Sexual development and hormonal function of the man depends on a complex control circuit from the hypothalamus, pituitary and testis includes and is regulated by the central nervous system. A male sexual dysfunction (man’s sexual dysfunction) or may be the consequence of a drug of hypogonadism, neurovascular or other disorders. Clinical Calculator: androgen deficiency in elderly men (ADAM) Screener physiology The hypothalamus produces gonadotropin-releasing hormone (GnRH), which is released in pulsatile form all 60-120 minutes. The target organ, the front Hypophysenanteil responds to each of these GnRH pulses with the corresponding release of luteinizing hormone (LH) and to a lesser extent of follicle stimulating hormone (FSH). When the GnRH pulses do not occur with the correct amplitude, frequency and daily variation, this can lead to hypogonadism. (Idiopathic hypogonadotropic hypogonadism). A continuous (as opposed to pulsed) stimulation by GnRH agonist (eg., For treatment of advanced prostate cancer) actually suppresses the release of LH and FSH from the pituitary gland and thus the production of testosterone. The Leydig cells of the testes to respond to a LH stimulation with production of 5-10 mg / day. Testosterone levels are highest in the early morning and lowest in the evening, but in older men this daily pattern can be mitigated. Testosterone is synthesized via several intermediates including dehydroepiandrosterone (DHEA) and androstenedione from cholesterol. The circulating testosterone is primarily bound to protein, determined to about 40% of the sex hormone binding globulin (SHBG) and 58% albumin. Thus, only about 2% of circulating testosterone is bioavailable than free testosterone. About 4-8% of the testosterone is converted into the target organs by the enzyme 5?-reductase into the more effective metabolite dihydrotestosterone (DHT). DHT has important metabolic effects in the prostate and mediates androgen alopecia. In adults, spermatogenesis sufficiently requires high intratesticular testosterone levels; the role of DHT in spermatogenesis is unclear. Testosterone and DHT have metabolic and other effects, including stimulation of protein anabolism (increasing muscle mass and bone density) stimulation of erythropoietin production in renal (increasing mass of red blood cells) stimulate the bone marrow stem cells (modulation of the immune system) Cutaneous effects (ie, sebum, hair growth) neural effects (typically perception, increase libido and possibly aggression) testosterone is converted to estradiol and DHT. Estradiol mediated in large part the effect of testosterone on organs like bone and brain. Testosterone, DHT and estradiol provide negative feedback on the hypothalamic-pituitary axis. In men estradiol the main inhibitor of LH production while both estradiol inhibin B, an image formed in the Sertoli cells of the testes peptide, production of FSH inhibit. Under the influence of testosterone, FSH stimulates the Sertoli cells and induces spermatogenesis. In spermatogenesis all germ cells (spermatogonia) which are adjacent to the Sertoli cells are differentiated in 16 primary spermatocytes, spermatids 4 each form. Each spermatid matures to a spermatozoon. Spermatogenesis takes 72 to 74 days, and every day are formed 100 million new sperm. After ripening, the spermatozoa are directed into the rete testis, where finally they enter the epididymis and the vas efferent. This hike takes another 14 days. During ejaculation, spermatozoa are mixed with secretions from the seminal vesicles, prostate and bulbo glands. Sexual differentiation and puberty Adrenarche In the embryo the presence of a Y chromosome, the development and growth of the testes triggers that start the seventh week of pregnancy with the secretion of testosterone and one the Mullerian ducts inhibiting hormone. The testosterone virilized the Wolffian ducts (which develop into the epididymis, vas deferens and seminal vesicles). DHT promotes the development of the external genital organs. The testosterone levels achieved during the second trimeter its peak and falls to birth almost to zero. Testosterone production increases during the first 6 months of life to short, then the testosterone levels remain low until puberty. LH and FSH are elevated at birth, but fall in the first months to low values ??to remain detectable low or not during the prepubertal years. The serum levels of adrenal androgens DHEA and DHEA sulfate begin to rise for several years before puberty by an unknown mechanism. Their conversion to low levels of testosterone initiates the growth of pubic and axillary (Adrenarche). Adrenarche can occur as early as age 9 or 10 years. The mechanisms that trigger puberty are unclear, but the hypothalamus in early puberty in relation to the inhibitory effect of sex hormones is less sensitive. This desensitization increases the secretion of LH and FSH, in accordance with the pulsating GnRH secretion and stimulates testosterone and sperm production. In boys, the elevated testosterone levels pubertal changes, of which the first growth of the testes and scrotum cause. Later increase penis length, muscle mass and bone density. The voice becomes deeper and the pubic and axillary hair is thicker and thicker (puberty when develop male sexual characteristics.). Puberty when male sexual characteristics develop. Bars indicate the standard ranges. There is no way for a change of habit available. Consequences of aging Aged both the hypothalamic secretion of GnRH and the Leydig cells, the response to FSH and LH diminish. In the elderly, the number of Leydig cells decreases. At about the age of 30 around the whole takes testosterone the man per year from 1-2%. The testosterone levels of men between 70 and 80 years amount to only half to two-thirds of the testosterone levels of men in the third decade of life. In addition, the SHBG levels increase with age, creating an even greater decrease of free and bioavailable testosterone caused. FSH and LH levels, however, remain normal to high normal. These age-related changes are sometimes referred to as andropause, although it does not lead to abrupt changes in hormone levels (and corresponding symptoms) is such as in menopause. The decline of testosterone may be due to a combination of symptoms that are known as androgen deficiency in the aging male (ADAM), arise which include :. Age-related muscle loss Increased fat deposition osteopenia loss of libido and erectile function Cognitive Decline When men have testosterone reflect these symptoms along with low serum, a hypogonadism diagnosed (Male hypogonadism) and are suitable for therapy with additional testosterone ? ?. The testosterone replacement therapy in men with low to normal testosterone levels is controversial. Some experts recommend trying a testosterone replacement therapy in older men with symptoms and signs of hypogonadism, in which the serum testosterone slightly lower mirror below the lower normal limit. No data favor a testosterone preparations specifically for use with ADAM, although daily transcutaneous applications seem to be the physio most logical and best to be most compatible.