question from a user
Hypoxia only effects erythropoietin levels to raise hematocrit. Testosterone raises hematocrit through multiple mechanisms. Since DHT was on your list, I did some googling about alpha 5 reductase inhibitors and hematocrit. There is some chatter about it lowering PCV, and I even found a proposed study where someone wanted to test using it to treat TRT induced erythrocytosis, but couldn't find the results (or even if the study had made it beyond proposal phase). Have you had any patients on TRT and then finasteride (either just for hair loss treatment, or as an experiment for PCV reduction) where you saw a marked decrease and/or elimination of their TRT induced erythrocytosis? Chronic hypoxia also causes other changes, which testosterone use does not. Specifically, the body creates more significantly more capillaries. These capillaries create more pathways for the thicker blood to go through, distributing the vessel wall burden, and also creating alternative pathways if a clot were to occur. When you say TRT usually does not do things such as alternate pathways, does that include patients who (either by ignoring doctors orders for blood donation or by going UGL) are on TRT for years, the whole time with high PCV? i.e. you're at risk initially, but if you survive for a few years without a heart attack, your body will adapt just like a person at altitude? Or even after years of TRT, it's just never gonna happen? Exogenous testosterone also causes downstream effects which hypoxia does not, such as thromboxane A2 receptor density and aggregation responses. The latest studies show that increased risk of arterial clotting is low with testosterone. However, the combination of increased blood viscosity along with increased platelet activity and thrombopoiesis triggered by testosterone can raise the risk of potential clots in those who ALSO have pre-existing coagulation or fibrinolysis dysfunction. Yeah, people seem to be talking about this more. Do you see the industry (or at least just your clinic) starting to shift away from blanket blood donation orders, and instead saying "we're just going to monitor your platelets every 6 months, and you're OK for now but if we start seeing changes in your platelets then you're going to have to start donating blood"?
AlphaMD's Answer
I have not personally seen any patients have a drop in hematocrit while using a 5-alpha reductase inhibitor, nor have I seen any studies on the matter, so I cannot speak to it.
What I meant regarding hypoxia and alternate pathways is that living at high altitude (or living with COPD, muscular dystrophy, cystic fibrosis or other chronic hypoxic condition) causes other changes in the lungs due to vascular remodeling and endothelial cell restructuring. This is caused from release of cytokines such as (TGF)-β, an important regulator of collagen synthesis in fibroblasts. Also, regarding capillary growth (see clubbed fingers), this is caused by hypoxia induced release of interleukins. Neither of these cytokines are released with testosterone use. They are specifically released from chronic hypoxia. So basically, even with chronic erythrocytosis from testosterone use, you will not get clubbed fingers or enlarged lungs.Most clinics are taking a less aggressive approach to blood donations regarding erythrocytosis. Less than a third of patients on TRT will have any problems with elevated hematocrit, and those that do often stay below the level of concern.
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