Glucocorticoids Inhibit Gonadotropin-releasing Hormone By Acting Directly At The Hypothalamic Level

[vulture]

I got low LH low FSH low T and was researching on possible causes. I got also at least two betametasone inyections, months ago, but who knows....anyway, found something that might be interesting for some of you.
Glucocorticoids inhibit gonadotropin-releasing hormone by acting directly at the hypothalamic level. - PubMed - NCBI

"Glucocorticoids, the end-product of the hypothalamic-pituitary-adrenal (HPA) axis, suppress gonadotropin release by acting at the level of the pituitary gland. However, experimental evidence suggests that they may also act at the hypothalamic level to suppress gonadotropin-releasing hormone (GnRH) release. The lack of a direct demonstration of this assumption, prompted us to evaluate the effects of glucocorticoids on hypothalamic GnRH release from individually-incubated hemi-hypothalami explanted from male rats. Since testosterone (T), dihydrotestosterone (DHT), and progesterone suppress GnRH release and androgens potentiate the effects of glucocorticoids on GnRH release, we studied also the interaction of these steroids with glucocorticoids on GnRH release. Corticosterone (B), the main glucocorticoid of the rodents with greater affinity for the type I glucocorticoid receptor, and dexamethasone (DEX), a synthetic type II glucocorticoid receptor agonist, were able to suppress basal GnRH release in a concentration-dependent fashion. DEX induced a more profound suppression of GnRH release. Neither T (0.1 nM) nor DHT (0.01 nM) modulated the suppressive effects of low (10 nM) or high (100 nM) concentrations of B on GnRH release. On the other hand, progesterone counteracted the suppressive effect of low concentrations of B (10 nM) on GnRH release, but had no effect on the suppression caused by a higher concentration of B (100 nM). The ability of glucocorticoids to inhibit directly GnRH release suggests that these stress-responsive hormones act also at the hypothalamic level to suppress the reproductive function. The suppressive effect of B was not modulated by androgens, but it was neutralized by progesterone, at least when B was used at low concentrations. We speculate that this steroid "protects" the GnRH-secreting neuron only during basal, but not stress-induced, HPA axis activity when the concentrations of glucocorticoids are more elevated."

 

[vulture]

Testosterone levels during systemic and inhaled corticosteroid therapy. - PubMed - NCBI

Testosterone levels during systemic and inhaled corticosteroid therapy.

 

[TreasureVibe]

I have once theorized that testicles output of T is normal or even high, but when varicocele is present, few of this T gets into the circulation at a proper saturation due to mobilization problems in the varicocele, showing on your blood test (taken from your arm) that your T is low even though your testes produce a healthy amount, and therefore LH and FSH could logically be low too as the body thinks there is no reason for it to increase it, as the testes produce healthy amounts of T.

Also testosterone blood level tests are not that reliable according to a piece written by Dr. Scally MD (even though he is a criticized expert) which can be seen here:

Examined changes over time have demonstrated a decrease in the total testosterone and an increase in SHBG levels. Because of this, the total testosterone might be normal, whereas the free or bioavailable testosterone is abnormal. If these alternative methods are used to diagnose hypogonadism, their utility during TRT is limited.

I would caution about the assay methodology used to calculate the free or bioavailable testosterone. The methods used to conduct the measurements vary in their accuracy, standardization, the extent of validation, and the reproducibility of results.

Bioavailable testosterone is measured or calculated in several ways. SHBG bound testosterone can be precipitated with ammonium sulfate and the remaining testosterone is then taken as the bioavailable.

Measures of free testosterone (FT) are controversial. The only standardized and validated method is equilibrium dialysis or by calculating free testosterone levels based on separate measurements of testosterone and SHBG. Other measures of free testosterone are less accurate.

Source: https://testosteronewisdom.com/2530...about-optimizing-testosterone-therapy-part-1/

I am against using pharmaceutical drugs to correct hypogonadism, personally. The natural route is always one a person should try first.

 

[vulture]

I have once theorized that testicles output of T is normal or even high, but when varicocele is present, few of this T gets into the circulation at a proper saturation due to mobilization problems in the varicocele, showing on your blood test (taken from your arm) that your T is low even though your testes produce a healthy amount, and therefore LH and FSH could logically be low too as the body thinks there is no reason for it to increase it, as the testes produce healthy amounts of T.

Also testosterone blood level tests are not that reliable according to a piece written by Dr. Scally MD (even though he is a criticized expert) which can be seen here:



Source: https://testosteronewisdom.com/2530...about-optimizing-testosterone-therapy-part-1/

I am against using pharmaceutical drugs to correct hypogonadism, personally. The natural route is always one a person should try first.

I read that Varicocele patients with low T, low LH, low FSH treated with T3 (specially hypothyroid) started to produce more LH and T. In a study it seemed irrelevant if you had varicoceles and in another seems peak levels were higher in post-varicoceletomy patient
Thing is I'm seriously considering, as an alternative to TRT, going on T3 + HCG with aromatase inhibitors