“Tren not that good for bulking”

Estradiol meaning straight up E2 without any test base at all?
Yes. I’ve actually felt like I’ve been on to something. It has a very specific use case and I wouldn’t advocate this for most people. But I think there is a reason why they use this combination to bulk up cattle.

I’m also using Anavar multiple days per week too on and off.

The disadvantage to this is that there is no DHT being produced it seems. And that peak strength seems to be enhanced when DHT is present. Anavar makes up for that to a degree I find, but at the same time, when I use testosterone gel which is short lived periodically, I notice greater drive and strength in the gym on those days when I use the testosterone gel instead of the Anavar as a pre workout androgen.

However this is a temporary protocol for me and I feel like I’ve learned a lot, drastically “improved” specific blood work parameters that I wanted to see if it would have a benefit.

The lack of DHT is the double edge sword because according to the careful bloodwork and testing, this lack seems to be responsible for the HDL increasing a lot, and SHBG as well which was important for me to try, because non crushed Shbg , I feel it has the potential to cause anabolism through another pathway and accelerate the growth effect of androgens when they are present. Now, im
Not saying just remove Test/DHT, but temporarily replace them maybe with something else to compensate while SHBG increases.

Also Elevated estradiol seems to increase IGF1 sensitivity or prolong it when using high doses of hgh/IGF1.
 
Estradiol meaning straight up E2 without any test base at all?
And the e2 is in the form of injectable estradiol valerate which I use at a dose that puts me e2 at 40pg/ml. I’ve gone higher earlier in this phase, but I’m attempting to dry out more and reduce collagen in my skin to thin it out and see if it works. I will go lower than 40 eventually also. I may drop the E2 completely the last 2 weeks of this phase.

I am still taking HCG semi regularly. And my test I just got back had my total T LCMS at 44 ng/Dl.
 
Tren requires rhGH (to ameliorate the decreased GH secretion that Tren induces) and Test (to potentiate the increase to systemic IGF-I) to serve bulking objectives. If you look at it simply in isolation it's better suited for cutting and recomp (of course Tren solo is not ideal for any purpose). But it can certainly be used to bulk in combination with the right compounds.
 
Tren requires rhGH (to ameliorate the decreased GH secretion that Tren induces) and Test (to potentiate the increase to systemic IGF-I) to serve bulking objectives. If you look at it simply in isolation it's better suited for cutting and recomp (of course Tren solo is not ideal for any purpose). But it can certainly be used to bulk in combination with the right compounds.
It's great for cutting as I lost no stength in steep deficit using enanthate only 200mg/week. Granted, I'm not very big, but still I was very impressed. Combined with stronger dht like winstrol and adding in more cals I notice my strength goes way up, perhaps due to aggression and cns over-stimulation (could be bro science idk).

However what sucks with tren for me is that when low on cals, usually eat less carbs I feel like death. I noticed you mentioned effects on insulin, it makes sense as the feeling is like hypoglycemia. Interesting steroid, that perhaps best served to pro bodybuilders or serious people who otherwise profit from using it.
 
It's great for cutting as I lost no stength in steep deficit using enanthate only 200mg/week. Granted, I'm not very big, but still I was very impressed. Combined with stronger dht like winstrol and adding in more cals I notice my strength goes way up, perhaps due to aggression and cns over-stimulation (could be bro science idk).

However what sucks with tren for me is that when low on cals, usually eat less carbs I feel like death. I noticed you mentioned effects on insulin, it makes sense as the feeling is like hypoglycemia. Interesting steroid, that perhaps best served to pro bodybuilders or serious people who otherwise profit from using it.
I agreed up until the last sentence. All of these features (augmented strength, insulin sensitization) also benefit bulking objectives (but Tren would be a compound used selectively and not run as the primary compound). I believe that Tren's intolerability is mostly dose-dependent, e.g., I think 50 - 150 mg is roughly optimal dosing (low to high dose). I think there'd be far fewer complaints of intolerability if guys viewed, as I do, 350 mg trenbolone acetate as profoundly androgenic, inducing aggression (but also increasing neural drive and strength).

