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<blockquote data-quote="Rand McClain DO" data-source="post: 102348" data-attributes="member: 90"><p>"Risk" with high H/H refers to what would be my first question. Risk of stroke? I have one patient with polycythemia rubra vera from an autoimmune disorder who has come in with a hemoglobin of 26 g/dL (I don't remember the hematocrit) and was and is doing fine constantly fighting to keep his levels down. I have other patients who either do not want to address their sleep apnea, submit to serial therapeutic phlebotomies, or (rarely) have a JAK2 gene mutation and have H/H assays above normal, and the worst symptoms I see are dizziness, lethargy, the "need" to take random deep breathes, and more pronounced post-prandial narcosis ("food coma"). The hematologists I have spoken with about this tell me that the issue is not about having this "thick blood" to which it is often referred, but whether you have a coagulation disorder (homologous for Leiden Factor V, eg) that could lead to "stickier" platelets and ultimately stroke. Yet, we also know that if one's blood gets more viscous, it makes it more difficult for the heart to pump which could lead to MI, stroke, hypertension or a venous thrombosis. So, I believe one consider all the avenues that might lead to these risks and address them intelligently.</p><p>I know of no mechanism by which estrogen leverages the production of RBC's (H/H increases).</p><p>Re T dosing, everyone is different. 60-80mg per week of testosterone (what form?) may work well for some and not for others, AND, it depends upon how we define "work" (eg, on libido, energy, anabolism, etc.). As for recommending more (or less), again, it depends upon for what purpose one is using T, but as for reducing benefit (as in some sort of accommodation taking place) I disagree. While androgen receptors can downregulate (or upregulate) to adjust to chronic T levels, the benefit of replacing T would not be diminished (one either needed it or did not and replacing either benefitted or did not). If more T than is necessary for replacement is used, then during a short period after which one stopped taking the exogenous T (for fertility, eg) then, yes, there is a short term reduction in benefit from HAVING TAKEN TRT because of downregulation of receptors (as well as there being less than "normal" (the original low T assay or less) T production temporarily until endogenous production resumes in its prior low but normal production) until these receptors upregulate to match the new level of T.</p></blockquote><p></p>
[QUOTE="Rand McClain DO, post: 102348, member: 90"] "Risk" with high H/H refers to what would be my first question. Risk of stroke? I have one patient with polycythemia rubra vera from an autoimmune disorder who has come in with a hemoglobin of 26 g/dL (I don't remember the hematocrit) and was and is doing fine constantly fighting to keep his levels down. I have other patients who either do not want to address their sleep apnea, submit to serial therapeutic phlebotomies, or (rarely) have a JAK2 gene mutation and have H/H assays above normal, and the worst symptoms I see are dizziness, lethargy, the "need" to take random deep breathes, and more pronounced post-prandial narcosis ("food coma"). The hematologists I have spoken with about this tell me that the issue is not about having this "thick blood" to which it is often referred, but whether you have a coagulation disorder (homologous for Leiden Factor V, eg) that could lead to "stickier" platelets and ultimately stroke. Yet, we also know that if one's blood gets more viscous, it makes it more difficult for the heart to pump which could lead to MI, stroke, hypertension or a venous thrombosis. So, I believe one consider all the avenues that might lead to these risks and address them intelligently. I know of no mechanism by which estrogen leverages the production of RBC's (H/H increases). Re T dosing, everyone is different. 60-80mg per week of testosterone (what form?) may work well for some and not for others, AND, it depends upon how we define "work" (eg, on libido, energy, anabolism, etc.). As for recommending more (or less), again, it depends upon for what purpose one is using T, but as for reducing benefit (as in some sort of accommodation taking place) I disagree. While androgen receptors can downregulate (or upregulate) to adjust to chronic T levels, the benefit of replacing T would not be diminished (one either needed it or did not and replacing either benefitted or did not). If more T than is necessary for replacement is used, then during a short period after which one stopped taking the exogenous T (for fertility, eg) then, yes, there is a short term reduction in benefit from HAVING TAKEN TRT because of downregulation of receptors (as well as there being less than "normal" (the original low T assay or less) T production temporarily until endogenous production resumes in its prior low but normal production) until these receptors upregulate to match the new level of T. [/QUOTE]
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