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]
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An international consensus document was recently published and provides guidance on the diagnosis, treatment and monitoring of late-onset hypogonadism (LOH) in men. The diagnosis of LOH requires biochemical and clinical components. Controversy in defining the clinical syndrome continues due to the high prevalence of hypogonadal symptoms in the aging male population and the non-specific nature of these symptoms. Further controversy surrounds setting a lower limit of normal testosterone, the limitations of the commonly available total testosterone result in assessing some patients and the unavailability of reliable measures of bioavailable or free testosterone for general clinical use. As with any clinical intervention testosterone treatment should be judged on a balance of risk versus benefit. The traditional benefits of testosterone on sexual function, mood, strength and quality of life remain the primary goals of treatment but possible beneficial effects on other parameters such as bone density, obesity, insulin resistance and angina are emerging and will be reviewed. Potential concerns regarding the effects of testosterone on prostate disease, aggression and polycythaemia will also be addressed. The options available for treatment have increased in recent years with the availability of a number of testosterone preparations which can reliably produce physiological serum concentrations.
In a recent study of male workers, men with low testosterone levels had an increased chance of severe erectile dysfunction (Kratzik et al 2005), although such a link had not been found previously (Rhoden et al 2002). Certainly erectile dysfunction is considered part of the clinical syndrome of hypogonadism, and questions regarding erectile dysfunction form part of the clinical assessment of patients with hypogonadism (Morley et al 2000; Moore 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
In a prospective, multicenter, single-armed study of ED patients who exhibited a suboptimal response to PDE5 inhibitors, the investigators found that percutaneous implantation of zotarolimus-eluting stents in focal atherosclerotic lesions was both safe and feasible and was associated with clinically meaningful improvement on subjective and objective measures of erectile function. [3]
When females have a higher baseline level of testosterone, they have higher increases in sexual arousal levels but smaller increases in testosterone, indicating a ceiling effect on testosterone levels in females. Sexual thoughts also change the level of testosterone but not level of cortisol in the female body, and hormonal contraceptives may affect the variation in testosterone response to sexual thoughts.[51]

For people who are worried about low or high testosterone, a doctor may perform a blood test to measure the amount of the hormone in the patient's blood. When doctors find low-T, they may prescribe testosterone therapy, in which the patient takes an artificial version of the hormone. This is available in the following forms: a gel to be applied to the upper arms, shoulders or abdomen daily; a skin patch put on the body or scrotum twice a day; a solution applied to the armpit; injections every two or three weeks; a patch put on the gums twice a day; or implants that last four to six months.


^ Jump up to: a b Lazaridis I, Charalampopoulos I, Alexaki VI, Avlonitis N, Pediaditakis I, Efstathopoulos P, Calogeropoulou T, Castanas E, Gravanis A (2011). "Neurosteroid dehydroepiandrosterone interacts with nerve growth factor (NGF) receptors, preventing neuronal apoptosis". PLoS Biol. 9 (4): e1001051. doi:10.1371/journal.pbio.1001051. PMC 3082517. PMID 21541365. 

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.
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."
Other factors leading to erectile dysfunction are diabetes mellitus, which is a well-known cause of neuropathy).[1] ED is also related to generally poor physical health, poor dietary habits, obesity, and most specifically cardiovascular disease, such as coronary artery disease and peripheral vascular disease.[1] Screening for cardiovascular risk factors, such as smoking, dyslipidemia, hypertension, and alcoholism is helpful.[1]

