high hematocrit/hemoglobin - what to do

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@ readalot You are responding to something I never said to create a gotcha-moment.

I did not claim absence of evidence equals evidence of no risk of high hematocrit on TRT, I merely pointed out that you have no evidence proving otherwise, although to an unaware reader your post implies you do.
 
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Two large pharmacoepidemiological studies have compared the rate of venous thromboembolism in men receiving testosterone treatment versus a control group (men not receiving testosterone treatment).39,40 The first study – which we have presented previously “Risk of Venous Thromboembolism in Men Receiving Testosterone Therapy” - showed that testosterone treatment is not associated with an increased risk of venous thromboembolism.39 The second study concluded that starting testosterone treatment is associated with an increased risk of venous thromboembolism during the first 6 months of testosterone treatment, and declines thereafter.40 A meta-analysis was recently conducted on these two studies.33 A meta-analysis is a statistical approach to combine the results from multiple studies in an effort to increase statistical power (over individual studies), improve estimates of the effect size and/or to resolve uncertainty when studies disagree.41,42 This meta-analysis showed that testosterone treatment is not associated with an increased risk of venous thromboembolism, even when the analysis was confined to the first 6 months of testosterone therapy. Risk of blood clots seems to be more strongly associated with estrogen and estrogen treatment. The contribution of estrogen as a causal factor in venous thromboembolism is supported by the World Professional Association for Transgender Health (WPATH), which report that the greatest risk factor of male-to-female estrogen hormone treatment is venous thromboembolism. This is not the case in female-to-male transsexuals, who are treated with testosterone.

 
You are responding to something I never said to create a gotcha-moment.
This comment does not follow from the previous posts we've had up above. My intention was not to create any gotcha moment. Have a good day/evening.

Best wishes.
 
I did not claim absence of evidence equals evidence of no risk of high hematocrit on TRT, I merely pointed out that you have no evidence proving otherwise, although to an unaware reader your post implies you do.

I have presented evidence that high Hct on TRT does pose risk. Whether that risk materializes for a given individual is a different matter.

Quite clearly I've spent a good portion of time up above laying that (antecedent: see underlined phrase above) all out in the goriest of detail you will find on the internet. Of course it does require someone to take the time to read the material. As shown in this thread, many times a person won't go to the trouble and instead prefers hand waving.

Caution seems in order.
 
where is the evidence that slightly 'elevated'(if you can define elevated) HCT can cause any issues?

Reposting from above:

Post #13

I really don't understand how @madman has the energy to repost/repeat the same stuff over and over and over and over again with the patience and persistence of a monk. This is tiresome.

My hats off to you @madman and @Nelson Vergel. @madman gets crap on here he's harsh but he must have a heart of gold.
 
Two large pharmacoepidemiological studies have compared the rate of venous thromboembolism in men receiving testosterone treatment versus a control group (men not receiving testosterone treatment).39,40 The first study – which we have presented previously “Risk of Venous Thromboembolism in Men Receiving Testosterone Therapy” - showed that testosterone treatment is not associated with an increased risk of venous thromboembolism.39 The second study concluded that starting testosterone treatment is associated with an increased risk of venous thromboembolism during the first 6 months of testosterone treatment, and declines thereafter.40 A meta-analysis was recently conducted on these two studies.33 A meta-analysis is a statistical approach to combine the results from multiple studies in an effort to increase statistical power (over individual studies), improve estimates of the effect size and/or to resolve uncertainty when studies disagree.41,42 This meta-analysis showed that testosterone treatment is not associated with an increased risk of venous thromboembolism, even when the analysis was confined to the first 6 months of testosterone therapy. Risk of blood clots seems to be more strongly associated with estrogen and estrogen treatment. The contribution of estrogen as a causal factor in venous thromboembolism is supported by the World Professional Association for Transgender Health (WPATH), which report that the greatest risk factor of male-to-female estrogen hormone treatment is venous thromboembolism. This is not the case in female-to-male transsexuals, who are treated with testosterone.


Clotting and hypercoagulation aren't the primary or even minor concern I'd have with elevated Hct from TRT.

But I've seen the topic used some times as a smokescreen to confuse the ignorant about the primary concerns.


You are only born with one heart and once you start having problems with it it really can get your attention.
 
Clotting and hypercoagulation aren't the primary or even minor concern I'd have with elevated Hct from TRT.

But I've seen the topic used some times as a smokescreen to confuse the ignorant about the primary concerns.


You are only born with one heart and once you start having problems with it it really can get your attention.
This is what I thought was interesting even though I don't know if it's true.

