HCG Articles 2

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Plasma testosterone response at 1st and 4th day after short- and long-term hCG stimulation test

            (Adiyaman, Ocal et al. 2004) Download

Human chorionic gonadotropin (hCG) stimulation test is a reliable dynamic test for the evaluation of testicular function during childhood. Several protocols have been recommended but their reliability is controversial. In order to decide the best timing to measure stimulated testosterone levels in short- and long-term hCG protocols, we evaluated 83 prepubertal patients in two group. In group A, 34 patients with isolated micropenis and in group B, 49 inguinal cryptorchidic patients were enrolled. In group A short-term hCG protocol (3000 IU/m2/im/3 days) and in group B long-term hCG protocol (1500 IU/m2/im; thrice a week for 3 weeks) was administered. Blood samples were drawn at the initiation of the test and then at the 1st and 4th days after the last hCG injection. Each case's peak stimulated testosterone (Tmax) and the incremenet in plasma testosterone (deltaT) were calculated and compared with the 1st and 4th day responses within the group. In the short-term protocol the 4th day responses were higher than the 1st day responses (p<0.01). Interestingly, while four patients had insufficient responses at the 1st day, three had sufficient Leydig cell response at the 4th day. In the long-term protocol group, in contrast to the short-term group, the 1st day responses were higher than the 4th day (p<0.01). According to our results, while performing hCG test in a patient, if a short-term protocol is planned, it is more convenient to check the 4th day testosterone response. On the other hand, in a long-term protocol it is best to check the 1st day response. We suggest that even if a patient's 1st day response is inadequate, the 4th day response should be checked in order to avoid misdiagnosis.

Gonadotropin modulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity in desensitized luteinized rat ovary

            (Azhar, Chen et al. 1984) Download

These studies were done to examine the effect of gonadotropin on rat luteal 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase activity (the rate-limiting step in cholesterol biosynthesis) in ovaries of pregnant mare's serum gonadotropin (PMSG)-human chorionic gonadotropin (hCG) primed rats. Administration of hCG stimulated HMG CoA reductase activity in a time- and dose-dependent manner: significant increases were noted within 4 h, with maximum effects (30-40-fold increases) seen 24 h after hCG (25 IU) administration. This effect was specific in that only LH, of several hormones tested, was as effective as hCG in stimulating HMG CoA reductase activity, and no change in the activity of either liver microsomal HMG CoA reductase or luteal microsomal NADPH-cytochrome c reductase was seen after hCG. The gonadotropin-induced increase in HMG CoA reductase activity seemed to be due to a net increase in enzyme activity, not to a change in the phosphorylated/dephosphorylated state of the enzyme. Pretreatment of animals with aminoglutethimide, an inhibitor of the conversion of cholesterol to steroid (pregnenolone), prevented the hCG-induced rise in HMG CoA reductase activity, whereas treatment with 4-aminopyrazolo[3,4-d]pyrimidine (4-APP), which depletes cellular cholesterol content, led to striking increases in enzyme activity. However, the combined effects of 4-APP and hCG were additive, suggesting that the stimulating effect of hCG on HMG CoA reductase activity is not entirely due to a depletion of cellular sterol content of luteinized ovaries. Similarly, cholesteryl ester and cholesterol syntheses as measured by [14C]acetate conversion were also increased by hCG and 4-APP treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Human chorionic gonadotrophin and weight loss. A double-blind, placebo-controlled trial

            (Bosch, Venter et al. 1990) Download

Low-dose human chorionic gonadotrophin (HCG) combined with a severe diet remains a popular treatment for obesity, despite equivocal evidence of its effectiveness. In a double-blind, placebo-controlled study, the effects of HCG on weight loss were compared with placebo injections. Forty obese women (body mass index greater than 30 kg/m2) were placed on the same diet supplying 5,000 kJ per day and received daily intramuscular injections of saline or HCG, 6 days a week for 6 weeks. A psychological profile, hunger level, body circumferences, a fasting blood sample and food records were obtained at the start and end of the study, while body weight was measured weekly. Subjects receiving HCG injections showed no advantages over those on placebo in respect of any of the variables recorded. Furthermore, weight loss on our diet was similar to that on severely restricted intake. We conclude that there is no rationale for the use of HCG injections in the treatment of obesity.