If you’re experiencing psychological ED, you may benefit from talk therapy. Therapy can help you manage your mental health. You’ll likely work with your therapist over several sessions, and your therapist will address things like major stress or anxiety factors, feelings around sex, or subconscious conflicts that could be affecting your sexual well-being.
This is similar to magnetic resonance imaging. Magnetic resonance angiography uses magnetic fields and radio waves to provide detailed images of the blood vessels. Doctors may inject a "contrast agent" into the person's bloodstream that causes vascular tissues to stand out against other tissues. The contrast agent provides for enhanced information regarding blood supply and vascular anomalies.
Dr. Shiel received a Bachelor of Science degree with honors from the University of Notre Dame. There he was involved in research in radiation biology and received the Huisking Scholarship. After graduating from St. Louis University School of Medicine, he completed his Internal Medicine residency and Rheumatology fellowship at the University of California, Irvine. He is board-certified in Internal Medicine and Rheumatology.
Sugar is to testosterone what kryptonite is to Superman. Eliminating sugar is probably the single most powerful way to increase your performance, in part because sugar absolutely devastates your testosterone levels (but all carbs do not, especially under heavy training.) In one study of 74 men, a 75g dose of sugar – about the equivalent of a bottle of soda – decreased serum testosterone by 25% in under an hour, and levels stayed low for at least 2 hours [7]. On top of that, 15% of the men who started with normal testosterone dipped into the hypogonadal range after they ate sugar – that’s the range in which doctors diagnose men’s testes and women’s ovaries as failing. When you do eat carbs, stick to Bulletproof ones like sweet potatoes and squash. My recommendations for types of carbs and how often to eat them are here.
Testosterone is an androgen hormone produced by the adrenal cortex, the testes (in men), and the ovaries (in women). It is often considered the primary male sex hormone. Testosterone stimulates the development of male secondary sex characteristics (like body hair and muscle growth) and is essential in the production of sperm. In women, testosterone plays a role in egg development and ovulation.
5. Medline Plus. US National Library of Medicine. NIH National Institutes of Health. Drugs that may cause impotence (updated 21 Jan 2015). http://www.nlm.nih.gov/medlineplus/ency/article/004024.htm (accessed Nov 2016). myDr myDr provides comprehensive Australian health and medical information, images and tools covering symptoms, diseases, tests, medicines and treatments, and nutrition and fitness.Related ArticlesImpotence treatmentsIf you have impotence (erectile dysfunction), the treatment your doctor recommends will depend on thErectile dysfunction: visiting your doctorFind out what questions a doctor may ask when discussing erectile dysfunction (ED, or impotenceGum disease linked to erectile dysfunctionAdvanced gum disease (periodontitis) has been linked to an increased risk of erectile dysfunction, wPeyronie's diseasePeyronie’s disease is condition where a band of scar tissue forms in the penis, causing aAdvertisement
The other component of that study is that the subjects ate much less saturated fat. Saturated fats are common in meat, butter, and coconut products, and they’re crucial for your body to function. Saturated fats keep the integrity of your cell membranes, and if you limit carbs and/or do Bulletproof Intermittent Fasting, saturated fats become a phenomenal source of energy for your brain.
The largest amounts of testosterone (>95%) are produced by the testes in men,[2] while the adrenal glands account for most of the remainder. Testosterone is also synthesized in far smaller total quantities in women by the adrenal glands, thecal cells of the ovaries, and, during pregnancy, by the placenta.[122] In the testes, testosterone is produced by the Leydig cells.[123] The male generative glands also contain Sertoli cells, which require testosterone for spermatogenesis. Like most hormones, testosterone is supplied to target tissues in the blood where much of it is transported bound to a specific plasma protein, sex hormone-binding globulin (SHBG).
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.
Testosterone is the principle sex hormone responsible for the development of reproductive function in male vertebrates. Testosterone is one of the hormones referred to as androgens, which are also known of as anabolic steroids. As a steroid hormone, testosterone is derived from cholesterol and the structure of this hormone is similar across all mammals, reptiles, birds and fish.
5. Medline Plus. US National Library of Medicine. NIH National Institutes of Health. Drugs that may cause impotence (updated 21 Jan 2015). http://www.nlm.nih.gov/medlineplus/ency/article/004024.htm (accessed Nov 2016). myDr myDr provides comprehensive Australian health and medical information, images and tools covering symptoms, diseases, tests, medicines and treatments, and nutrition and fitness.Related ArticlesImpotence treatmentsIf you have impotence (erectile dysfunction), the treatment your doctor recommends will depend on thErectile dysfunction: visiting your doctorFind out what questions a doctor may ask when discussing erectile dysfunction (ED, or impotenceGum disease linked to erectile dysfunctionAdvanced gum disease (periodontitis) has been linked to an increased risk of erectile dysfunction, wPeyronie's diseasePeyronie’s disease is condition where a band of scar tissue forms in the penis, causing aAdvertisement
The hypogonadal-obesity-adipocytokine cycle hypothesis. Adipose tissue contains the enzyme aromatase which metabolises testosterone to oestrogen. This results in reduced testosterone levels, which increase the action of lipoprotein lipase and increase fat mass, thus increasing aromatisation of testosterone and completing the cycle. Visceral fat also promotes lower testosterone levels by reducing pituitary LH pulse amplitude via leptin and/or other factors. In vitro studies have shown that leptin also inhibits testosterone production directly at the testes. Visceral adiposity could also provide the link between testosterone and insulin resistance (Jones 2007).
Even before the study yields its findings, Dr. Swerdloff said a few important points should be emphasized. "I want to make it clear that this is not a made-up disease," he said. "It is well known in younger men that if you have a failure to produce normal testosterone, there are certain signs and symptoms that create a kind of syndrome. Treatment for low testosterone has been documented to be beneficial."

