yeah I'm not with ya on the after 40 more red blood cells being bad
Two of these you can read for free. Bhasin is the leader in this research. I usually prefer not to get into heated debates about AAS these days but this one is pretty important especially as our TRT. HRT and AAS users age. It doesn't happen to everyone but does to a lot of older guys.
J Clin Endocrinol Metab. 2008 Mar;93(3):914-9. Epub 2007 Dec 26.
[h=1]
Effects of graded doses of testosterone on erythropoiesis in healthy young and older men.[/h]
Coviello AD[SUP]1[/SUP],
Kaplan B,
Lakshman KM,
Chen T,
Singh AB,
Bhasin S.
[h=3]
Author information [/h]
[h=3]Abstract[/h][h=4]CONTEXT:[/h]Erythrocytosis is a dose-limiting adverse effect of testosterone therapy, especially in older men.
[h=4]OBJECTIVE:[/h]Our objective was to compare the dose-related changes in hemoglobin and hematocrit in young and older men and determine whether age-related differences in erythropoietic response to testosterone can be explained by changes in erythropoietin and soluble transferrin receptor (sTfR) levels.
[h=4]DESIGN:[/h]We conducted a secondary analysis of data from a testosterone dose-response study in young and older men who received long-acting GnRH agonist monthly plus one of five weekly doses of testosterone enanthate (25, 50, 125, 300, or 600 mg im) for 20 wk.
[h=4]SETTING:[/h]The study took place at a General Clinical Research Center.
[h=4]PARTICIPANTS:[/h]Participants included 60 older men aged 60-75 yr and 61 young men aged 19-35 yr.
[h=4]OUTCOME MEASURES:[/h]Outcome measures included hematocrit and hemoglobin and serum erythropoietin and sTfR levels.
[h=4]RESULTS:[/h]Hemoglobin and hematocrit increased significantly in a linear, dose-dependent fashion in both young and older men in response to graded doses of testosterone (P<0.0001). The increases in hemoglobin and hematocrit were significantly greater in older than young men. There was no significant difference in percent change from baseline in erythropoietin or sTfR levels across groups in either young or older men. Changes in erythropoietin or sTfR levels were not significantly correlated with changes in total or free testosterone levels.
[h=4]CONCLUSIONS:[/h]Testosterone has a dose-dependent stimulatory effect on erythropoiesis in men that is more pronounced in older men. The testosterone-induced rise in hemoglobin and hematocrit and age-related differences in response to testosterone therapy may be mediated by factors other than erythropoietin and sTfR.
<dl class="rprtid"><dt>PMID:</dt><dd>18160461</dd><dd> [PubMed - indexed for MEDLINE] </dd><dd>
</dd><dt>PMCID:</dt><dd>PMC2266950</dd><dd>
</dd></dl>
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[h=3]
Publication Types, MeSH Terms, Substances, Grant Support[/h]
<input name="EntrezSystem2.PEntrez.PubMed.Pubmed_ResultsPanel.Pubmed_RVAbstract.uid" id="UidCheckBox24158761" value="24158761" type="checkbox">2.
J Gerontol A Biol Sci Med Sci. 2014 Jun;69(6):725-35. doi: 10.1093/gerona/glt154. Epub 2013 Oct 24.
[h=1]
Testosterone Induces Erythrocytosis via Increased Erythropoietin and Suppressed Hepcidin: Evidence for a New Erythropoietin/Hemoglobin Set Point.[/h]
Bachman E[SUP]1[/SUP],
Travison TG[SUP]2[/SUP],
Basaria S[SUP]3[/SUP],
Davda MN[SUP]2[/SUP],
Guo W[SUP]2[/SUP],
Li M[SUP]2[/SUP],
Connor Westfall J[SUP]3[/SUP],
Bae H[SUP]3[/SUP],
Gordeuk V[SUP]2[/SUP],
Bhasin S[SUP]4[/SUP].
[h=3]
Author information [/h]
[h=3]Abstract[/h][h=4]BACKGROUND:[/h]The mechanisms by which testosterone increases hemoglobin and hematocrit remain unclear.
[h=4]METHODS:[/h]We assessed the hormonal and hematologic responses to testosterone administration in a clinical trial in which older men with mobility limitation were randomized to either placebo or testosterone gel daily for 6 months.
