Comparative Erythropoiesis (Increases to Hematocrit) by & between AAS Including What We Know about EQ & the Apparent Counterexample of Trenbolone

[Type-IIx]

I used to walk around thinking I was about to drop dead at any moment, going out of my way to look for different blood donation centers (I crashed my ferritin in the process). But now it’ll range between 56-60% on TRT depending on the blood draw. Been this way for close to 10 years now. I’m a bit health obsessed so I’m religious about checking all my other bio markers and I have no other risk factors. No clotting mutations. Platelets around 200-250. So I just deal with it. The alternative is crashing my testosterone.

The risks of venous thromboembolic events are in the thousands of person-years per each 1% elevation in the region of mild/moderate elevations (e.g., 54% - 58%). The risks are possibly (IMO, probably) in the decades of person-years per each 1% elevation in the region of severe elevations (>= 60%).

One paper has quantified the risks we're talking about here. In terms of relative risk, for every 5% ↑ in haematocrit, there was a 33% ↑ in the probability for a venous thromboembolic event in men, adjusted for age, BMI, and smoking. In terms of absolute risk: for men with average haematocrit (43 - 46%), there is a 0.16% probability for such an event within 10 years (1.6 per 1,000 person-years). If haematocrit ↑ by 5%, that chance ↑ by 33% to 0.21% within the next 10 years (2.1 per 1,000 person-years).

This study did not, however, attempt to quantify risks into the outer/extreme-rightmost regions of these elevations (e.g., >= 60%), however.

Miguel Indurain, multiple winner of the Tour de France, was jokingly referred to as "Mr. Sixty" by fellow competitors for walking around with HCT at 60%. He's still alive. Hell, the odds are in your favour that you don't suffer stroke or embolism in the next couple decades.

But, that risk could be reduced to virtually nil by keeping your HCT in the more mild range of elevations. Do you see what I am saying? Low probability, extremely high severity is still high risk.

Hey, if you feel good with, say somewhat arbitrarily, 6:1 odds against a major stroke in the next 20 years because you don't like low iron/ferritin levels and having to phlebotomize, I won't judge you. It just wouldn't comport with my own risk tolerance, given the minor nuisance vs. catastrophic, life-altering 1/7 risk.

 

[NotHuman]

The risks are in the thousands of person-years per each 1% elevation in the region of mild/moderate elevations (e.g., 54% - 58%). The risks are possibly (IMO, probably) in the decades of person-years per each 1% elevation in the region of severe elevations (>= 60%).

One paper has quantified the risks we're talking about here. In terms of relative risk, for every 5% ↑ in haematocrit, there was a 33% ↑ in the probability for a venous thromboembolic event in men, adjusted for age, BMI, and smoking. In terms of absolute risk: for men with average haematocrit (43 - 46%), there is a 0.16% probability for such an event within 10 years (1.6 per 1,000 person-years). If haematocrit ↑ by 5%, that
chance ↑ by 33% to 0.21% within the next 10 years (2.1 per 1,000 person-years).

This study did not, however, attempt to quantify risks into the outer/leftmost regions of these elevations (e.g., >= 60%), however.

Miguel Indurain, multiple winner of the Tour de France, was jokingly referred to as "Mr. Sixty" by fellow competitors for walking around with HCT at 60%. He's still alive. Hell, the odds are in your favour that you don't suffer stroke or embolism in the next couple decades.

But, that risk could be reduced to virtually nil by keeping your HCT in the more mild range of elevations. Do you see what I am saying? Low probability, extremely high severity is still high risk.

Well I’d love to drop my H/H if I could, but nothing I do helps. I’m on a hefty dose of nattokinase (10,000FU) for insurance. Some say Telmisartan helps lower H//H but I’ve been taking that for almost 10 years and it definitely doesn’t for me.

Any suggestions?

 

[Type-IIx]

Well I’d love to drop my H/H if I could, but nothing I do helps. I’m on a hefty dose of nattokinase (10,000FU) for insurance. Some say Telmisartan helps lower H//H but I’ve been taking that for almost 10 years and it definitely doesn’t for me.

