Sexual Medicine Society of North America, Inc.


Position Statements

The Position Statements are listed below. Please click on any of the titles below to view the statements.

The Position Statements are listed below. Please click on any of the titles below to view the statements.

Surgical and non-surgical treatments of sexual dysfunction should be standard benefits of all medical insurance programs


The Sexual Medicine Society of North America (SMSNA) believes that treatment of sexual dysfunction is an essential and necessary element of good healthcare and produces significant improvements not only in sexual function but also in overall health, work productivity and life satisfaction. SMSNA strongly supports the concept that all standard treatments for sexual dysfunction, including implantation of penile prostheses, should be covered by Medicare and other medical insurance programs.


Many good quality scientific studies clearly demonstrate the safety, efficacy and value of standard treatments of sexual dysfunction in men and women.

In general, medical insurance programs grant benefits for treatments that are medically necessary. Medically necessary services are often defined as treatments which replace, improve or restore a dysfunctional, missing or impaired body part. Examples of non-life-threatening conditions which are routinely granted medical insurance benefits are breast reconstruction after treatment for breast cancer, bariatric surgery for treatment of obesity, genital reconstructive surgery for treatment of transgender conditions and joint replacement for treatment of pain and disability due to arthropathy.

The most commonly treated sexual dysfunction is erectile dysfunction (ED). ED is not primarily a psychological problem although there are significant secondary psychological effects of ED. ED is usually a physical problem, which is very often caused by diabetes mellitus, treatments for prostate cancer, hypertension, dyslipidemia, vasculopathy, smoking and various forms of cardiovascular disease. There are several safe and effective treatments for ED due to these conditions. These treatments include oral therapy with PDE5 inhibitors, intracavernous injections, intraurethral prostaglandin, vacuum therapy and implantation of penile prostheses.

SMSNA believes that treatments for ED, as well as other forms of sexual dysfunction, fit the definition of medical necessity and should be routine benefits of medical insurance programs. Treatment of sexual dysfunction is as deserving of insurance benefits as reconstructive breast surgery, transgender reconstructive genital surgery and other conditions which compromise quality of life. SMSNA believes that it is inconsistent for medical insurance benefits to be denied for treatment of sexual dysfunction, which may have a devastating effect on quality of life but granted for breast and genital reconstruction and other dysfunctions which are not life-threatening. When ED is due to prostate cancer treatments, diabetes mellitus and other underlying conditions, SMSNA strongly supports the provision of medical insurance benefits for all standard treatments, including implantation of penile prostheses.

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SMSNA Consensus Statement and White Paper Executive Summary: Adult Onset Hypogonadism (AOH)

Click here to download the PDF version (version 1 – October 31, 2015)

In August 2015, a colloquium of experts commissioned by the Sexual Medicine Society of North America (SMSNA) convened in Washington, DC, to discuss the common clinical scenario of men who present with low testosterone (T) and associated signs and symptoms accompanied by low or normal gonadotropin levels.  This syndrome is not classical primary (testicular failure) or secondary (pituitary or hypothalamic failure) hypogonadism because low T may be the result of both testicular and pituitary-hypothalamic failure.  The Panel designated this syndrome Adult Onset Hypogonadism (AOH) because it occurs commonly in men of middle-age and older.

The Panel consisted of 17 experts in men’s health, sexual medicine, urology, endocrinology, and methodology.  All colloquium participants declared potential conflicts of interest; participants were both members and non-members in the SMSNA.  The Panel deliberated regarding a rigorous diagnostic process to document signs and symptoms of AOH, the rationale for treatment with T, and a monitoring protocol for T-treated patients.     

The SMSNA recognizes that the evaluation and management of hypogonadal syndromes have been addressed in recent publications (i.e., the Endocrine Society, Bhasin et al., 2010; the American Urological Association, Paduch et al., 2013; the International Society for Sexual Medicine, Dean et al., 2015).  The primary purpose of this document is to support health care professionals in the development of a deeper understanding of AOH, particularly in how it differs from classical primary and secondary hypogonadism, and to provide a conceptual framework to guide its diagnosis, treatment, and follow-up

Consensus statement:  AOH is a measurable syndrome characterized by low T, associated symptoms, and low or normal gonadotropin levels.  Men with AOH who are candidates for treatment with T should be counseled regarding the benefits and risks of treatment.  Patients who are treated should be monitored regularly.

Section 1: Conceptualization of AOH. 

