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Beyond this, it is critical for maintaining muscle mass, bone density, red blood cell production, and libido. It drives the development of male secondary sexual characteristics during puberty, such as deepening of the voice and growth of body hair. They are distinct molecules with unique roles, yet their pathways are intimately intertwined within the body's sophisticated regulatory system.
A final scenario is a patient who presents for VR for which he is otherwise a good candidate, who has a history of hypogonadism currently or previously treated with TRT. A second scenario is a patient who wishes to preserve existing spermatogenesis before beginning TRT or AAS use. CC is cost effective and has been more effective as a combined therapy in this setting, with less extensive data to support it as a monotherapy.80 If the patient exhibits a low T/E ratio, an AI could be prescribed, with anastrozole 1 mg oral twice weekly is a reasonable starting dose that may be titrated up or down according to the response. Data from the male contraception literature indicate a reasonable probability of recovery in 67%, 90%, 96%, and 100% of men at 6, 12, 16, and 24 months, respectively, with a median time to recovery of 20 × 106 ml-1 sperm in 3–6 months.13,30,31 Yet, many men will not tolerate discontinuation either due to severe hypogonadal symptoms, uncertainty of recovery, and/or timing issues, and these men may require some form of alternate androgen supplementation. If the patient and his partner are willing to wait and his hypogonadal symptoms are manageable without TRT or AAS, the patient could simply discontinue the use of TRT or AAS to allow spontaneous recovery.
It has been discovered in studies that the issue of recovery of the Leydig cells following anabolic steroid use is not due to a lack of LH, but due instead to the desensitization of the Leydig cells to LH. In any case, no matter how mild or severe an anabolic steroid exerts HPTA suppression, all anabolic steroids when utilized for typical cycle lengths of weeks at a time will eventually cause the HPTA to shut down, or at the very least severely suppress its hormonal signal processes. While some individuals might experience absolutely no HPTA suppression or shutdown at all, other individuals might experience severe HPTA suppression and shutdown to the extent where they might require far longer periods of time to ensure full recovery than most. Length of cycle (degree of testicular desensitization) With anabolic steroid use, there are several different major determining factors in how much difficulty an individual will experience in recovery of their HPTA and endogenous Testosterone function during PCT.
Both FSH and maintenance of high intratesticular testosterone (ITT) levels (50–100 fold higher than serum) in response to LH are critical for normal spermatogenesis to occur.21,22,23,24 Historically, Sertoli cell-produced androgen-binding protein was thought to be responsible for such high ITT levels, but recent data suggest that other factors are also involved.25 Interestingly, animal studies have demonstrated that the absence of FSH signaling results in impaired spermatogenesis whereas loss of sufficiently high ITT levels results in the absence of spermatogenesis.26 Both TRT and AAS use can lead to suppression of the hypothalamic-pituitary-gonadal (HPG) axis, resulting in a diminution of spermatogenesis and potential infertility. Both TRT and AAS can suppress the hypothalamic-pituitary-gonadal (HPG) axis resulting in diminution of spermatogenesis. The use of testosterone replacement therapy (TRT) for hypogonadism continues to rise, particularly in younger men who may wish to remain fertile. This intrinsic production contributes other hormones and precursors that are part of the natural testicular output, such as pregnenolone and other prohormones. To truly grasp why combining these two substances is even a consideration, one must understand the body's exquisite feedback loop for regulating testosterone, known as the HPTA. This is often when testosterone replacement therapy (TRT) is introduced under medical supervision to restore levels to a healthy, physiological range.