[h=4]RESULTS:[/h]The 7%-10% increase in hemoglobin and hematocrit, respectively, with testosterone administration was associated with significantly increased erythropoietin (EPO) levels and decreased ferritin and hepcidin levels at 1 and 3 months. At 6 months, EPO and hepcidin levels returned toward baseline in spite of continued testosterone administration, but EPO levels remained nonsuppressed even though elevated hemoglobin and hematocrit higher than at baseline, suggesting a new set point. Consistent with increased iron utilization, soluble transferrin receptor (sTR) levels and ratio of sTR/log ferritin increased significantly in testosterone-treated men. Hormonal and hematologic responses were similar in anemic participants. The majority of testosterone-treated anemic participants increased their hemoglobin into normal range.
[h=4]CONCLUSIONS:[/h]Testosterone-induced increase in hemoglobin and hematocrit is associated with stimulation of EPO and reduced ferritin and hepcidin concentrations. We propose that testosterone stimulates erythropoiesis by stimulating EPO and recalibrating the set point of EPO in relation to hemoglobin and by increasing iron utilization for erythropoiesis.
© The Author 2013. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail:
[email protected].
[h=4]KEYWORDS:[/h]Erythropoietin; Ferritin.; Hepcidin; Testosterone
<dl class="rprtid"><dt>PMID:</dt><dd>24158761</dd><dd> [PubMed - in process] </dd><dd>
</dd><dt>PMCID:</dt><dd>PMC4022090</dd><dd> [Available on 2015/6/1]</dd></dl>
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[h=3]
Grant Support[/h]
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Aging Cell. 2013 Apr;12(2):280-91. doi: 10.1111/acel.12052. Epub 2013 Feb 28.
[h=1]
Testosterone administration inhibits hepcidin transcription and is associated with increased iron incorporation into red blood cells.[/h]
Guo W[SUP]1[/SUP],
Bachman E,
Li M,
Roy CN,
Blusztajn J,
Wong S,
Chan SY,
Serra C,
Jasuja R,
Travison TG,
Muckenthaler MU,
Nemeth E,
Bhasin S.
[h=3]
Author information [/h]
[h=3]Abstract[/h]Testosterone administration increases hemoglobin levels and has been used to treat anemia of chronic disease. Erythrocytosis is the most frequent adverse event associated with testosterone therapy of hypogonadal men, especially older men. However, the mechanisms by which testosterone increases hemoglobin remain unknown. Testosterone administration in male and female mice was associated with a greater increase in hemoglobin and hematocrit, reticulocyte count, reticulocyte hemoglobin concentration, and serum iron and transferrin saturation than placebo. Testosterone downregulated hepatic hepcidin mRNA expression, upregulated renal erythropoietin mRNA expression, and increased erythropoietin levels. Testosterone-induced suppression of hepcidin expression was independent of its effects on erythropoietin or hypoxia-sensing mechanisms. Transgenic mice with liver-specific constitutive hepcidin over-expression failed to exhibit the expected increase in hemoglobin in response to testosterone administration. Testosterone upregulated splenic ferroportin expression and reduced iron retention in spleen. After intravenous administration of transferrin-bound (58) Fe, the amount of (58) Fe incorporated into red blood cells was significantly greater in testosterone-treated mice than in placebo-treated mice. Serum from testosterone-treated mice stimulated hemoglobin synthesis in K562 erythroleukemia cells more than that from vehicle-treated mice. Testosterone administration promoted the association of androgen receptor (AR) with Smad1 and Smad4 to reduce their binding to bone morphogenetic protein (BMP)-response elements in hepcidin promoter in the liver. Ectopic expression of AR in hepatocytes suppressed hepcidin transcription; this effect was blocked dose-dependently by AR antagonist flutamide. Testosterone did not affect hepcidin mRNA stability. In conclusion, testosterone inhibits hepcidin transcription through its interaction with BMP/Smad signaling. Testosterone administration is associated with increased iron incorporation into red blood cells.
© 2013 The Authors Aging Cell © 2013 Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland.
<dl class="rprtid"><dt>PMID:</dt><dd>23399021</dd><dd> [PubMed - indexed for MEDLINE] </dd><dd>
</dd><dt>PMCID:</dt><dd>PMC3602280</dd><dd>
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