AOH is a clinical and biochemical syndrome characterized by a deficiency of T with symptoms and signs that can be caused by testicular and/or hypothalamic-pituitary (HP) dysfunction; AOH is therefore clinically distinct from classical primary and secondary hypogonadism. This syndrome is characterized by T deficiency and the failure to mount an adequate compensatory pituitary response to low T levels; gonadotropin levels are low or in the normal range.

AOH is well-illustrated by hypogonadal men in the European Male Ageing Study (EMAS) (Tajar et al., 2010; see Figure 1).  Approximately 2.0% of men had primary hypogonadism (low T, high LH), 9.5% had “compensated” hypogonadism (normal T, high LH), and 11.8% of men were classified as having secondary hypogonadism with low T accompanied by low or normal LH – a presentation consistent with AOH.


Figure 1. Subgroups of men by gonadal status and by decade of age from the European Male Ageing Study (EMAS) (Tajar et al., 2010).

In the EMAS study, the prevalence of hypogonadism was 13.8%; of these men, 85.5% were classified as having secondary hypogonadism (Tajar et al., 2010).  Similar prevalences of secondary hypogonadism have been reported among men seeking care for sexual dysfunction (Guay et al., 2010; Maseroli et al., 2015). 

Importantly, among men with secondary hypogonadism in the EMAS sample, only 11% had a specific medical condition (e.g., genetics, surgery, radiotherapy, trauma) that could account for the hypogonadism; the etiology in the remaining 89% was unknown (Corona & Maggi, 2015). The term AOH could be applied to the overwhelming majority of these men, many of whom also had concomitant metabolic disease (i.e., obesity, type 2 diabetes, or metabolic syndrome). 

Hypogonadism prevalence in general may increase with age (e.g., the Baltimore Longitudinal Study of Aging, BLSA, Harman et al., 2001).  The prevalence may be higher among men ≥ 65 years of age although prevalence rates by decade up to age 84 have been reported as statistically indistinguishable (range 34% to 45.5%) (Mulligan et al., 2006).  Patterns are similar when symptoms are considered.  In the Massachusetts Male Aging Study (MMAS), symptomatic AD prevalence was similar for men aged 40 to 49 years (4.1%) and 50 to 59 years (4.5%) but was increased among men aged 60 to 70 years (9.4%) (Araujo et al., 2004).  In the Boston Area Community Health (BACH) study prevalence rates of symptomatic AD by decade among men aged 30 to 69 years ranged from 3.1% to 7.0% and were statistically indistinguishable; the prevalence rate for men aged 70 to 79 years, however, was 18.1% (Araujo et al., 2007).  Some studies suggest that AOH, unlike overall hypogonadism, is less likely to be influenced by age.  In the EMAS study, the prevalence of men with primary hypogonadism increased significantly with age but not among men with low T and normal LH levels – men likely to have AOH (Tajar et al., 2010).


Among healthy aging men, hypothalamic-pituitary-gonadal function may be maintained (i.e., Nieschlag et al., 1982; Yeap et al., 2009; Sartorius et al., 2012).  In a broader population of men, however, beginning at 20-30 years of age T levels decline by 0.3% to 1.4% per year (Wu et al., 2008).  It is believed that declining T levels are partly the result of primary testis failure – the Leydig cells become less responsive to exogenous gonadotropin stimulation (Rubens et al., 1974) and the number of Leydig cells declines (Neaves et al., 1984).      

The relationship between secondary hypogonadism and aging is complex.   Production of GnRH decreases with age and GnRH/LH pulse amplitude diminishes (Araujo et al., 2011; Takahashi et al., 2005).  In addition, androgen negative feedback suppression of LH secretion may be increased (Winters & Atkinson, 1997).  Sex hormone binding globulin (SHBG) levels tend to rise in older men, causing free T levels to decline (Feldman et al., 2002).  T levels are higher in the morning than in the evening and there is a dampening of this diurnal rhythm as men grow older (Zumoff et al., 1982).

Section 2:  AOH and Common Comorbidities

AOH more often occurs in men who have chronic disease states that are more common as men age, making it difficult to separate the influence of comorbidities from the influence of aging.  High BMI, central adiposity, and the metabolic syndrome are associated with low serum total T and low free T levels (Wang et al., 2011; Allan & McLachlan, 2010; MacDonald et al., 2010; Brand et al., 2011; Laaksonen et al., 2004, 2005).  Low total and free T levels are associated with an increased risk of developing metabolic syndrome, independent of age and obesity (Wang et al., 2011; Allan & McLachlan, 2010; MacDonald et al., 2010; Brand et al., 2011).  In the EMAS study, BMI was significantly associated with risk for secondary hypogonadism and the risk for secondary hypogonadism increased as a man’s number of comorbidities increased (Tajar et al., 2010). 