Risk of blood clots seems to be more strongly associated with estrogen and estrogen treatment.
 
I have presented evidence that high Hct on TRT does pose risk. Whether that risk materializes for a given individual is a different matter.

You did not. The studies you posted were not about people on TRT, so why was their HCT elevated in the first place? It matters.

You are focussing on a symptom, ignoring it’s specific medical context, to draw a conclusion for a fundamentally different medical context. Ironically, the only fact to conclude is that the symptom presented itself outside of the context of TRT.
Doing so, you are actually applying a research model of the human body with fixed variables because it is easier to understand and it makes it possible to draw conclusions from the data that is already there (elevated HCT equals higher blood viscosity equals cvd).
To me it is a mistake often made in medical research and it sets us back by creating false dogma’s that hurt patients while trying to help them.

In my opinion, the only conclusion to draw from this is that we need specific research to create guidelines that aren’t arbitrary and to not be dogmatic about doing so. Until then it is risk to calculate depending on the medical context of the patient.
You make these calculations based on the assumption that high HCT is the culprit, I make them based on other known culprits such as hypertension, crp-levels, insuline resistance, etc.

I will leave it at that because I feel we are going in circles. I appreciate our discussion about this. Best wishes to you as well!
 
You did not. The studies you posted were not about people on TRT, so why was their HCT elevated in the first place? It matters.
Ok, I see. We must suspend our knowledge of the relationships between Hct, blood viscosity, endothelial shear stress, NO production, vasodilation, etc, etc since those relationships may not hold for a subject on TRT? We must wait for the RCTs specific to TRT patients before we urge caution in regard to any risks of elevated Hct for TRT patients?

If I understand you correctly, elevated Hct is merely a symptom so we must ignore the fundamental physical relationships between Hct and blood viscosity and in turn viscosity's impact on the cardiovascular system since somehow those relationships would not apply or be drastically altered in the context of TRT?

The diagram below must be completely disregarded in the context of TRT? TRT would have some compensatory, yet currently unknown, mechanism to ameliorate the concerns?



We have no constitutive framework with which to work?




Yes, you are correct on your point we are going in circles. Take care.
 
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EDIT:
@Nelson Vergel

i really enjoyed how they treated the concept of optimal Hct at rest vs under constraint of constant cardiac power. Perhaps something to weave into your articles emphasizing the ramifications for TRT patients in different demographic and age groups.

===

My 2 cents...
An excellent recent article that examines the tradeoffs associated with longevity vs performance. Hedge accordingly based on your specific circumstances.



Abstract​

In humans and higher animals, a trade-off between sufficiently high erythrocyte concentrations to bind oxygen and sufficiently low blood viscosity to allow rapid blood flow has been achieved during evolution. Optimal hematocrit theory has been successful in predicting hematocrit (HCT) values of about 0.3–0.5, in very good agreement with the normal values observed for humans and many animal species. However, according to those calculations, the optimal value should be independent of the mechanical load of the body. This is in contradiction to the exertional increase in HCT observed in some animals called natural blood dopers and to the illegal practice of blood boosting in high-performance sports. Here, we present a novel calculation to predict the optimal HCT value under the constraint of constant cardiac power and compare it to the optimal value obtained for constant driving pressure. We show that the optimal HCT under constant power ranges from 0.5 to 0.7, in agreement with observed values in natural blood dopers at exertion. We use this result to explain the tendency to better exertional performance at an increased HCT.



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ok, since hematocrit definitely matters, what is the max hematocrit level you would be comfortable being at (max)

See post #32:



See last highlighted portion. Have your physician assess your inflammation status, plasma viscosity, heart history, PAH status, etc. and work together to determine how much you can tolerate?

General rule of thumb:

Hct(max) (as you refer to it) for old dude with reduced vasodilation capacity is lower than for young stud without the wear and tear. You'll get a variety of opinions. Hope this gives some food for thought. An old man doping his blood to give the Hct of a tour-de-france cylist ain't my idea of of appropriate treatment. You have to look at what's the rate limiting step in each person. A cyclist's heart may be able to take the additional beating; a heart patient?

My intention here is to counter the blanket statement that TRT-induced erythrocytosis is harmless. That is a dangerous statement [my opinion]. But it's your heart.
 
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Beyond Testosterone Book by Nelson Vergel
readalot: thank you. hard decision. i think for a 43 year old me, with no heart issues, no family heart issues, a clean calcium score CT scan, somewhere around the upper limit seems acceptable to me. things might change of course in the future
 
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