"I am very cautious about committing someone for life to medication," said Dr. Kathleen L. Wyne, who directs research on diabetes and metabolism at Houston's Methodist Hospital Research Institute and serves on the Sex Hormone and Reproductive Endocrinology Scientific Committee for the American Association of Clinical Endocrinologists. "That does frustrate patients because they have heard about [Low T] from TV and friends."


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.
^ Butenandt A, Hanisch G (1935). "Uber die Umwandlung des Dehydroandrosterons in Androstenol-(17)-one-(3) (Testosterone); um Weg zur Darstellung des Testosterons auf Cholesterin (Vorlauf Mitteilung). [The conversion of dehydroandrosterone into androstenol-(17)-one-3 (testosterone); a method for the production of testosterone from cholesterol (preliminary communication)]". Chemische Berichte (in German). 68 (9): 1859–62. doi:10.1002/cber.19350680937.
One study examined the role of testosterone supplementation in hypogonadal men with ED. These men were considered nonresponders to sildenafil, and their erections were monitored by assessing nocturnal penile tumescence (NPT). After these men were given testosterone transdermally for 6 months, the number of NPTs increased, as did the maximum rigidity with sildenafil. [18] This study suggests that a certain level of testosterone may be necessary for PDE5 inhibitors to function properly.

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."
Stanley A Brosman, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Association for the Advancement of Science, American Association for Cancer Research, American College of Surgeons, American Medical Association, American Urological Association, Society for Basic Urologic Research, Society of Surgical Oncology, Society of Urologic Oncology, Western Section of the American Urological Association, Association of Clinical Research Professionals, American Society of Clinical Oncology, International Society of Urology, International Society of Urological Pathology
Once a complete sexual and medical history has been completed, appropriate laboratory studies should be conducted. In the initial evaluation of ED, sophisticated laboratory testing is rarely necessary. For example, serum testosterone (and sometimes prolactin) is typically only useful when the patient demonstrates hypogonadal features or testicular atrophy, or when clinical history is suggestive. Additional hormonal evaluation may include thyroid stimulating hormone in those with a clinical suspicion of hypothyroidism or appropriate diabetes screening in those presenting with a concern for impaired glucose metabolism. If the patient has not been evaluated with a lipid panel and hyperlipidemia is suspected, measurement and appropriate referral to internal medicine or cardiology is recommended. In most cases, a tentative diagnosis can be established with a complete sexual and medical history, physical examination, and limited or no laboratory testing.
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.
This evidence, together with the beneficial effects of testosterone replacement on central obesity and diabetes, raises the question whether testosterone treatment could be beneficial in preventing or treating atherosclerosis. No trial of sufficient size or duration has investigated the effect of testosterone replacement in primary or secondary prevention cardiovascular disease. The absence of such data leads us to examine the relationship of testosterone to other cardiovascular risk factors, such as adverse lipid parameters, blood pressure, endothelial dysfunction, coagulation factors, inflammatory markers and cytokines. This analysis can supply evidence of the likely effects of testosterone on overall cardiovascular risk. This has limitations, however, including the potential for diverging effects of testosterone on the various factors involved and the resultant impossibility of accurately predicting the relative impact of such changes.
Currently available testosterone preparations in common use include intramuscular injections, subcutaneous pellets, buccal tablets, transdermal gels and patches (see Table 2). Oral testosterone is not widely used. Unmodified testosterone taken orally is largely subject to first-pass metabolism by the liver. Oral doses 100 fold greater than physiological testosterone production can be given to achieve adequate serum levels. Methyl testosterone esters have been associated with hepatotoxicity. There has been some use of testosterone undecanoate, which is an esterified derivative of testosterone that is absorbed via the lymphatic system and bypasses the liver. Unfortunately, it produces unpredictable testosterone levels and increases testosterone levels for only a short period after each oral dose (Schurmeyer et al 1983).
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.
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