Human chorionic gonadotropin treatment of nonorganic erectile failure and lack of sexual desire: a double-blind study

            (Buvat, Lemaire et al. 1987) Download

Forty-five cases of nonorganic failure (n = 39) or lack of sexual desire (LSD, n = 6) were treated for one month, either with human chorionic gonadotropins (HCG, 5,000 IU I.M. twice per week) or with placebo using a double-blind method. HCG gave better results than placebo (47% vs 12%, p less than 0.05) and improved a higher number of sexual parameters (6/7) than placebo (2/7). HCG effect on sexual behavior did not correlate with the increase in plasma testosterone level: it seems HCG is a useful option in sexologic treatment of erectile failure and LSD.

The action of chorionic gonadotrophin in the obese

            (Carne 1961) Download

Hyperglycosylated hCG

         (Cole 2007) Download

Hyperglycosylated hCG (hCG-H) is a glycosylation variant of the hormone hCG. Here we review all that is known about this independently functioning molecule. As discussed, it is a very different molecule to the hormone hCG. First, hCG-H is produced by cytotrophoblast cells while regular hCG is made in syncytiotrophoblast cell. Second, it is an autocrine acting directly on the cells which produce it, while regular hCG is an endocrine acting on maternal corpus luteal cells. Third, hCG-H has minimal biological activity in promoting progesterone production compared to regular hCG. Fourth, hCG-H functions unlike regular hCG as an invasion promoter, whether invasion as in choriocarcinoma and testicular germ cell malignancies, or as in implantation of pregnancy. These functions seemingly occur through action on cytotrophoblast cell TGFbeta receptors. Fifth, hCG-H is an essential component for successful human implantation to prevent early pregnancy loss and spontaneous abortion. Sixth, hCG-H is critical for promoting the midtrimester hemochorial implantation, and for preventing preeclampsia. Seventh, measurements of hCG-H have advantages over measurements of regular hCG or total hCG, in detecting pregnancy, pregnancy outcome (failing or term pregnancy), predicting preeclampsia in pregnancy, or as a tumor marker for gestational trophoblastic diseases.

In vitro induction of human suppressor T cells by a chorionic gonadotropin preparation

            (Fuchs, Hammarstrom et al. 1981) Download

Human chorionic gonadotropin (hCG) in physiological retroplacental concentration has been shown to possess the capacity of inducing human lymphocytes which are subsequently competent to depress an antibody response induced by purified protein derivative of tuberculin, phytohemagglutinin, lipopolysaccharide and pokeweed mitogen. These suppressor cells inhibited the T cell-dependent mitogen-induced activation of lymphocytes synthesizing IgM, IgG and IgA. No suppression by hCG-induced cells was observed in Epstein-Barr virus activated cell cultures, indicating a T cell origin of the target cell. It is suggested that this may represent a mechanism for the cellular basis of an hCG-induced immunosuppressive effect in pregnancy.

Sex-dependent induction of human suppressor T cells by chorionic gonadotropin

         (Fuchs, Hammarstrom et al. 1982) Download

Human chorionic gonadotropin (hCG) in physiological retroplacental concentration has been shown to induce human female lymphocytes which suppress the proliferation and differentiation of B cells stimulated by purified protein derivative of tuberculin. To test whether the hCG-induced suppression was sex dependent parallel experiments using female and male peripheral lymphocytes were performed. hCG did not induce cells capable of suppressing purified protein derivative induced B cell proliferation in lymphocytes from males, which was in contrast to lymphocytes from females where a statistically significant suppression was found. A similar hCG-induced suppressive effect was found before menarche, after the menopause and in two patients with Turner's syndrome, suggesting that a gene(s) on the Y chromosome exerts a regulatory function and thus prevents the hormone from inducing suppressor T cells.

