Long Term GnRH suppression --> downregulation/reduction GnRH Receptor ?

[living2die]

I am well aware that after long term AAS use, the LH receptors in the body (namely sex organs, brain, etc) become downregulated/suppresses/reduced in number do to the low/non existing circulating LH levels.

Does the same occur with GnRH receptors ? If one had been continuously using AAS for extended periods, using HCG to stimulate the hormonal pathway (as an LH analog), would GnRH receptors also be reduced in number, as well as suffer from downregulation due to the complete or near to complete absence of GnRH ?

I know that when someone has been taking AAS long term without concomitant HCG use, after beginning to supplement w/ HCG, it will take a while for the testes and the like to respond to the HCG circulating in the body because the body has downregulated/reduced in capacity the number of LH receptors...however in time, the body will 're-grow/reactivate' LH receptors within the body after x amount of time using HCG.

If this analogy of HCG can be applied to GnRH supplementation, I wonder how long it would take for the body to 'reactivate/regrow' GnRH receptors after prolonged absence of a GnRH signal due to long term AAS use?

 

[Michael Scally MD]

Once again, I do not have the time to elaborate on this topic. However, GnRH dysfunction is a real problem in AAS induced hypogonadism. As this case study shows, use of GnRH (LH-RH) may prove curative. I have included the article as an attachment to set you on your way.


van Breda E, Keizer HA, Kuipers H, Wolffenbuttel BH. Androgenic anabolic steroid use and severe hypothalamic-pituitary dysfunction: a case study. Int J Sports Med 2003;24(3):195-6.

The data of the present case demonstrate that the abuse of androgenic anabolic steroids (AAS) may lead to serious health effects. Although most clinical attention is usually directed towards peripheral side effects, the most serious central side effect, hypothalamic-pituitary-dysfunction, is often overlooked in severe cases. Although this latter central side-effect usually recovers spontaneously when AAS intake is discontinued, the present case shows that spontaneous recovery does not always take place. We suggest that hypothalamic-pituitary dysfunction should always be considered in the differential diagnosis in athletes seen with typical presentation of anabolic steroid use. In order to regain normal hypothalamic-pituitary function, supraphysiological doses of 200 microg LH-RH should be considered when the physiological challenge test with LH-RH (50 microg) fails to show an acceptable response.

 

[living2die]

Currently taking GnRH, after reading this literature provided by Dr. Scally (thanks Scally !) I decided that as I have had next to nil GnRH circulating, due to prolonged AAS induced dysfunction of my HPTA axis, I thought I should rev up the dose of GnRH. I took 1 shot of [2000mcg - 2MG vial] / mL yesterday, and I did report feeling an increase in wellbeing. The only negative is GnRH is that taken for too long at too high doses (same situation as with HCG over prolonged periods and at high doses) GnRH can actually desensitize GnRH receptors (I doubt I have a problem with this as I have had nil GnRH circulation within the last four years).

Once again, I do not have the time to elaborate on this topic. However, GnRH dysfunction is a real problem in AAS induced hypogonadism. As this case study shows, use of GnRH (LH-RH) may prove curative. I have included the article as an attachment to set you on your way.


van Breda E, Keizer HA, Kuipers H, Wolffenbuttel BH. Androgenic anabolic steroid use and severe hypothalamic-pituitary dysfunction: a case study. Int J Sports Med 2003;24(3):195-6.

The data of the present case demonstrate that the abuse of androgenic anabolic steroids (AAS) may lead to serious health effects. Although most clinical attention is usually directed towards peripheral side effects, the most serious central side effect, hypothalamic-pituitary-dysfunction, is often overlooked in severe cases. Although this latter central side-effect usually recovers spontaneously when AAS intake is discontinued, the present case shows that spontaneous recovery does not always take place. We suggest that hypothalamic-pituitary dysfunction should always be considered in the differential diagnosis in athletes seen with typical presentation of anabolic steroid use. In order to regain normal hypothalamic-pituitary function, supraphysiological doses of 200 microg LH-RH should be considered when the physiological challenge test with LH-RH (50 microg) fails to show an acceptable response.