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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Basics & Questions
Trt protocal - advice needed
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<blockquote data-quote="RobRoy" data-source="post: 265296" data-attributes="member: 42893"><p>Everything you have posted is a baseline study. It has nothing to do with raising estradiol by giving testosterone. In every study that mean we're giving testosterone get raised estradiol (unless it was a study where they were blocking estradiol). In all of those studies where they gave testosterone and therefore raised estradiol it did not result in erectile dysfunction. But when you give testosterone and block estradiol, those studies did result in adverse effects such as erectile dysfunction. Testosterone works through its active metabolites which are DHT and estradiol. When you block those active metabolites you block the beneficial effects of testosterone at the tissue level where they are generated. What you measure in the serum does not reflect the levels in the tissues of either estradiol or DHT. People are making adjustments on serum levels that don't have an effect at the tissue level when on testosterone.</p><p>The reason for this highlights fundamentally important control mechanisms in androgen target tissues that finely regulate pathways for androgen synthesis and degra- dation to maintain DHT homeostasis. These in- tracellular processes do not appear to be affected by circulating DHT concentrations. Circulating levels of DHT in response to testosterone do not correlate with those found an androgen sensitive tissues such as the prostate, adipose tissue, and muscle due to local regulatory mechanisms that tightly control intracellular androgen homeostasis.</p><p>Same holds true for estrogen.</p><p>In comparing blood levels of E2 and testosterone with biologic effects, it is important to recognize that E2 is produced locally from aromatase in target tissues and acts in a paracrine fashion (Simpson 2003). In healthy men and in studies of medically castrated men undergoing graded testosterone add-back, serum levels of E2 reflect the total E2 that has diffused into the blood from all tissues having been synthesized by aromatase and escaped local tissue metabolism. These blood levels, no matter how</p><p>accurately measured, are an indirect reflection of total estrogen signalling which is further locally modulated by sulphoconjugation and deconjugation of estrogens (Song 2001).</p><p>So when we take an aromatase inhibitor or a five alpha reductase inhibitor we will decrease levels in the serum but most importantly we're decreasing them in the tissues where they're needed therefore we are blocking the beneficial effects of testosterone in the tissues and that's why we see negative effects with aromatase inhibitors and five alpha reductase inhibitor's.</p><p>So what you're measuring in the serum with regard to DHT and estradiol when you're on testosterone does not have an effect in the tissues themselves because estradiol and DHT are generated intracellularly. Their levels are tightly controlled intracellularly. So men on testosterone are completely different than baseline studies or observations in men that are not on testosterone. They are not the same and it is comparing apples to oranges</p></blockquote><p></p>
[QUOTE="RobRoy, post: 265296, member: 42893"] Everything you have posted is a baseline study. It has nothing to do with raising estradiol by giving testosterone. In every study that mean we're giving testosterone get raised estradiol (unless it was a study where they were blocking estradiol). In all of those studies where they gave testosterone and therefore raised estradiol it did not result in erectile dysfunction. But when you give testosterone and block estradiol, those studies did result in adverse effects such as erectile dysfunction. Testosterone works through its active metabolites which are DHT and estradiol. When you block those active metabolites you block the beneficial effects of testosterone at the tissue level where they are generated. What you measure in the serum does not reflect the levels in the tissues of either estradiol or DHT. People are making adjustments on serum levels that don't have an effect at the tissue level when on testosterone. The reason for this highlights fundamentally important control mechanisms in androgen target tissues that finely regulate pathways for androgen synthesis and degra- dation to maintain DHT homeostasis. These in- tracellular processes do not appear to be affected by circulating DHT concentrations. Circulating levels of DHT in response to testosterone do not correlate with those found an androgen sensitive tissues such as the prostate, adipose tissue, and muscle due to local regulatory mechanisms that tightly control intracellular androgen homeostasis. Same holds true for estrogen. In comparing blood levels of E2 and testosterone with biologic effects, it is important to recognize that E2 is produced locally from aromatase in target tissues and acts in a paracrine fashion (Simpson 2003). In healthy men and in studies of medically castrated men undergoing graded testosterone add-back, serum levels of E2 reflect the total E2 that has diffused into the blood from all tissues having been synthesized by aromatase and escaped local tissue metabolism. These blood levels, no matter how accurately measured, are an indirect reflection of total estrogen signalling which is further locally modulated by sulphoconjugation and deconjugation of estrogens (Song 2001). So when we take an aromatase inhibitor or a five alpha reductase inhibitor we will decrease levels in the serum but most importantly we're decreasing them in the tissues where they're needed therefore we are blocking the beneficial effects of testosterone in the tissues and that's why we see negative effects with aromatase inhibitors and five alpha reductase inhibitor's. So what you're measuring in the serum with regard to DHT and estradiol when you're on testosterone does not have an effect in the tissues themselves because estradiol and DHT are generated intracellularly. Their levels are tightly controlled intracellularly. So men on testosterone are completely different than baseline studies or observations in men that are not on testosterone. They are not the same and it is comparing apples to oranges [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Basics & Questions
Trt protocal - advice needed
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