I've only ran Tren (as acetate) at 350 mg or higher myself, but it's been many years. I would use it again at 75 mg to start if Balkan still produced Parabolan.

While deriving an income from one's physique certainly weighs more favorably for risk tolerance, it is still rational for many to use so effective a drug as Tren depending on that risk tolerance. Nobody can stand in another's shoes and make that risk/reward tradeoff assessment.
 
I agreed up until the last sentence. All of these features (augmented strength, insulin sensitization) also benefit bulking objectives (but Tren would be a compound used selectively and not run as the primary compound). I believe that Tren's intolerability is mostly dose-dependent, e.g., I think 50 - 150 mg is roughly optimal dosing (low to high dose). I think there'd be far fewer complaints of intolerability if guys viewed, as I do, 350 mg trenbolone acetate as profoundly androgenic, inducing aggression (but also increasing neural drive and strength).

I've only ran Tren (as acetate) at 350 mg or higher myself, but it's been many years. I would use it again at 75 mg to start if Balkan still produced Parabolan.

While deriving an income from one's physique certainly weighs more favorably for risk tolerance, it is still rational for many to use so effective a drug as Tren depending on that risk tolerance. Nobody can stand in another's shoes and make that risk/reward tradeoff assessment.
The community elevates tren to a certain status and abuses it as a result.

My most successful prep used a MAX of 350 tren and only for 6 weeks. Drug dependency needs to go. Especially for adding size; food and training are far more important than what drugs make up the total mg and drugs chosen for tolerance (general well-being, apettire and GERD, fatigue and organ impacts, etc) are going to outperform those that are more harsh. People just use the harsh, big hitter drugs as a crutch for not eating, training, and resting like they should.
 
The community elevates tren to a certain status and abuses it as a result.

My most successful prep used a MAX of 350 tren and only for 6 weeks. Drug dependency needs to go. Especially for adding size; food and training are far more important than what drugs make up the total mg and drugs chosen for tolerance (general well-being, apettire and GERD, fatigue and organ impacts, etc) are going to outperform those that are more harsh. People just use the harsh, big hitter drugs as a crutch for not eating, training, and resting like they should.
Absolutely, I view the drugs as important once advanced no doubt. I view them as the linchpin that ties together training and nutrition. But that means they are the most dispensible of the three factors.

Training with progressive overload, hitting optimal (not simply ever increasing) volumes, tactical use of intensification methods (e.g., DC or myo-reps, muscle rounds), and dedicated training blocks for volume over tension methods and for heavy load over volume methods (periodization, basically) is foundational. Nutrition literally provides the energy to do this work and determines your body composition (basic building blocks as nutrients and energy to perform work/train/function; basic as in foundational, not easy).

No doubt, after ~2.5 years of perfectly (emphasis because virtually nobody exists that perfectly designs and implements training) implemented resistance training, the addition of AAS will present a novel stimulus that is synergistic (greater than additive) to the training adaptations (i.e., increased muscle size).

And yet, what one actually uses with respect to the PEDs has only subtle influences.

The optimal approach is the one that you, Mac, take, to use the minimal doses necessary to elicit sane increases in muscle size and strength without spillover/side effects and selective use of the harsher compounds to bust through plateaus. The long-term focus is continuous and steady gains.

The minimal effective dose strategy > maximal tolerable dose strategy. Show me ONE guy that does the latter in his prime years (say 20 - 40) that both A) has his health later in life, and B) isn't still working on that pro card. Usually, in fact universally IMO, judging by their complaints, demeanor, lifestyle, etc. their doses are beyond tolerable anyhow.

I also believe thaatthe PEDs are clearly vital in that they can determine outcomes at the VERY HIGHEST LEVEL (I include yours in this). Please correct me if this is contrary to your experience:

I believe that in a sense, at the highest level of a competitive endeavor that is enhanced by PED use like pro bodybuilding, that discussions about drugs are typically obfuscated; competitors tend to be less that forthcoming about their usage because, whether rooted in fact or not, it is a sort of war based on asymmetry (there is incomplete information about your competitors' protocols, dosing, compounds, etc.), and obfuscation and withholding of facts is just a strategy to, whether true or merely perceived, fortify your position against the adversaries.

