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Although steroids suppress testosterone production primarily by lowering the level of gonadotropic hormones, the big roadblock to a restored HPTA after we come off steroids is surprisingly not LH, testosterone, or FSH but the levels of sex hormones in the circulation. In this case, what the patients are receiving are either estrogen replacement therapy or HRT, which is estrogen-progestin-receptor-negative. But since these hormones have been proven by laboratory studies to have the same or enhanced efficacy as HRT in treating the same reproductive problems, it is reasonable to assume that it can similarly have the same effects on fertility, just in a different manner. Follicle Stimulating Hormone (FSH) has proven to be the major testosterone receptor agonist, and it has a higher affinity for the binding of testosterone than for LH, a similar affinity is obtained by the synthetic analogue 2-ethyl-6 alpha-methyltestosterone. Thus, it acts like FSH on testosterone. Estradiol stimulates the gonadotrophs (ovaries and testis) like estrogen. It binds to the transcription factors, which can be stimulated by testosterone and the LH of estrogen. It is then converted to the more potent estradiol by estrogen-dependent enzyme systems. However, since the conversion process is dependent on LH, the level at which it is elevated in the serum is a function of the target hormone. The mechanism of estradiol action in men who respond to FSH is similar to that in men who respond to testosterone, and has been studied extensively. It is not a question of determining the amount of FSH that is sufficient to stimulate the gonads but rather of finding estrogenic substrates that are highly expressed and that are able to respond to FSH. However, it is important to establish if the estradiol receptors available to the FSH receptor are high or low, because higher levels can only increase the amount of FSH. Many other studies have found that a very small, highly concentrated dose of estradiol has little effect on the LH receptor. In women, some evidence has also been seen for an inhibitory action on the LH receptor, which is probably not caused by the amount of estradiol but was reported by other investigators. For a discussion of the mechanism of estrogen-associated effects (including the effects of testosterone on the same receptors), please see this article. Progesterone also binds to the estrogen receptors (and also testosterone receptors) of the ovary, pituitary, and hypothalamus, and this potent estrogen-dependent action appears to be independent of the estrogen receptors. What

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