T Nation

Testosterone + Nandrolone + Drostanolone is a Good Lean-Bulk Stack

Shbg is a glycoprotein that binds to androgens and estrogens. It inhibits the function of androgens and estrogens on various tissues and whatnot, hence why bodybuilders say it’s better to have low SHBG as more bioavailable + free T is available for use at any given moment.
That’s what I think anyway

I’m 25; MS of Pharmacy = MPharm = Master’s of Sciences of Pharmacy.

I haven’t competed in BB yet. From 15 to 22 y.o. I was road cycling and even won several races (174 cm, 55-60 kg mountain chamois). I’ve started BB’ing & powerlifting (big words) around 2 years ago - currently sitting at 88 kg, 9% BF and with results in BP 5x110, LB SQ 5x170, DL 5x200, running a hypertrophy mesocycle on the juice from title’s thread (oxy or tren will join his friends soon). My studies limits faster development successfully, but I’m happy with the results anyway. Productivity, however, while on AAS is through the roof.

From one point of view, SHBG is a body’s reservoir of T and E2, as stated above. Too much SHBG (liver diseases, elevated E2, another hormonal disturbances) leads to free T deficiency. Too low SHBG leads to elevated rate of T metabolism. The result of both circumstances is hypogonadism.

What’s really interesting about the protein is that it’s complex with DHT and it’s derivatives probably interacts with specific membrane receptors leading to an anti-estrogenic effects (another argument for DHT anti-estrogenic properties).

174kg and 55kg? That’s a hell of a transformation you’ve made, congratulations. Do you enjoy the studying?

waaaaaaaaaaait a minute, it isn’t actually true that people with low SHBG legitimately require more frequent injections is it? I have insulin resistence (for absolutely no… god damn reason), my SHBG has always tested very low (however SHBG tends to fluctuate daily in regular people, my labs have shown my SHBG to fluctuate by as much as 200%) As to liver diseases and high SHBG, low SHBG is actually associated with NAFLD, however high SHBG holds true to the rest when regarding liver disease. I was under the impression the metabolisation and elimination rate of testosterone was predetermined by the livers rate of biotransformation (metabolising test into inactive metabolites).

How is it a reservoir when T that’s bound to SHBG is said to be inert, gone, lost, down the drain (as opposed to albumin, from which it can break away)?

I happen to have lowish SHBG. Does this have any implication on my TRT (+Blast 'n Cruise maybe) path other than indication for more frequent injections?
Could this (by a long stretch of imagination) maybe even a reason for me being a person with considerable highs and lows pretty much all my life in performance, mood, etc.?

T + SHBG > SHBG-T (inactive T)
SHBG-T > SHBG + T (active T)

The reaction is reversible, stays in a dynamic equilibrium (to keep 1-3% of free T in the blood). In physiology only 2-10 mg of T is produced, it isn’t much, SHBG-T complex serves as an additional source of the hormone (so obviously this inactive T isn’t lost).

Low SHBG = faster T metabolism = higher aromatization = HPTA suppresion = vicious circle (another secondary hypogonadism origin).

Faster T metabolism due to lowered SHBG doesn’t literally means you need to inject more frequent (hello, long esters half life’s are long enough even in this case - you should inject your enanthate/cypionate e3d-e4d anyway). It means that you should inject more for given T level and increase you AI dosage.

Thanks a lot! This makes sense.
Quite many sources indicate that T bound to SHBG is lost. That made me wonder why the hell did evolution end up with the enzyme that serves to make the body’s job more difficult? :slight_smile: It seemed like the idea of putting the heating in your room on high but opening the window. Now, I understand that it’s not the case.

So now that I’ve abused your thread anyways, this may be forgiven as well: What compound would you recommend instead of Nandro that:

  • doesn’t mess with CNS
  • is relatively safe in general
  • provides nice lean gains
  • goes well with T (and Drostanolone)

Phew thank god, I’ve been arguing with people on the T replacement forum as to why injections shouldn’t be dictated by SHBG as it’s bullshit and has nothing to do with it (I stated the half life arguement and that SHBG doesn’t increase the excretion rate of test, it’s up to individual metabolism to inactive metabolites and elimination of the drug), if I was wrong that’d have been… Very embarrassing

