Atomini's all-you-need-to-know about TREN and how to use it effectively thread!

[hsvcraig]

Hey mate, I was thinking about doing 20 weeks on with tren e, low dose test, is this a stupid idea? I'd cut the tren from weeks 1-12 then start again after to prevent receptors being flooded, I also recover ok with a good pct. what's your thoughts?

[Oubowtie06]

Writing this up as an example Cycle. Looking to do it in 6 months after i do some natural cutting


Week 1-8 Test 250 a week divided by two pins
Week 1-8 Tren 500 a week pinning every other day

Week 1-8 Arimadex .25 mg Every other day if needed and adjust if needed
Week 1-8 Prami .5-1 MG per day From Day 1



Nolvadex start 14 days after last injection.
40Mg first 2 weeks
20MG last 2 Weeks

[Atomini]

Hey mate, I was thinking about doing 20 weeks on with tren e, low dose test, is this a stupid idea? I'd cut the tren from weeks 1-12 then start again after to prevent receptors being flooded, I also recover ok with a good pct. what's your thoughts?

Yes it's a stupid idea. What is the need to run a cycle of anything this long, especially considering the benefit:risk ratio begins to shift into the negative proportion after week 8-10? By that point, you're just getting diminishing gains for the risk you're taking on such a long cycle. Also, the idea of 'receptor saturation' and 'receptors being flooded' is a complete myth. Your diminishing gains do not result from the myth of 'receptor saturation'. As a matter of fact, the exact OPPOSITE happens when you use anabolic steroids .

The myth of receptor saturation has been disproven in a number of studies I saw, where it was noted that the number of androgen receptors actually INCREASED in response to supraphysiological doses of anabolic steroids and grew FASTER in individuals administered high doses of AAS. There is no such thing as androgen receptor 'downregulation', 'burnout', or the need to 'clean' receptors. All of those propositions sound absolutely absurd in the face of the evidence brought forth by the medical studies cited above that all display total opposite operation regarding how androgen receptors work.

Now, some people might be wondering still why the effectiveness of anabolic steroids simply decrease and level out over time as well as over the course of a cycle. Well, the reason why we 'cycle' is of course to avoid any long term damage from using supraphysological amounts of AAS. We all already know this. The idea with cycling is to get on, make your gains, and then get off before the body can, for the lack of a better term, 'catch on' to what is going on. With prolonged use of AAS, not only can you encounter permanent health issues, but the effectiveness of the anabolic steroid decreases over time, but NOT because of receptor 'downregulation' or 'saturation' or 'burn out' or whatever quirky whaky name you want to give it. The reason gains diminish over time is for a couple of primary reasons:

1. It happens because your body has begun secreting and producing hormones and proteins that are antagonistic to the anabolic steroids you are using (this is what I meant, going back to what I said about your body 'catching on'). Hormones and proteins such as: cortisol, myostatin, SHBG, estrogen and various other factors all increase the longer you are on a cycle. The only way to prevent this is either to use ancilliaries that will somewhat combat the rise of these antagonistic devices, OR to simply get off cycle and allow the body to 'normalize' itself.

2. Lets be realistic here. A 5'10" 170lb. male at 10% bodyfat hopping on a cycle is going to obviously be able to slap on a whole lot more amount of muscle mass than a 5'10" 210 lbs. at 10% bodyfat. The latter subject has far more muscle mass on him, and therefore is closer to his genetic limitations than the former subject. The more cycles you do, the more mass you gain, the closer you reach your limit and therefore the slower the gains will come on every subsequent cycle. If you were to build yourself up to 225 lbs. at 10% bodyfat, and lets say you are very close to your genetic limit... and suddenly a life situation strikes and you lose a lot of muscle, leaving you at lets say 180 lbs., if you were to do a cycle to get yourself back up, the gains would then be dramatic again. Muscle growth never really occurs in a linear consistent fashion. If that were the case, we'd all be champion bodybuilders after a handful of cycles.

Read this:

Taking issue with the idea of androgen receptor down-regulation.
By Bryan Haycock MS.