Any suggestions?

Phlebotomy is what works straightforwardly, a daily aspirin to reduce clotting risks but increase bleeding risks... besides just getting off TRT/AAS altogether if that is indeed the cause (presumably).

 

[Iron_Yuppie]

Since MENT is not potently androgenic, then it would be expected to increase HCT/Hb more significantly than tetosterone at equipotent dose/durations.

It doesn’t. In both the existing studies and in my own experience it has no effect on HCT.

 

[Iron_Yuppie]

This is purely anecdotal AND from Reddit posters…(don’t yell at me)

But there are a few guys with lab work to back up their findings that MENT only HRT I think they were using 3-5mg daily ?? Droped their HCT significantly compared to 150-200mg testosterone TRT.

If I can find the thread I’ll PM
You the link

You don’t have to PM me the link, I’m one of the guys who posted about that.

 

[NotHuman]

It doesn’t. In both the existing studies and in my own experience it has no effect on HCT.

At what dosage? Even high dosages won’t raise HCT? I’ve never used more than 15mg a day alongside my TRT test dose.

 

[Type-IIx]

It doesn’t. In both the existing studies and in my own experience it has no effect on HCT.

Well that's not true with respect to the studies, which show precisely the opposite.

There was a trend difference between MENT & testosterone on hematocrit at doses trialled (~ 2 mg/w vs. 120 mg/w, respectively) at 12 weeks, with MENT increasing hematocrit greater than testosterone (0.46 vs. 0.44, respectively) with a statistically significant between-group difference (95% confidence interval) for hemoglobin that MENT increased at 12 weeks, but testosterone did not significantly. Further, MENT provoked a striking increase in systolic blood pressure where testosterone had no effect. [1].

Since the only part of your statement that is actually testable has been easily falsified, and since you do not provide any supporting evidence of your own experience, not to mind in a valid form subjected to statistical & probabilistic methods to establish confidence to distinguish any measurement of yours from mere random chance, I'm going to go ahead and say, actually, MENT has a demonstrable clear effect on HCT.

[1] Walton, M. J., Kumar, N., Baird, D. T., Ludlow, H., & Anderson, R. A. (2007). 7 -Methyl-19-Nortestosterone (MENT) vs Testosterone in Combination With Etonogestrel Implants for Spermatogenic Suppression in He althy Men. Journal of Andrology, 28(5), 679–688. doi:10.2164/jandrol.107.002683

 

[NotHuman]

The increase in systolic BP is very real. I have to triple my dosages of Nebivolol and Telmisartan when using it.

 

[TheBootstrap]

Well that's not true with respect to the studies, which show precisely the opposite.

There was a trend difference between MENT & testosterone on hematocrit at doses trialled (~ 2 mg/w vs. 120 mg/w, respectively) at 12 weeks, with MENT increasing hematocrit greater than testosterone (0.46 vs. 0.44, respectively) with a statistically significant between-group difference (95% confidence interval) for hemoglobin that MENT increased at 12 weeks, but testosterone did not significantly. Further, MENT provoked a striking increase in systolic blood pressure where testosterone had no effect. [1].

Since the only part of your statement that is actually testable has been easily falsified, and since you do not provide any supporting evidence of your own experience, not to mind in a valid form subjected to statistical & probabilistic methods to establish confidence to distinguish any measurement of yours from mere random chance, I'm going to go ahead and say, actually, MENT has a demonstrable clear effect on HCT.

[1] Walton, M. J., Kumar, N., Baird, D. T., Ludlow, H., & Anderson, R. A. (2007). 7 -Methyl-19-Nortestosterone (MENT) vs Testosterone in Combination With Etonogestrel Implants for Spermatogenic Suppression in He althy Men. Journal of Andrology, 28(5), 679–688. doi:10.2164/jandrol.107.002683

I scanned the relevant part of the cited paper, and I believe the above statements regarding the study's hematocrit results are incorrect, but perhaps I am missing something. Where do you see any between-group analysis? The only information on that topic I see is the footnote of Table 2 that says:

"There were no significant differences between the MENT and testosterone groups in any of these variables."

