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

[NotHuman]

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?

Test cyp (200mg/ml) straight from Walgreens. 3/5 of a cc on a slin pin is 12mg so I inject that every day. I do daily injections since they are much better for stable blood levels and to avoid much of a difference between peak and trough.

 

[Type-IIx]

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?

Yes, from memory of a conversation you and I had some time ago on this very same topic, I recall that 120 mg/w testosterone enanthate/cypionate is roughly where I would think that risks of long-term use to cardiac maladaptations outweigh the benefits for healthspan for all individuals; but lower is less risky, as is youth. For older men & those with elevated CV risks, we might be averse to even 85 mg/w.

The recommendations for proper TRT dose titration based on biochemical measures are to start with 250 mg every 21 days (i.e., an initial 3 week interval) of testosterone enanthate/cypionate. Measure the mid-point (i.e., day 14) total testosterone. Titrate dose & frequency up or down to a mid-interval TT of 500 - 800 ng/dL. Rely on biochemical and objective (e.g., truncal hair growth, muscular strength) measures, only referring to subjective (e.g., energy, well-being, sexual activity) measures where adequacy of the regimen has been established and cleared of psychological impairments by a clinician (i.e., after psychiatrist's evaluation).

I think that breaks from use of hormones benefits endogenous production, so fertility of course as well as not being life-long dependent on exogenous application in some form) and has psychological benefits, especially after an extended blast on a frequent administration schedule.

 

[Type-IIx]

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.

There's not enough evidence to say with certainty without its being measured in a valid model that permits comparison between agents, e.g., Gorshein's 72 h Fe incorporation & reticulocyte count.

But there are reasons to believe that it probably does potently stimulate HCT/Hb because it is a relatively attenuated/weak androgen (inversely related to hematinic potency) & while a weak association, it is also an androsta-1,4-diene-3-one, a member of the same class of AAS that Dianabol belongs to, an ideal hematinic agent.

 

[Iron_Yuppie]

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.

What exactly would you like? I could post blood work if I was inclined to comb through the various piles of paperwork I have, some in print form, some in PDFs, but then what? You could simply say those were made up or that they didn’t belong to me. I’d have no way of proving anything. I’m giving my personal experience, it’s entirely up to you and anyone else to decide whether or not I’ve staged an elaborate lie from which I derive no benefit.

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

It was. That was unnecessary on my part. You were implying—whether intentionally or not—that I was simply making something up. That rubbed me the wrong way. I could have given you the benefit of a good faith argument but instead I presumed you were being an asshole and responded as such. I apologize for that.

I've said that differences between measurement values could be due to random chance; a far cry from fucking magical thinking.

If cause and effect can no longer be observed and reported on then you have no way to measure anything because random externalities come and go all the time. I have years worth of data showing how using testosterone affects my HCT. I have nine months of data showing how not using testosterone and instead taking MENT affects my HCT. I have ~20 months of data showing the impact of various doses of valsartan has had on my HCT. At no point in time have I said that those data apply to every single human being on the planet, but they damn sure apply to me. My objection to your argument is that you are using a study to refute objective reality.

 

[Type-IIx]

What exactly would you like? I could post blood work if I was inclined to comb through the various piles of paperwork I have, some in print form, some in PDFs, but then what?

Yes, please! I intimated you that I am interested, at the first moment you mentioned this. I still am.

You could simply say those were made up or that they didn’t belong to me. I’d have no way of proving anything. I’m giving my personal experience, it’s entirely up to you and anyone else to decide whether or not I’ve staged an elaborate lie from which I derive no benefit.

I could, but I won't. I'll only qualify that we cannot readily attribute cause/effect to two data points, and it needs to be informed by other relevant compound use & doses.

I really, truly, am not just trying to be right on the internet bro.

It was. That was unnecessary on my part. You were implying—whether intentionally or not—that I was simply making something up. That rubbed me the wrong way. I could have given you the benefit of a good faith argument but instead I presumed you were being an asshole and responded as such. I apologize for that.

Thank you, I accept the apology.

If cause and effect can no longer be observed and reported on then you have no way to measure anything because random externalities come and go all the time. I have years worth of data showing how using testosterone affects my HCT. I have nine months of data showing how not using testosterone and instead taking MENT affects my HCT. I have ~20 months of data showing the impact of various doses of valsartan has had on my HCT. At no point in time have I said that those data apply to every single human being on the planet, but they damn sure apply to me. My objection to your argument is that you are using a study to refute objective reality.

I rely on bloodwork all the damn time to make decisions; I qualify it as nonauthoritative evidence (where published, replicable data subjected to rigorous study design & statistical/probabilistic methods to root out data from random chance are authoritative), but it's still usually more valuable than no data, and in the right context can be good evidence.