As to e4d, I shoot my test e7d, no issues. I don’t use AI, I was on 1mg of adex/day when I was like 14 prescribed for short stature due to precocious puberty, my TT was 1000+Ng/DL (this was with impaired glucose tolerance, so likely low SHBG, FT through the roof naturally), test taken before using the adex, twas baseline testing. The adex caused a lot of issues for me, joint pain, countless injuries (some which never healed), osteopenia in parts of my spine now (was on for years), broken ankle that required surgery, trashed lipids (went back to normal when I went off). I’m aware 7mg/wk is a reckless dose to be prescribed. Anyhow after I went off (I had chronic debilitating pain at this point) my TT dropped from 1000+ to low 400s, to 200s, to eventually 100s before I was put on TRT (was in the 2-300s for the better part of a year, my Testostrone production wasn’t recovering. I was the last person I’d expected this shit to happen to given my precocious puberty (age 9), but I guess life sometimes deals shitty hands, there’s people way, way, way, waaay worse off though so I can’t complain. there’s no way to pinpoint exactly what caused it, I’ve been exposed to a fair bit of radiation, however I doubt that was the culprit, I wasn’t (chronically) exposed to any meds known to cause hypogonadism.

Estrogen within ratio to my testosterone doesn’t seem to give me symptoms of high E therefore I don’t worry about it. That and AI+androgens tend to potentiate the negative impact on cholesterol caused by androgens as estrogen is important for cholesterol metabolism.

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Why idiots who prescribe such high doses of an AI have right to practice medicine?

What are your T, freeT, SHBG and E2 levels?

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Well it was an endocrinologist who prescribed it because due to the precocious puberty my ephysial plates were closing at an accelerated rate. I ended up short anyway, stopped growing at around 15-16 at 5’5 (165-166cm). I was like 1.5cm over the requirement for GH… They wouldn’t give it to me (granted it probably would’ve made me diabetic lol).

110mg/wk has me peak in the low 500s and nadir in the low 300s, I was only able to get 140mg prescribed after a YEAR (I primarily self medicate due to the status of TRT in Aus). My E2 tends to stay around 20, it never fully bounced back after the AI use, which was strange, but then again who knows what consistently crushing estrogen down to damn near zero will do to a developing adolescents endocrine system. SHBG ranges from 13-27. I tend to feel better the higher I go (dose wise) hence after these bloods I’m going to cruise on 200-210mg/wk (alternating between the two doses every couple weeks to prevent my body from achieving homeostasis). Resident endo on this board (when he gets back from Asia I’m sure he will be eager to talk to you) reccomends such a protocal (regarding the slight dosage changes).

Although it’s a feelings game, not a numbers game (I do feel better at higher doses though), I find it irritating that instead of trying to aim for the numerous bloods I had when I was 14, it seems like “hmmmm, lets get you to 400ng/dl”…

If e5d protocol suits you, that’s cool. However, in pharmacokinetics we usually pursue to achieve as stable medicine concentration in the blood as possible (Css - concentration steady state), so more frequent injections allows us to achieve this.

Obviously, fluctuations like 20% from Css,min to Css,max, or even more during TRT, won’t practically change anything (this happens in physiology as well). Too big differences between Css,min and Css,max would increase T’s variability in plasma concentration leading to several uncomfortable effects (mainly cus of E2 peaks and downs).

Basing on TE’s half life, Cmax and tmax (200 mg/wk of TE we assume):

  1. e2d protocol leads to ~22% of Css fluctuations
  2. e3d - ~33%
  3. e4d - ~43%
  4. e5d - ~55%

I’ve found myself that e3d-e4d injections of TE while on TRT (100-120 mg/wk) and daily AI administration give stable bloodwork and feelings. It’s given SC, so no damage to muscle tissue.

I’m very aware of this (stable blood concentrations, what Cmax and Cmin is) , however I prefer keeping things simple. Why overcomplicate things when I feel good shooting every 7 days?

E2 spikes come with a spike in testosterone. I personally don’t see the issue with a spike in E2 if it’s accompanied by elevated testosterone, the ratio is the bodies equilibrium, if I’m already screwing with my test (going slightly over physiologic levels), why would I want to further mess with the ratios of my hormones?

I don’t see the point in using an AI because I don’t have gyno, water retention, fatigue, moodiness, HBP or any of the sides one would expect to see with high E2. If I was to get gyno I’d use a serm before I used an AI (personal choice, I’m aware of the potential risk for ocular nerve damage, however a SERM positively impacts the lipid profile as it acts as an estrogen with regards to helping with cholesterol metabolism, stimulating bone density etc while an AI tends to tank HDL, decrease bone density if you accidentally crash you’re E2 (which isn’t very hard to do considering how powerful these drugs are).

As to sub Q shots, primoteston (no matter where I shoot it) causes large amounts swelling, UGL test doesn’t do this, primoteston does, it’s a bad reaction to one of the solvents in the oil, given I don’t have a choice I just put up with it. Sub Q shots of primoteston tend to cause massive, fat knotty lumps of irritation (normal for sub Q shots) however they stick around for about a month, swelling from shooting primoteston only sticks around for two weeks or so.