There is as much misinformation about steroids as there is good information had among bodybuilding enthusiasts. Go to any gym and you will hear some kid spouting off to his buddies about how steroids do this, or how they do that, or whatever. This soon starts somewhat of a pissing contest (excuse the expression) as to who knows more about steroids. It's the same kind of titillating and infectious banter that adolescent boys get into about girls and sex. With steroid banter you hear all the popular terms like Deca , Test, GH, gyno , zits, raisins, "h-u-u-u-ge", roid, freak, monster, roid-rage, "I knew this guy once", etc., etc.. If by some rare chance they are smart and have been reading this or some other high quality bodybuilding site on the net, they may actually get a few details right. More often than not they know just enough to be dangerous. Fortunately steroids haven't proven to be all that dangerous. Not only that, but most of these guys who are infatuated with steroids won't ever use or even see them except in magazines.

This kind of ego driven gym talk doesn't really bother me until they begin giving advice to other clueless people who actually have access to them. Spewing out steroid lingo gives other less experienced kids the impression that these kids actually know what they are talking about. That's how all of the psuedo-science folklore about steroids perpetuates. This is also why most people who actually use steroids know little about them. This last fact should bother anyone who cares about bodybuilding and/or bodybuilders.

I started out with this article planning on giving some textbook style explanation as to why using steroids doesn't down regulate androgen receptors (AR). Then after considering some of my critics views that I tend to write articles that hardly anyone can read, I decided to write an easy to read, yet informative explanation about what androgens actually do and how this precludes androgen receptor down regulation. I still have a few references but not so many that it looks like a review paper.

Androgen receptors down-regulate….Don't they?
One misunderstood principle of steroid physiology is the concept of androgen receptors (AR), sometimes called "steroid receptors", and the effects of steroid use on their regulation. It is commonly believed that taking androgens for extended periods of time will lead to what is called AR "down regulation". The premise for this argument is; when using steroids during an extended cycle , you eventually stop growing even though the dose has not decreased. This belief has persisted despite the fact that there is no scientific evidence to date that shows that increased levels of androgens down regulates the androgen receptor in muscle tissue.

The argument for AR down-regulation sounds pretty straightforward on the surface. After all, we know that receptor down-regulation happens with other messenger-mediated systems in the body such as adrenergic receptors. It has been shown that when taking a beta agonist such as Clenbuterol , the number of beta-receptors on target cells begins to decrease. (This is due to a decrease in the half-life of receptor proteins without a decrease in the rate that the cell is making new receptors.) This leads to a decrease in the potency of a given dose. Subsequently, with fewer receptors you get a smaller, or diminished, physiological response. This is a natural way for your body to maintain equilibrium in the face of an unusually high level of beta-agonism.

In reality this example using Clenbuterol is not an appropriate one. Androgen receptors and adrenergic receptors are quite different. Nevertheless, this is the argument for androgen receptor down-regulation and the reasoning behind it. The differences in the regulation of ARs and adrenergic receptors in part show the error in the view that AR down-regulate when you take steroids . Where adrenergic receptor half-life is decreased in most target cells with increased catecholamines, AR receptors half-live's are actually increased in many tissues in the presence of androgens.1

Let me present a different argument against AR down-regulation in muscle tissue. I feel that once you consider all of the effects of testosterone on muscle cells you come to realize that when you eventually stop growing (or grow more slowly) it is not because there is a reduction in the number of androgen receptors.

Testosterone : A multifaceted anabolic
Consider the question, "How do anabolic steroids produce muscle growth?" If you were to ask the average bodybuilding enthusiast I think you would hear, "steroids increase protein synthesis." This is true, however there is more to it than simple increases in protein synthesis. In fact, the answer to the question of how steroids work must include virtually every mechanism involved in skeletal muscle hypertrophy. These mechanisms include:

Enhanced protein synthesis

Enhanced protein synthesis

Enhanced growth factor activity (e.g. GH, IGF -1, etc.)