Example A: I doubt that you are posting your coach's protocols for the internet and potential competitor to see.

I believe this is more pronounced during phases in the cycle where novel compounds/drug classes become available that enhance performance.

Example B: Right now the GLP-1 & GIP agonists are likely being used by your competitors, but they probably are mum on this fact, and you may even hear users of these drugs deriding them as a crutch for the weak, not needed for the disciplined, etc.

And yet, these are going to be used by many competitors right now.

My unpopular opinion, after many years of involvement in sport, is that the least talented athletes always are the ones using drugs to begin with and/or the most drugs, but that you simply cannot turn a donkey into a racehorse.
 
Absolutely, I view the drugs as important once advanced no doubt. I view them as the linchpin that ties together training and nutrition. But that means they are the most dispensible of the three factors.

Training with progressive overload, hitting optimal (not simply ever increasing) volumes, tactical use of intensification methods (e.g., DC or myo-reps, muscle rounds), and dedicated training blocks for volume over tension methods and for heavy load over volume methods (periodization, basically) is foundational. Nutrition literally provides the energy to do this work and determines your body composition (basic building blocks as nutrients and energy to perform work/train/function; basic as in foundational, not easy).

No doubt, after ~2.5 years of perfectly (emphasis because virtually nobody exists that perfectly designs and implements training) implemented resistance training, the addition of AAS will present a novel stimulus that is synergistic (greater than additive) to the training adaptations (i.e., increased muscle size).

And yet, what one actually uses with respect to the PEDs has only subtle influences.

The optimal approach is the one that you, Mac, take, to use the minimal doses necessary to elicit sane increases in muscle size and strength without spillover/side effects and selective use of the harsher compounds to bust through plateaus. The long-term focus is continuous and steady gains.

The minimal effective dose strategy > maximal tolerable dose strategy. Show me ONE guy that does the latter in his prime years (say 20 - 40) that both A) has his health later in life, and B) isn't still working on that pro card. Usually, in fact universally IMO, judging by their complaints, demeanor, lifestyle, etc. their doses are beyond tolerable anyhow.

I also believe thaatthe PEDs are clearly vital in that they can determine outcomes at the VERY HIGHEST LEVEL (I include yours in this). Please correct me if this is contrary to your experience:

I believe that in a sense, at the highest level of a competitive endeavor that is enhanced by PED use like pro bodybuilding, that discussions about drugs are typically obfuscated; competitors tend to be less that forthcoming about their usage because, whether rooted in fact or not, it is a sort of war based on asymmetry (there is incomplete information about your competitors' protocols, dosing, compounds, etc.), and obfuscation and withholding of facts is just a strategy to, whether true or merely perceived, fortify your position against the adversaries.

Example A: I doubt that you are posting your coach's protocols for the internet and potential competitor to see.

I believe this is more pronounced during phases in the cycle where novel compounds/drug classes become available that enhance performance.

Example B: Right now the GLP-1 & GIP agonists are likely being used by your competitors, but they probably are mum on this fact, and you may even hear users of these drugs deriding them as a crutch for the weak, not needed for the disciplined, etc.

And yet, these are going to be used by many competitors right now.

My unpopular opinion, after many years of involvement in sport, is that the least talented athletes always are the ones using drugs to begin with and/or the most drugs, but that you simply cannot turn a donkey into a racehorse.
More or less

I try to be as transparent as possible here with my own protocols; my take is what I say here isn’t cookie cutter read and apply to yourself. 5 bodybuilders could use the same exact plan and have 5 different outcomes.

What my coach specifically does I don’t outline 1:1 here.

I think any possible benefit of showing reality and a moderate usage model overshadows any benefit of concealing what I do for the most part.

The landscape in the industry has changed tho as guys realize they can monetize everything and the deeper look people get the more interested they are. Are these guys being fully transparent? Your guess is as good as mine.

