Thyroid hormones do this via binding to thyroid hormone receptors (THR), activating a range of changes inside the cell (in a nutshell, though it’s obviously more complex than this). I’m sure many of you know that Thyroid hormones are renown for ‘burning fat’, in addition to muscle (when thyroid hormones are in excess). Thyroid hormones, triiodothyronine (T3) & thyroxine (T4) are based and released by the thyroid gland. There’s also inhibin, activin, leptin (hormone produce by fat tissue), insulin and ghrelin (hunger hormone), and kisspeptin which all play their role in this cycle. This is quite evidently enough time for the hormonal imbalance to wreak havoc on the body and result in any individual losing most or all of the newly gained muscle during this time. Today it is a very different story, where scientific and medical understanding of anabolic steroid use has soared exponentially since the old ‘golden era’ days of bodybuilding and anabolic steroid use in athletics. The concept of PCT did not exist prior to the late 1980s and early 1990s, as the understanding of the mechanisms by which anabolic steroids affected the body were not completely understood during the 1950s, 1960s, and 1970s. Low leptin levels contribute to the disruption of normal GnRH secretion, as leptin is needed for proper hypothalamic function and the initiation of puberty. The altered GnRH pulsatility leads to a decrease in the frequency and amplitude of LH and FSH release from the pituitary gland. In contrast to the stimulatory effects of leptin and insulin, ghrelin exerts predominantly inhibitory effects on GnRH secretion. Insulin, another metabolic hormone, also plays a significant role in modulating GnRH secretion. At the pituitary level, leptin directly stimulates the release of LH and, to a lesser extent, FSH via nitric oxide synthase activation in gonadotropes. Leptin, an adipocyte-derived hormone, exerts a stimulatory effect on GnRH secretion through multiple mechanisms. By stimulating GnRH release, kisspeptin indirectly promotes the secretion of LH and FSH from the pituitary gland. 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. Prenatal exposure to alcohol can affect the hormones regulating fetal development resulting in foetal alcohol spectrum disorder. Starvation from anorexia nervosa or bulimia causes the HPG axis to deactivate causing women's ovarian and uterine cycles to stop. Although often described as preventing pregnancy by mimicking the pregnancy state, hormonal birth control is effective because it works on the HPG axis to mimic the luteal phase of a woman's cycle. Chromosomal mutations tend to affect the androgen production rather than the HPG axis.citation needed During development, hormones help determine how neurons synapse and migrate to result in sexual dimorphisms. As males age, the testes begin to produce less testosterone, leading to a condition known as post-pubertal hypogonadism. Fluctuations in this axis cause changes in the hormones produced by each gland and have various local and systemic effects on the body. After testicular salvage therapy, the authors demonstrated an 83% overall success rate with VR, which was 100% if at least one vasovasostomy was performed.60 In that case series, if improvement in testicular volume on physical exam and increase in gonadotropin levels was appreciated, VR was performed; however, testicular sperm aspiration was performed in two of the six men to confirm spermatogenesis before VR due to insufficient testis volume improvement and/or lack of improvement of the HPG axis on serum hormone testing. A series evaluating anastrozole for treatment of secondary hypogonadism in 69 older men followed for 1 year confirmed a generally low rate of adverse events although one instance each of new diagnosis hepatitis, pulmonary embolism, and embolic stroke was reported.91 A similar observation of pulmonary embolism incidence was confirmed in a more recent series after only 12 weeks of treatment.90 In addition, some data have suggested potentially worse skeletal bone health with anastrozole use in older men, presumably based upon lower estrogen levels.92 Taken collectively, AIs may result in a positive influence on the HPG axis after TRT or AAS use, but in the absence of more robust clinical data and an uncertain side effect profile with long-term use, AI use may be limited to an adjunctive role only in those who have abnormally low T/E ratios. Inhibin B levels have been considered a surrogate for spermatogenesis; for example, men with spermatogenetic defects express lower inhibin B levels.27 Additional autocrine, paracrine, and endocrine factors within the hypothalamus, pituitary, and testis can function to further modulate the HPG axis in complex ways including endocannabinoids, GnRH, kisspeptin, norepinephrine, growth hormone, interleukins, and TGF-β.28 Therefore, the HPG axis represents a dynamic, but tightly regulated, system at multiple levels resulting in spermatogenesis, among other things. Endogenous testosterone directly inhibits GnRH and LH release at the hypothalamus and pituitary levels, respectively, leading to downstream attenuation of testosterone production. Significantly reducing this time and increasing the body's testosterone during the therapy process is the only way to stop treatment that makes sense, which means that some type of post-cycle therapy (PCT) plan is a sensible approach. You will stop taking testosterone and continue with HCG. Part 2- HCG Mono-therapy (4 week duration) This idea faded when many men using testosterone discovered that they could still get a woman pregnant. There was a time in history not long ago when it was thought that exogenous testosterone would be promoted as a male contraceptive. You don't want to give up testosterone all at once, as this will cause unnecessary symptoms that could last for many months. Over the past few years, the huge increase in testosterone prescriptions and TRT clinics has sadly led many men who have been misdiagnosed with low testosterone but to be given TRT when they might not need it in the first place. Do you think this adds much to the recovery timeframe? The theory behind adding HCG to a testosterone protocol is to mitigate the negative side effects caused by the HPTA shutdown. This is a well-known and expected side effect of testosterone-only therapy. I now commit the cardinal sin…… I cycle on and off purely for aesthetics as medically I don’t need TRT, my levels are mid range. With that being said, hormones aren’t fully understood by anyone yet. After 30 days, as long as your testosterone levels are high, you can discontinue hCG and adjust tamoxifen. For those who decide to stop taking TRT, there are protocols that can help restore the body's natural hormonal axis. External testosterone turns off the brain’s LH and FSH signaling, which lowers intratesticular testosterone, shrinks the testes, and halts sperm production. These can be positive effects as well as negative effects. However, at the end of the 21 week period, LH levels were observed to rise within 3 weeks once the exogenous Testosterone administration stopped, but Testosterone levels did not rise until many weeks later in most of the test subjects. In one study in which exogenous Testosterone was administered to male test subjects for 21 weeks, LH levels were suppressed shortly after beginning administration.
