using alcohol in moderation: "In small amounts, alcohol can relieve anxiety and may help with erectile dysfunction, but if you drink too much, it can cause erectile dysfunction or make the problem worse."
Professional-athlete-turned-biohacker Maximilian Gotzler gave a speech about boosting testosterone at the 2015 Bulletproof Conference. He started by leading the room through the Haka, a Maori war dance that New Zealand’s pro rugby team has made popular. The Pasadena Conference Center trembled as over 100 people shouted and stomped in unison. It was awesome.
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.
It may also become a treatment for anemia, bone density and strength problems. In a 2017 study published in the journal of the American Medical Association (JAMA), testosterone treatments corrected anemia in older men with low testosterone levels better than a placebo. Another 2017 study published in JAMA found that older men with low testosterone had increased bone strength and density after treatment when compared with a placebo. 
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.
According to a review of all randomized controlled trials evaluating sildenafil by the American Urological Association (AUA) Consensus Panel on Erectile Dysfunction, 36% to 76% of patients receiving the drug were "able to achieve intercourse" during treatment. For tadalafil, four randomized controlled trials revealed that 11% to 47% of patients were "able to achieve intercourse." Similar efficacy has been observed with vardenafil, although studies are fewer.19 A meta-analysis published in 2013 clearly demonstrated increased efficacy over placebo for all PDE5 inhibitors.24 Head-to-head comparison suggested that tadalafil outperforms sildenafil on validated measures of erectile dysfunction, including the international index of erectile function and sexual encounter profile-2 and -3.
There is a dirty little secret about testosterone cream that almost no one knows, and I’m going to share it here. Please don’t abuse it. If you take a vanishingly small dose of testosterone cream and apply it to your labia and the vulva (or your partner’s), you will witness a form of vasodilation rarely seen no matter how good you are in bed. It has a profound local effect and will produce a night you won’t forget for years.
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.
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]
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."
The development of an erection is a complex event involving integration of psychologic, neurologic, endocrine, vascular, and local anatomic systems. Positron emission tomography scanning studies have suggested that sexual arousal is activated in higher cortical centers that then stimulate the medial preoptic and paraventricular nuclei of the hypothalamus.5 These signals ultimately descend through a complex neural network involving the parasympathetic nervous system and eventually activate parasympathetic nerves in the sacral area (S2 to S4).

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.


Patients at high cardiovascular risk should not be treated for ED until their cardiac condition is stabilize. These conditions include unstable or refractory angina, myocardial infarction or cerebrovascular accident within the past 2 weeks, uncontrolled hypertension, New York Heart Association (NYHA) Functional Classification III-IV congestive heart failure, high-risk arrhythmias, hypertrophic obstructive cardiomyopathies, and moderate-to-severe valvular disease.25 This class of drugs is also contraindicated in patients who use nitroglycerin or nitrate-containing compounds.26, 27
The amount of testosterone synthesized is regulated by the hypothalamic–pituitary–testicular axis (see figure to the right).[125] When testosterone levels are low, gonadotropin-releasing hormone (GnRH) is released by the hypothalamus, which in turn stimulates the pituitary gland to release FSH and LH. These latter two hormones stimulate the testis to synthesize testosterone. Finally, increasing levels of testosterone through a negative feedback loop act on the hypothalamus and pituitary to inhibit the release of GnRH and FSH/LH, respectively.

The vascular processes that produce an erection are controlled by the nervous system and certain prescription medications may have the side effect of interfering with necessary nerve signals. Among the possible culprits are a variety of stimulants, sedatives, diuretics, antihistamines, and drugs to treat high blood pressure, cancer, or depression. But never stop a medication unless your doctor tells you to. In addition, alcohol, tobacco, and illegal drugs, such as marijuana, may contribute to the dysfunction.
Cross-sectional studies conducted at the time of diagnosis of BPH have failed to show consistent differences in testosterone levels between patients and controls. A prospective study also failed to demonstrate a correlation between testosterone and the development of BPH (Gann et al 1995). Clinical trials have shown that testosterone treatment of hypogonadal men does cause growth of the prostate, but only to the size seen in normal men, and also causes a small increase in prostate specific antigen (PSA) within the normal range (Rhoden and Morgentaler 2005). Despite growth of the prostate a number of studies have failed to detect any adverse effects on symptoms of urinary obstruction or physiological measurements such as flow rates and residual volumes (Snyder et al 1999; Kenny et al 2000, 2001). Despite the lack of evidence linking symptoms of BPH to testosterone treatment, it remains important to monitor for any new or deteriorating problems when commencing patients on testosterone treatment, as the small growth of prostate tissue may adversely affect a certain subset of individuals.