Clinical review: The rationale for banning human chorionic gonadotropin and estrogen blockers in sport

            (Handelsman 2006) Download

CONTEXT: The objective of the study was to review the rationale underlying the banning of human chorionic gonadotropin (hCG) and estrogen blockers (antiestrogens, specific estrogen receptor modulators, aromatase inhibitors) in sports for male and female athletes in the light of gender differences in regulation of reproductive physiology. EVIDENCE ACQUISITION: We reviewed well-controlled clinical studies of exogenous testosterone effects on human muscle size and strength in men and all available evidence relevant to the effects of hCG and estrogen blockers on blood testosterone in men and women. EVIDENCE SYNTHESIS: Well-designed placebo-controlled clinical studies in men with suppressed pituitary-testicular axis establish a strong case that, across a wide range from sub- to supraphysiological doses, muscle growth and strength is proportional to exogenous testosterone dose and resulting blood testosterone concentrations. In men, there is unequivocal evidence that hCG and estrogen blockers cause consistent and sustained rise in blood testosterone concentrations. In women, although there has been no direct testing of ergogenic or myotrophic properties of exogenous testosterone in healthy women, either hCG or estrogen blockers do not produce any consistent or biologically significant increase blood testosterone concentrations. CONCLUSIONS: In men undergoing potential stimulation of endogenous blood testosterone concentrations, blood testosterone concentration is a reasonable surrogate measure for muscle growth and increased strength in men. Because hCG and estrogen blockers produce marked increase in blood testosterone concentration in men, this provides strong evidence to support the banning of hCG and estrogen blockers in men. In women, however, the negligible effect on blood testosterone suggests that drug-induced performance enhancement by hCG or estrogen blockers is highly unlikely. Furthermore, routine urinary hCG testing in young women risks invasion of privacy by detecting unrecognized pregnancy. These considerations suggest that prohibition of hCG and estrogen blockers should be restricted to men in which they are well justified.

Chorionic gonadotropin and obesity

            (Hutton 1970) Download

Does hCG or hCGbeta play a role in cancer cell biology?

            (Iles, Delves et al. 2010) Download

The role that hCG might play in the oncogenic process in cancer is certainly complex. We know that the expression of hCG and its beta subunit is a widespread phenomenon which has been described in many cancer subtypes. However, hCG's involvement in breast cancer has been antithetical: the detection of ectopically expressed hCG(beta) by breast tumors has been employed as a biomarker of malignancy, and hCG has been proposed as a ligand vehicle for toxic drugs, with the aim of targeting the LH/hCG receptor which is reported to be expressed by malignant breast tissue. However, it has also been proposed that hCG is a protective agent against the development of breast cancer, leading some to advocate hCG administration to non-pregnant women as a prophylactic measure against cancer. Nevertheless, suggestions that hCG is involved in the angiogenesis, metastasis and immune escape that are central to cancer progression - are phenomena which clearly apply to breast cancer. Indeed, a tumor vaccine based upon hCG has very recently been shown to protect against mammary tumors in mice. We propose that this apparent paradox is resolved if the free beta subunit of hCG produced by tumors acts as an autocrine anti-apoptotic and angiogenic growth factor, whilst intact heterodimeric hCG, as in pregnancy, is part of developmental signaling that initiates tissue differentiation (including breast ductal tissue development), and hence reduces the population of stem-like cells which are susceptible to oncogenic factors.


Human chorionic gonadotropin (hCG) and prevention of breast cancer

            (Janssens, Russo et al. 2007) Download

Animal and 'in vitro' experiences learned that human chorionic gonadotropin (hCG) is capable to protect from breast cancer. Receptors for hCG/luteinizing hormone (LH) are present on human female and male breast cancer cells. hCG decreases proliferation and invasion of breast cancer MCF-7 cells by inhibiting NF-kappa B, AP-1 activation and other genes. Doxorubicin toxicity is enhanced by conjugation with beta-hCG in MCF-7 cells. All these pieces of evidence suggest that hCG is active in human breast cancer. Direct proof however is missing. We performed a pilot study phase I trial for testing the inhibitory effects or recombinant hCG (rhCG) on primary breast cancer. Twenty-five postmenopausal women with newly diagnosed breast cancers of more than 1.5 cm were biopsied before randomization to receive either 500 microg rhCG (n=20) or placebo. After 2 weeks, surgery was done and tissues were analysed with regard to morphological, immunohistochemical and biochemical changes in tissues and plasma. rhCG reduces significantly the proliferative index and the expression of both the oestrogen receptor and progesterone receptor. rhCG does not modify the hormonal level of estradiol, progesterone, inhibin and follicle stimulating hormone (FSH) but increases significantly the level of LH. In a second pilot study, we tested the clinical efficacy through an open-label single centre study in 13 postmenopausal women with metastatic breast cancer. A 500 microg rhCG once every 2 days shows activity in postmenopausal metastatic breast cancer. The time to progression is relatively short. Response to previous hormonal treatment is indicative for rhCG activity. Given the data in primary and metastatic breast cancer rhCG further large scale investigation is highly warranted. rhCG can be an realistic option in (chemo-) prevention trials.