Your mention of GLP agonists is an interesting point here. That’s the next frontier to be unveiled, but as with any attempt to leverage new and exciting drugs…we’ll see use prior to understanding and I cannot imagine there aren’t some drawbacks. I for one don’t intend to use them, but we’ll see.
 
Absolutely, I view the drugs as important once advanced no doubt. I view them as the linchpin that ties together training and nutrition. But that means they are the most dispensible of the three factors.

Training with progressive overload, hitting optimal (not simply ever increasing) volumes, tactical use of intensification methods (e.g., DC or myo-reps, muscle rounds), and dedicated training blocks for volume over tension methods and for heavy load over volume methods (periodization, basically) is foundational. Nutrition literally provides the energy to do this work and determines your body composition (basic building blocks as nutrients and energy to perform work/train/function; basic as in foundational, not easy).

No doubt, after ~2.5 years of perfectly (emphasis because virtually nobody exists that perfectly designs and implements training) implemented resistance training, the addition of AAS will present a novel stimulus that is synergistic (greater than additive) to the training adaptations (i.e., increased muscle size).

And yet, what one actually uses with respect to the PEDs has only subtle influences.

The optimal approach is the one that you, Mac, take, to use the minimal doses necessary to elicit sane increases in muscle size and strength without spillover/side effects and selective use of the harsher compounds to bust through plateaus. The long-term focus is continuous and steady gains.

The minimal effective dose strategy > maximal tolerable dose strategy. Show me ONE guy that does the latter in his prime years (say 20 - 40) that both A) has his health later in life, and B) isn't still working on that pro card. Usually, in fact universally IMO, judging by their complaints, demeanor, lifestyle, etc. their doses are beyond tolerable anyhow.

I also believe thaatthe PEDs are clearly vital in that they can determine outcomes at the VERY HIGHEST LEVEL (I include yours in this). Please correct me if this is contrary to your experience:

I believe that in a sense, at the highest level of a competitive endeavor that is enhanced by PED use like pro bodybuilding, that discussions about drugs are typically obfuscated; competitors tend to be less that forthcoming about their usage because, whether rooted in fact or not, it is a sort of war based on asymmetry (there is incomplete information about your competitors' protocols, dosing, compounds, etc.), and obfuscation and withholding of facts is just a strategy to, whether true or merely perceived, fortify your position against the adversaries.

Example A: I doubt that you are posting your coach's protocols for the internet and potential competitor to see.

I believe this is more pronounced during phases in the cycle where novel compounds/drug classes become available that enhance performance.

Example B: Right now the GLP-1 & GIP agonists are likely being used by your competitors, but they probably are mum on this fact, and you may even hear users of these drugs deriding them as a crutch for the weak, not needed for the disciplined, etc.

And yet, these are going to be used by many competitors right now.

My unpopular opinion, after many years of involvement in sport, is that the least talented athletes always are the ones using drugs to begin with and/or the most drugs, but that you simply cannot turn a donkey into a racehorse.
So what's your preferred method to find minimal effective dose? Start low and choose the dose whereby you start seeing progress? And do you keep titrating up until you see sides (and then at that point, cut back the dose and/or add an alternate compound?)
 
So what's your preferred method to find minimal effective dose? Start low and choose the dose whereby you start seeing progress? And do you keep titrating up until you see sides (and then at that point, cut back the dose and/or add an alternate compound?)
Finding an optimal dose is more art than science. My process is basically as follows:

I often build out a risk/reward profile (tradeoffs) for novel compounds that possess a high degree of uncertainty or potential risk (e.g., DNP, MENT, insulin). This considers the benefits and the potential harms (i.e., tolerability; prevalence; severity) and weighs the harms.

