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

[NotHuman]

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.

I did recently as well. 16mg per day (112mg weekly) and somehow I was above the range for TT and FT. It was confused since that doesn’t normally put me that high.

 

[NotHuman]

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.



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

When I was using heavy AAS doses, I never had a problem with HCT. It never went over 51%. It wasn’t until I dropped down to low test and then TRT that it became much higher. Then then donating blood all the time made it go up even more once the blood came back.

my testosterone levels are all over the place since I’ve tested them 100s of times but usually my TT is in the 900s and FT about 25ish. They were higher more recently as I pointed out above but that was an accident. I have seen a 58-60% HCT many times in blood test results despite trying to drink water first thing in the morning. However, all my other health markers are optimal. I’m not really worried since I’ve researched the subject but I am worried enough that I hardly ever go on blasts anymore. Sometimes I’ll add 5-15mg MENT and it doesn’t seem to raise it above 60% luckily.

 

[Jin23]

When I was using heavy AAS doses, I never had a problem with HCT. It never went over 51%. It wasn’t until I dropped down to low test and then TRT that it became much higher. Then then donating blood all the time made it go up even more once the blood came back.

my testosterone levels are all over the place since I’ve tested them 100s of times but usually my TT is in the 900s and FT about 25ish. They were higher more recently as I pointed out above but that was an accident. I have seen a 58-60% HCT many times in blood test results despite trying to drink water first thing in the morning. However, all my other health markers are optimal. I’m not really worried since I’ve researched the subject but I am worried enough that I hardly ever go on blasts anymore. Sometimes I’ll add 5-15mg MENT and it doesn’t seem to raise it above 60% luckily.

Those are high levels and what's the lab range on that free t? Also, why are your T levels all over the place? And is that 900 peak or through?

 

[NotHuman]

Those are high levels and what's the lab range on that free t? Also, why are your T levels all over the place? And is that 900 peak or through?

8.7-25 is the range for Free Test.

Ok maybe not all over the place but there will always be some variance the more you get blood tests. Those are generally averages. I inject daily and haven’t noticed much of a difference in levels whether it’s peak or trough, but I try to get my blood checked at the trough so 24 hours after the last injection.

If I get my HCT tested in the afternoon, it’s definitely a few percentage points lower since I’ve had more hydration but it’s still high.

 

[Jin23]

8.7-25 is the range for Free Test.

Ok maybe not all over the place but there will always be some variance the more you get blood tests. Those are generally averages. I inject daily and haven’t noticed much of a difference in levels whether it’s peak or trough, but I try to get my blood checked at the trough so 24 hours after the last injection.

If I get my HCT tested in the afternoon, it’s definitely a few percentage points lower since I’ve had more hydration but it’s still high.

Well, there you go. 900 ngdl is your average serum level which is high and so is your free T. Lab ranges aren't magical, as in, if you stay just below it's high range, you'll be magically o.k. 900 ng/dl with free T hoovering just at the upper physiological limit is high. Normal, I repeat; Normal, ranges are almost half of where you're at.

 

[NotHuman]

Well, there you go. 900 ngdl is your average serum level which is high and so is your free T. Lab ranges aren't magical, as in, if you stay just below it's high range, you'll be magically o.k. 900 ng/dl with free T hoovering just at the upper physiological limit is high. Normal, I repeat; Normal, ranges are almost half of where you're at.

Somehow I doubt my hematocrit level would drop ~10% if I went from a total testosterone level of 900 down to 500.

 

[Jin23]

Somehow I doubt my hematocrit level would drop ~10% if I went from a total testosterone level of 900 down to 500.

I don't think so either, but it definitely would drop to a more manageable level. You also might be at significantly higher free T level then that lab result you had. Also, how is your iron panel looking? And where is your e2 at, do you need to use small doses of an Ai to keep it in check?

 

[NotHuman]

I don't think so either, but it definitely would drop to a more manageable level. You also might be at significantly higher free T level then that lab result you had. Also, how is your iron panel looking? And where is your e2 at, do you need to use small doses of an Ai to keep it in check?

My iron panel is at manageable levels now that I’ve recovered my ferritin back up from being deficient thanks to pointless and harmful phlebotomies.

Estradiol is always high (40-50), which I think could be another contributing factor to my secondary erythrocytosis. My DHT is always elevated too.

Another thing I notice is my O2% is a little on the lower side of 95-97% depending on when I check

So it is possible I am using too much testosterone like you suggested which is why I lowered my dose to 12mg per day. I’m getting labs on Monday for the first time on this dose. Curious what the results will be.