Also, there are no confidence intervals in the paper. There are +/- standard errors in Table 2. Did you mean to refer to those?

Unfortunately, since this is a comparative experiment and they didn't present any between-group analysis (again, unless I missed it), nothing can be concluded about whether or how MENT affects hematocrit, either in comparison to the testosterone treatment or non-treatment.

 

[Iron_Yuppie]

There was a trend difference between MENT & testosterone on hematocrit at doses trialled (~ 2 mg/w vs. 120 mg/w, respectively) at 12 weeks, with MENT increasing hematocrit greater than testosterone (0.46 vs. 0.44, respectively) with a statistically significant between-group difference (95% confidence interval) for hemoglobin that MENT increased at 12 weeks, but testosterone did not significantly.

You didn’t cite the whole section on hematology. Here, I’ll help out:

“Hemoglobin concentrations were significantly increased in the MENT group at 12 weeks, but this did not persist at 24 weeks (Table 2). A similar pattern was also seen in hematocrit, Hemoglobin concentrations were significantly increased in the MENT group at 12 weeks, but this did not persist at 24 weeks (Table 2). A similar pattern was also seen in hematocrit, but this did not reach statistical significance. In the testosterone group a slower progressive rise in hemoglobin concentration (P = .0006) was observed that only became significantly at 48 weeks. There was also a significant overall rise in hematocrit (P = .009) in the testosterone group, although none of the individual treatment time points were significantly different from pretreatment (Table 2).”

So MENT caused a statistically insignificant rise in HCT, which at week 12 ceased, at 24 weeks was lower than baseline, and post treatment HCT was still lower than pretreatment baseline.

Interesting how you left those parts out. Im sure it was just an oversight.

I'm going to go ahead and say, actually, MENT has a demonstrable clear effect on HCT.

I guess mine went from 59.6 to 54.2 on 12 weeks of MENT alone by magic then. I suppose after nearly nine months on MENT my HCT further—by the powers of magic that you’re implying exist—went lower than it was, even prior to trt, to 48. I don’t know, instead of armchair sciencing maybe touch some grass and talk to live humans who have some experience with these things in the real world.

 

[HB_22]

Alright, so I’ll ask the question that’s probably too simplistic but nonetheless is of interest to me: as someone who has struggled with HCT simply from my trt dose, what would be the most effective compounds to use if the goal was growth while minimizing the increase in HCT?

Disclaimer: You’re not my physician and I will not hold you responsible for the answer. I’m asking merely your opinion within this context.

Angiotensin receptor blockers (ARBs) and ACE inhibitors are known to inhibit erythrocytosis, thereby leading to reduced plasma levels of erythrozyts, hemoglobin and hematocrit.
According to studies these drug classes are relatively safe as the incidence rate of adverse events for most of these ARBs and ACEIs were comparable to the incidence rate of the Placebo group. If struggling with high hgb, hct or erythrozyts then a low dose approach could be worth a try, imho.


But again, this not medical advise, this is just my personal opinion.

 

[Jin23]

How are soo many people having issues with hematocrit while on trt? I find it really hard to believe that whilst having normal physiological serum levels of androgens (500 - 700 ngdl), the prevalence of excessive erythropoiesis would be this high.

The increase in systolic BP is very real. I have to triple my dosages of Nebivolol and Telmisartan when using it.

Where are your levels really at; TT and free T?

 

[Millard]

How are soo many people having issues with hematocrit while on trt? I find it really hard to believe that whilst having normal physiological serum levels of androgens (500 - 700 ngdl), the prevalence of excessive erythropoiesis would be this high.

TRT has become somewhat of a meaningless phrase on forums like this as something quite different from real therapeutic TRT taken to maintain normal physiological testosterone levels.

Instead, TRT has become a euphemism for many who want to cycle year round with 200-400mg test per week. Or TRT is used to described by people who blast year round and "bridge" with 200-400mg per week between blasts.

Having said that however, there are more than a few people on therapeutic, physiological level TRT dosages who push beyond the upper range of normal for hematocrit %.

