They are made up of testosterone with an attached ester including the propionate (TP), enanthate (TE), cypionate (TC) and undecanoate (TU) formulated with an oil plus other excipients to enhance the solubility of the ester. Currently, testosterone injections and testosterone gel preparations are more commonly used in the US. Testosterone preparations that are currently available include injections, transdermal patches and gels, oral testosterone, buccal tablets, oral capsules and testosterone implants (Table 3). Elevation of hematocrit above the reference range may lead to increased blood viscosity, which may increase thrombotic complications such as stroke, myocardial infarction, deep vein thrombosis and pulmonary embolism. Gynecomastia may occur with the administration of testosterone because of its conversion to estradiol. The decrease in central adiposity and minor improvements in insulin sensitivity and hemoglobin A1C have also been reported in individuals with hypogonadism and metabolic syndrome and/or type 2 diabetes 2,57,58,61-66. There is conflicting information regarding the ability of testosterone to improve erectile dysfunction independent of the effects on libido 31,34-38.
In addition to hCG and testosterone replacement therapy, there are other medications that stimulate the production of endogenous testosterone. Many patients with congenital hypogonadotropic hypogonadism require hCG and FSH to complete spermatogenesis while acquired hypogonadotropic hypogonadism may be managed with hCG alone 143,144. If the patient desires fertility, replacement of LH is usually achieved by using human chorionic gonadotropin (hCG).
Literally everyone I’ve ever seen on here doing HCG monotherapy eventually switched to TRT and they don’t switch back. HCG monotherapy hasn’t shown great results in itself but doing very small doses would be extra horrible. 100iu/day of HCG only would not be enough to bring levels up high enough. HCG Monotherapy means therapy only using HCG. 3 х 1500ui is a fertility protocol, not for optimizing t. HCG therapy resulted in a satisfactory biochemical and symptomatic response in 40 men (95.2%). 24 men (50.7%) were on clomiphene citrate or T prior to switching to hCG therapy.
The more common causes of primary hypogonadism or hypergonadotropic hypogonadism include chromosomal defects (e.g., Klinefelter syndrome), testicular injury (e.g., chemotherapy, radiation, surgery, trauma) and infection. Primary hypogonadism results from disorders of the testes that lead to low testosterone production and impaired spermatogenesis. The decreased functional ability of the testis to produce adequate amounts of testosterone and/or mature spermatozoa can be due to defects in the testis, pituitary and/or hypothalamus, or at multiple levels. The options of testosterone delivery systems (injections, transdermal patches/gels, buccal tablets, capsules and implants) have increased in the last decade. You can see the same threads on all forums all over again every day - the guy has the symptoms but he is refused treatment because he is in range. And all of them should go on TRT to increase their levels to above 1000 ng/dl to get ‘there’?
Early findings suggest that hCG treatment may cause fewer side effects than traditional testosterone replacement therapy (TRT). The strength of this study is that it is the first to quantify the safety of hCG in patients with previous T therapy. HCG may serve as a potential method of T therapy in patients who do not qualify for exogenous T, even those with former T use.

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