Enhanced activation of myogenic stem cells (i.e. satellite cells)

Enhanced myonuclear number (to maintain nuclear to cytoplasmic ratio)

New myofiber formation

Starting with enhanced growth factor activity, we know that testosterone increases GH and IGF-1 levels. In a study by Fryburg the effects of testosterone and stanozolol were compared for their effects on stimulating GH release.2 Testosterone enanthate (only 3 mg per kg per week) increased GH levels by 22% and IGF-1 levels by 21% whereas oral stanozolol (0.1mg per kg per day) had no effect whatsoever on GH or IGF-1 levels. This study was only 2-3 weeks long, and although stanozolol did not effect GH or IGF-1 levels, it had a similar effect on urinary nitrogen levels.

What does this difference in the effects of testosterone and stanozolol mean? It means that stanozolol may increase protein synthesis by binding to AR receptors in existing myonuclei, however, because it does not increase growth factor levels it is much less effective at activating satellite cells and therefore may not increase satellite cell activity nor myonuclear number directly when compared to testosterone esters. I will explain the importance of increasing myonuclear number in a moment, first lets look at how increases in GH and IGF-1 subsequent to testosterone use effects satellite cells.

Don't forget Satellite cells!
Satellite cells are myogenic stem cells, or pre-muscle cells, that serve to assist regeneration of adult skeletal muscle. Following proliferation (reproduction) and subsequent differentiation (to become a specific type of cell), satellite cells will fuse with one another or with the adjacent damaged muscle fiber, thereby increasing the number of myonuclei for fiber growth and repair. Proliferation of satellite cells is necessary in order to meet the needs of thousands of muscle cells all potentially requiring additional nuclei. Differentiation is necessary in order for the new nucleus to behave as a nucleus of muscle origin. The number of myonuclei directly determines the capacity of a muscle cell to manufacture proteins, including androgen receptors.

In order to better understand what is physically happening between satellite cells and muscle cells, try to picture 2 oil droplets floating on water. The two droplets represent a muscle cell and a satellite cell. Because the lipid bilayer of cells are hydrophobic just like common oil droplets, when brought into proximity to one another in an aqueous environment, they will come into contact for a moment and then fuse together to form one larger oil droplet. Now whatever was dissolved within one droplet (i.e. nuclei) will then mix with the contents of the other droplet. This is a simplified model of how satellite cells donate nuclei, and thus protein-synthesizing capacity, to existing muscle cells.

Enhanced activation of satellite cells by testosterone requires IGF-1. Those androgens that aromatize are effective at not only increasing IGF-1 levels but also the sensitivity of satellite cells to growth factors.3 This action has no direct effect on protein synthesis, but it does lead to a greater capacity for protein synthesis by increasing fusion of satellite cells to existing fibers. This increases the number of myonuclei and therefore the capacity of the cell to produce proteins. That is why large bodybuilders will benefit significantly more from high levels of androgens compared to a relatively new user.

Testosterone would be much less effective if it were not able to increase myonucleation. There is finite limit placed on the cytoplasmic/nuclear ratio, or the size of a muscle cell in relation to the number of nuclei it contains.4 Whenever a muscle grows in response to training there is a coordinated increase in the number of myonuclei and the increase in fiber cross sectional area (CSA). When satellite cells are prohibited from donating viable nuclei, overloaded muscle will not grow.5,6 Clearly, satellite cell activity is a required step, or prerequisite, in compensatory muscle hypertrophy, for without it, a muscle simply cannot significantly increase total protein content or CSA.

More myonuclei mean more receptors
So it is not only true that testosterone increases protein synthesis by activating genetic expression, it also increases the capacity of the muscle to grow in the future by leading to the accumulation of myonuclei which are required for protein synthesis. There is good reason to believe that testosterone in high enough doses may even encourage new fiber formation. To quote the authors of a recent study on the effects of steroids on muscle cells:

"Intake of anabolic steroids and strength-training induce an increase in muscle size by both hypertrophy and the formation of new muscle fibers. We propose that activation of satellite cells is a key process and is enhanced by the steroid use."7

Simply stated, supraphysiological levels of testosterone give rise to increased numbers of myonuclei and thereby an increase in the number of total androgen receptors per muscle fiber. Keep in mind that I am referring to testosterone and testosterone esters. Not the neutered designer androgens that people take to avoid side effects . This is not an argument to rapidly increase the dosages you use. It takes time for these changes to occur and the benefits of higher testosterone levels will not be immediately realized.

