ICA Symposium - Endocrinology of Aging in Males
Barry Zirkin (USA) presented data on testicular endocrinology of the Brown Norway rat. As in the human, in this animal model serum levels of testosterone and FSH decrease and there is spontaneous prostatic overgrowth with aging. The ability of Leydig cells to produce steroids and LH to stimulate Leydig cells also decline with aging. Interestingly, if the "old" Leydig cells are abolished using the Leydig cell cytotoxic drug, ethylene dimethyl sulphonate (EDS), the new generation of Leydig cells reappearing has functional characteristics of "young" Leydig cells. These features are, however, lost fairly soon, and the reason may be the increased production of reactive oxygen species in the aging testis.
Unlike most other rat strains, the Brown Norway rat responds with hypertrophy of all prostatic lobes to androgen treatment. The increase is greater in old rats. It was therefore concluded that the Brown Norway rat is a useful model for understanding human prostatic overgrowth and age-related reduction of testicular androgen production.
Joyce Tenover (USA) reviewed the current knowledge on age-related androgen deficiency in men and the current status of androgen replacement therapy of aging men. It is clear that androgen levels decline with aging and a significant proportion of aging men become androgen-deficient. Changes are seen in androgen target organs such as bone, muscle, central nervous system and reproductive organs. The prevalence of androgen deficiency (i.e. testosterone below 11 nmol/L) is 22% in men aged 60-80 years and 35% in men over 80 years. One clear sign of the androgen deficiency is the increase of fracture frequency in aging men. The data on benefits and risks of testosterone replacement therapy of aging men are still insufficient. It was concluded that androgen replacement therapy may be beneficial for bone and muscle function of aging men. The beneficial effects on cognition are still insufficiently documented. Likewise, effects on longevity remain unknown, as well as risks of long-term treatment, which may be related to prostatic and cardiovascular functions.
The third talk of this symposium was give by Gerhard Lunglmayr (Austria). He presented results on a survey of androgen deficiency and related symptoms in aging men. The goals of the study were to identify the hypogonadal men in the aging population, to assess the symptoms related to androgen deficiency, to determine the impact of chronic illnesses on sex hormone production, and to investigate the effects of hypoandrogenism on health.
About 800 apparently healthy men over 50 years of age were studied. The main findings were: A total of 11.4% of the men, mostly in the oldest age-groups, display suppressed testosterone levels (less than 11 nmol/l). Men with documented other diseases had lower testosterone levels. There was negative correlation of most aspects of sexual function with age, except for sexual performance and erectile function which did not show this correlation. Symptoms allegedly due to androgen deficiency (hot flushes, insomnia and fatigue) were not related with the low T levels. Rating of questions related to general health and well-being were correlated with age and prevalence of chronic illnesses but not with the hormone levels. A testosterone replacement therapy trial with a smaller subgroup of the men is currently pending. One conclusion from this study is that despite the age-related decline of testosterone, correlation of the apparent symptoms of androgen deficiency with low testosterone levels was not apparent. More studies on this contentious topic are needed before conclusions can be drawn on the clinical significance of the age-related hypoandrogenism and the need for androgen replacement therapy.
Ilpo Huhtaniemi, Finland