Bryan said:
docj077 said:
Testosterone and DHT cause negative feedback upon the hypothalamus and the anterior pituitary. They inhibits the release of GnRH and pituitary gonadotropes.
With no DHT production, testosterone levels increase in the blood and hinder the release of GnRH, LH, and FSH.
Nope. As I said before, it
raises LH and FSH, and testosterone as a result.
docj077 said:
The metabolite of testosterone, estrogen, also directly inhibits the release of GnRH, LH, and FSH. So, we have more testosterone initially lowing gonadotrope levels which lowers testosterone levels. As those levels fall, LH release will increase to bring it back up. Unfortunately, that testosterone is converted to estrogen which once again negatively effects the release of previously mentioned hormones. So, no matter what the body does, testosterone levels will eventually become lower after an initial spike.
Sorry, it doesn't work that way. It doesn't go up and down like a yo-yo.
Bryan
Well, I'm not going to argue any more with you. The way I type it is the way that every medical professional is taught to learn it. I just took medical physiology at the M.D. level not more than three months ago.
Testosterone does not raise LH and FSH. That's why men who go through andropause have decreased testosterone, but increased LH and FSH as the negative feedback mechansims are no longer in place.
Taken from MDConsult.com
Causes of hypogonadism vary with age. Boys and young men with hypogonadism often have a congenital abnormality, most commonly Klinefelter's syndrome, a primary testicular disorder resulting in small, undeveloped testes and elevated serum gonadotropins. Most hypogonadal men aged 30 to 50 years have a combination of primary and secondary hypogonadism.
There is both a gradual increase in LH serum concentration indicating a degree of primary hypogonadism as well as blunting of LH secretory bursts indicating a degree of secondary hypogonadism. As men age, serum testosterone decreases approximately 1% to 2% a year after age 30 and, accompanied by an age-associated decrease in SHBG resulting in an even lower free T concentration, eventually resulting in a condition some have termed ADAM, or androgen deficiency in the aging male. Others call this period of life andropause or EDAM (endocrine decline in aging males). This period is characterized also by an increase in SHBG and a decrease in Leydig cell count, which, along with declining testosterone production, result in increased body fat, decreased bone mineral density, mood and memory problems, decreased sexual desire, and diminished strength and energy. The existence of this period of declining hormone reproduction is clear, but the presence of a characteristic syndrome that can be identified in all men is less certain. Some men over age 70 years still have T levels in the upper third of males 20 to 40 years of age [64]. Symptoms of this syndrome, including all those noted in Box 5, may also result from aging shifts of other hormones including growth hormone, melatonin, and leptins [65]. Measurement of all these other hormones is probably not useful in the context of the man with sexual problems since normal levels and management protocols have not been worked out.
Emergency Medicine Clinics of North America
Volume 23 • Number 3 • August 2005
Copyright © 2005 W. B. Saunders Company
Anabolic Steroids: What Should the Emergency Physician Know?
James T. Brown, MD
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OSF Saint Francis Medical Center, 530 N.E. Glen Oak, Peoria, IL 61637, USA
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E-mail address:
JBrown5005@aol.com
REPRODUCTIVE/ENDOCRINE
In men, anabolic steroid use leads to hypogonadotropic hypogonadism, resulting from the suppression of LH and follicle stimulating hormone (FSH) mediated through the negative feedback loop of the hypothalamic–pituitary–gonadal axis [1]. Because LH and FSH are essential for spermatogenesis, the resulting physiologic effects of anabolic steroid use include decreased sperm density and sperm count, decreased sperm motility, abnormal sperm morphology, testicular atrophy, and no change in libido [1]. Increasing doses of anabolic steroids will lead to oligospermia and infertility [31]. Nomalization generally occurs within 1 year of cessation of the anabolic steroids [32], [33]. Feminization in males can occur from the conversion of testosterone to estrogen metabolites (aromatization) [20]. The increased estrogens may result in increased voice pitch and gynecomastia.
In women, anabolic steroid use leads to hirsutism, acne, deepening of the voice, clitoral hypertrophy, decreased breast mass, decreased menstruation or amenorrhea, increased appetite, and male pattern baldness. Even after discontinuation of the causative agent, these effects are sometimes irreversible [34].
Anabolic steriods refer to androgen-based substances.
Not only that, but the decrease in testosterone levels also decreases estrogen levels leading to eventual osteoporosis in the male.
Also, it does go up and down like a yo-yo. That's why GnRH antagonists that are used for prostate cancer must be long lasting and are given weekly to monthly depending on the staging. If it wasn't, the hypothalamic-pituitatry axis would once again restart. The fluctuations are also seasonal.
It says the exact same thing that I've been saying in my medical physiology book that I have from the Sanford School of Medicine at the University of South Dakota where I'm a student. Endocrinology is a required course within the medical physiology component of first year.
Taken from First Aid USMLE Step 1:
Testosterone:
Differentiates male genitalia, has anabolic effects on protein metabolism, maintains gametogenesis, maintains libido, inhibits GnRH, and fuses epiphyseal plates in bone.
Figure 1. Schematized notion of postulated feedback actions of testosterone in the normal male GnRH-LH-gonadal axis. In situ denotes feedback mediated by putative central (hypothalamic-pituitary) aromatization of testosterone to estradiol, rather than by peripheral blood estradiol levels. Other nonaromatizable androgens act like DHT on the hypothalamus to suppress the action of GnRH (Gonadotropin Releasing Hormone) secreting neurons as well as acting on the pituitary to suppress LH. Gonadotropes are LH/FSH secreting pituitary cells. The lower block illustrates testosterone and estradiol secreted from the testes. Adapted from Schnorr JA, Bray MJ, Veldhuis JD. J Clin Endocrinol Metab. 2001 Jun; 86(6):2600-6.
You guys are very, very wrong about this one.