Human chorionic gonadotropin is an immune modulator and can prevent autoimmune diabetes in NOD mice

            (Khil, Jun et al. 2007) Download

AIMS/HYPOTHESIS: Expression of T helper (Th)1 cytokine mRNA in pregnant women is known to be inversely correlated with serum human chorionic gonadotropin (hCG). Type 1 diabetes is a Th1-mediated autoimmune disease, in which intervention at an early stage of the autoimmune process can prevent disease progression. We hypothesised that immune modulation by treating young NOD mice with hCG may prevent diabetes. METHODS: Female NOD mice were treated with hCG or recombinant hCG from 3 to 15 weeks of age and the incidence of diabetes and development of insulitis was determined. CD4(+) and CD8(+) T cell populations, T cell proliferation, cytokine production and CD4(+)CD25(+) regulatory T cells were examined and adoptive transfer experiments were performed. RESULTS: Both purified and recombinant hCG prevented development of diabetes in NOD mice. hCG decreased the proportion and number of CD4(+) and CD8(+) T cells and inhibited T cell proliferative responses against beta cell antigens. hCG treatment suppressed IFN-gamma production, but increased IL-10 and TGF-beta production in splenocytes stimulated with anti-CD3 antibody. hCG treatment also suppressed TNF-alpha production in splenocytes stimulated with lipopolysaccharide. Furthermore, hCG treatment increased the CD4(+)CD25(+)/CD4(+) T cell ratio in spleen and pancreatic lymph nodes. Depletion of CD4(+)CD25(+) T cells from splenocytes of hCG-treated NOD mice abolished their preventive effect on diabetes transfer. CONCLUSIONS/INTERPRETATION: We conclude that hCG has an immunomodulatory effect by downregulating effector cells, including Th1 cells, CD8(+) T cells and macrophages, and increasing the CD4(+)CD25(+)/CD4(+) T cell ratio, thus preventing autoimmune diabetes in NOD mice.

The action of chorionic gonadotrophin in the obese

(Lebon 1961) Download

Upregulation of human chorionic gonadotrophin-induced steroidogenic acute regulatory protein by insulin-like growth factor-I in rat Leydig cells

            (Lin, Wang et al. 1998) Download

Insulin-like growth factor-I (IGF-I) plays an essential role in reproductive function. Leydig cells express specific IGF-I receptors, and IGF-I enhances human chorionic gonadorphin (hCG)-induced testosterone formation. In the present study, we evaluate the effect of IGF-I on the gene expression and protein levels of steroidogenic acute regulatory protein (StAR), the rate-limiting step in steroidogenesis. StAR mRNA is expressed in rat Leydig cells as two major transcripts of 3.8 and 1.7 kb. StAR mRNA levels (both 3.8 and 1.7 kb) were markedly induced about 20-fold by hCG (10 ng/mL). Concomitant addition of IGF-I (50 or 100 ng/mL) and hCG (10 ng/mL) resulted in significant increases in StAR and cytochrome P450 side-chain cleavage (P450scc) mRNA levels, whereas lower doses of IGF-I (1 or 10 ng/ mL) had small effects. Synergistic effects of IGF-I and hCG on StAR mRNA levels were confirmed by ribonuclease protection assay (RPA). IGF-I (100 ng/mL) enhanced hCG- and 20 OH-cholesterol + hCG-induced testosterone formation, whereas the conversions of pregnenolone, 17-OH pregnenolone, dehydroepiandrosterone, and androstenedione to testosterone were not affected. This suggests that the major effect of IGF-I is at the steps of StAR and P450scc, whereas other steroidogenic enzymes are not affected. To evaluate whether increased StAR mRNA levels induced by IGF-I and hCG are associated with increased StAR protein levels, we carried out Western blot analyses. Basal StAR protein levels were low after 24 h in culture. hCG (10 ng/mL) increased StAR protein by 4.5-fold. In the presence of IGF-I (100 ng/mL), hCG-induced StAR protein levels were further increased. In conclusion, our present study demonstrated that IGF-I enhances Leydig cell steroidogenesis by upregulating hCG-induced StAR gene expression and protein production.

