Still feeling like crap months after cycle
Read a post somewhere on here about guys running power restarts 2500 iu of hcg e0d then clomid at 50 for 30 days and nolva at 20mg for 45
And had great success with it
Did blood work multiple times test always low fsh and lh pretty low as well.
To much hcg or should I stick to it?
Talked a a known bodybuilder he suggested 1000iu of hcg eod for 14 days
I did talk to multiple doctors endo and urologist and both were kind of clueless
Hey, good luck to you. From the papers I posted in the other thread:
For the clinician using hCG and FSH to induce spermatogenesis, the clinical question is how to determine the optimal dose and timing based on normal physiology. One can start by looking back at studies that show that there is a linear relationship between GnRH secretion and resultant LH production (17). Unfortunately, some studies on LH and FSH pulsatility suggest great variation among subjects in terms of secretory dose and pulsatility when measured in short time intervals. In fact it is even debated whether there are FSH pulses (5,18-20). Small-scale studies on hCG (or recombinant LH) may imply that low dose hCG divided into several doses (300 IU over 5 days) may be more effective at producing an optimal testosterone to estradiol ratio compared to a single larger dose (1,500 IU ×1 dose) (21). In contrast, one study shows that hCG induces a biphasic response in testosterone production resulting in a peak at 2–4 hours and a higher one at 48 to 72 hours after one administration of hCG (22). This finding would indicate that every third or fourth day dosing would be ideal. Guidance on FSH dosing is even more elusive as the clinically useful outcome, spermatogenesis, is typically checked at 2.5 to 3 months intervals making it difficult to study multiple FSH doses and regimens. Therefore, the optimal dosing regimen for either hormone remains elusive and is likely patient specific.
In our experience, the subcutaneous route of administration is as effective as the intramuscular route for both gonadotropins and significantly increases patient compliance. Therapy is typically initiated with hCG alone at a dose of 1,000 IU on alternate days and the dose titrated based on trough testosterone levels and testicular growth (149). Alternatively, recombinant human hCG can also be administered subcutaneously from a prefilled syringe. In some patients the dose of hCG can be decreased over time as testicular size increases. In the majority of patients with larger testes at baseline, spermatogenesis can be initiated with hCG alone most likely due to residual FSH secretion (140, 150). Once there is a plateau in the response to hCG which typically occurs at around 6 months, therapy with FSH (in one of the three forms described above) should be added at a dose of 75 IU on alternate days. If sperm output and testicular growth remain suboptimal the dose of FSH can be gradually increased to 150 U daily. Continuation of this combined regimen for 12-24 months induces testicular growth in almost all patients, spermatogenesis in approximately 80% and pregnancy rates in the range of 50% (151-153). In an Australian study of 75 men with HH treated with gonadotropins the median time for sperm to appear in the ejaculate was 7.1 months and for conception was just over 28 months (152). Similar data were reported in a compilation of clinical trial data from Asian, European, Australian and American patients (153). Factors predictive of better outcome include larger baseline testicular size and absence of cryptorchidism. The Australian study reported that prior androgen use is also a negative prognostic indicator of response (152). While the study investigators propose that gonadotropin therapy be considered to induce puberty based on their results, confirmation that such an approach is superior to the conventional practice of giving testosterone would require a large clinical trial the logistics of which would be challenging given the rarity of this patient population. Gynecomastia is the most common side effect of gonadotropin therapy and is due to hCG stimulation of aromatase causing increased secretion of estradiol. This undesirable side effect can be prevented by using the lowest dose of hCG capable of maintaining serum testosterone levels towards the lower end of the normal range.
In my own experience which may be meaningless for you, I’ve had good response using 500 IU 3x per week of u-hCG after coming off TRT. What was your status before AAS use?