When the hypothalamus detects excess levels of Testosterone and/or Estrogen in the body (either from the use of exogenous androgens on an anabolic steroid cycle or otherwise), the hypothalamus will act to attempt to restore a balance by essentially doing the opposite of what was previously described. In the case of post cycle therapy, the concern is primarily with the negative feedback loop of the HPTA. The HPTA is the Hypothalamic Pituitary Testicular Axis, which is an axis of interconnected endocrine glands in the body that deal with and control Testosterone production. Furthermore, the attempt to allow the body to recover on its own will present a very high probability of long-term endocrine damage to the HPTA over time whereby the individual will develop anabolic steroid induced hypogonadism (the inability to manufacture proper levels of Testosterone for the rest of their life). SHBG (Sex Hormone Binding Globulin) is also a concern here as well, which is a protein that binds to sex hormones (Testosterone) and renders them inactive, essentially ‘handcuffing’ them and preventing them from exerting their effects. With Testosterone levels low and Cortisol levels in the normal (or high) range, Cortisol now becomes a threat to the newly created muscle that was created during the recent anabolic steroid cycle (Testosterone properly suppresses and counteracts Cortisol’s catabolic effects on muscle tissue).
This is why fertility concerns are common in men on long-term TRT and why a thoughtful approach to hormone therapy is essential. When levels are low, it ramps production back up. If you’re exploring or already on testosterone replacement therapy (TRT), you’ve probably come across the term HPTA. While the protocol can be effective, it’s important to consult with a specialist and monitor hormone levels closely to ensure the best possible. Another study published in the Journal of Andrology found that clomiphene citrate was effective in stimulating the release of LH and FSH and increasing testosterone levels in men with low testosterone. Also, it’s always advisable to consult with an endocrinologist or specialist in hormone replacement therapy before starting or discontinuing any hormone therapy.
HCG is essentially an analogue of LH, and the testes after a prolonged anabolic steroid cycle would be as equally desensitized to HCG as they are to LH. It has been mentioned already that much of the difficulty in recovering the HPTA following an anabolic steroid cycle is the result of Leydig cell desensitization. The majority of anabolic steroid users from the 1960s – mid 1980s did not even utilize any compounds for the purpose of hormonal recovery, and the term PCT did not even exist at that time. Therefore, HCG must be utilized with a SERM and especially an aromatase inhibitor, as HCG has demonstrated to increase aromatase activity in the testes, resulting in rising Estrogen levels. What results is an increase in Testosterone production via stimulation of the Leydig cells by HCG. It is a protein hormone manufactured in high amounts by pregnant females that contains a protein subunit that is 100% identical to LH, and therefore when administered to men, it will mimic the action of LH in target tissues, such as the testes. The other importance of aromatase inhibitors is the ability to mitigate the Estrogenic effects of HCG, which will be explained shortly.
The only following issue to cover now is that of stimulating and maintaining proper endogenous LH release so as to carry recovery along until the body can become self-sufficient once again. Estrogen rising is of course undesirable during PCT, as it has already been explained that Estrogen will trigger suppression of endogenous Testosterone production, and there is no doubt that any individual wishes to encounter Estrogenic side effects during PCT either. The human body, however, produces LH amounts on its own that are far too inefficient for proper and rapid Testosterone production. HCG should never be utilized alone, as its nature as a gonadotropin will itself trigger a negative feedback loop whereby once HCG is utilized, the pituitary gland will halt output of LH until HCG use has discontinued. By way of lowering total circulating blood plasma Estrogen levels, AIs will engage the negative feedback loop in a positive manner and result in the release of LH and FSH for the manufacture and secretion of more Testosterone. Rather than block the activity of Estrogen at the cellular level in different tissues, aromatase inhibitors (AIs) serve to lower total circulating Estrogen levels in the body by way of inhibiting the aromatase enzyme, which is the enzyme responsible for the conversion of androgens into Estrogen.
The HPG axis operates through a feedback loop, where the levels of testosterone and estrogen provide feedback to the hypothalamus and pituitary gland to regulate hormone production. However, long-term use of TRT can lead to suppression of the body’s own testosterone production, making it difficult for the individual to discontinue therapy and resume normal hormone levels. The HPTA (hypothalamic-pituitary-testicular axis) restart protocol is a method used to help the body resume its natural testosterone production after discontinuing testosterone replacement therapy (TRT). When estrogen levels are reduced, the body may increase testosterone production to compensate. The HPG axis is a hormonal feedback loop that regulates the production and secretion of sex hormones, including testosterone, in men.

Gender: Female