 

[Jin23]

My iron panel is at manageable levels now that I’ve recovered my ferritin back up from being deficient thanks to pointless and harmful phlebotomies.

Estradiol is always high (40-50), which I think could be another contributing factor to my secondary erythrocytosis. My DHT is always elevated too.

Another thing I notice is my O2% is a little on the lower side of 95-97% depending on when I check

So it is possible I am using too much testosterone like you suggested which is why I lowered my dose to 12mg per day. I’m getting labs on Monday for the first time on this dose. Curious what the results will be.

A high estradiol is for sure a sign of androgen excess, ofc high dht means the same. There is no question your dose is too high.

Idk when you lowered your dose, but hct wont fall in a weeks time ... If you're pinning ed try to hit somewhere around 650 ngdl. I know it's psychologically hard to lower the dose, but high dosages really are unsustainable so in reality you really don't have a choice anyway.

And just measure shbg and albumin then calculate free t using TruT calc.

 

[NotHuman]

A high estradiol is for sure a sign of androgen excess, ofc high dht means the same. There is no question your dose is too high.

Idk when you lowered your dose, but hct wont fall in a weeks time ... If you're pinning ed try to hit somewhere around 650 ngdl. I know it's psychologically hard to lower the dose, but high dosages really are unsustainable so in reality you really don't have a choice anyway.

And just measure shbg and albumin then calculate free t using TruT calc.

It's not intentionally high. I've used a slightly higher dose of 20mg per day and gotten lower testosterone numbers before. It's bizarre.

I think if the HCT does go down, it'll prob take 3 months. The thing is even if I do accomplish this, I will just want to blast some MENT at that point anyway lol.

I will have lowered it from 16mg to 12mg daily for 4 weeks when I get re-tested. I would have waited longer but I am going away for a month the following day so I want to get it out of the way first. Can always test again when I get back.

 

[Type-IIx]

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.

Sorry bro, I didn't even realize that post was in reply to you, I treated you like someone else. Besides that, I was in a cunty mood when I replied to you, can't handle Tren like I used to.

 

[Type-IIx]

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:



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.

I think I was referring to hemoglobin and not hematocrit, there was a trend in hematocrit changes at 12 weeks and statistical significance in hemoglobin changes.

Here's what I wrote in my own notes on this study:

Haematologic effects
Hemoglobin concentrations were significantly increased (149 ± 2.9 g/L → 154 ± 3.3; effect size: 1.724; %Δ: +3.35%; 95% confidence interval) by MENT (~ 2 mg/w) at 12 weeks, and a similar pattern (0.44 to 0.46; effect size: 2; %Δ: +4.5%; not significant) was seen in hematocrit, but this did not reach statistical significance. [8].

In the testosterone group (~ 120 mg/w) a slower progressive rise in hemoglobin concentration was observed that only became significant at 48 weeks. There was also a significant overall rise in hematocrit in the testosterone group, although none of the individual treatment time points were significantly different from pre-treatment (0.45 ± 0.01).

Recall that haemoglobin (Hb) measures reflect binding protein in erythrocytes (RBCs) for O₂ (Hb 13.5-17 g/dL [men], 12-15.5 g/dL [women])

Haematocrit (HCT) is the % of blood volume occupied by erythrocytes (RBCs) [men 41-51%, women 36-47%]

 

[Type-IIx]

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:



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.

Sorry I clearly did make a mistake here when I initially glanced at the Table; this was all very haphazard and quick, and you can tell I edited at least one mistake in what I initially responded with, given the editing history of the post. While I recall thinking that it a very unusual way to present such a thing, I incorrectly read the legend initially as saying that the † & ‡ symbols referred to between-group differences.

The confidence intervals are associated with the P values, 0.05 & 0.01. That is, 95% & 99% confidence intervals.

 

[malfeasance]

Somehow I doubt my hematocrit level would drop ~10% if I went from a total testosterone level of 900 down to 500.

It takes months for hematocrit levels to drop, especially if you are middle aged or older.

The lifespan of a red blood cell is around 120 days, so once you stop stimulating their production by injecting supraphsyiological levels of hormones, older red blood cells that die off will not be replaced with excessively high numbers of artificially stimulated red blood cells almost immediately, but it would be December / January before you know your real hematocrit number as a result of the change.

 

[malfeasance]

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

That is not even close to normal levels of testosterone that the body produces naturally, even for a 25 year old male.

