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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
How fast can hematocrit rise?
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<blockquote data-quote="Nelson Vergel" data-source="post: 46083" data-attributes="member: 3"><p>Here is the only study that showed a hematocrit graph using 125 mg per week of testosterone enanthate injections (they gave a group finasteride to see if blocking DHT may suppress hematocrit increase, which it did not).</p><p></p><p>Hematocrit increased from an avg of around 43 to 48 after 6 months. This is lower than what we see in the field but shows that hematocrit can indeed level off.</p><p></p><p>[ATTACH]2279[/ATTACH]</p><p></p><p>Abstract</p><p>Testosterone (T) stimulates erythropoiesis and regulates iron homeostasis. However, it remains unknown whether the (type II) 5α-reduction of T to dihydrotestosterone (DHT) mediates these androgenic effects, as it does in some other tissues. Our purpose was to determine whether inhibition of type II 5α-reductase (via finasteride) alters red blood cell (RBC) production and serum markers of iron homeostasis subsequent to testosterone-enanthate (TE) administration in older hypogonadal men. Sixty men aged ≥60 yr with serum T <300 ng/dl or bioavailable T <70 ng/dl received treatment with TE (125 mg/wk) vs. vehicle paired with finasteride (5 mg/day) vs. placebo using a 2 × 2 factorial design. Over the course of 12 mo, TE increased RBC count 9%, hematocrit 4%, and hemoglobin 8% while suppressing serum hepcidin 57% (<em>P</em> < 0.001 for all measurements). Most of the aforementioned changes occurred in the first 3 mo of treatment, and finasteride coadministration did not significantly alter any of these effects. TE also reduced serum ferritin 32% (<em>P</em> = 0.002) within 3 mo of treatment initiation without altering iron, transferrin, or transferrin saturation. We conclude that TE stimulates erythropoiesis and alters iron homeostasis independently of the type II 5α-reductase enzyme. These results demonstrate that elevated DHT is not required for androgen-mediated erythropoiesis or for alterations in iron homeostasis that would appear to support iron incorporation into RBCs.</p><p></p><p><a href="http://ajpendo.physiology.org/content/307/5/E456" target="_blank">http://ajpendo.physiology.org/content/307/5/E456</a></p></blockquote><p></p>
[QUOTE="Nelson Vergel, post: 46083, member: 3"] Here is the only study that showed a hematocrit graph using 125 mg per week of testosterone enanthate injections (they gave a group finasteride to see if blocking DHT may suppress hematocrit increase, which it did not). Hematocrit increased from an avg of around 43 to 48 after 6 months. This is lower than what we see in the field but shows that hematocrit can indeed level off. [ATTACH=CONFIG]2279[/ATTACH] Abstract Testosterone (T) stimulates erythropoiesis and regulates iron homeostasis. However, it remains unknown whether the (type II) 5α-reduction of T to dihydrotestosterone (DHT) mediates these androgenic effects, as it does in some other tissues. Our purpose was to determine whether inhibition of type II 5α-reductase (via finasteride) alters red blood cell (RBC) production and serum markers of iron homeostasis subsequent to testosterone-enanthate (TE) administration in older hypogonadal men. Sixty men aged ≥60 yr with serum T <300 ng/dl or bioavailable T <70 ng/dl received treatment with TE (125 mg/wk) vs. vehicle paired with finasteride (5 mg/day) vs. placebo using a 2 × 2 factorial design. Over the course of 12 mo, TE increased RBC count 9%, hematocrit 4%, and hemoglobin 8% while suppressing serum hepcidin 57% ([I]P[/I] < 0.001 for all measurements). Most of the aforementioned changes occurred in the first 3 mo of treatment, and finasteride coadministration did not significantly alter any of these effects. TE also reduced serum ferritin 32% ([I]P[/I] = 0.002) within 3 mo of treatment initiation without altering iron, transferrin, or transferrin saturation. We conclude that TE stimulates erythropoiesis and alters iron homeostasis independently of the type II 5α-reductase enzyme. These results demonstrate that elevated DHT is not required for androgen-mediated erythropoiesis or for alterations in iron homeostasis that would appear to support iron incorporation into RBCs. [url]http://ajpendo.physiology.org/content/307/5/E456[/url] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
How fast can hematocrit rise?
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