Section 3: Clinical Signs and Symptoms of AOH

AOH is often overlooked because hypogonadal men ignore their symptoms (Dandona & Rosenberg, 2010).  T influences all the steps of the male sexual response; sexual dysfunctions are a prominent symptom of AOH and are often the presenting symptom. These symptoms may include: hypoactive sexual desire (HSD), reduced nocturnal and morning erections, reduced sex-induced erections, delayed ejaculation and reduced semen volume (Buvat et al., 2013; Mulligan et al., 2006).  The Endocrine Society and the American Association of Clinical Endocrinologists (AACE) suggest that physicians should measure the T levels of men with any of the symptoms and signs in Table 1.

Table 1:  Conditions in which serum T measurement is suggested

(adapted from Bhasin et al., 2010)


Osteoporosis, low trauma fracture

Type 2 diabetes

Glucocorticoids, ketoconazole, opioid or other medications that affect T metabolism or production

Moderate to severe COPD

Sellar mass, radiation to the sellar region, or other diseases of the sellar region

End-stage renal disease, maintenance hemodialysis

HIV-associated weight loss

Section 4:  Diagnosis and Monitoring

Men presenting with possible signs and symptoms of AOH must be systematically evaluated, accurately diagnosed, carefully counseled regarding the risks and benefits of treatment, and followed regularly if T replacement is initiated.  The process recommended by the panel is summarized in Figures 2 and 3.

Risks and Safety of T.  There are two challenges to understanding the risks of T replacement in appropriately selected men.  The first challenge is the lack of definitive evidence derived from properly-designed prospective studies.  The second challenge is the existence of mixed evidence that is not definitive from the literature that is available.  In the absence of definitive evidence regarding risks, patients must be monitored regularly for adverse events.

Cardiovascular risksDefinitive evidence regarding the short- and long-term cardiovascular risks of T replacement is not yet available because the published prospective trials were not designed or powered to examine cardiovascular endpoints.  The available trials and meta-analyses report mixed findings, with some finding no risks associated with T replacement and others reporting risks associated with T replacement.  The need for definitive trials that can yield unambiguous findings is underscored by several recent publications using retrospective data that report possible risks of T replacement (i.e., Layton et al., 2015; Finkle et al., 2014; Vigen et al., 2013).  The clinical utility of these data is unclear because of the inherent limitations of these studies (e.g., lack of assessment of whether men met criteria for T replacement, failure to compare event rates to those in non-T-using men, and statistical limitations).  Therefore, it is critically important that men administered T be monitored regularly.

Prostate cancer risks.  No appropriately designed and powered study has been conducted to assess prostate cancer-related risks of T replacement.  The available evidence has yielded mixed findings although most studies have found no risk associated with T replacement (e.g., Hsing et al., 2001; EHPCCG, 2008; Calof et al., 2005).  Given the absence of definitive evidence, men administered T should be monitored regularly.

Erythrocytosis.  During TRT, levels of hemoglobin (Hb) and hematocrit (Hct) rise for the first 5-6 months, then tend to plateau (Swerdloff & Wang, 2003; Wang et al., 2004). Injectable T formulations are associated with the greatest treatment-induced increases in Hb and Hct (Dobs et al., 1999; Rhoden & Morgentaler, 2004; Vorkas et al., 2012; Jick & Hagberg 2013).  Although it has been hypothesized that enhanced blood viscosity poses a threat for ischemic sequela, the direct relationship between TRT-induced erythrocytosis and subsequent risk for cardiovascular (CV) events has not been demonstrated through prospective randomized controlled trials (Schreijer et al., 2010; Braekkan et al., 2010; Vaya & Suescun 2013; De Stef et al., 2008; Glueck et al. 2014).  Therefore, in the absence of sufficient information regarding risk, men administered T should be monitored regularly.

