Many young men with erectile dysfunction wrongly assume that low testosterone must be to blame. This is highly unlikely as very little testosterone is need to achieve an erection, many ED studies show no correlation with testosterone, and T supplementation is only effective in severely hypogonadal patients.
Plasma testosterone levels of sexually functional and dysfunctional men.
Arch Sex Behav. 1980 Oct;9(5):355-66.
Schwartz MF, Kolodny RC, Masters WH.
Abstract
Plasma testosterone levels in a group of 341 men with sexual dysfunction were compared to those in 199 men with normal sexual function. All subjects were participants in a 2-week intensive conjoint sex therapy program at the Masters & Johnson Institute. Testosterone determinations were made using radioimmunoassay methods after column chromatography; all blood samples were obtained on the second day of therapy between 8:00 and 9:00 a.m. after an overnight fast. Circulating levels of testosterone in men with normal sexual function (mean 635 ng/dl) were not significantly different from testosterone values in sexually dysfunctional men (mean 629 ng/dl). However, men with primary impotence (N = 13) had significantly higher testosterone levels than men with secondary impotence (N = 180), with mean levels of 710 and 574 ng/dl, respectively (p < 0.001). The mean testosterone level for men with ejaculatory imcompetence was 660 ng/dl (N = 15), while for men with premature ejaculation the mean was 622 ng/dl (N = 91). Plasma testosterone concentrations were not related to therapy outcome but were correlated negatively with age of patients.
Pituitary gonadal system function in patients with erectile impotence and premature ejaculation.
Arch Sex Behav. 1979 Jan;8(1):41-8.
Pirke KM, Kockott G, Aldenhoff J, Besinger U, Feil W.
Abstract
The pituitary testicular system was studied in men with psychogenic impotence. Eight patients with primary erectile impotence age 22–36 years, eight men with secondary erectile impotence age 29–55 years, and 16 men with premature ejaculation age 23–43 years were studied. The last group was further divided into two subgroups: E1 (n = 7) patients without and E2 (n = 9) patients with anxiety and avoidance behavior toward coital activity. Sixteen normal adult men age 21–44 served as a control group. Diagnosis was made after psychiatric and physical examinations. Patients complaining primarily of loss of libido were not considered in the study. Ten consecutive blood samples were obtained over a period of 3 hr from each patient. Luteinizing hormone (LH), total testosterone, and free (not protein-bound) testosterone were measured. Statistical analysis revealed no significant differences between patients and normal controls.
Plasma testosterone and testosterone binding affinities in men with impotence, oligospermia, azoospermia, and hypogonadism.
Br Med J. 1974 Mar 2;1(5904):349-51.
Abstract
Mean plasma testosterone levels (+/- S.D.), using Sephadex LH-20 and competitive protein binding, were 629 +/- 160 ng/100 ml for a group of 27 normal adult men, 650 +/- 205 ng/100 ml for 27 impotent men with normal secondary sex characteristics, 644 +/- 178 ng/100 ml for 20 men with oligospermia, and 563 +/- 125 ng/100 ml for 16 azoospermic men. None of these values differ significantly. For 21 men with clinical evidence of hypogonadism the mean plasma testosterone (+/- S.D.), at 177 +/- 122 ng/100 ml, differed significantly (P < 0.001) from that of the normal men.The mean testosterone binding affinities (as measured by the reciprocal of the quantity of plasma needed to bind 50% of (3)H-testosterone tracer) were similar for normal, impotent, and oligospermic men. Though lower for azoospermic men the difference was not significant (P >0.1). For 12 of the 16 hypogonadal males the testosterone binding affinity was normal, but raised binding affinities, similar to those found in normal adult females or prepubertal boys (about twice normal adult male levels), were found in four cases of delayed puberty. These findings help to explain why androgen therapy is usually useless in the treatment of impotence.
Does testosterone have a role in erectile function?
Am J Med. 2006 May;119(5):373-82.
PURPOSE:
Despite the well-established role of testosterone in enhancing libido, its exact contribution to erections in men remains unclear. The main objectives of this review are to clarify the role of testosterone in erectile function and evaluate its therapeutic value in men with erectile dysfunction (ED).
METHODS:
Review of the relevant literature (English, French, and Spanish) from 1939 to June 2005 was conducted using data sources from MEDLINE, endocrinology text books, and hand searching of cross-references from original articles and reviews. Clinical trials, animal studies, case reports, reviews, and guidelines of major associations were included.
RESULTS:
Animal and preliminary human studies suggest that testosterone may facilitate erection by acting as vasodilator of the penile arterioles and cavernous sinusoids. Following castration, most, but not all, men had partial or complete loss of erection. Hypogonadism is not a common finding in ED, occurring in about 5% of cases, and in general, there is lack of association between serum testosterone levels, when present in normal or moderately low levels, and erectile function.
Most trials using testosterone for treatment of ED in hypogonadal men suffer from methodological problems and report inconsistent results, but overall, suggest that testosterone may be superior to placebo. Erectile function is more likely to improve with testosterone therapy in patients with severe degrees of hypogonadism.
Testosterone treatment may ameliorate the response to the phosphodiesterase 5 (PDE5) inhibitors in hypogonadal men and men with low-normal serum testosterone. Repeated measurement of morning serum total testosterone is a fairly accurate and easy method to evaluate androgenecity, but measurement of free or bioavailable testosterone is recommended in conditions that alter the levels of sex-hormone-binding globulin (SHBG), such as in the elderly and in obesity.
CONCLUSIONS:
Available data suggest that in most men circulating levels of testosterone, well below the normal range, are essential for normal erection and that higher levels of serum testosterone may not have major impact on erectile function. Screening for hypogonadism in all men with ED is necessary to identify cases of severe hypogonadism and some cases of mild to moderate hypogonadism, who may benefit from testosterone treatment.
Significance of hypogonadism in erectile dysfunction.
World J Urol. 2006 Dec;24(6):657-67.
Abstract
To review the role and significance of hypogonadism, defined as a low testosterone (T) level, in erectile dysfunction (ED). Review of literature.
Serum T is below 3 ng/ml in 12% of ED patients, including 4% before and 15% after the age of 50. Replacement studies in men with severe hypogonadism demonstrate that sexual desire and arousal, as well as the frequency of sexual activity and spontaneous erections are clearly T-dependant. Psychic erections are partly T-dependant. The effects of T upon sexual function are dose-dependant up to a threshold level that is consistent within an individual, but markedly variable between individuals, ranging from 2 to 4.5 ng/ml. More evidence is required to confirm a significant impact of T on the intrapenile vascular mechanisms of erections in men as it is the case in animals.
No convincing association of T with ED has been found in epidemiological studies. As concerns clinical experience, although a meta-analysis of the randomized controlled trials established that T therapy consistently restores erectile function in young hypogonadal patients with T below 3.46 ng/ml, the effects of this treatment have been mostly disappointing when used alone in older patients consulting for ED who are subsequently diagnosed to have hypogonadism following routine T measurement. These poor results may probably be explained by the high prevalence of co-morbidities, and by the fact that ED itself may induce hypogonadism.
Combination therapy with T and PDE5 inhibitor (PDE5I) may be effective in the hypogonadal ED patients when T therapy alone fails. However, more evidence is required to confirm the hypothesis that a minimum level of T is required for a complete effect of PDE5I in certain men, since a PDE5I was able to restore complete erections in severely hypogonadal men. Though a low T level is not always the only cause of ED in hypogonadal ED patients, there are important benefits in screening for hypogonadism in ED. A low T level justifies a 3 month trial of T therapy, before combining a PDE5I if T therapy alone fails.
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