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    We aim to provide consumers with helpful, in-depth information about nutrition and weight-loss products. All product names, logos and brands are property of their respective owners. We support the operation of our site through the sale of our all-natural, premium products, which include Burn TS and Boost, as well as through Amazon affiliate links (Amazon Associates Program). Whether we make money or not on a certain page does not influence the core mission of our writers and medical reviewers, which is to publish content that is accurate and informative. All our own products are made with premium ingredients supported by science and formulated in the United States in GMP-certified facilities. For more information, see our full Advertising Disclosure. Boosting testosterone levels is big business these days. A: The administration of antiestrogens is a common treatment because anti-estrogens interfere with the normal negative feedback of sex steroids at hypothalamic and pituitary levels in order to increase endogenous gonadotropin-releasing hormone secretion from the hypothalamus and FSH and LH secretion directly from the pituitary. In turn, FSH and LH stimulate Leydig cells in the testes, and this has been claimed to lead to increased local testosterone production, thereby boosting spermatogenesis with a possible improvement in fertility. There may also be a direct effect of antiestrogens on testicular spermatogenesis or steroidogenesis. Clomid is a mixed agonist/antagonist for the estradiol receptor. Clomid acts as an estrogen, rather than an antiestrogen, by sensitizing pituitary cells to the action of Gn RH. Although tamoxifen is almost as effective as Clomid in binding to pituitary estrogen receptors, tamoxifen has little or no estrogenic activity in terms of its ability to enhance the Gn RH-stimulated release of LH. The estrogenic action of Clomid at the pituitary represents a unique feature of this compound and that tamoxifen may be devoid of estrogenic activity at the pituitary level. Perusal of the literature thus indicates that clomiphene acts in several ways in the human male; (a) due to its similarity of structure to stilbesterol it binds with receptor sites in the hypothalamus and pituitary, (b) It stimulates gonadotrophin secretion by acting on the hypothalamo-hypophyseal system, (c) the inhibitory effects of high levels of circulating estrogens (produced under the influence of clomiphene) on hypothalamo-hypophyseal axis are possibly prevented by its potent antiestrogenic behaviour. The result of these varied effects of clomiphene is an overall increase in gonadotrophin and estrogen secretion and accounts for their increase under clinical conditions.

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