High T and High red blood count Q
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madman
Super Moderator
The use of exogenous T has an erythropoietic stimulating effect.
Testosterone Induces Erythrocytosis via Increased Erythropoietin and Suppressed Hepcidin: Evidence for a New Erythropoietin/Hemoglobin Set Point
Testosterone use in men has increased markedly over the past 15 years—reaching nearly $1.7 billion in prescription sales in 2012—due to numerous factors, including the increased awareness of androgen deficiency syndromes in men and the growing off-label use of testosterone for age-related decline in testosterone levels (1). Increased red blood cell mass (erythrocytosis) is the most common adverse event associated with testosterone therapy in clinical practice and in testosterone trials (2,3). Thus, understanding the mechanism of testosterone-induced erythrocytosis is important within the context of its safety, especially in older men, who experience greater increments in hemoglobin and hematocrit in response to testosterone administration than young men (4).
madman
Super Moderator
Erythrocytosis Following Testosterone Therapy
Samuel J. Ohlander, MD, Bibin Varghese, and Alexander W. Pastuszak
Conclusions
Erythrocytosis is often a limiting variable in patients on TTh. Direct and indirect effects related to supraphysiologic T levels are thought to mediate the effects on erythrocytosis. The true mechanism of erythrocytosis and its role on thromboembolic events remains unclear, though few data support an increased risk of CV events resulting from testosterone-induced erythrocytosis. Large multicenter randomized controlled trials are required to study TTh, its effects on Hb and Hct, and the clinical significance of treatment induced elevations in red blood cell mass.
Samuel J. Ohlander, MD, Bibin Varghese, and Alexander W. Pastuszak
Conclusions
Erythrocytosis is often a limiting variable in patients on TTh. Direct and indirect effects related to supraphysiologic T levels are thought to mediate the effects on erythrocytosis. The true mechanism of erythrocytosis and its role on thromboembolic events remains unclear, though few data support an increased risk of CV events resulting from testosterone-induced erythrocytosis. Large multicenter randomized controlled trials are required to study TTh, its effects on Hb and Hct, and the clinical significance of treatment induced elevations in red blood cell mass.
madman
Super Moderator
Here is an older post from Dr. Saya that is very sound advice regarding erythrocytosis.
#28
There are valid points on both sides of this.
Fact: polycythemia vera and erythrocytosis are COMPLETELY different phenomena and should not be confused (though the terms are often erroneously used interchangeably). Polycythemia vera is without a doubt MORE risky, but that doesn't mean erythrocytosis comes without (longterm) risk.
Fact: though the physiology is similar, erythrocytosis from TRT is NOT a physiologic erythrocytosis, but is IATROGENIC. Though physiologically similar, the ethics and medico-legal considerations are certainly much different.
Fact: there is no solid data of increased risk of MI, DVT, etc that is attributable directly to appropriate TRT (I know we all agree on this one).
My take: as I've said before, it is not concern for MI, DVT that presents itself to me with TRT-induced erythrocytosis, but more the LONG TERM vascular consequences. To be clear, I'm generally referring to HCT >53 which is about where I draw the line LONG TERM. Most folks at high altitude DO in fact have higher H/H than their counterparts at sea level, however most are NOT HCT > 53 unless they have multiple exacerbating factors contributing (smoker, high iron levels/intake, OSA - this is a BIG one, COPD, + TRT). We all agree higher HCT = more viscous blood. If we look at simple fluid dynamics and the laws of physics, thicker fluid (blood) inside of a pipe (vessel) = higher pressure (blood pressure). I've seen this countless times in patients requiring blood donation or therapeutic phlebotomy -- BP drops, sometimes dramatically, afterwards and generally remains at the lower levels until (if/when) HCT rises again.
Now of course we also have the other end of the equation with enhanced nitric oxide production - which helps as it dilates the pipe (vessel) - consequently counterbalancing the increase in pressure. The problem is that this vasodilation from nitric oxide is VARIABLE over time, whereas the increased HCT is more constant...meaning that this teeter-totter of "thicker blood" counterbalanced by nitric oxide vasodilation, will certainly present times when the viscosity side of the equation is at a distinct advantage. Thinking of it another way, the body is able to adapt REMARKABLY to many differing situations (one of which noted above with the vasodilation), but nonetheless has it's functional limits. Think of it as an airplane that flies at 60-70% of its functional engine capacity (just estimates as I'm not a pilot!) - this piece of machinery has the capacity to utilize a higher percentage of its capacity, but keeping the "normal operating capacity" of the plain at 60-70% gives that added safety margin. The plain can then "throw it into overdrive" and utilize a higher percentage (temporarily) of its capacity when the situation calls for it. This is a crude analogy, but hopefully will make some sense. For the human side - the human body has a capacity to TOLERATE (probably the best term) HCT levels very high under certain situations as an adaptive mechanism, but the higher the HCT goes you are eating into that safety margin for the max capacity of the cardiovascular system and thus reduce the ability of the cardiovascular to remain plastic and adaptable to other changing conditions or insults. For instance, all may be well when the "teeter-totter" of viscosity/nitric oxide is all balanced, but what about when the patient experiences times of reduced nitric oxide production (or other reasons that the pipe won't dilate...like atherosclerosis as they age)...well then the equation is shifted squarely in favor of the higher viscosity = higher BP --> increased shear forces on arterial walls --> increased risk of macro and microvascular pathology, etc.