Around 7mg a day is produced by the normal male, and the body is constantly busy binding up some of it and metabolizing all of it. But do the math. 7mg x 7 = around 49 mg a week.

7 x 7 = 49

Guys doing 150-200 mg a week and calling it TRT are fooling themselves.

 

[malfeasance]

It's not intentionally high. I've used a slightly higher dose of 20mg per day and gotten lower testosterone numbers before. It's bizarre.

I think if the HCT does go down, it'll prob take 3 months. The thing is even if I do accomplish this, I will just want to blast some MENT at that point anyway lol.

I will have lowered it from 16mg to 12mg daily for 4 weeks when I get re-tested. I would have waited longer but I am going away for a month the following day so I want to get it out of the way first. Can always test again when I get back.

Wow, really close to what I posted above (3 months v. 4 months).

Your daily injections - are they no ester or with an ester? If your testosterone has an ester, then I am curious as to your reasoning for dosing it daily?

I am also curious how you measure such small amounts to know the difference between 16 and 12 mg?

 

[Type-IIx]

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.

Here's what I wrote in my own notes on this study:

Haematologic effects
Hemoglobin concentrations were significantly increased (149 ± 2.9 g/L → 154 ± 3.3; effect size: 1.724; %Δ: +3.35%; 95% confidence interval) by MENT (~ 2 mg/w) at 12 weeks, and a similar pattern (0.44 to 0.46; effect size: 2; %Δ: +4.5%; not significant) was seen in hematocrit, but this did not reach statistical significance. [8].

In the testosterone group (~ 120 mg/w) a slower progressive rise in hemoglobin concentration was observed that only became significant at 48 weeks. There was also a significant overall rise in hematocrit in the testosterone group, although none of the individual treatment time points were significantly different from pre-treatment (0.45 ± 0.01).

Recall that haemoglobin (Hb) measures reflect binding protein in erythrocytes (RBCs) for O₂ (Hb 13.5-17 g/dL [men], 12-15.5 g/dL [women])

Haematocrit (HCT) is the % of blood volume occupied by erythrocytes (RBCs) [men 41-51%, women 36-47%]

Right, I gave you the study I referenced so that you can challenge my presentation of the same data. No oversight; my perspective on the same evidence. Do note that I did err by saying that the confidence intervals referred to between-group differences, that is not so, but rather to base-line levels.

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.

How am I to assess this for reliability? It's just a declarative statement that you attribute cause/effect to, but without any supporting materials.

The fact that you are putting words of "magic" in my mouth is a real cunty fucking argument tactic.

I've said that differences between measurement values could be due to random chance; a far cry from fucking magical thinking. Not to mind, any host of factors that affect measurement (e.g., season, iron status, liver health, etc. affect HbA1c measurements with statistical if not clinical significance) despite there being no increase in mean glycosylated hemoglobin, etc.

 

[malfeasance]

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.

Does your research inform you about any recommendations you can make for us in plain English? I see you recommend blood draining in this thread.

Anything else? Maybe TRT level recommendations?

For those who cycle, abuse, for putting on size, does taking a break (not cruise, no TRT, but injecting nothing at all) help?

 

[malfeasance]

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

Author: Type-IIx

Comparative potencies to increase hematocrit (HCT) & hemoglobin (Hb)

Nandrolone (decanoate > phenylpropionate) > Anadrol (Oxymetholone) > Testosterone (propionate > cypionate > enanthate). [1].

Discussion

While Testosterone is modestly erythropoietic, this effect becomes significant at doses greater than peak myotrophic‡ & androgenic response. [2]. Methyltestosterone is not significantly erythropoietic and highly androgenic, the same goes for Cheque drops & Halotestin (potently androgenic and not significantly erythropoietic). [2].

Dianabol possesses ideal features as a hematinic agent: at doses equating to 0.6 mg per k.g. daily in man, significant myotrophic and erythropoietic activity is observed (in rodent) without androgenicity. [2]. Masteron's erythropoietic potency is significant in man [3] and rat [4]. This feature of Masteron is dissociated from its relatively weakened myotrophic potency.

Anadrol is consistently demonstrated as a potent stimulator of erythropoiesis in man [3] and rat [4], though is associated with considerable hepatotoxicity. In aplastic anemia cases, 80% of patients saw mild-to-marked alterations in liver function given 17AAs Dianabol & Anadrol versus a mere 26% given Masteron & Primo Ace (oral) at doses ranging from 0.25 - 3.0 mg/kg/day [3]. Noteworthy, however, is the high background of liver dysfunction comorbid with aplastic anemia (24%); as well as normalization of liver function in patients switched from the 17AAs (Anadrol & Dianabol) to non-17AA oral androgens Masteron & Primo Ace [3].

