There’s a YouTube video linked in the log, the guy restarted after heavy cycles for 10 years. The important thing to note here is that your natural levels at 20 years old probably wont be your natural levels at 34 years old. Theoretically it would take a month to reach steady state levels. Quite similar age, time on TRT and natural levels to my own.
Self-administering this combination without medical supervision is strongly discouraged due to the risks of hormonal imbalance and side effects. If preserving testicular size and function and maintaining the possibility of fathering a **** are priorities, then the combination is vastly superior to testosterone alone. In this transitional phase, taking HCG does make a critical difference in the efficacy and speed of recovery. After a course of HCG, medications are then introduced to stimulate the pituitary to produce its own LH. The challenge is that the testes have been dormant and may be unresponsive to the body's naturally slowly returning LH signal. More importantly, this stimulation supports the ongoing process of spermatogenesis, significantly improving the chances of preserving fertility.
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 **** 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).
Several options could be discussed depending on the severity of his hypogonadal symptoms, timing in which he and his partner wish to achieve pregnancy, and assuming there is no clinical evidence of primary hypogonadism. A patient who presents for treatment of male factor infertility, indicated by oligospermia or nonobstructive azoospermia, who either reports a recent history or current use of TRT and/or AAS is a common scenario faced by a male fertility specialist. Certain clinical scenarios are commonly encountered, and a brief discussion of these authors’ recommendations for treatment in each scenario follows.
Following the use of exogenous anabolic steroids, the majority of users will experience what has been dubbed a "hormonal crash" or "post cycle crash", which is a bodily environment in which key hormones essential to the retention of the newly created muscle mass has been suppressed or shut down. It is important to remember humans are the only species to hide their fertile period, but this effect is a difference in the effect of the hormones rather than a difference in the HPG axis. Depending on which hormone and receptor are unable to bind different effects occur but all alter the HPG axis.citation needed

Gender: Female

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