Successful treatment of acquired undescended testes with human chorionic gonadotropin

            (Meijer, Hack et al. 2001) Download

Human chorionic gonadotrophin therapy may have its place in the management of acquired undescended testes and surgery should be reserved for those who fail to respond to therapy. Further studies are necessary to evaluate these preliminary results.

Successful treatment of anabolic steroid-induced azoospermia with human chorionic gonadotropin and human menopausal gonadotropin

            (Menon 2003) Download

OBJECTIVE: To document for the first time the successful treatment using human chorionic gonadotropin (hCG) and human menopausal gonadotropins (hMG) of anabolic steroid-induced azoospermia that was persistent despite 1 year of cessation from steroid use. DESIGN: Clinical case report. SETTINGS: Tertiary referral center for infertility. PATIENT(S): A married couple with primary subfertility secondary to azoospermia and male hypogonadotropic hypogonadism. The husband was a bodybuilder who admitted to have used the anabolic steroids testosterone cypionate, methandrostenolone, oxandrolone, testosterone propionate, oxymetholone, nandrolone decanoate, and methenolone enanthate. INTERVENTION(S): Twice-weekly injections of 10,000 IU of hCG (Profasi; Serono) and daily injections of 75 IU of hMG (Humegon; Organon) for 3 months. MAIN OUTCOME MEASURE(S): Semen analyses, pregnancy. RESULT(S): Semen analyses returned to normal after 3 months of treatment. The couple conceived spontaneously 7 months later. CONCLUSION(S): Steroid-induced azoospermia that is persistent after cessation of steroid use can be treated successfully with hCG and hMG.

Human chorionic gonadotropin as an angiogenic factor in breast cancer during pregnancy

            (Michel, Aguilar et al. 2007) Download

Breast cancer associated with pregnancy is defined as the one in which the diagnosis is made in a pregnancy or within one year of delivery. Breast cancer is the second most common malignancy during pregnancy and it is generally considered to have a worse prognosis than the one that is not associated with pregnancy. The average patient is between 32 and 38 years of age. Steroid hormone receptor-positive cell populations comprise 80% of breast cancers, however, estrogen receptor levels in pregnancy-associated tumors are often low or absent. Extensive laboratory data suggest that angiogenesis plays an essential role in breast cancer development, invasion, and metastasis. One of the most powerful stimulatory factors, vascular endothelial growth factor (VEGF), functions in autocrine/paracrine pathways. Current research, generally has validated the poor prognosis and early relapse that are associated with increasing microvessel density, which is related to VEGF expression in tumoral cells. During pregnancy, human chorionic gonadotropin (hCG) induces neovascularization in various tissues, one of them being the placenta. Its receptors have been detected in epithelial cells in breast carcinoma tissue, and breast cancer cell lines. According to this premise the hCG normally produced during pregnancy could induce the synthesis of VEGF and by this means stimulate the development and metastatic potential of breast cancer cells in the pregnancy period. Thus, research involving hCG and VEGF would help us understand the physiopathology of breast cancer during pregnancy, as well as provide us with probable prognostic tools.

The effects of crude and purified human gonadotropin on in vitro stimulated human lymphocyte cultures

            (Morse, Stearns et al. 1976) Download

Feedback and hormonal regulation of hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase: the concept of cholesterol buffering capacity