Benign Prostatic Hypertrophy (BPH)/Lower Urinary Tract Symptoms (LUTS).  The preponderance of evidence indicates that T replacement has no effect on BPH and LUTS symptoms or improves symptoms (Amano et al., 2010; Francomano et al., 2014; Haider et al., 2009; Kalinchenko et al., 2008; Karazindiyanogly & Cayan, 2008; Pearl et al., 2013; Shigehara et al., 2011).

Section 5:  Conclusion

AOH is a diagnosable clinical syndrome in which men experience signs and symptoms associated with low T levels and low or normal gonadotropin levels.  Its etiology appears to include failure at the testicular and hypothalamic-pituitary levels, making it distinct from classical primary and secondary hypogonadism.  The AOH presentation is more common among men with prevalent comorbidities such as obesity, metabolic syndrome, and diabetes.  AOH is a more accurate diagnosis for the group of adult men most frequently diagnosed with hypogonadism.  Men with AOH who are candidates for treatment with T should be counseled regarding the risks and benefits of treatment.  Men who are treated with T should be monitored regularly given that definitive evidence regarding potential short-term and long-term risks of T is not yet available. 

Acknowledgements and Disclosures

The SMSNA is a not-for-profit society established in 1994 to promote, encourage and support the highest standards of practice, research, education and ethics in the study of the anatomy, physiology, pathophysiology, diagnosis and treatment of human sexual function and dysfunction.  The SMSNA strives to support the free exchange and discussion of new ideas, thoughts and concepts in sexual medicine. 

The colloquium was funded by the SMSNA Foundation through an unrestricted grant from Repros Therapeutics, Inc. SMSNA required complete independence from industry during the development of this document.  No industry representatives were present in the closed meeting, there was no industry participation in the evidence selection, discussion, or creation of this document, and there was no attempt by industry to influence its content.


Allan CA, McLachlan RI Androgens and obesity. Curr Opin Endocrinol Diabetes Obes 2010;17:224–232

Amano T, Imao T, Takemae K, Iwamoto T, Nakanome M. Testosterone replacement therapy by testosterone ointment relieves lower urinary tract symptoms in late onset hypogonadism patients. Aging Male: Off J Int Soc Study Aging Male. 2010;13(4):242–6

Araujo AB, et al. Prevalence and Incidence of Androgen Deficiency in Middle-Aged and Older Men: Estimates from the Massachusetts Male Aging Study. J Clin Endocrinol Metab; 2004; 89(12):5920–592

Araujo AB, et al. Prevalence of symptomatic androgen deficiency in men. J Clin Endocrinol Metab 92(11):4241–4247, 2007

Araujo ABDixon JMSuarez EAMurad MHGuey LTWittert GA. Endogenous testosterone and mortality in men: a systematic review and meta-analysis. J Clin Endocrinol Metab. 2011 Oct;96(10):3007-19

Bhasin S, Cunningham GR, Hayes FJ, et al. Testosterone therapy in men with androgen deficiency syndromes: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab; 2010;95:2536-2559

Braekkan SK, Mathiesen EB, Njølstad I, Wilsgaard T, Hansen JB. Hematocrit and risk of venous thromboembolism in a general population. The Tromso study. Haematologica. 2010;95: 270-5

Brand, J. S., van der Tweel, I., Grobbee, D. E., Emmelot-Vonk, M. H. & van der Schouw, Y. T. Testosterone, sex hormone-binding globulin and the metabolic syndrome: a systematic review and meta-analysis of observational studies. Int. J. Epidemiol. 40, 189–207 (2011)

Buvat J, et al. Testosterone Deficiency in Men: Systematic Review and Standard Operating Procedures for Diagnosis and Treatment J Sex Med 2013;10: 245–284

Calof OM, Singh AB, Lee ML, et al. Adverse events associated with testosterone replacement in middle-aged and older men: a meta-analysis of randomized, placebo-controlled trials. J Gerontol A Biol Sci Med Sci. 2005;60: 1451-7

Corona, G., & Maggi, M. Perspective:  Regulatory agencies’ changes to testosterone product labeling.  J Sex Med; 2014; 12; 1690-1693

Dandona, M. T. Rosenberg A practical guide to male hypogonadism in the primary care setting P. Int J Clin Pract, May 2010, 64, 6, 682–696.

Dean, JD et al., The International Society for Sexual Medicine’s Process of Care for the Assessment and Management of Testosterone deficiency in adult men.  J. Sex Med; 2015; 12(8); 1660-1686.