He said it's also important to point out there may be different thresholds for different people. "One man might get low libido at 325 milligrams per deciliter, while another might not get low libido until 450," he said. As for doctors who say that every man of a certain age will benefit from TRT, Dr. Swerdloff said, "It should not be treatment based on age. It should be treatment based on the best available laboratory and clinical data. Those patients who don't meet the criteria for treatment should not be treated unless there is some logical reason why they are outliers from the usual type of pattern."


In a randomized double-blind, parallel, placebo-controlled trial, sildenafil plus testosterone was not superior to sildenafil plus placebo in improving erectile function in men with ED and low testosterone levels. [19] The objective of the study was to determine whether the addition of testosterone to sildenafil therapy improves erectile response in men with ED and low testosterone levels.
Osteoporosis refers to pathological loss of bone density and strength. It is an important condition due to its prevalence and association with bone fractures; most commonly of the hip, vertebra and forearm. Men are relatively protected from the development of osteoporosis by a higher peak bone mass compared with women (Campion and Maricic 2003). Furthermore, women lose bone at an accelerated rate immediately following the menopause. Nevertheless, men start to lose bone mass during early adult life and experience an increase in the rate of bone loss with age (Scopacasa et al 2002). Women of a given age have a higher prevalence of osteoporosis in comparison to men but the prevalence increases with age in both sexes. As a result, men have a lower incidence of osteoporotic fractures than women of a given age but the gap between the sexes narrows with advancing age (Chang et al 2004) and there is evidence that hip fractures in men are associated with greater mortality than in women (Campion and Maricic 2003).
Testosterone is a sex hormone that plays important roles in the body. In men, it’s thought to regulate sex drive (libido), bone mass, fat distribution, muscle mass and strength, and the production of red blood cells and sperm. A small amount of circulating testosterone is converted to estradiol, a form of estrogen. As men age, they often make less testosterone, and so they produce less estradiol as well. Thus, changes often attributed to testosterone deficiency might be partly or entirely due to the accompanying decline in estradiol.

More can be learned from a large, randomized, placebo-controlled trial of finasteride treatment in 18,800 men aged 55 or more. Finasteride is a 5α-reductase inhibitor which acts to prevent the metabolism of testosterone to dihydrotestosterone (DHT) – the most active androgen in the prostate. The trial showed a greater overall incidence of prostate cancer in the control group, but men treated with finasteride were more likely to have high grade tumors (Thompson et al 2003), suggesting that reduced androgen exposure of the prostate may delay the presentation of prostate cancer and/or promote advanced disease in some other way.

Epidemiological studies have also assessed links between serum testosterone and non-coronary atherosclerosis. A study of over 1000 people aged 55 years and over found an inverse correlation between serum total and bioavailable testosterone and the amount of aortic atherosclerosis in men, as assessed by radiological methods (Hak et al 2002). Increased intima-media thickness (IMT) is an early sign of atherosclerosis and has also been shown to predict cardiovascular mortality (Murakami et al 2005). Cross-sectional studies have found that testosterone levels are negatively correlated with carotid IMT in independently living men aged 74–93 years (van den Beld et al 2003), diabetic men (Fukui et al 2003) and young obese men (De Pergola et al 2003). A 4-year follow up study of the latter population showed that free testosterone was also inversely correlated with the rate of increase of IMT (Muller et al 2004).
Do erectile dysfunction exercises help? Many people have erectile dysfunction (ED), but it is often possible to reverse this with exercises to strengthen muscles in the area. These include pelvic floor exercises. ED can often be due to lifestyle factors including obesity and low physical activity levels. Learn more about exercises for ED here. Read now
Interestingly, the Belgian company Solvay, acquired for €4.5 billion in 2010 by American pharmaceutical giant Abbott, didn't put its own or its product's name on the website. As AdWeek pointed out when the campaign launched, "One of the advantages of taking the unbranded route for Androgel is that the company does not have to warn consumers quite so prominently about Androgel's side effects."

