Endogenous Testosterone

Endogenous Testosterone

Testosterone is an anabolic/androgenic hormone. Although it is normally thought as a male hormone, it is naturally produced in both men and women. Its anabolic properties include the maintenance and growth of muscle and bone tissue (Sutton, Coleman, Casey, & Lazarus, 1973). Increase in muscular size appears to be due to the effect of testosterones upon protein synthesis (Griggs, Kingston, Jozefowicz, Herr, Forbes, & Halliday, 1989). Testosterone increases skeletal muscle size through hypotrophy (Boone, Lambert, Flynn, Michaud, Rodriguez-Zayas, & Andres, 1990); not by hyperplasia (Mooradian, Morely, & Korenman, 1987). Testosterone has been reported to enhance glycogen synthesis, reabsorption of sodium in the kidneys, and secretion of sebaceous glands (Mooradian, Morely, & Korenman, 1987). Testosterone is also associated with bone growth, calcium retention, sodium reabsorption, and increased metabolic rate. Testosterone levels have been linked to aggressive behavior in animals and humans (Bahrke, Barke, & Strauss, 1990).

The negative feedback loop of the hypothalamic-pituitary-testicular axis regulates the production of endogeneous testosterone. The hypothalamus secretes gonadotropin releasing hormone (GnRH), which stimulates luteinizing hormone (LH) and follicle stimulating hormone (FSH) from the anterior pituitary. LH can then stimulate the membrane receptors of the Leydig cells in the testes to stimulate the production of testosterone (Kraemer, 1988).

Resting testosterone values for mature males range from 14.0 to 28.0 nmol/L (Kraemer, 1988). Approximately 97 to 99 percent of testosterone is transported in the blood bound to plasma proteins such as sex hormone binding globulin (SHBG) and albumin. The remaining 1 to 3% is the biologically active, free testosterone. Testosterone circulates in the blood approximately 15 to 30 minutes until it is either bound to receptors or metabolized into inactive products by the liver and subsequently excreted through the urine.

Testosterone can be converted to estradiol through aromatization in adipose tissue, certain brain tissue, and other specific tissues (Mooradian, Morely, & Korenman, 1987). Testosterone is also converted to dihydrotesterone in the gonads and certain peripheral tissues (Di Pasquale, 1992a; Mooradian, Morely, & Korenman, 1987). In normal men, plasma levels of dihydrotestosterone (DHT) are approximately 55 ng/100 ml. The production of dyhydrotestosterone is 1/20th of the production of testosterone. Dihydrotestosterone is related to facial hair, genetic balding, prostate growth, and the development of male external genitalia. Dihydrotestesterone does not aromatize and has less of an antigonadotropic effect than testosterone. In high levels, dihydrotestosterone can assume the function of testosterone, and testosterone can assume the function of dihydrotestosterone (Di Pasquale, 1992a).

Testosterone decreases by approximately 1% per year after age 30 (Brawer 2004, Harris 2011) whereas both free and albumin-bound testosterone declined at about 2% per year. Sex hormone-binding globulin (SHBG) increase at 1.6% per year. The increase in SHBG likely results in a further decline in testosterone levels. Dehydroepiandrosterone, dehydroepiandrosterone sulfate, cortisol, and estrone showed significant declines, whereas dihydrotestosterone (DHT), follicle-stimulating hormone (FSH), luteinizing hormone (LH), and prolactin increased over time. (Harris 2011)

The level of testosterone appears to influence sexual function. Declining testosterone may cause a decline in libido, Erectile Dysfunction (ED), and difficulty achieving ejaculation. Testosterone replacement therapy can improve erectile function for hypogonadal men. (Harris 2011)

Exogenous testosterone can have severe adverse effects on spermatogenesis by suppressing intratesticular testosterone production (Harris 2011, Crosnoe 2013). Therapies that protect the testis involve Human Chorionic Gonadotropin (hCG) therapy or selective estrogen receptor modulators (SERMs) such as clomiphene citrate (Crosnoe 2013). Most men on hormonal contraception therapy return to normal sperm production within 1 year after discontinuation (Crosnoe 2013).

See production of testosterone in testes. Also see BPA and other Hormone Disruptors.

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