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.
Some men report being helped by an oral medication called yohimbine, which comes from the bark of a tree that grows in India and Africa. This drug, which needs to be taken every day, has been reported to help about 20 to 25 percent of the men taking it. A relatively new but widely used oral medication called Viagra requires a careful medical evaluation by your doctor.
Hypogonadism is a disease in which the body is unable to produce normal amounts of testosterone due to a problem with the testicles or with the pituitary gland that controls the testicles. Testosterone replacement therapy can improve the signs and symptoms of low testosterone in these men. Doctors may prescribe testosterone as injections, pellets, patches or gels.

Look, ED can have many causes. Most of the time, it’s physiological. But there are also lots of psychological reasons why someone may experience ED. Treating ED isn’t all about medication. Dealing with some of these psychological issues can help you battle ED, too. I’m talking about depression, anxiety, loss of desire, sense of inadequacy, guilt, fatigue, anger, relationship dysfunction. Working through these types of psychological challenges can help you achieve the happy, healthy manhood you deserve.

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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).

Other factors leading to erectile dysfunction are diabetes mellitus, which is a well-known cause of neuropathy).[1] ED is also related to generally poor physical health, poor dietary habits, obesity, and most specifically cardiovascular disease, such as coronary artery disease and peripheral vascular disease.[1] Screening for cardiovascular risk factors, such as smoking, dyslipidemia, hypertension, and alcoholism is helpful.[1] 

Cosgrove et al reported a higher rate of sexual dysfunction in veterans with posttraumatic stress disorder (PTSD) than in veterans who did not develop this problem. [42] The domains on the International Index of Erectile Function (IIEF) questionnaire that demonstrated the most change included overall sexual satisfaction and erectile function. [43, 44] Men with PTSD should be evaluated and treated if they have sexual dysfunction.

Several treatments were promoted in the pre-PGE1, pre-prostaglandin era, including yohimbine, trazodone, testosterone, and various herbal remedies. None of these is currently recommended under the updated American Urological Association Guidelines for the Treatment of Erectile Dysfunction.15 Testosterone supplementation is only recommended for men with low testosterone levels.

Several treatments were promoted in the pre-PGE1, pre-prostaglandin era, including yohimbine, trazodone, testosterone, and various herbal remedies. None of these is currently recommended under the updated American Urological Association Guidelines for the Treatment of Erectile Dysfunction.15 Testosterone supplementation is only recommended for men with low testosterone levels.

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