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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
SHBG finally increased, but the hematocrit increased, ferritin decreased. Thyroid?
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<blockquote data-quote="madman" data-source="post: 200672" data-attributes="member: 13851"><p>[URL unfurl="true"]https://www.excelmale.com/forum/threads/mechanisms-underlying-the-metabolic-actions-of-t-in-the-human.21879/[/URL]</p><p></p><p></p><p><strong>Hematocrit</strong></p><p></p><p><em><strong>The stimulatory effect of testosterone on hematocrit has been known for a long time (59). </strong></em>Hypogonadal states are characterized by a mild normocytic normochromic anemia which reverses following testosterone treatment (2). <em><strong>The mechanism underlying this effect has been thought to be due to an increase in erythropoietin synthesis in the kidney. However, more recently, it has been shown that hepcidin concentration is suppressed by testosterone (60, 61). <u>Hepcidin suppresses the expression of ferroportin, the membrane protein responsible for the absorption of iron by the enterocyte, and the release of iron stored in the monocytes and macrophages of the reticuloendothelial system (62). Thus ferroportin has a cardinal role in increasing the bio-availability of iron</u>.</strong></em> <strong><em><u>Recent investigations have also revealed that with the suppression of hepcidin, testosterone therapy increases the expression of ferroportin along with that of transferrin receptor and plasma transferrin concentrations</u> (63). <u>Plasma iron and ferritin concentrations fall</u>. <u>These findings are consistent with the release of iron from the stores with an increase in ferroportin and the transport of iron to erythropoietic cells through transferrin and the uptake of iron by erythropoietic tissues through the transferrin receptor</u>. These effects, in addition to the stimulatory effect of testosterone on erythropoietin production, enhance hemoglobin production following testosterone therapy.</em></strong></p><p><strong></strong></p><p><strong></strong></p><p><strong></strong></p><p><strong></strong></p><p><strong>Erythrocytosis:</strong> <strong><em>Erythrocytosis is a known adverse effect of testosterone administration.</em></strong> A randomized placebo-controlled trial of transdermal testosterone therapy for one year in elderly men found a 2% incidence of polycythemia (2). <em><strong><u>The effect is dose-dependent and is seen more commonly in those with supra-normal levels of testosterone</u>. Hematocrit above 55% increases blood viscosity and could exacerbate vascular disease in the coronary, cerebrovascular, or peripheral vascular circulation. Periodic hematological assessment is therefore indicated (1). <u>In those with other causes of secondary polycythemia </u></strong></em><u><em><strong>(such as smoking or sleep apnoea)</strong></em></u><em><strong><u>, dose adjustment and/or periodic phlebotomy may be necessary to keep the hematocrit below 55%</u>.</strong></em></p></blockquote><p></p>
[QUOTE="madman, post: 200672, member: 13851"] [URL unfurl="true"]https://www.excelmale.com/forum/threads/mechanisms-underlying-the-metabolic-actions-of-t-in-the-human.21879/[/URL] [B]Hematocrit[/B] [I][B]The stimulatory effect of testosterone on hematocrit has been known for a long time (59). [/B][/I]Hypogonadal states are characterized by a mild normocytic normochromic anemia which reverses following testosterone treatment (2). [I][B]The mechanism underlying this effect has been thought to be due to an increase in erythropoietin synthesis in the kidney. However, more recently, it has been shown that hepcidin concentration is suppressed by testosterone (60, 61). [U]Hepcidin suppresses the expression of ferroportin, the membrane protein responsible for the absorption of iron by the enterocyte, and the release of iron stored in the monocytes and macrophages of the reticuloendothelial system (62). Thus ferroportin has a cardinal role in increasing the bio-availability of iron[/U].[/B][/I][U] [/U][B][I][U]Recent investigations have also revealed that with the suppression of hepcidin, testosterone therapy increases the expression of ferroportin along with that of transferrin receptor and plasma transferrin concentrations[/U] (63). [U]Plasma iron and ferritin concentrations fall[/U]. [U]These findings are consistent with the release of iron from the stores with an increase in ferroportin and the transport of iron to erythropoietic cells through transferrin and the uptake of iron by erythropoietic tissues through the transferrin receptor[/U]. These effects, in addition to the stimulatory effect of testosterone on erythropoietin production, enhance hemoglobin production following testosterone therapy.[/I] Erythrocytosis:[/B] [B][I]Erythrocytosis is a known adverse effect of testosterone administration.[/I][/B] A randomized placebo-controlled trial of transdermal testosterone therapy for one year in elderly men found a 2% incidence of polycythemia (2). [I][B][U]The effect is dose-dependent and is seen more commonly in those with supra-normal levels of testosterone[/U]. Hematocrit above 55% increases blood viscosity and could exacerbate vascular disease in the coronary, cerebrovascular, or peripheral vascular circulation. Periodic hematological assessment is therefore indicated (1). [U]In those with other causes of secondary polycythemia [/U][/B][/I][U][I][B](such as smoking or sleep apnoea)[/B][/I][/U][I][B][U], dose adjustment and/or periodic phlebotomy may be necessary to keep the hematocrit below 55%[/U].[/B][/I] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
SHBG finally increased, but the hematocrit increased, ferritin decreased. Thyroid?
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