 

[Type-IIx]

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

What? Fuck no. Never said anything of the sort.

There's more to consider beyond the hematinic potency of, say 50 mg/w tren vs. 250 mg/w test when it comes to safety.

Like cardiovascular risks (way worse for Tren). Psychological risks (if not direct, then indirect, by effects on sleep, ulcerogenic risks/"heartburn"). Fuck, I think some of my posts in this very thread, probably including this one, are a testament to how much of a prick 100 mg/w tren enanthate can make someone who's usually semi-tolerable.

And I'm having a good day.

 

[malfeasance]

Test cyp (200mg/ml) straight from Walgreens. 3/5 of a cc on a slin pin is 12mg so I inject that every day. I do daily injections since they are much better for stable blood levels and to avoid much of a difference between peak and trough.

3/5 of a cc is not equal to 12mg no matter what sort of pin you put it in. 3/50 is.

3/5 of a cc is 3/5 of 200, which is 120 mg.

Maybe you mean 3/5 of one tenth of a cc? (3/50 of a cc)

Slin pins come in 1 cc, .5 cc, and .3 cc. I assume you are using one of these and measuring 3/50 of a cc somehow.

In the smallest one, it is very difficult to control for air bubble with oil (slin is thinner, watery).

So six one unit clicks on the 0.3 cc syringe, maybe?

 

[NotHuman]

3/5 of a cc is not equal to 12mg no matter what sort of pin you put it in. 3/50 is.

3/5 of a cc is 3/5 of 200, which is 120 mg.

Maybe you mean 3/5 of one tenth of a cc? (3/50 of a cc)

Slin pins come in 1 cc, .5 cc, and .3 cc. I assume you are using one of these and measuring 3/50 of a cc somehow.

In the smallest one, it is very difficult to control for air bubble with oil (slin is thinner, watery).

So six one unit clicks on the 0.3 cc syringe, maybe?

Pardon me, yes. I meant 3/5 of one tenth of a cc. I visualize it in my brain so instinctively that I forget the exact math.

 

[TheBootstrap]

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.

Makes sense.

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

Oh, ok. I was confused since I haven't seen things put in that manner before. It's a bit unusual since confidence intervals are, generally speaking, constructed by inverting hypothesis tests and therefore secondary to p-values (being primary), and thus if you're doing "statistically significant" error-control type statistics, most would simply cite the p-value being less than the stated alpha value.

I'm a big fan of confidence intervals and consider them to be a thousand times better than p-values when used in an estimation context vs null hypothesis significance testing. Here I agree it makes no difference vs p-values since you're using them in the testing context. As I said, just a bit unusual way to use them from what I've seen.

Thanks for the clarifications.

 

[S.B.C]

"cunty mood" that sounds very British.

 

[malfeasance]

Yes, from memory of a conversation you and I had some time ago on this very same topic, I recall that 120 mg/w testosterone enanthate/cypionate is roughly where I would think that risks of long-term use to cardiac maladaptations outweigh the benefits for healthspan for all individuals; but lower is less risky, as is youth. For older men & those with elevated CV risks, we might be averse to even 85 mg/w.

The recommendations for proper TRT dose titration based on biochemical measures are to start with 250 mg every 21 days (i.e., an initial 3 week interval) of testosterone enanthate/cypionate. Measure the mid-point (i.e., day 14) total testosterone. Titrate dose & frequency up or down to a mid-interval TT of 500 - 800 ng/dL. Rely on biochemical and objective (e.g., truncal hair growth, muscular strength) measures, only referring to subjective (e.g., energy, well-being, sexual activity) measures where adequacy of the regimen has been established and cleared of psychological impairments by a clinician (i.e., after psychiatrist's evaluation).

I think that breaks from use of hormones benefits endogenous production, so fertility of course as well as not being life-long dependent on exogenous application in some form) and has psychological benefits, especially after an extended blast on a frequent administration schedule.

So, now I know I just have to get younger, and all this will work out.

 

[Type-IIx]

"cunty mood" that sounds very British.

Could be. Could be spending time on the UK Muscle board and they're rubbing off on me. God knows they've got better banter, even if shittier food. Could be that I think cunt, as a word at least as versatile as fuck, should be rehabilitated and no longer maligned by pearl-clutching Americans.

So, now I know I just have to get younger, and all this will work out.