If my risk/reward analysis favors use, I next, if available, start with the dose that maximally stimulates N retention from the literature and compare that versus clinical trials that measured tolerability as an outcome (e.g., stage 3/4 hepatotoxicity). I sort of assess response (whether a hyper- or hypo- responder) by whether it visually results in > or < mean changes & blood work (just once for the compound on the time-frame that is applicable to the time-course of changes [different for rhGH at a constant dose for IGF-I changes vs. GGT changes at a constant dose for Halo], to refer to for future comparisons in an ecologically valid manner).

For compounds without human trial data on anabolism (i.e., N retention or DEXA or occasionally caliper outcomes), I look into the compound's relative potency to transactivate the AR (Houtman's bioluminescene data) and compute testosterone-equivalent dosing, and then factor in some considerations like TBG (thyroxine-binding globulin) changes if available. The decrease in TBG reflects anabolic potency quite well. I look too to its effects on the other (nuclear family) steroid receptors, consider anything Peter Bond's Book on Steroids has to say about the compound (e.g., cardiovascular risks, lipid risks), and to the Houtman data on its metabolites where available.

I never extrapolate from animal data, it's completely inapplicable. It's better to draw inferences from assays that compare different compounds in terms of nuclear retention or potency. Differences in metabolism are profound (e.g., peripheral metabolism of androgens by 3α-HSD in human skeletal muscle severely weakens parent androgens subject to it unlike in animals; relative central output from animal to man of different releasing and active hormones or releasing-hormones; exogenous E2 potentiates GH response/increases IGF-I unlike in man, etc.) and the Hershberger assay is completely inapplicable to man (not least of all because the levator ani is the dorsal bulbocavernous, a sex organ responsive to androgenic & anabolic effects), or rather any use beyond initial screening for potentially favorable anabolism and/or androgenicity worthy of human trials.

I might use human equivalent dosing to highlight a remarkable difference between human and animal use (e.g., Tren, where < 10 mg weekly is equivalent to that delivered by a Synovex implant, and where bovid are less AR-dense than humans in skeletal muscle; but without consideration for metabolic differences, that might cause orders of magnitude discrepancies in net anabolism).

I eventually then fall back to using reasonable doses that align with the product's contents/dose (e.g., if an Anavar tablet is 10 mg I might start with that or 2; if an Anadrol tablet is 50 mg I might start with 1/2).

This all proceeds relatively informally, but this is the process for me to find an optimal dose (rather than a minimally effective one).
 
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Finding an optimal dose is more art than science. My process is basically as follows:

I often build out a risk/reward profile (tradeoffs) for novel compounds that possess a high degree of uncertainty or potential risk (e.g., DNP, MENT, insulin). This considers the benefits and the potential harms (i.e., tolerability; prevalence; severity) and weighs the harms.

If my risk/reward analysis favors use, I next, if available, start with the dose that maximally stimulates N retention from the literature and compare that versus clinical trials that measured tolerability as an outcome (e.g., stage 3/4 hepatotoxicity). I sort of assess response (whether a hyper- or hypo- responder) by whether it visually results in > or < mean changes & blood work (just once for the compound on the time-frame that is applicable to the time-course of changes [different for rhGH at a constant dose for IGF-I changes vs. GGT changes at a constant dose for Halo], to refer to for future comparisons in an ecologically valid manner).

For compounds without human trial data on anabolism (i.e., N retention or DEXA or occasionally caliper outcomes), I look into the compound's relative potency to transactivate the AR (Houtman's bioluminescene data) and compute testosterone-equivalent dosing, and then factor in some considerations like TBG (thyroxine-binding globulin) changes if available. The decrease in TBG reflects anabolic potency quite well. I look too to its effects on the other (nuclear family) steroid receptors, consider anything Peter Bond's Book on Steroids has to say about the compound (e.g., cardiovascular risks, lipid risks), and to the Houtman data on its metabolites where available.

I never extrapolate from animal data, it's completely inapplicable. It's better to draw inferences from assays that compare different compounds in terms of nuclear retention or potency. Differences in metabolism are profound (e.g., peripheral metabolism of androgens by 3α-HSD in human skeletal muscle severely weakens parent androgens subject to it unlike in animals; relative central output from animal to man of different releasing and active hormones or releasing-hormones; exogenous E2 potentiates GH response/increases IGF-I unlike in man, etc.) and the Hershberger assay is completely inapplicable to man (not least of all because the levator ani is the dorsal bulbocavernous, a sex organ responsive to androgenic & anabolic effects), or rather any use beyond initial screening for potentially favorable anabolism and/or androgenicity worthy of human trials.