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. 

Diabetes is an example of an endocrine disease that can cause a person to experience impotence. Diabetes affects the body’s ability to utilize the hormone insulin. One of the side effects associated with chronic diabetes is nerve damage. This affects penis sensations. Other complications associated with diabetes are impaired blood flow and hormone levels. Both of these factors can contribute to impotence.
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Treatment depends on the underlying cause. In general, exercise, particularly of the aerobic type, is effective for preventing ED during midlife. Exercise as a treatment is under investigation.[22]:6, 18–19 For tobacco smokers, cessation often results in a significant improvement.[23] Oral pharmacotherapy and vacuum erection devices are first-line treatments,[22]:20, 24 followed by injections of drugs into the penis, as well as penile implants.[22]:25–26 Vascular reconstructive surgeries are beneficial in certain groups.[24]

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.
ED can also occur among younger men. A 2013 study found that one in four men seeking their first treatment for ED were under the age of 40. The researchers found a stronger correlation between smoking and illicit drug use and ED in men under 40 than among older men. That suggests that lifestyle choices may be a main contributing factor for ED in younger men.
More can be learned from a large, randomized, placebo-controlled trial of finasteride treatment in 18,800 men aged 55 or more. Finasteride is a 5α-reductase inhibitor which acts to prevent the metabolism of testosterone to dihydrotestosterone (DHT) – the most active androgen in the prostate. The trial showed a greater overall incidence of prostate cancer in the control group, but men treated with finasteride were more likely to have high grade tumors (Thompson et al 2003), suggesting that reduced androgen exposure of the prostate may delay the presentation of prostate cancer and/or promote advanced disease in some other way.
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.

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."

TT may help you but it may have adverse (harmful) results. (See discussion of these side effects below.) The Federal Drug Administration (FDA) has said that testosterone drug labels should state that there is a risk for heart disease and stroke for some men using testosterone products. All men should be checked for heart disease and stroke before, and periodically while on, TT. The AUA however, on careful review of evidence-based peer review literature, has stated that there is no strong evidence that TT either increases or decreases the risk of cardiovascular events.


If you have symptoms of ED, it’s important to check with your doctor before trying any treatments on your own. This is because ED can be a sign of other health problems. For instance, heart disease or high cholesterol could cause ED symptoms. With a diagnosis, your doctor could recommend a number of steps that would likely improve both your heart health and your ED. These steps include lowering your cholesterol, reducing your weight, or taking medications to unclog your blood vessels.
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.
Hormone deficiency or hypogonadism, whether primary or secondary, has been thought to impact erectile function. Approximately a third of men in the European Male Aging Study demonstrated low testosterone, suggesting that hypogonadism is overrepresented among men with ED.11 Hormone deficiency, however, is less frequently the cause of ED than diabetes or vascular disease. Many entities with a strong relationship to ED also diminish bioavailable testosterone, including obesity, diabetes, and opioid use. Other hormones involved in testosterone metabolism or availability, like thyroid stimulating hormone and gonadotropins, also may impact erectile quality, presumably through regulating bioavailable testosterone. Understanding the relationship between testosterone and ED has been impaired by a lack of standardized measurement of this hormone and the cyclic nature of its release and consumption.