Maintenance of the kind of muscle mass seen in top-level bodybuilders today requires a given level of androgens in the body. That level will vary from individual to individual depending on their genetics. Nevertheless, if the androgen level drops, or if they were to "cycle off" the absolute level of lean mass will also drop. Likewise, as the level of androgens goes up, so will the level of lean mass that individual will be able to maintain. All of this happens without any evidence of AR down regulation. More accurately it demonstrates a relationship between the amount of androgens in the blood stream and the amount of lean mass that you can maintain. This does not mean that all you need is massive doses to get huge. Recruitment of satellite cells and increased myonucleation requires consistent "effective" training, massive amounts of food, and most importantly, time. Start out with reasonable doses. Then, as you get bigger you can adjust your doses upwards.

References:

Kemppainen JA, Lane MV, Sar M, Wilson EM. Androgen receptor phosphorylation, turnover, nuclear transport, and transcriptional activation. Specificity for steroids and antihormones. J Biol Chem 1992 Jan 15;267(2):968-74

Fryburg DA., Weltman A., Jahn LA., et al: Short-term modulation of the androgen milieu alters pulsatile, but not exercise- or growth hormone releasing hormone -stimulated GH secretion in healthy men: Impact of gonadal steroid and GH secretory changes on metabolic outcomes. J Clin Endocrinol. Metab. 82(11):3710-37-19, 1997

Thompson SH., Boxhorn LK., Kong W., and Allen RE. Trenbolone alters the responsiveness of skeletal muscle satellite cells to fibroblast growth factor and insulin -like growth factor-I. Endocrinology. 124:2110-2117, 1989

Rosenblatt JD, Yong D, Parry DJ., Satellite cell activity is required for hypertrophy of overloaded adult rat muscle. Muscle Nerve 17:608-613, 1994

Rosenblatt JD, Parry DJ., Gamma irradiation prevents compensatory hypertrophy of overloaded extensor digitorum longus muscle. J. Appl. Physiol. 73:2538-2543, 1992

Phelan JN, Gonyea WJ. Effect of radiation on satellite cell activity and protein expression in overloaded mammalian skeletal muscle. Anat. Rec. 247:179-188, 1997

Kadi F, Eriksson A, Holmner S, Thornell LE. Effects of anabolic steroids on the muscle cells of strength-trained athletes. Med Sci Sports Exerc 1999 Nov;31(11):1528-34

This is why I don't support long cycle lengths. If anything, they're simply a waste of the money you spent on your gear as positive returns simply diminish after the 8-10 week mark (and it varies between people). The longer you remain on, the more your body will flood itself with hormones and proteins that are antagonistic to muscle growth and the AAS you are using.

Writing this up as an example Cycle. Looking to do it in 6 months after i do some natural cutting


Week 1-8 Test 250 a week divided by two pins
Week 1-8 Tren 500 a week pinning every other day

Week 1-8 Arimadex .25 mg Every other day if needed and adjust if needed
Week 1-8 Prami .5-1 MG per day From Day 1



Nolvadex start 14 days after last injection.
40Mg first 2 weeks
20MG last 2 Weeks

Looks like a very solid straightforward cycle to me! This should be an example cycle to show most of the newcomers on here that this is how cycles should be! Simple, effective, and straight to the point. No fancy elaborate stacks of 3+ compounds or complex cycles that would require a PhD to understand.

[Oubowtie06]

My last few weeks of reading seems to be paying off then lol

[lance1337]

Hello Atomini. Thank you for the thread first of all. The most consistent and helpful post about Tren I've read so far.

I would like to hear your opinion on a few issues which I can't fully understand.