I might use human equivalent dosing to highlight a remarkable difference between human and animal use (e.g., Tren, where < 10 mg weekly is equivalent to that delivered by a Synovex implant, and where bovid are less AR-dense than humans in skeletal muscle; but without consideration for metabolic differences, that might cause orders of magnitude discrepancies in net anabolism).

I eventually then fall back to using reasonable doses that align with the product's contents/dose (e.g., if an Anavar tablet is 10 mg I might start with that or 2; if an Anadrol tablet is 50 mg I might start with 1/2).

This all proceeds relatively informally, but this is the process for me to find an optimal dose (rather than a minimally effective one).
Do you have logs or detailed postings about your cycles/usage?

I’d be very curious to see how you operate and your stats, diet day to day life etc.
 
Do you have logs or detailed postings about your cycles/usage?

I’d be very curious to see how you operate and your stats, diet day to day life etc.
I don't, and I'm surprised you'd be interested heh. I'm entirely uninteresting in this regard, just a retired athlete that doesn't put myself through the rigors of bodybuilding prep and am, therefore, fat (compared to bodybuilders). I do have extensive AAS personal experience (and peptides, rhGH, I've used all the AAS on the market including many designer steroids like methylstenbolone, Epistane, furazadrol, but not (because my research told me they're not for me) slin, MENT, 1-Test/"DHB" (I've used its 17AA counterpart M1T), & DNP.
 
This is a great thread. Guys who have used nandrolone, could similar gains be made with double the dose of something mild like primo? For example: 700mg of primo as potent as 350 NPP?
I’m too old for 19-nors.
 
This is a great thread. Guys who have used nandrolone, could similar gains be made with double the dose of something mild like primo? For example: 700mg of primo as potent as 350 NPP?
I’m too old for 19-nors.
Nope.

To start, Deca is 2.43x as potent as Primo at the AR. Then, you factor in human metabolism and Primo's (but not Deca's) being susceptible to metabolism (breakdown) by muscle 3α-HSD, and Deca's whole-body and protein anabolic effects by stimulating IGF-I. The conclusion you're left with is that the two aren't even really comparable.
 
Tren requires rhGH (to ameliorate the decreased GH secretion that Tren induces) and Test (to potentiate the increase to systemic IGF-I) to serve bulking objectives. If you look at it simply in isolation it's better suited for cutting and recomp (of course Tren solo is not ideal for any purpose). But it can certainly be used to bulk in combination with the right compounds.
Nope.

To start, Deca is 2.43x as potent as Primo at the AR. Then, you factor in human metabolism and Primo's (but not Deca's) being susceptible to metabolism (breakdown) by muscle 3α-HSD, and Deca's whole-body and protein anabolic effects by stimulating IGF-I. The conclusion you're left with is that the two aren't even really comparable.
Curious how does this apply to orals with low AR affinity known to cause growth ?
 
Nope.

To start, Deca is 2.43x as potent as Primo at the AR. Then, you factor in human metabolism and Primo's (but not Deca's) being susceptible to metabolism (breakdown) by muscle 3α-HSD, and Deca's whole-body and protein anabolic effects by stimulating IGF-I. The conclusion you're left with is that the two aren't even really comparable.
I’m not surprised to get this answer. Thanks for breaking it down.
 
Curious how does this apply to orals with low AR affinity known to cause growth ?
Some (e.g., Anadrol) principally act as a prohormone to a more active compound (17α-methyl-5α-androstane-3α,17β-diol for Anadrol); some serve principally to exert their action by a combination of AR, GR, and ER-β modulation (e.g., Anavar), etc. I would just note also that we're not rabbits nor rats, so the affinity data in those species are not applicable to man.
 
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