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.
Findings that improvements in serum glucose, serum insulin, insulin resistance or glycemic control, in men treated with testosterone are accompanied by reduced measures of central obesity, are in line with other studies showing a specific effect of testosterone in reducing central or visceral obesity (Rebuffe-Scrive et al 1991; Marin, Holmang et al 1992). Furthermore, studies that have shown neutral effects of testosterone on glucose metabolism have not measured (Corrales et al 2004), or shown neutral effects (Lee et al 2005) (Tripathy et al 1998; Bhasin et al 2005) on central obesity. Given the known association of visceral obesity with insulin resistance, it is possible that testosterone treatment of hypogonadal men acts to improve insulin resistance and diabetes through an effect in reducing central obesity. This effect can be explained by the action of testosterone in inhibiting lipoprotein lipase and thereby reducing triglyceride uptake into adipocytes (Sorva et al 1988), an action which seems to occur preferentially in visceral fat (Marin et al 1995; Marin et al 1996). Visceral fat is thought to be more responsive to hormonal changes due to a greater concentration of androgen receptors and increased vascularity compared with subcutaneous fat (Bjorntorp 1996). Further explanation of the links between hypogonadism and obesity is offered by the hypogonadal-obesity-adipocytokine cycle hypothesis (see Figure 1). In this model, increases in body fat lead to increases in aromatase levels, in addition to insulin resistance, adverse lipid profiles and increased leptin levels. Increased action of aromatase in metabolizing testosterone to estrogen, reduces testosterone levels which induces further accumulation of visceral fat. Higher leptin levels and possibly other factors, act at the pituitary to suppress gonadotrophin release and exacerbate hypogonadism (Cohen 1999; Kapoor et al 2005). Leptin has also been shown to reduce testosterone secretion from rodent testes in vitro (Tena-Sempere et al 1999). A full review of the relationship between testosterone, insulin resistance and diabetes can be found elsewhere (Kapoor et al 2005; Jones 2007).
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.
It also had a purpose. It turns out posing in powerful stances causes your testosterone to increase within 20 minutes [13,14]. In those two studies, power posing for just a few minutes also dropped cortisol and boosted confidence. It’s a great way to start your day, or to give yourself an edge before a job interview or a big presentation. They don’t call it “warrior pose” for nothing!

Intramuscular testosterone injections were first used around fifty years ago. Commercially available preparations contain testosterone esters in an oily vehicle. Esterification is designed to retard the release of testosterone from the depot site into the blood because the half life of unmodified testosterone would be very short. For many years intramuscular preparations were the most commonly used testosterone therapy and this is still the case in some centers. Pain can occur at injection sites, but the injections are generally well tolerated and free of major side effects. Until recently, the available intramuscular injections were designed for use at a frequency of between weekly and once every four weeks. These preparations are the cheapest mode of testosterone treatment available, but often cause supraphysiological testosterone levels in the days immediately following injection and/or low trough levels prior to the next injection during which time the symptoms of hypogonadism may return (Nieschlag et al 1976). More recently, a commercial preparation of testosterone undecanoate for intramuscular injection has become available. This has a much longer half life and produces testosterone levels in the physiological range throughout each treatment cycle (Schubert et al 2004). The usual dose frequency is once every three months. This is much more convenient for patients but does not allow prompt cessation of treatment if a contraindication to testosterone develops. The most common example of this would be prostate cancer and it has therefore been suggested that shorter acting testosterone preparations should preferably used for treating older patients (Nieschlag et al 2005). Similar considerations apply to the use of subcutaneous implants which take the form of cylindrical pellets injected under the skin of the abdominal wall and steadily release testosterone to provide physiological testosterone levels for up to six months. Problems also include pellet extrusion and infection (Handelsman et al 1997).
In addition to its role as a natural hormone, testosterone is used as a medication, for instance in the treatment of low testosterone levels in men and breast cancer in women.[10] Since testosterone levels decrease as men age, testosterone is sometimes used in older men to counteract this deficiency. It is also used illicitly to enhance physique and performance, for instance in athletes.

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]
In non-human primates, it may be that testosterone in puberty stimulates sexual arousal, which allows the primate to increasingly seek out sexual experiences with females and thus creates a sexual preference for females.[39] Some research has also indicated that if testosterone is eliminated in an adult male human or other adult male primate's system, its sexual motivation decreases, but there is no corresponding decrease in ability to engage in sexual activity (mounting, ejaculating, etc.).[39]
Dr. Wyne told me that although she has seen an increase in male patients asking about low testosterone, she hasn't seen an actual increase in the condition itself. "I do see an increase in guys who are fatter," she said. "The question is whether, if you lose 15 or 20 pounds, your testosterone would revert [to normal]. We know that even 15 pounds makes a huge difference to their level. Most of these guys actually have 50 pounds to lose."

Low testosterone levels may contribute to decreased sex drive, erectile dysfunction, fragile bones, and other health issues. Having low testosterone levels may also indicate an underlying medical condition. See your doctor if you suspect you have low testosterone. A simple blood test is all it takes to check if your testosterone falls within the normal range.
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