Sure, e5d or even e7d could be a good solution as well. Personally, I’ve found that more frequent injections works just better on me and some of guys I consult. Whatever you like.

SERM’s topic is way oversimplied in BB circle. It’s not that easy. I know that AI calibration is hard as well (e1d administration when 0.025 mg plus or minus daily matters), but it’s much better option in most cases.

Monday has just started, good luck this week guys.


Wait, my original post dissapeared, I was just trying to link physio to the thread

It’s nearly Tuesday here!!! I’m in the future.

By SERMS being oversimplified are you talking about how they’re not nearly as benign as people think they are? Are you talking about the potential neurotoxicity or the mental sides from clomiphenes antigonadotrophic and inherently estrogenic isomer zuclomiphene. Or the liver toxicity and increased risk of hepatic cancer? They’re agents for chemotherapy, they’ve been shown to be cytotoxic in a myriad of cells in vitro, so I do get what you’re saying in that people seem to think they’re benign, when in fact they are potentially one of the more dangerous ancillaries. (Or am I interpreting what you said wrong). Serms don’t decrease estrogen either, I guess that’s another misconception with them as (you know this I don’t know why I’m describing this now) they bind to the ER competitively and thus block the effects of estrogen in tissues sensitive to the effects of estrogen such as breast tissue, yet they mimick estrogen in many ways too (bone density, lipid metabolism etc.) And clomiphene is actually two drugs (two isomers) zuclomiphene and enclomiphene, Tamoxifen is a pro-drug that in itself has very little affinity to the ER so derp, I believe it’s hepatically metabolised via CYP2D6 (interesting fact, I’m an extreme CYD2D6 hypermetaboliser, I’ve had testing done) and (cyp2a4? Correct me if I’m wrong there), I forget the names of the active metabolites, one of them was enoxifen or something. (Edit endoxifen… Close enough, rewarded half marks… And afimoxefene)

Which part was the area that is simplified in bodybuilding?

The neuro effects are dose dependant I believe, doses usedin studies like thesehttps://link.springer.com/article/10.1023/A:1005826323652
Arent exactly relevant to me using 10mg/day to treat gyno.Granted I wouldnt be over the moon about taking a SERM(but Id rather take it than an AI) its personal preference.Think about it like this, say you smoked a marijuana cigaretteand had an acute psychotic episode as a result of themarijuana, why on EARTH would you smoke it again? Ivehad a terrible experience with AIs, Im aware the dose wasextreme but my god I couldnt take it if my joint pain gotworse again, its irritating enough as it is!

This is a great thread :slight_smile: nice conversation guys

Long story short (crazy week) - SERM work in muscle tissue as well. Elevating E2 for muscle tissue building purposes while loading SERM (even at low doses) to prevent gyno and/or excess water retention and/or elevated BP isn’t the best approach.

Yeet, so whats you’re opinion on DHEA (dehydroepiandrosterone), natural production doesn’t seem to plummet until 30s, however I’m curious as to whether there’s any benefit supplementing with it. Given its secreted by the adrenals and administration of Corticosteroids diminishes the production of DHEA, would taking exogenous DHEA diminish the production of endogenous Corticosteroids? That’s not exactly a bad thing unless cortisol dips too low.

Appears to improve insulin sensitivity in various studies with older subjects.

Yes, and is no less important for CNS (more about that this weekend, maybe).

hCG as an agent for “natural” DHEA production (if testes work, although a little).

Is the yes related to decreased production of endogenous Corticosteroids or benefit with regard to supplementation.

…but Masteron (and another DHT derivatives) doesn’t lower your E2 because it’s such a potent SHBG inactivator, thus elevates your wet compounds in an unbound state (T for example) ready for aromatisation (more difficult, but still).

The effect of blocking SHBG is probably more important than inhibiting aromatase, regarding to final E2 level in the blood. Here’s what I’ve found on myself (E2 levels):

2.XI - 184 pmol/L
9.XI - 181 pmol/L
16.XI - 178 pmol/L (just after the blood was taken, first drostanolone’s shot entered)
30.XI (today) - 203 pmol/L (+12%, significant difference)

Observations & conclusion: after including drostanolone into my cycle I’ve gained significant strenght, vascularization and libido (no fake, anti-E2 effect achieved). I’ve noticed significant LBM increase as well. So, the mechanism must be lying in DHT’s E2-antagonistic role on a level of gene transcription (blocking/inducing transcription factors/coagonists/corespresors just before gene reading competing with E2 mediated pathways).

BTW, after 4 weeks of cycling (just below 2 g/wk of compounds) my RBC, HCT, INR and liver markers decreased. I’m simply born to do this, LOL.