Forensic Sciences ; Hormones ; pharmacology ; physiology ; Humans ; Sports

Late onset hypogonadism was originally perceived as an academic topic. In the course of two decades it has become an issue impacting on everyday urology. For long time clinical conditions, such as cardiovascular disease, diabetes mellitus type 2, sexual dysfunction and urological complaints affecting the aging male, were regarded as independent clinical entities, treated by a number of medical specialists. Over the last decade their close interrelationship could be convincingly demonstrated. Declining testosterone levels in elderly appear to be central to the above pathologies. Epidemiological studies show that prostate disease occurs at an age when serum testosterone levels decline. It is now clear that erectile dysfunction is a local expression of endothelial dysfunction of the cardiovascular system. Testosterone deficiency is associated with an increased incidence of cardiovascular disease and diabetes mellitus, sequels of the metabolic syndrome. There is a relationship between the metabolic syndrome and lower urinary tract symptoms (LUTS). The pathophysiology of LUTS has much in common with the pathological substrate of erectile dysfunction with regard to vascular factors and the role of nitric oxide, explaining why phosphodiesterase type 5 inhibitors have often a beneficial effect on LUTS. It must be regarded an omission not to include testosterone measurements in the work-up of the LUTS, erectile dysfunction, cardiovascular disease and diabetes mellitus type 2. These conditions hinge on testosterone deficiency, and if testosterone deficiency can be proven, testosterone treatment can improve these conditions. There are many sites in the lower urinary tract where testosterone exerts effects.
Aged ; Aging ; Cardiovascular Diseases ; Cardiovascular System ; Diabetes Mellitus ; Erectile Dysfunction ; Humans ; Hypogonadism ; Incidence ; Lower Urinary Tract Symptoms ; Male ; Metabolic Syndrome X ; Nitric Oxide ; Phosphodiesterase 5 Inhibitors ; Prostate ; Specialization ; Testosterone ; Urinary Tract ; Urination Disorders ; Urology

Sex segregation in competitive sports is regarded as fair. Before puberty boys and girls do not differ in height, muscle and bone mass. Testosterone (T) exposure during puberty leads to an ultimate average greater height in men of 12-15 cm, longer and larger bones and muscle mass and strength and higher hemoglobin levels. Postpubertal androgen ablation reverses, at least in part, previous anabolic effects of T on muscle, bone mineral density and hemoglobin but the long bones remain longer and wider. T administration dose dependently increases muscle mass and maximal voluntary strength. Therefore, exogenous androgens, being performance enhancing drugs, are banned for all athletes. An issue is the participation in competitive sports of people with errors of sexual differentiation and particularly transsexuals who have been sex-reassigned. In view of the effects of T, a clear demarcation is whether sex reassignment has taken place before or after hormonal puberty. Pubertal effects of T are in part reversible but there is no reliable evidence as to its completeness. The International Olympic Committee (IOC) has taken an inevitably arbitrary decision with regard to participation of sex-reassigned transsexuals in elite sports: sex reassignment must have taken place at least two years earlier, hormone treatment must be appropriate for the reassigned sex and the reassigned sex must be legally recognized. The IOC policy is not binding for other organizations.
Female ; Humans ; Male ; Sports ; Testosterone ; administration & dosage ; Transsexualism

Erectile response is centrally and peripherally regulated by androgens. The original insights into the mechanisms of action of androgens were that androgens particularly exert effects on libido and that erections in response to erotic stimuli were relatively androgen-independent. It was shown that sexual functions in men required androgen levels at the low end of reference values of testosterone. So it seemed that testosterone was not useful treatment for men with erectile difficulties, particularly following the advent of the phosphodiesterase type 5 (PDE5) inhibitors. However, approximately 50% of those treated with PDE5 inhibitors discontinue their treatment. A number of recent developments shed new light on testosterone treatment of erectile dysfunction (ED) in aging men. (1) A recent insight is that, in contrast to younger men, elderly men might require higher levels of testosterone for normal sexual functioning. (2) Several studies have indicated that PDE5 inhibitors are not always sufficient to restore erectile potency in men, and that testosterone improves the therapeutical response to PDE5 inhibitors considerably. (3) There is growing insight that testosterone has profound effects on tissues of the penis involved in the mechanism of erection and that testosterone deficiency impairs the anatomical and physiological substrate of erectile capacity, reversible upon androgen replacement. The synthesis of PDE5 is upregulated by androgens, and the arterial inflow into the penis is improved by giving androgen. The above invites a re-examination of the merits of giving testosterone to aging men with ED. The beneficial effects of PDE5 inhibitors may only be optimally expressed in a eugonadal environment.
3',5'-Cyclic-GMP Phosphodiesterases ; Aging ; physiology ; Animals ; Cyclic Nucleotide Phosphodiesterases, Type 5 ; Humans ; Male ; Middle Aged ; Penile Erection ; drug effects ; physiology ; Penis ; anatomy & histology ; drug effects ; Phosphodiesterase Inhibitors ; pharmacology ; therapeutic use ; Phosphoric Diester Hydrolases ; physiology ; Piperazines ; therapeutic use ; Purines ; Sildenafil Citrate ; Sulfones ; Testosterone ; blood ; physiology