Shorter Ester = Bigger Sides?

We have trolls that come and go, but some just return from time to time to remind us they exist and annoy us. They kinda evolve, there seems to be a new breed of hybrid trolls or some shit. OP as a troll you either adapt or you perish, choose your fate.
 
We have trolls that come and go, but some just return from time to time to remind us they exist and annoy us. They kinda evolve, there seems to be a new breed of hybrid trolls or some shit. OP as a troll you either adapt or you perish, choose your fate.

I'm perplexed at the amount of knowledge this kids have and that they actually have the balls to use aas. Goes to shove how normalized aas have become - a big part owning to people like derek ... First he created a yt channel so he could push tony huge sarm's, then when that passed he just contributed to the normalization of aas and now he has his own trt clinic, where all the kids whom in large part learned about aas and went on aas because of him, can go and pay big money to get sorted out. This is marketing 101: create demand and then supply the product.

He doesn't even believe this study and still choses to believe some misinformed mpmd video.

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"Plasma testosterone concentrations were most rapidly and completely suppressed within the first week after injections of the phenylpropionate ester, but this suppression was sustained for the shortest time. The duration of suppression was significantly longest after the gluteal 1-ml injection. Plasma testosterone concentrations returned to base line by day 13 after the phenylpropionate ester but required >20 days to return to base-line levels after the decanoate ester." Minto CF, Howe C, Wishart S, Conway AJ, Handelsman DJ. Pharmacokinetics and pharmacodynamics of nandrolone esters in oil vehicle: effects of ester, injection site and injection volume. J Pharmacol Exp Ther. 1997 Apr;281(1):93-102.
- FSH suppression occurred rapidly (day 3 or 4) but returned to base-line practically immediately after phenylpropionate (IM gluteal) and after about a week with decanoate (Table 6, Inhibin, p. 100)

But nandrolone (as hexyloxyphenylpropionate; Anadur) at 200 mg every 21 days was unable to maintain suppression of spermatogenesis whereas 100 mg testoterone (as enanthate) was able. Behre, H. M., Kliesch, S., Lemcke, B., von Eckardstein, S., & Nieschlag, E. (2001). Suppression of spermatogenesis to azoospermia by combined administration of GnRH antagonist and 19-nortestosterone cannot be maintained by this non-aromatizable androgen alone. Human Reproduction, 16(12), 2570–2577. doi:10.1093/humrep/16.12.2570. Swerdloff, R. S., Bagatell, C. J., Wang, C., Anawalt, B. D., Berman, N., Steiner, B., & Bremner, W. J. (1998). Suppression of Spermatogenesis in Man Induced by Nal-Glu Gonadotropin Releasing Hormone Antagonist and Testosterone Enanthate (TE) Is Maintained by TE Alone1. The Journal of Clinical Endocrinology & Metabolism, 83(10), 3527–3533. doi:10.1210/jcem.83.10.5184

LH suppression was mostly reversed by week 6 post-cycle with 250 mg Test Cyp per week versus week 10 post-cycle in 500 mg group.

This is from a 2018 paper titled Population PK/PD Modeling of Testosterone Cypionate in Healthy Male Subjects by Bi, Perry, Ellerby, et al.

In conclusion, if you're just basically worried about which nandrolone ester is going to give you the most grief with recovery of HPG axis functioning, you're simply worried about the wrong thing if you consider testosterone to be a smooth recovery. Deca is worse than NPP in this regard, but even the Anadur (21-day half life) is unable to fully suppress HPG axis functioning at 200 mg every 21 days unlike testosterone enanthate or cypionate at 100 mg every week.
 
And for the love of god don't use clomid. Use enclomiphene and if you can't source it use tamox. And don't use large dosages, you'll just suffer sides. Use 25mg enclom or 20mg tamox. As I said, you are probably half way recovered already so no need for large dosages.
Why such disdain for clomid?

Don’t get me wrong, it is well known that quite a few people suffer sides from it, so that’s probably where you’re going with this; but I’m curious if you’d elaborate on why such a determined shut down of it?

Like any drug, personal reaction is a thing. For myself, it was a hell of a drug. Well rounded sense of well being and balls swelled up like nobody’s business.
 
For myself, it was a hell of a drug. Well rounded sense of well being and balls swelled up like nobody’s business.

A well round sense of well being is definitely not a typical response to clomid.

Why the disdain? It's basically two drugs in one and the problem is due to it's isomer zuclomiphene, which has a HL measured in days - while enc has a HL measured in hours, specifically, 10h. ZU is basically a strong estrogen and at higher dosages will prevent your gonads from recovering. The longer HL of zu leads to much higher levels of zu in comparison to enc over a period of time.