Is EQ is Particularly Erythropoietic?

From [2], we can say that there is no class effect of androst-1,4-dien-3-ones (e.g., EQ, Dianabol) in augmenting erythropoiesis. While the most potent hematinic agent assayed was of this class (Dianabol), 17β-hydroxy-2-methyl-androst-1,4-dien-3-one (a 2-methyl generally decreases androgenicity; an apparent exception to this, then, is present here) and 11β,17β-dihydroxy-17-methyl-androst-1,4-dien-3-one (an 11β-hydroxyl substituent added to an androst-1,4-dien-3-one serves only to hinder potency unlike in the 19-nortestosterone series or in the presence of a 9α-fluoro substituent) lacked any particular potency in this regard. [2]. See †, below.

General Rule (Androgenicity is Inversely Related to Hematopoietic Potency)

Nandrolone, Anadrol, Dianabol, Masteron, and Primobolan are more potent stimulators of erythropoiesis than Testosterone. Halotestin, Cheque drops, and Methyltestosterone, while potently androgenic, do not significantly stimulate hematinic activity.

If there is a general rule with respect to AAS’ hematopoietic potencies, it is that androgenic potency is inversely related to hematopoietic potency.

Still, if AAS are used at doses that are above those which are maximally stimulatory of N retention‡ (i.e., > peak myotropic response), one should expect that this general rule will not necessarily hold.

Trenbolone as an Apparent Exception to the Rule

The case of Trenbolone presents an illustration of this phenomenon of the general rule not applying at very high doses. To reiterate, AAS used at doses that are above those which are maximally stimulatory of N retention‡ (i.e., > peak myotropic response), one should expect that this general rule will not necessarily hold.

Trenbolone, as acetate, is according to bro-science, to be used at a 350 mg/w dose for a novice. This is, however, a remarkably high dose for this drug. On a molar (per-mg) basis, 350 mg of trenbolone acetate posesses approximately 5.5-fold the AR activation potency as 350 mg of testosterone enanthate. That is to say, 350 mg of trenbolone acetate is equivalent in AR potency to > 1,900 mg/w of testosterone enanthate. Since the hazards or health risks germane to trenbolone are mostly AR-mediated, but (e.g., cardiovascular risks, electrolyte disturbances and therefore renal/kidney risks) are also mediated by its antagonism of the MR (mineralocorticoid receptor). An often reported side effect by trenbolone users is appetite supression. This is indicative of acute toxicity. Since AAS (at therapeutic doses) increase appetite as a class effect, the experience of reduced appetite is indicative of excessive dosing and acute toxicity.

†: By this rule, EQ, being particularly well tolerated in practice by women, one might – speculatively – follow through on this line of reasoning to consider EQ as a candidate for inclusion into this class of weak (or “attenuated”) androgens, and by extension, potent hematinic agents.

‡: Maximal stimulation of N retention is not the only mechanism by which AAS exert their effects on muscle size (↑) and fat mass (↓).

______________________
References:

[1] Gorshein, D., Murphy, S., & Gardner, F. H. (1973). Comparative study on the erythropoietic effects of androgens and their mode of action. Journal of Applied Physiology, 35(3), 376–378. doi:10.1152/jappl.1973.35.3.376
[2] Molinari PF, Rosenkrantz H. Erythropoietic activity and androgenic implications of 29 testosterone derivatives in orchiectomized rats. J Lab Clin Med. 1971 Sep;78(3):399-410.
[3] Sanchez-Medal L, Gomez-Leal A, Duarte L, Guadalupe Rico M. Anabolic androgenic steroids in the treatment of acquired aplastic anemia. Blood. 1969 Sep;34(3):283-300.
[4] Duarte, L., Sanchez Medal, L., Labardini, J., & Arriaga, L. (1967). The Erythropoietic Effects of Anabolic Steroids. Experimental Biology and Medicine, 125(4), 1030–1032. doi:10.3181/00379727-125-32268

I read it, twice, and I cannot figure out what it is saying about EQ.

So EQ does or does not live up to its reputation for driving hematocrit up to 100% (ok, joking about 100%, but is EQ especially bad for hematocrit, or what?)

My anecdotal observation is that EQ drives up my hematocrit levels really high.

Which is too bad because I like the way I look on high levels of EQ and moderate testosterone.

 

[malfeasance]

So it's safer for us all to be injecting tren?