We don't have long term data (and likely will not for a long time to come) for MANY of the interesting and debatable talking points related to TRT and other hormonal treatments. We can just weigh the current data we have, use our own clinical judgment and understanding of the physiology of the human body, and sprinkle in a little common sense from time to time to make the decisions we feel are in the best interest of our patients long term.
I personally would not feel forthright in telling one of my 30-40-50 year old patients that sustaining an iatrogenic erythrocytosis with HCT >53 for the next two, three, or four decades of their life will not present any long term risk...but it's a debatable topic and one for which each provider (and patient) must determine where they stand and approach it accordingly.
#28
There are valid points on both sides of this.
Fact: polycythemia vera and erythrocytosis are COMPLETELY different phenomena and should not be confused (though the terms are often erroneously used interchangeably). Polycythemia vera is without a doubt MORE risky, but that doesn't mean erythrocytosis comes without (longterm) risk.
Fact: though the physiology is similar, erythrocytosis from TRT is NOT a physiologic erythrocytosis, but is IATROGENIC. Though physiologically similar, the ethics and medico-legal considerations are certainly much different.
Fact: there is no solid data of increased risk of MI, DVT, etc that is attributable directly to appropriate TRT (I know we all agree on this one).
My take: as I've said before, it is not concern for MI, DVT that presents itself to me with TRT-induced erythrocytosis, but more the LONG TERM vascular consequences. To be clear, I'm generally referring to HCT >53 which is about where I draw the line LONG TERM. Most folks at high altitude DO in fact have higher H/H than their counterparts at sea level, however most are NOT HCT > 53 unless they have multiple exacerbating factors contributing (smoker, high iron levels/intake, OSA - this is a BIG one, COPD, + TRT). We all agree higher HCT = more viscous blood. If we look at simple fluid dynamics and the laws of physics, thicker fluid (blood) inside of a pipe (vessel) = higher pressure (blood pressure). I've seen this countless times in patients requiring blood donation or therapeutic phlebotomy -- BP drops, sometimes dramatically, afterwards and generally remains at the lower levels until (if/when) HCT rises again.
Now of course we also have the other end of the equation with enhanced nitric oxide production - which helps as it dilates the pipe (vessel) - consequently counterbalancing the increase in pressure. The problem is that this vasodilation from nitric oxide is VARIABLE over time, whereas the increased HCT is more constant...meaning that this teeter-totter of "thicker blood" counterbalanced by nitric oxide vasodilation, will certainly present times when the viscosity side of the equation is at a distinct advantage. Thinking of it another way, the body is able to adapt REMARKABLY to many differing situations (one of which noted above with the vasodilation), but nonetheless has it's functional limits. Think of it as an airplane that flies at 60-70% of its functional engine capacity (just estimates as I'm not a pilot!) - this piece of machinery has the capacity to utilize a higher percentage of its capacity, but keeping the "normal operating capacity" of the plain at 60-70% gives that added safety margin. The plain can then "throw it into overdrive" and utilize a higher percentage (temporarily) of its capacity when the situation calls for it. This is a crude analogy, but hopefully will make some sense. For the human side - the human body has a capacity to TOLERATE (probably the best term) HCT levels very high under certain situations as an adaptive mechanism, but the higher the HCT goes you are eating into that safety margin for the max capacity of the cardiovascular system and thus reduce the ability of the cardiovascular to remain plastic and adaptable to other changing conditions or insults. For instance, all may be well when the "teeter-totter" of viscosity/nitric oxide is all balanced, but what about when the patient experiences times of reduced nitric oxide production (or other reasons that the pipe won't dilate...like atherosclerosis as they age)...well then the equation is shifted squarely in favor of the higher viscosity = higher BP --> increased shear forces on arterial walls --> increased risk of macro and microvascular pathology, etc.
We don't have long term data (and likely will not for a long time to come) for MANY of the interesting and debatable talking points related to TRT and other hormonal treatments. We can just weigh the current data we have, use our own clinical judgment and understanding of the physiology of the human body, and sprinkle in a little common sense from time to time to make the decisions we feel are in the best interest of our patients long term.
I personally would not feel forthright in telling one of my 30-40-50 year old patients that sustaining an iatrogenic erythrocytosis with HCT >53 for the next two, three, or four decades of their life will not present any long term risk...but it's a debatable topic and one for which each provider (and patient) must determine where they stand and approach it accordingly.
Thanks for that. The Dr's statements on NO lead me to beleive that daily supplementing with NO (beets, etc) help the vessels with plasticity to accommodate blood volume. Also, Vit E thins blood and provides other health benefits aspirin doesn't provide. Do many TRT patents take Vit E? When giving blood, it may be best to do so just before your next labs so that you get an updated iron level to see how giving blood effects that, no?
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