 

[Jin23]

TRT has become somewhat of a meaningless phrase on forums like this as something quite different from real therapeutic TRT taken to maintain normal physiological testosterone levels.

Instead, TRT has become a euphemism for many who want to cycle year round with 200-400mg test per week. Or TRT is used to described by people who blast year round and "bridge" with 200-400mg per week between blasts.

Having said that however, there are more than a few people on therapeutic, physiological level TRT dosages who push beyond the upper range of normal for hematocrit %.

Yeah, it's what I was insinuating. But also 150 to 200mg's, I find it hard to believe that such dosages fall in the range of normal androgen levels, which again I equate to 700ngdl at Tmax. Ofc some people metabolize test poorly, where they might need 150mg's weekly (split 75 x 2) to achieve a serum peak level of 750 ngdl, but according to the internet, almost everybody falls into this category ...

 

[Juggy3838]

I'm not going to "yell" at you, but I will give you a stern instruction that you have to do a hell of a lot better than this. At the very least, don't bother posting vague unsubstantiated claims when you cannot provide the supporting materials, especially when your claim runs totally contrary to the evidence that I actually did take the time to provide here in this thread.

Since MENT is not potently androgenic, then it would be expected to increase HCT/Hb more significantly than tetosterone at equipotent dose/durations.

Vague unsubstantiated claims? My claims? I never claimed MENT is better for HCT than testosterone. And a few people from a forum with one set of before/after labs each means very little for evidence anyways. There are dozens of variables that could influence HCT. I mean for fucks sake, there are studies showing HCT changes in a population due to yearly climate (April vs August).

I was just making the comment due to it being an interesting result. I don’t see the reason for a defensive response.

 

[HB_22]

Yeah, it's what I was insinuating. But also 150 to 200mg's, I find it hard to believe that such dosages fall in the range of normal androgen levels, which again I equate to 700ngdl at Tmax. Ofc some people metabolize test poorly, where they might need 150mg's weekly (split 75 x 2) to achieve a serum peak level of 750 ngdl, but according to the internet, almost everybody falls into this category ...

I agree. I had above the lab reference range elevated free testosterone and total testosterone levels with just 105mg per week, split into daily 15mg injections.

 

[Iron_Yuppie]

Angiotensin receptor blockers (ARBs) and ACE inhibitors are known to inhibit erythrocytosis, thereby leading to reduced plasma levels of erythrozyts, hemoglobin and hematocrit.
According to studies these drug classes are relatively safe as the incidence rate of adverse events for most of these ARBs and ACEIs were comparable to the incidence rate of the Placebo group. If struggling with high hgb, hct or erythrozyts then a low dose approach could be worth a try, imho.


But again, this not medical advise, this is just my personal opinion.

Valsartan has helped my HCT for sure. Unfortunately the reason I needed it was because MENT gave me high BP which persisted for ~18 months after cessation.

 

[Iron_Yuppie]

How are soo many people having issues with hematocrit while on trt? I find it really hard to believe that whilst having normal physiological serum levels of androgens (500 - 700 ngdl), the prevalence of excessive erythropoiesis would be this high.

How many people on trt have levels between 500-700? What percentage do you think? My money is on it landing somewhere in the lower quintile.

 

[NotHuman]

Angiotensin receptor blockers (ARBs) and ACE inhibitors are known to inhibit erythrocytosis, thereby leading to reduced plasma levels of erythrozyts, hemoglobin and hematocrit.
According to studies these drug classes are relatively safe as the incidence rate of adverse events for most of these ARBs and ACEIs were comparable to the incidence rate of the Placebo group. If struggling with high hgb, hct or erythrozyts then a low dose approach could be worth a try, imho.


But again, this not medical advice, this is just my personal opinion.

I keep seeing people say these drugs lower hematocrit but I’ve been on Telmisartan for 10 years on and off and it sure as crap doesn’t reduce mine.

 

[NotHuman]

Valsartan has helped my HCT for sure. Unfortunately the reason I needed it was because MENT gave me high BP which persisted for ~18 months after cessation.

18 months?? That’s wild. Mine dropped maybe a day or two after stopping.