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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Basics & Questions
so what *are* the possible causes of late-onset secondary hypogonadism?
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<blockquote data-quote="Aki" data-source="post: 138092" data-attributes="member: 14084"><p>[USER=15043]@Gman86[/USER] and [USER=38109]@Cataceous[/USER] - appreciate the responses</p><p></p><p>I too have some recollection of the feedback mechanism whereby LH/FSH production is signalled. And if I remember correctly, clomid works by blocking the estrogen receptors, fooling the pituitary into producing more LH and FSH and consequently more testosterone (assuming one's testicles still function). Now the question is, what was fooling the pituitary in the first place into sensing an excess of estrogen that didn't exist? In this regard, I think Gman86's explanation (of estrogen-like pollutants/mimics) has merit, although obviously it isn't entirely satisfactory either.</p><p>(And if it in fact is the primary explanation, raises another bunch of questions that need answering.)</p><p></p><p>Or could it just be that for some reason the pituitary has become more sensitive to estrogen so that even a small amount causes greater than normal negative feedback?</p><p></p><p>I also wonder why SHBG appears to behave "conspiratorially" and seeks to undo the testosterone rise induced by clomid.. like if you have a T-level of ~250 ng/dL with an SHBG of 15 nmol/L before taking clomid, and a low dose of clomid raises your T to 500-600 but your SHBG also creeps up to 30 nmol/L, it seems you've wiped out most (if not all) of your free-T gains; and this doesn't even take into account clomid's own estrogenic side effects.</p><p></p><p>Also (since GMan86 mentioned GnRH) I've heard of references made to tertiary and secondary hypogonadism, but don't know why in case of low LH/FSH, secondary hypogonadism rather than tertiary is assumed. (Maybe there's an obvious reason for it, but I don't know it.)</p><p></p><p>Interesting topic for discussion, although I'm not sure if we laypeople (or I, in any case) will make much progress without going through books and research papers.</p></blockquote><p></p>
[QUOTE="Aki, post: 138092, member: 14084"] [USER=15043]@Gman86[/USER] and [USER=38109]@Cataceous[/USER] - appreciate the responses I too have some recollection of the feedback mechanism whereby LH/FSH production is signalled. And if I remember correctly, clomid works by blocking the estrogen receptors, fooling the pituitary into producing more LH and FSH and consequently more testosterone (assuming one's testicles still function). Now the question is, what was fooling the pituitary in the first place into sensing an excess of estrogen that didn't exist? In this regard, I think Gman86's explanation (of estrogen-like pollutants/mimics) has merit, although obviously it isn't entirely satisfactory either. (And if it in fact is the primary explanation, raises another bunch of questions that need answering.) Or could it just be that for some reason the pituitary has become more sensitive to estrogen so that even a small amount causes greater than normal negative feedback? I also wonder why SHBG appears to behave "conspiratorially" and seeks to undo the testosterone rise induced by clomid.. like if you have a T-level of ~250 ng/dL with an SHBG of 15 nmol/L before taking clomid, and a low dose of clomid raises your T to 500-600 but your SHBG also creeps up to 30 nmol/L, it seems you've wiped out most (if not all) of your free-T gains; and this doesn't even take into account clomid's own estrogenic side effects. Also (since GMan86 mentioned GnRH) I've heard of references made to tertiary and secondary hypogonadism, but don't know why in case of low LH/FSH, secondary hypogonadism rather than tertiary is assumed. (Maybe there's an obvious reason for it, but I don't know it.) Interesting topic for discussion, although I'm not sure if we laypeople (or I, in any case) will make much progress without going through books and research papers. [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Basics & Questions
so what *are* the possible causes of late-onset secondary hypogonadism?
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