De Stef, et al.  Recurrent thrombosis in patients with polycythemia vera and essential thrombocythemia: incidence, risk factors, and effect of treatments. Haematologica 2008;93:372–80

Dobs AS, Meikle AW, Arver S, Sanders SW, Caramelli KE, Mazer NA. Pharmacokinetics, efficacy, and safety of a permeation-enhanced testosterone transdermal system in comparison with bi-weekly injections of testosterone enanthate for the treatment of hypogonadal men. J Clin Endocrinol Metab. 1999;84: 3469-78.

Endogenous Hormones and Prostate Cancer Collaborative Group. Endogenous sex hormones and prostate cancer: a collaborative analysis of 18 prospective studies. J Natl Cancer Inst. 2008;100(3):170-183

Feldman HA, Longcope C, Derby CA, Johannes CB, Araujo AB, Coviello AD, Bremner WJ, McKinlay JB. Age trends in the level of serum testosterone and other hormones in middle-aged men: longitudinal results from the Massachusetts male aging study. J Clin Endocrinol Metab. 2002 Feb;87(2):589-98

Finkle WD, Greenland, S., Ridgeway, GK, Adamas, JL, Frasco, MA, Cook, MB, Fraumeni Jr., JF, Hoover, RN.  Increased risk of non-fatal myocardial infarction following testosterone therapy prescription in men. PLoS ONE. 2014; 9(1); e85805

Francomano D, Ilacqua A, Bruzziches R, Lenzi A, Aversa A. Effects of 5-year treatment with testosterone undecanoate on lower urinary tract symptoms in obese men with hypogonadism and metabolic syndrome. Urology. 2014;83(1):167–73

Glueck, CJ, Friedman, J, Hafeez, A., Hassan, A., Wang, P.  Testosterone, thrombophilia, thrombosis.  Blood Coagul Fibrinolysis; 2014; 25; 683-687

Guay, A., Seftel, A., Traish, A. Hypogonadism in men with erectile dysfunction may be related to a host of chronic illnesses.  Int J Impot Res; 2010; 22; 9-19

Haider A, Gooren LJ, Padungtod P, Saad F. Concurrent improvement of the metabolic syndrome and lower urinary tract symptoms upon normalisation of plasma testosterone levels in hypogonadal elderly men. Andrologia. 2009;41(1):7–139

Harman, S.M., Metter, E.J., Tobin, J.D., Pearson, J., Blackman, M.R. Longitudinal effects of aging on serum total and free testosterone levels in healthy men.  J Clin Endocrinol Metabol 2001; 86; 724-731

Hsing AW.  Hormones and prostate cancer:  what’s next? Epidemiol Rev 2001; 23(1); 42-58. 

Jick SS, Hagberg KW. The risk of adverse outcomes in association with use of testosterone products: a cohort study using the UK-based general practice research database. Br J Clin Pharmacol. 2013;75: 260-70

Kalinchenko S, Vishnevskiy EL, Koval AN, Mskhalaya GJ, Saad F. Beneficial effects of testosterone administration on symptoms of the lower urinary tract in men with late-onset hypogonadism: a pilot study. Aging Male: Off J Int Soc Study Aging Male. 2008;11(2): 57–61

Karazindiyanoglu S, Cayan S. The effect of testosterone therapy on lower urinary tract symptoms/bladder and sexual functions in men with symptomatic late-onset hypogonadism. Aging Male: Off J Int Soc Study Aging Male. 2008;11(3):146–9

Laaksonen DE, Niskanen L, Punnonen K, et al The metabolic syndrome and smoking in relation to hypogonadism in middle-aged men: a prospective cohort study. J Clin Endocrinol Metab 2005;90:712–719

Layton, JB, Meier, CR, Sharpless, JL, Sturmer, T, Jick, SS, Brookhart, MA.  Comparative safety of testosterone dosage forms.  JAMA Intern Med; 2015; 175(7), 1187-1196

MacDonald AA, Herbison GP, Showell M, Farquhar CM The impact of body mass index on semen parameters and reproductive hormones in human males: a systematic review with meta-analysis. Hum Reprod Update 2010;16:293–311

Maseroli, E., Corona, G., Rastrelli, G., Lotti, F., Cipriani, S., Forti, G., Mannucci, E., Maggi, M. Prevalence of endocrine and metabolic disorders in subjects with erectile dysfunction:  A comparative study.  J Sex Med; 2015; 12: 956-965

Mulligan T, et al. Prevalence of hypogonadism in males aged at least 45 years: the HIM study Int J Clin Pract, July 2006, 60, 7, 762–769).