Reasonable. There is a period, probably before 40, where low-dose anabolics (i.e., AAS, rhGH & GH secretagogues) might make you look/feel a bit younger as part of a well-rounded exercise program, but they tend to oppose longevity & healthspan as you age past mid-life, or where it would be without modern medicine. After that, Metformin & reducing IGF-I, and exercise aimed at just mitigating muscle function & bone mineral losses with resistance training, and doing more to enhance or at least maintain VO2max, muscle power mostly in the lower body, and basic balance, become more important. A sick joke, this whole existence & death thing that we are blessed with full foreknowledge & awareness of.

 

[Juggy3838]

@Type-IIx

“Metformin & reducing IGF-I, and exercise aimed at just mitigating muscle function & bone mineral losses with resistance training, and doing more to enhance or at least maintain VO2max”

You ever listen to Peter Attia podcasts? He has some great guests speaking on how powerful raising your VO2 max is on life span. It’s pretty absurd. I think he cited that the difference in risk of all-cause mortality between the bottom 25% and top 2.5% for VO2 max is like 400%

Ok ADHD moment over. Back to the thread.

 

[Type-IIx]

@Type-IIx

“Metformin & reducing IGF-I, and exercise aimed at just mitigating muscle function & bone mineral losses with resistance training, and doing more to enhance or at least maintain VO2max”

You ever listen to Peter Attia podcasts? He has some great guests speaking on how powerful raising your VO2 max is on life span. It’s pretty absurd. I think he cited that the difference in risk of all-cause mortality between the bottom 25% and top 2.5% for VO2 max is like 400%

Ok ADHD moment over. Back to the thread.

Yes, I am familiar with Peter Attia & his media/content.

His training methods for longevity & healthspan make tremendous sense, though his nutrition dogma (keto, basically; though he may have walked that back or qualified it in multiplicity) is flimsy at best. He has a tendency to hyperfixate on some myopic aspect of some general concept (i.e., the topic) and take discussions off onto absurd tangents. But basically, I think his training material – not particularly original, but that he has become associated with – hits the mark for longevity/healthspan, and that he's a highly intelligent and productive person worthy of admiration.

 

[Juggy3838]

Yes, I am familiar with Peter Attia & his media/content.

His training methods for longevity & healthspan make tremendous sense, though his nutrition dogma (keto, basically; though he may have walked that back or qualified it in multiplicity) is flimsy at best. He has a tendency to hyperfixate on some myopic aspect of some general concept (i.e., the topic) and take discussions off onto absurd tangents. But basically, I think his training material – not particularly original, but that he has become associated with – hits the mark for longevity/healthspan, and that he's a highly intelligent and productive person worthy of admiration.

It’s funny you say that, he has a few podcasts where he talks about changing his mind on keto and his prior views on diet/fasting. Definitely a mixed diet guy now. I got hooked on his podcasts when I was trying to tease out the implications and the current literature on cholesterol numbers when my dad went carnivore.

I’m a fan, pretty decent time fillers while driving or on a jog.

 

[malfeasance]

@Type-IIx

“Metformin & reducing IGF-I, and exercise aimed at just mitigating muscle function & bone mineral losses with resistance training, and doing more to enhance or at least maintain VO2max”

You ever listen to Peter Attia podcasts? He has some great guests speaking on how powerful raising your VO2 max is on life span. It’s pretty absurd. I think he cited that the difference in risk of all-cause mortality between the bottom 25% and top 2.5% for VO2 max is like 400%

Ok ADHD moment over. Back to the thread.

You can't train yourself into the top 2.5% of VO2 max - it is genetic at that level. If you do not have the genetics, then you will never get there.

You can, however, improve your VO2 max, and it will improve the most for the folks at the bottom of the spectrum.

 

[hungryalways]

For those with high HCT, it's worth checking how long it's taking before your sample reaches the lab for analysis. I had some high levels from a local company here, for which samples are sent in the mail (which takes 24 to 48 hours) - it turns out this delay was artificially raising the value.

This study shows around an 8% increase in HCT over 48 hours when the blood was stored at 23 °C: Stability of hematological analytes during 48 hours storage at three temperatures using Cell-Dyn hematology analyzer

Afterward, I had my bloods done locally and everything was normal. I emailed my theory over to the company that did the original labs, and their hematology department replied. According to them, they'd run similar tests, and after two days at room temperature, they see 14% changes in HCT, MCV and MCHC.

TLDR: Make sure your blood is getting to the lab ASAP.

 

[readalot]

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.

Ok checking in. Have you gotten bigger and veiny-er?

Excellent like to post count ratio. Well done!

 

[readalot]

This thread is great. Well done fellas LOL.

I have spent too much time debating the wrong group. Bravo on the kcals exerted in this thread.

 

[Iron_Yuppie]

Ok checking in. Have you gotten bigger and veiny-er?

Excellent like to post count ratio. Well done!

I’m sorry, who are you and what are you talking about?