The Use of HCG to Prevent / Reverse Testicular Shrinkage and Preserve FertilityHuma n Chorionic Gonadotropin From the book Testosterone: A Mans Guide, amazon. Hcg treatment for testicular atrophy chorionic gonadotropin HCG not to be confused with human growth hormone, or HGH is a glycoprotein hormone that mimics LH luteinizing hormoneproduced in pregnancy by the developing embryo soon after conception, and later hcg treatment for testicular atrophy part of the placenta. Its role is to prevent the disintegration of the corpus steroid shot for cyst acne of the treatmsnt and to maintain the progesterone production critical for pregnancy in women. HCG is used to cause ovulation and to treat infertility in women. But in men, HCG is also used in young boys when their testicles have not dropped down into the scrotum normally.
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Human chorionic gonadotropin HCG is used as a hormonal therapy to utilize the effects of pituitary derived endogenous gonadotropins, including luteinizing hormone LH and follicle stimulating hormone FSH. HCG is a glycoprotein composed of amino acids. HCG has a half-life in the range of hours while LH has a half-life in the range of minutes. The half-life of LH is physiologically important and allows for a pulsatile LH systemic exposure. LH and HCG are widely regarded as analogous hormones due to the similarity in the structure of the hormones, including the similar alpha subunits which exhibit similar biologic activities when associated with the beta subunit.
The beta subunit is unique to HCG. LH and HCG share a mutual receptor, however events after receptor binding are different between the two hormones. Human chorionic gonadotropin HCG and a recombinant formulation, called choriogonadotropin alfa r-HCG , is a gonad-stimulating polypeptide hormone normally secreted by the placenta during pregnancy.
The non-recombinant products are obtained from the urine of pregnant women. HCG has been used to treat cryptorchidism or hypogonadotropic hypogonadism in males, sometimes in combination with menotropins or follitropin. Interestingly, HCG was introduced for the treatment of cryptorchidism in , and remained the only hormonal agent available to treat the condition until the 's, when gonadotropin-releasing hormone GnRH analogs also became a treatment option. Urine-derived HCG was first approved by the FDA in , and received subsequent approval for additional indications in HCG binds to receptors that are present in reproductive tissues in the male, regulating fertility.
HCG is increasingly used in combination with Testosterone Therapy. When exogenous Testosterone is administered it influences the balance of the hypothalamus — pituitary — gonadal HPG axis. Estrogenic and androgenic mediated negative-feedback reduces the secretion and activity of gonadotropin releasing hormone GnRH and therefore reduces gonadotropin secretion.
Gonadotropins control the functionality of the gonads, including their production of hormones and physiological processes. More specifically, the reduction in LH and FSH activity reduce testicular spermatogenesis and testicular produced testosterone. Testicular atrophy is resultant of insufficient gonadotropin signaling.
HCG is commonly used during and after testosterone therapy to maintain and restore testicular size, endogenous testosterone production and spermatogenesis. HCG administration acts as supplemental gonadotropin, replacing absent LH activity. During testosterone therapy HCG has been found to maintain the level of intratesticular testosterone, and maintain normal spermatogenesis.
In idiopathic hypogonadotrophic hypogonadism patients, ranging in age from 12 to 24, HCG 1,, IU was administrated intramuscularly, 3 times per week, for 8 weeks. The HCG treatment increased the serum testosterone level, penile length, and testicular volume in idiopathic hypogonadotrophic hypogonadism patients. The mechanism of action of human chorionic gonadotropin HCG depends upon the purpose for which it is being used, the sex of the patient, and the level of maturity of the patient to whom it is administered.
Adult and adolescent males: In adult and adolescent men with hypogonadotropic hypogonadism, HCG acts like LH and stimulates testosterone production in the Leydig cells and spermatogenesis in the seminiferous tubules.
Stimulation of androgen production by HCG causes development of secondary sex characteristics in males e. Human chorionic gonadotropin HCG also stimulates the Leydig cells to produce estrogens; increased estrogen levels may produce gynecomastia in some males.
Once HCG is initiated, it takes at least 70—80 days for germ cells to reach the spermatozoal stage. Response to treatment is also noted by the development of masculine features and the normalization of serum testosterone levels. Induction of testicular growth and increased sperm volumes may help to restore fertility in these men after many months to years of treatment, which is then sometimes combined with the use of either menotropins or follitropin. In select females with infertility , human chorionic gonadotropin has actions essentially identical to those of luteinizing hormone LH.
Human chorionic gonadotropin HCG also appears to have additional, though minimal, follicle-stimulating hormone FSH activity. By administering HCG after follitropin, menotropins, or clomiphene, the normal LH surge that precedes ovulation can be mimicked. Human chorionic gonadotropin HCG promotes the development and maintenance of the corpus lutetium and the production of progesterone. Following HCG administration, final luteinization or maturation of the oocytes occurs and either ovulation can ensue for timed insemination techniques, or oocyte retrieval can take place for assisted reproductive technology ART procedures such as in vitro fertilization IVF.
Once pregnancy takes place, endogenous HCG is normally secreted by the placenta to support the continued secretion of female hormones and the corpus luteum. Male infants and children: In the male infant, normal testicular descent is complete by 3 months of age. Testicular descent occurs secondary to an endogenous testosterone surge stimulated by pituitary gonadotropins in response to the discontinued exposure to maternal circulating estrogens upon birth; this testosterone surge peaks within 60 days postnatally.
In male infants and children with cryptorchidism, HCG acts like LH and causes the Leydig cells of the testes to produce a testosterone surge and induce the descent of palpable testes. Hormonal therapies like HCG have not replaced the primary surgical treatment for the condition, which is orchiopexy within the first 1—2 years of life. Early animal studies have suggested that HCG may be used as an adjunct to orchiopexy to help preserve fertility, but human data is lacking.
Activity on body composition all sexes: Human chorionic gonadotropin has no known effects on appetite, or on mobilization or distribution of body fat. It is not an effective treatment for obesity. In sport, athletes use HCG as an 'undetectable' anabolic steroid; HCG increases the body's production of testosterone and epitestosterone without increasing the ratio of the two hormones in the urine above normal values.
Urinary testing is being developed which should allow for discriminate testing of HCG doping in sport. Role in Testosterone Replacement Therapy HCG binds to receptors that are present in reproductive tissues in the male, regulating fertility.
Testes- contains Leydig cells and Sertoli cells. Produces testosterone which is metabolized into a cascade of metabolites most importantly including estrogen and progesterone.
Luteinizing Hormone LH - binds with receptors on Leydig cells and interstitial cells in the testis, and promote the secretion of androgens by the Leydig cells.
Follicle-Stimulating Hormone FSH - binds with Sertoli cells which build the microenvironment of spermatogenesis, regulates the maturation of spermcells. Estrogen- estrogen receptors in the hypothalamus and these receptors direct the negative feedback of GnRH secretion, negatively regulate at a pituitary level and gonadal cell level in an autocrine manner.
Androgens- androgen receptors in the hypothalamus direct the negative feedback of GnRH secretion, regulate hormonal synthesis at gonadal cell level in an autocrine manner. Androgens have strong suppressive effects on gonadotropin synthesis in the anterior pituitary. Progesterone- negatively regulates the organizing hormone synthesis. HCG - mimics the functions of LH. Mechanism of Action The mechanism of action of human chorionic gonadotropin HCG depends upon the purpose for which it is being used, the sex of the patient, and the level of maturity of the patient to whom it is administered.