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HCG and it's Use in Functional Medicine!

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  • #31
    Contrary to what is posted on the net HCG does not promote weight loss at all.

    Ineffectiveness of human chorionic gonadotropin in weight reduction: a double-blind study.

    Stein MR, Julis RE, Peck CC, Hinshaw W, Sawicki JE, Deller JJ Jr.

    Our investigation was designed to retest the hypothesis of the efficacy of human chorionic gonadotropin (HCG) on weight reduction in obese women in a clinic setting. We sought to duplicate the Asher-Harper study (1973) which had found that the combination of 500 cal diet and HCG had a statistically significant benefit over the diet and placebo combination as evidenced by greater weight loss and decrease in hunger. Fifty-one women between the ages of 18 and 60 participated in our 32-day prospective, randomized, double-blind comparison of HCG versus placebo. Each patient was given the same diet (the one prescribed in the Asher-Harper study), was weighed daily Monday through Saturday and was counselled by one of the investigators who administered the injections. Laboratory studies were performed at the time of initial physical examinations and at the end of the study. Twenty of 25 in the HCG and 21 of 26 patients in the placebo groups completed 28 injections. There was no statistically significant difference in the means of the two groups in number of injections received, weight loss, percent of weight loss, hip and waist circumference, weight loss per injections, or in hunger ratings. HCG does not appear to enhance the effectiveness of a rigidly imposed regimen for weight reduction.

    PMID: 786001 [PubMed - indexed for MEDLINE]
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    • #32
      This study on rats shows a refractory period of 60-96 hours after HCG administration. This may lend support to every 3-4 day injects of HCG rather than eod.



      Testicular steroidogenesis after human chorionic gonadotropin desensitization in rats.

      Chasalow F, Marr H, Haour F, Saez JM.

      When a single injection of 500 I.U. of human chorionic gonadotropin (hCG) is given to rats there is an initial acute rise of plasma testosterone and of testicular content for both cyclic AMP and testosterone. This response correlates with an increase in both lyase and 17 alpha-hydroxylase activities. Thereafter both plasma and testicular testosterone decline and do not increase after a second injection of hCG. During this period of desensitization, isolated Leydig cells were insensitive to the steroidogenic stimulatory effect of both hCG and dibutyryl cyclic AMP. The post-cyclic AMP block is not due to an alteration of the cyclic AMP-dependent protein kinase but it is correlated with a decrease in both lyase and 17 alpha-hydroxylase activities of the Leydig cell's microsomes. This decrease is not caused by the absence of the recently described cytosol activator of this enzyme because its addition did not restore the enzymatic activity. Within 60 to 96 h after hCG injection there was a spontaneous increase of both plasma and testicular testosterone and this parallels the recovery of lyase and 17 alpha-hydroxylase activities. These results suggest that both enzymatic activities are regulated, directly or indirectly, by hCG, and that this is partly responsible for the hCG-induced steroidogenic refractoriness of Leydig cells.

      PMID: 221476 [PubMed - indexed for MEDLINE]

      full study
      http://www.jbc.org/content/254/13/5613.full.pdf
      All posts are for entertainment and may contain fiction. Consult a doctor before using any medication.

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      • #33
        The potential roles of estrogens in regulating Leydig cell development and function: A review

        References and further reading may be available for this article. To view references and further reading you must purchase this article.

        Tom O. Abney, , a

        a Department of Physiology and Endocrinology, Medical College of Georgia, Augusta, Georgia 30912, USA

        Available online 10 September 1999.

        Abstract
        It is generally agreed that estrogens, principally estradiol-17β, are synthesized by and act in the testis of mammals, including humans. The site of estradiol synthesis in the testis is generally believed to begin in the Sertoli cell and switch to the Leydig cell during neonatal development where a gonadotropin-regulated aromatase is present. Numerous studies suggest that the primary target cell of estradiol in the testis at all ages is the Leydig cell. In fact, the Leydig cell is known to possess an estrogen receptor that binds estradiol in the classic manner. The mechanism of estradiol action and the role of its receptor in the testis, however, remain unresolved. In Leydig cells, estradiol appears to induce several alterations that are dependent in large part on the developmental stage of the Leydig cell. In the fetal and neonatal testes, estradiol appears to block the ontogenic development of Leydig cells from precursor cells. There is also evidence that estradiol similarly blocks the regeneration of Leydig cells in the testis of mature, ethane dimethylsulfonate-treated animals. Evidence indicates that the precursor cell possesses high levels of estrogen receptors relative to that of the Leydig cell. It is postulated that estradiol is a paracrine factor involved in regulating the interstitial population of Leydig cells. Evidence also indicates that estradiol acts directly in the mature testis to block androgen production. It appears to do so by inhibiting the activities of several steroidogenic enzymes involved in testosterone synthesis. Although the more conventional receptor-mediated mode of action is feasible, several studies have suggested that this action might entail direct competitive inhibition of key steroidogenic enzymes by estradiol. In summary, the net biologic effect of estradiol in the testis appears to be inhibition of androgen production, either by limiting development and growth of the Leydig cell population or through direct action in the Leydig cell.
        All posts are for entertainment and may contain fiction. Consult a doctor before using any medication.

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        • #34
          Originally posted by heavyiron View Post
          Contrary to what is posted on the net HCG does not promote weight loss at all.

          Ineffectiveness of human chorionic gonadotropin in weight reduction: a double-blind study.
          HCG is not supposed to promote weight loss : it just changes where you lose weight to mainly fat while promoting muscle gain (even on 500 Cal/day). This is caused mainly by increase in the testosterone (and E2 in women) . In men a steroid cycle would probably work as well. This study forgot to measure body fat content, or they would have seen a significant difference.

          In uncontrolled settings HCG may result is greater weight loss caused by the improved motivation and ability to stick to this draconian 500 cal/day diet when you see inches melt away where it counts (rather than appearing to lose mainly muscle strength without HCG). Not having your muscle waste away will also make it easier to excercise and lose additional weight that way.

          500 Cal/day is dangerous without medical supervision since you will have a hard time eating enough protein, vegetables and fruit to cover basic nutritional requirements. There is no reason not to use HCG with a safer 1000+ Cal/day (low-carb) diet though.

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