Why some people suffer major sides from clomid and some don't is probably multifactorial. No doubt variances in pharmacodynamics between individuals play a role, but I'd wager the different kinetics of zuclomiphene between individuals is what drives the heaviest burden of experiencing sides. While it has been shown that enc blood levels don't vary that much between individuals, the zu levels can vary a lot.

"The ratio of ZUC:ENC ranged from 1.43 to 88.3 in our patient population. Review of ENC and ZUCvalues individually reveals that, with the exception of a few patients, there was little variation in ENCconcentration with 93% of patients demonstrating an ENC concentration less than 15 ng/mL and80% with an ENC concentration less than 4 ng/mL. In contrast, ZUC concentration demonstrated ahigh degree of interpatient variability. ZUC concentration ranged from 27.6 to 109.0, with 73% ofpatients having a ZUC concentration between 20 and 60 ng/mL."

So as you can see, some individuals can have a small enc to zu ratio of 4 ng/ml to 27.6 ng/ml, while others can have a ratio over 4 ng/ml to 109 ng/ml and there is a very good chance the high zu levels are what's causing the issues.

Helo, Sevann; Mahon, Joseph; Ellen, Joseph; Wiehle, Ron; Fontenot, Gregory; Hsu, Kuang; Feustel, Paul; Welliver, Charles; McCullough, Andrew (2016). Serum levels of enclomiphene and zuclomiphene in hypogonadal men on long-term clomiphene citrate treatment. doi:10.1111/bju.13625
 
I'm perplexed at the amount of knowledge this kids have and that they actually have the balls to use aas. Goes to shove how normalized aas have become - a big part owning to people like derek ... First he created a yt channel so he could push tony huge sarm's, then when that passed he just contributed to the normalization of aas and now he has his own trt clinic, where all the kids whom in large part learned about aas and went on aas because of him, can go and pay big money to get sorted out. This is marketing 101: create demand and then supply the product.

He doesn't even believe this study and still choses to believe some misinformed mpmd video.
Those new to AAS are the same generation that never knew a time before YouTube, and that believes firmly that the 'Tube is a high quality source of information and that books are outmoded by it. They wouldn't have a million followers if they didn't know a thing or two, bro!!
 
Those new to AAS are the same generation that never knew a time before YouTube, and that believes firmly that the 'Tube is a high quality source of information and that books are outmoded by it. They wouldn't have a million followers if they didn't know a thing or two, bro!!

Must be quite scary, not having that critical distance, knowing how it was before social media. I've no idea what I'd do if I had kid ...

Btw, I found this guy, he's an md and not quite sure if he's an er doc or has a private trt practice alongside it, but I've found his info solid and objective. Think you might approve of him a bit more.


View: https://www.youtube.com/watch?v=CvYVNNlWkLo
 
@Jin23

Appreciate the detailed response about why you’re not a fan of Clomid. It’ll give me something to dig into a bit.

What are your thoughts round Ralox as a PCT drug? More commonly used to combat gyno, but does it have a place in pct?
 
@Jin23

Appreciate the detailed response about why you’re not a fan of Clomid. It’ll give me something to dig into a bit.

What are your thoughts round Ralox as a PCT drug? More commonly used to combat gyno, but does it have a place in pct?

I know it works for pct, but haven't delved in to it specifically, so I can't comment for real ...
 
I believe your friend is wrong. Pinning everyday like you plan on will provide very stable blood levels. Pinning test prop once or twice a week would cause the spikes he is talking about. He probably knows just enough to be dangerous as they say. Good luck my friend
This
 
To actually answer the question posed:

Indeed, shorter esters are associated with more side effects and reduced tolerability. Naturally, more frequent injections result in more soreness, swelling, pain at the injection site.

But also, shorter esters mean a lower Tmax (time to Cmax, peak concentration, which is Css, steady-state concentration at a constant weekly dose after 5 t1/2s or haf lives). This is associated with more erythropoietic activity and therefore erythrocytosis/polycythymia. It also results in an increased # of peaks.

Administering every t1/2, or even more frequently, any AAS i.m. formulation does not result in a "smoothening" of the release pharmacokinetics, but rather it results in a substantial increase to the # of peaks & a decreased time to peak concentration. Plotting the release pharmacokinetics wrt time with a tool like SteroidPlotter will show you that this is the case, there will be more spiking but no smoothness to the curve.

There is no reliable (i.e., confidence intervals sufficient to distinguish cause/effect from random chance) evidence that the slope (degree of change) or the difference in concentrations ("fluctuations") are related to any effect whatsoever.

It may be true that peak concentrations elicit some rapid nongenomic effects, e.g., on strength/neural drive and may explain why oral 17AA drugs can serve as a pre-workout. This is related to efficacy rather than to tolerability, however.
 
Short esters will provide bigger peaks than long esters.
 

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