            (Ness and Chambers 2000) Download

Regulation of the expression of hepatic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase by the major end product of the biosynthetic pathway, cholesterol, and by various hormones is critical to maintaining constant serum and tissue cholesterol levels in the face of an ever-changing external environment. The ability to downregulate this enzyme provides a means to buffer the body against the serum cholesterol-raising action of dietary cholesterol. The higher the basal expression of hepatic HMG-CoA reductase, the greater the "cholesterol buffering capacity" and the greater the resistance to dietary cholesterol. This review focuses on the mechanisms of feedback and hormonal regulation of HMG-CoA reductase in intact animals rather than in cultured cells and presents the evidence that leads to the proposal that regulation of hepatic HMG-CoA reductase acts as a cholesterol buffer. Recent studies with animals have shown that feedback regulation of hepatic HMG-CoA reductase occurs at the level of translation in addition to transcription. The translational efficiency of HMG-CoA reductase mRNA is diminished through the action of dietary cholesterol. Oxylanosterols appear to be involved in this translational regulation. Feedback regulation by dietary cholesterol does not appear to involve changes in the state of phosphorylation of hepatic HMG-CoA reductase or in the rate of degradation of this enzyme. Several hormones act to alter the expression of hepatic HMG-CoA reductase in animals. These include insulin, glucagon, glucocorticoids, thyroid hormone and estrogen. Insulin stimulates HMG-CoA reductase activity likely by increasing the rate of transcription, whereas glucagon acts by opposing this effect. Hepatic HMG-CoA reductase activity undergoes a significant diurnal variation due to changes in the level of immunoreactive protein primarily mediated by changes in insulin and glucagon levels. Thyroid hormone increases hepatic HMG-CoA reductase levels by acting to increase both transcription and stability of the mRNA. Glucocorticoids act to decrease hepatic HMG-CoA reductase expression by destabilizing reductase mRNA. Estrogen acts to increase hepatic HMG-CoA reductase activity primarily by stabilizing the mRNA. Deficiencies in those hormones that act to increase hepatic HMG-CoA reductase gene expression lead to elevations in serum cholesterol levels. High basal expression of hepatic HMG-CoA reductase, whether due to genetic or hormonal factors, appears to result in greater cholesterol buffering capacity and thus increased resistance to dietary cholesterol.

Enhancement of radiosensitivity of the MCF-7 breast cancer cell line with human chorionic gonadotropin

            (Pond-Tor, Rhodes et al. 2002) Download

Secretion of human chorionic gonadotropin (hCG) during pregnancy induces differentiation of the mammary gland, thereby making breast tissue less susceptible to carcinogenesis. HCG binds to specific hCG receptors on mammary epithelial cells inducing changes in gene expression that can inhibit cell proliferation and, therefore, interfere with tumorigenesis. Since breast cancer cells also contain a relatively high level of the hCG receptor, hCG has potential as a therapeutic agent. We postulated that hCG might also enhance the radiosensitivity of breast cancer cells and, therefore, be useful as an adjunctive therapy. In the present study, MCF-7 breast cancer cells grown in cell culture were treated with hCG (0.2-5 IU/ml) for 24 h prior to exposing the cells to 0 Gy, 3 Gy, 4 Gy, or 5 Gy of radiation. Following irradiation, the MCF-7 cells were incubated either in the presence or absence of hCG. Cell survival was monitored with an MTT assay 1 day, 4 days, and 7 days after irradiation. All of the concentrations of hCG tested enhanced radiosensitivity of MCF-7 cells. The maximum enhancement occurred with MCF-7 cells that had been exposed to 2 IU/ml of hCG for at least 24 h prior to irradiation with 4 Gy. The use of higher concentrations of hCG or a higher dose of radiation did not increase the enhancement effect. Treatment of MCF-7 cells with hCG for only 24 h was sufficient to achieve the maximum effect. However, maintaining the cells in hCG beyond 24 h increased the effectiveness of the lowest hCG concentration. Using a linear-quadratic equation to analyze the data, we determined that the use of hCG would result in an 8-10% reduction in MCF-7 cell survival at a dose of 2 Gy, a typical dose used in conventional cancer therapy.

By the way, doctor. I've been trying to lose weight for a long time and nothing seems to work. What do you know about the HCG diet?

            (Robb-Nicholson 2010) Download

The action of chorionic gonadotrophin in the obese

            (Simeons 1954) Download

Chorionic gonadotropin in weight control. A double-blind crossover study

         (Young, Fuchs et al. 1976) Download

Two hundred two patients participated in a double-blind random cross-over study of the effectiveness of human chorionic gonadotropin (HCG) vs placebo in a wieght reduction program. Serial measurements were made of weight, skin-fold thickness, dropout rates, reasons for dropping out, and patient subjective response. There was no statistically significant difference between those receiving HCG vs placebo during any phase of this study (P greater than .1).


References

Adiyaman, P., G. Ocal, et al. (2004). "Plasma testosterone response at 1st and 4th day after short- and long-term hCG stimulation test." Turk J Pediatr 46(4): 309-14.

