I posted some similar information over at another forum. Here’s was a response:
None of this matters. Testosterone INCREASES NO production and dilates blood vessels to account for any blood thickening essentially cancelling out any negative side effects. Hence no one on TRT us dropping dead. If this was not true, one would see an increase in blood pressure and heart rate due to thicker blood. From my personal experience over the years my vitals have not changed. Rating heart rate 59 bpm. Blood pressure 100/65. Hematocrit around 52-54. As high as 58.
Read the testosterone impact on Nitric oxide production. If high hct was bad for guys on trt imagine how many guys would drop dead? I agree most people can react differently but the testosterone pharmacology is the same in everyone.
Want to share the same information I shared over there in my response. Happy to think about/entertain any critique/errors in my presentation. My intent is to learn and provide forum for educated discussion.
Thank you.
My summarized response:
You’ve got some false dilemma and circular reasoning fallacy going on here.
So with this logic, there’s no concern with competing effects since testosterone increases NO production, end of story. You can run your Hct as high as you want with impunity since testosterone will increase NO production. So why is it some men see a >20-30 point increase in systolic BP with their Hct rising from 45 to 54% on TRT? Everyone has your cardiovascular response to TRT?
If raising Hct with TRT is bad for guys, then we’d be seeing them dropping dead. So if we don’t observe them “dropping dead”, then no problem with elevated Hct.
Interesting.
Watch from 46:30 till the end:
Testosterone and Estrogen in Men: Good, Bad or Indifferent?
As Dr. Rouzier mentions, men observed at high alititude suffering (i.i., side effects) from excessive erythrocytosis (EE) already have significantly higher testosterone levels than those that don’t have EE. He uses this to justify TRT induced erythrocytosis since it’s testosterone mediated and these guys aren’t “dropping dead”.
Your claim is that use of exogenous testosterone should cancel out any and all increase in viscosity due to increased Hct from the testosterone? So should we give these guys with EE at high altitude more testosterone? They must not be making enough. They need more? Or is it that they need exogenous testosterone since their endogenous testosterone (which is already high compared to control population) is not high enough?
Take a read:
High serum testosterone levels are associated with excessive erythrocytosis of chronic mountain sickness in men
I’ve read over and over the claim that people at altitude have high Hct and they are fine. They aren’t “dropping dead”. Therefore, guys with high Hct from TRT are fine. I took the time to post some recent mechanistic study of why running Hct up too high can be problematic and posted before why all Hct values are not created equal (marked variation in blood viscosity vs Hct depending on plasma viscosity status).
So if you don’t want to read, that’s up to you. But for others trying to make sense of all this, the concern I am trying to daylight is not an acute event, “dropping dead”, or even clotting issue leading to stroke. It’s long term wear and tear on the heart leading to early failure. When you die prematurely from heart failure there may be no one there pointing out “see, he ran his Hct too high for 10 years.”
I summed this up in a thread on another forum (edited for length):
The primary concern with elevated blood viscosity is hypertension, increased shear stress to the lumen (I’m sure you are familiar with what that does), and risk of ischemia and reduced perfusion for compromised patients / older patients. Also, what’s the concern with young person running high blood viscosity for years? Ask AAS abusers what the long term implications of elevated Hct are? Integrate out over 20 years the cost of making your heart do extra, measurably more work. Combine that with a patient who has limited vasodilation ability.
So according to this logic, no worries with elevating serum viscosity, just let it ride? For a patient with plenty of mileage on the heart, pre-CHF or CHF, no worries with cranking up the blood viscosity? Harmless?
This response is lazy and avoids having to discuss the fact the heart is a pump and a pump is designed to operate on a pump curve (just to keep it simple). Depending on the viscosity of the fluid the pump is pumping, you will land on a point on that curve. Surely you understand the long term implications of running a pump too high on the gpm vs hp curve? Any concerns for long term issues if you want that pump in service for a while? We aint talking about a pump in a manufacturing facility that can be replaced rather easily. We are talking about a heart.
For folks who talk about optimization, you seem to not understand or ignore the penalty function associated with performance vs longevity. For readers, I’ve shared what I think is important for you to consider. Take care of your cardiovascular system. That means use reasonable caution. Running your Hct above 50, or even 55 is not that. But given the TT levels you guys are recommending, I can see how this little inconvenience causes an issue. Elevated Hct has to be harmless in your practice otherwise you have to have your patients doing an oil drain on a regular, painful basis.