Neaves WB, Johnson L, Porter JC, et al. Leydig cell numbers, daily sperm production, and serum gonadotropin levels in aging men. J Clin Endocrinol Metab 1984;59:756–63

Nieschlag E, Lammers U, Freischem CW, Langer K, Wickings EJ. Reproductive functions in young fathers and grandfathers. J Clin Endocrinol Metab. 1982;55:676-81.

Paduch, DA., Brannigan, RE., Fuchs, EF., Kim, ED., Marmar, JL., Sandlow, JI.  White Paper: The laboratory diagnosis of testosterone deficiency.  2013. American Urological Association.

Pearl, JA, Berhanu, D, Francois, N, Masson, P, Zargaroff, S, Cashy, J, et al. Testosterone supplementation does not worsen lower urinary tract symptoms. J Urol. 2013;190(5):1828–33

Rhoden EL, Morgentaler A. Risks of testosterone-replacement therapy and recommendations for monitoring. N Engl J Med. 2004;350: 482-92

Rubens R, Dhont M,Vermeulen A. Further studies on Leydig cell function in old age. J Clin Endocrinol Metab 1974;39:40–5

Sartorius G, Spasevska S, Idan A, et al. Serum testosterone, dihydrotestosterone and estradiol concentrations in older men self-reporting very good health: the healthy man study. Clin Endocrinol (Oxf). 2012;77:755-63

Schreijer AJ, Reitsma PH, Cannegieter SC. High hematocrit as a risk factor for venous thrombosis. Cause or innocent bystander? Haematologica. 2010;95: 182-40

Shigehara K, Sugimoto K, Konaka H, Iijima M, Fukushima M, Maeda Y, et al. Androgen replacement therapy contributes to improving lower urinary tract symptoms in patients with hypogonadism and benign prostate hypertrophy: a randomised controlled study. Aging Male: Off J Int Soc Study Aging Male. 2011;14(1):53–8

Swerdloff RS, Wang C. Three-year follow-up of androgen treatment in hypogonadal men: preliminary report with testosterone gel. Aging Male. 2003;6: 207-11

Tajar A and the EMAS Group. Characteristics of Secondary, Primary, and Compensated Hypogonadism in Aging Men: Evidence from the European Male Aging Study. J Clin Endocrinol Metab, April 2010, 95(4):1810–1818

Takahashi PY, Liu PY, Roebuck PD, et al. Graded inhibition of pulsatile luteinizing hormone secretion by a selective gonadotropin- releasing hormone (GnRH)-receptor antagonist in healthy men: evidence that age attenuates hypothalamic GnRH outflow. J Clin Endocrinol Metab 2005;90:2768–745

Vaya A, Suescun M. Hemorheological parameters as independent predictors of venous thromboembolism. Clin Hemorheol Microcirc. 2013;53: 131-41

Vigen R, O'Donnell CI, Barón AE, Grunwald GK, Maddox TM, Bradley SM, Barqawi A, Woning G, Wierman ME, Plomondon ME, Rumsfeld JS, Ho PM. Association of testosterone therapy with mortality, myocardial infarction, and stroke in men with low testosterone levels.JAMA. 2013;310:1829-36

Vorkas CK, Vaamonde CM, Glesby MJ. Testosterone replacement therapy and polycythemia in HIV-infected patients. AIDS. 2012;26: 243-5.

Wang C, Cunningham G, Dobs A, et al. Long-term testosterone gel (AndroGel) treatment maintains beneficial effects on sexual function and mood, lean and fat mass, and bone mineral density in hypogonadal men. J Clin Endocrinol Metab. 2004;89: 2085-98

Wang C, Jackson G, Jones TH, Matsumoto AM, Nehra A, Perelman MA, Swerdloff RS,

Traish A, Zitzmann M, Cunningham G. Low testosterone associated with obesity and

the metabolic syndrome contributes to sexual dysfunction and cardiovascular disease risk in men with type 2 diabetes. Diabetes Care. 2011 Jul;34(7):1669-75

Winters, SJ; Atkinson, L. Serum LH concentrations in hypogonadal men during transdermal testosterone replacement through scrotal skin: further evidence that ageing enhances testosterone negative feedback.  Clinical Endocrinology; 1997; 47(3); 317-322.