Azhar, S., Y. D. Chen, et al. (1984). "Gonadotropin modulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity in desensitized luteinized rat ovary." Biochemistry 23(20): 4533-8.

Bosch, B., I. Venter, et al. (1990). "Human chorionic gonadotrophin and weight loss. A double-blind, placebo-controlled trial." S Afr Med J 77(4): 185-9.

Buvat, J., A. Lemaire, et al. (1987). "Human chorionic gonadotropin treatment of nonorganic erectile failure and lack of sexual desire: a double-blind study." Urology 30(3): 216-9.

Carne, S. (1961). "The action of chorionic gonadotrophin in the obese." Lancet 2(7215): 1282-4.

Cole, L. A. (2007). "Hyperglycosylated hCG." Placenta 28(10): 977-86.

Craig, L. S., R. E. Ray, et al. (1963). "Chorionic gonadotropin in the treatment of obese women." Am J Clin Nutr 12: 230-4.

Fuchs, T., L. Hammarstrom, et al. (1981). "In vitro induction of human suppressor T cells by a chorionic gonadotropin preparation." J Reprod Immunol 3(2): 75-84.

Fuchs, T., L. Hammarstrom, et al. (1982). "Sex-dependent induction of human suppressor T cells by chorionic gonadotropin." J Reprod Immunol 4(4): 185-90.

Handelsman, D. J. (2006). "Clinical review: The rationale for banning human chorionic gonadotropin and estrogen blockers in sport." J Clin Endocrinol Metab 91(5): 1646-53.

Hutton, J. H. (1970). "Chorionic gonadotropin and obesity." Am J Clin Nutr 23(3): 243-4.

Iles, R. K., P. J. Delves, et al. (2010). "Does hCG or hCGbeta play a role in cancer cell biology?" Mol Cell Endocrinol 329(1-2): 62-70.

Janssens, J. P., J. Russo, et al. (2007). "Human chorionic gonadotropin (hCG) and prevention of breast cancer." Mol Cell Endocrinol 269(1-2): 93-8.

Khil, L. Y., H. S. Jun, et al. (2007). "Human chorionic gonadotropin is an immune modulator and can prevent autoimmune diabetes in NOD mice." Diabetologia 50(10): 2147-55.

Lebon, P. (1961). "The action of chorionic gonadotrophin in the obese." Lancet.

Lin, T., D. Wang, et al. (1998). "Upregulation of human chorionic gonadotrophin-induced steroidogenic acute regulatory protein by insulin-like growth factor-I in rat Leydig cells." Endocrine 8(1): 73-8.

Meijer, R. W., W. W. Hack, et al. (2001). "Successful treatment of acquired undescended testes with human chorionic gonadotropin." Eur J Pediatr 160(1): 66-7.

Menon, D. K. (2003). "Successful treatment of anabolic steroid-induced azoospermia with human chorionic gonadotropin and human menopausal gonadotropin." Fertil Steril 79 Suppl 3: 1659-61.

Michel, R. M., J. L. Aguilar, et al. (2007). "Human chorionic gonadotropin as an angiogenic factor in breast cancer during pregnancy." Med Hypotheses 68(5): 1035-40.

Morse, J. H., G. Stearns, et al. (1976). "The effects of crude and purified human gonadotropin on in vitro stimulated human lymphocyte cultures." Cell Immunol 25(2): 178-88.

Ness, G. C. and C. M. Chambers (2000). "Feedback and hormonal regulation of hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase: the concept of cholesterol buffering capacity." Proc Soc Exp Biol Med 224(1): 8-19.

Pond-Tor, S., R. G. Rhodes, et al. (2002). "Enhancement of radiosensitivity of the MCF-7 breast cancer cell line with human chorionic gonadotropin." Breast Cancer Res Treat 72(1): 45-51.

Robb-Nicholson, C. (2010). "By the way, doctor. I've been trying to lose weight for a long time and nothing seems to work. What do you know about the HCG diet?" Harv Womens Health Watch 17(9): 8.

Simeons, A. T. (1954). "The action of chorionic gonadotrophin in the obese." Lancet 267(6845): 946-7.

Young, R. L., R. J. Fuchs, et al. (1976). "Chorionic gonadotropin in weight control. A double-blind crossover study." JAMA 236(22): 2495-7.