Wu FC, Tajar A, Pye SR et al.: Hypothalamic-pituitary-testicular axis disruptions in older men are differentially linked to age and modifiable risk factors: the European Male Aging Study. J Clin Endocrinol Metab 2008, 93:2737-4508

Yeap, BB, Almeida, OP, Hyde, Z, Norman, PE, Chubb, SAP, Jamrozik, K., Hankey, GJ, Flicker, L.  Healthier lifestyle predicts higher circulating testosterone in older men:  The Health In Men Study.  Clinical Endocrinol; 2009; 70; 455-463

Zumoff B, Strain GW, Kream J, et al. Age variation of the 24 hour mean plasma concentration of androgens, estrogens, and gonadotropins in normal adult men. J Clin Endocrinol Metab 1982; 54:534-538

Click here to download the PDF version (version 1 – October 31, 2015)

5-alpha reductase inhibitors and sexual side effects

The statement below is based on a meeting convened in November 2011 by the Sexual Medicine Society of North America. The meeting consisted of a panel of internationally recognized experts in men's health, sexual medicine, endocrinology and prostate disease. The participants were charged with reviewing the medical literature as it stands at this time on the link between 5-alpha reductase inhibitors and persistent sexual side effects.

Five alpha-reductase inhibitors, a class of medication used to treat the symptoms of certain prostate conditions as well as male-pattern hair loss, are known to be associated with undesired sexual symptoms during treatment. Some of these symptoms may last for many years after stopping these medications. The Sexual Medicine Society of North America (SMSNA) recognizes that an association exists between these drugs and persistent undesirable symptoms after termination of treatment and that men with these symptoms are suffering. However, at this time, human scientific evidence does not allow us to define the prevalence or the cause of these symptoms. The medical literature is limited, and as such, it is currently impossible to definitively link, as cause and effect, these medications to the long-lasting symptoms these men experience. Future research is required to differentiate whether such symptoms are an association with or are the result of the use of these medications. SMSNA are committed to developing a better understanding of this problem, to defining which research avenues may be of most benefit and to developing clinical care pathways for such patients.

Razors and Preoperative Preparation of the Male Genitalia

The Sexual Medicine Society of North America (SMSNA), a specialty society of the American Urological Association, supports in general the recent nationwide initiative to reduce peri-operative infections by the use of clippers rather than razors for preoperative hair removal. However, the delicate, irregular, and elastic skin of the male genitalia is ill-suited for clippers, which tend to produce multiple skin breaks, in contrast with razors, which have been used with good success for decades. In the absence of any evidence to the contrary, the SMSNA recommends that surgeons be permitted their choice of razors or clippers for preoperative preparation of the male genitalia.

Medicaid Benefits for Erectile Dysfunction

Certain states have recently denied Medicaid therapy for erectile dysfunction to men who have been convicted of sexual offenses. The Sexual Medicine Society of North America, Inc. (SMS) acknowledges governments' need to protect its citizens from sexual predators. Denial of Medicaid benefits for erectile dysfunction is appropriate in the case of sexual predators.

SMS believes it is unwise and illogical to deny effective treatment of erectile dysfunction to all Medicaid beneficiaries.

Erectile dysfunction often results from certain serious organic diseases, including heart disease, high blood pressure, diabetes and high cholesterol. Current medical and surgical treatments of erectile dysfunction are safe and highly effective and can restore an essential bodily function.

Smoking and Erectile Dysfunction

Cigarette smoking is a risk factor for erectile dysfunction. Men who smoke have a greater chance of developing erectile dysfunction than men who do not smoke.

Diagnostic Evaluation of Impotence

Diagnostic studies used to evaluate the pathophysiology of impotence should be individualized for each patient.

A generic or standard list of diagnostic tests for all patients is not an appropriate practice.

Studies used for the diagnostic evaluation of impotence should be limited in general to the tests which are needed to identify the treatment options available to each patient, taking into account each patient's unique clinical status and treatment preferences.

The patient who wishes to identify the cause or causes of his erectile dysfunction as organic and/or psychogenic, nocturnal penile tumescence and rigidity (NPTR) monitoring, vascular and other testing are useful, but the patient must be provided information permitting an informed decision to seek testing which is not essential to the selection of treatment options.NPTR monitoring and extensive vascular testing are not indicated for the diagnostic evaluation of every impotent patient.

Ethical medical practice requires that diagnostic, therapeutic and other decisions must be made solely for the benefit of the patient and must be made without regard for the benefit of the health care provider.

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