What is the connection between estrogen-prolactin, estrogen-progesterone, progesterone-prolactin?
How does each of these effect male breast tissue and gyno?
Does estradiol have direct impact on gynecomastia or just through raising prolactin? I don't know why but I thought high estro itself just gives you more fat in your breast and that gyno develops because of high prolactin which is caused by high estro.
Does progesterone always convert to prolactin?

And what do you think of my cycle

Week 1-10 Test prop 50mg e3d - I can't run it eod cause I've got 50mg ampules and I'd like to have the dose around 100mgs a week like you suggested
Week 1-10 Tren Ace 50mg ed
Week 1-10 arimidex 0,25mcg ed - I'm very prone to gyno and I feel like I can get it even from 350mgs of test a week without an AI. Though I'm not sure if I should use an AI at all at such a low dose of test. What would you suggest?
I will have prami on hand in case of gyno (caber is very very expensive where I live)

PCT in case I'm able to get some aromasin
1-10 day HCG 500ius
1-10 day Aromasin 12,5mgs ed
1-10 day Nolva 20mgs ed
11-28 day Nolva 40mgs ed

I'f I won't get aromasin I'll just run a-dex solo 0,25mgs ed. Or is it a bad idea and I would rather use just Nolva?

Hope you understood what I was asking about and thank you in advance.

[Atomini]

lance1337,

Whew, okay... The issue of Progestins and elevated Prolactin is an interesting one.

Increases in Prolactin can be kept in control by keeping Estrogen levels from rising, and can also be controlled from the use of a Prolactin antagonist as you probably already know. What's also strange is that Progestins are actually SUPPOSED TO INHIBIT PROLACTIN SECRETION, but for some reason, Progestins such as Trenbolone and Nandrolone end up causing an increase in prolactin in varying numbers of users. We all know how things are SUPPOSED to be in theory, but in practice it can be very different, especially in a game like this where every individual reacts differently to different compounds compared to the next person. Progestins, in vitro (and in theory) are actually INHIBITORS of prolactin secretion. However... Trenbolone in varying degrees between users DOES increase prolactin secretion and the only evidence we have unfortunately is anecdotal, but its there with bloodwork and all. Trenbolone SHOULDN'T cause prolactin secretion and should actually suppress it due to its Progestogenic nature, but the fact is that in some people for unknown reasons it does increase Prolactin secretion, even in conditions where Estrogen levels are kept to a minimum and controlled. And the reason why I support using a prolactin antagonist while running any Progestogenic 19-nor is to keep those levels down in the first place - prolactin has an intense inhibitory effect on libido, sex drive, and the ability to achieve orgasms. We see constant reports of people having sex drive and libido issues when using compounds like Trenbolone and Deca , and when a prolactin antagonist is inserted into the mix, it solves their libido issues.

I ran Trenbolone once (with 400mg/week of Testosterone ) and waited until week 3 to begin using my standard 1mg/week of Cabergoline - no AI used. At the end of week 2 I had bloodwork done, and prolactin was in the 300s. Taking 1mg of caber took me down to 4. What's strange is that bloodwork in an identical Trenbolone cycle later on with 400mg/week of Testosterone and no AI showed no increase in Prolactin. For unknown reasons in humans, the issue of Prolactin secretion is a dodgy one and different people respond differently at different times, even. As an overall precaution, I always run Cabergoline regardless on any Trenbolone cycle. I'll always run a prolactin antagonist when running Trenbolone regardless. I will take zero chances with this.

I wish there were studies done on humans with Trenbolone that we could look at and finally know the truth behind this, but unfortunately there aren't any and likely won't be any in the near future. There isn't a whole lot of data or solid data on Prolactin LEVELS raising from 19-Nors, but it is strongly speculated that the Estrogen receptor is a co-binding factor in Prolactin receptor expression (PRLR). This can make us far more sensitive to Prolactin even if its not increased or wildly out of range. This theory also fits well with the Estrogen receptor being the causitive factor in Prolactin issues. This is also why for the most part, controlling E2 levels should control Prolactin. It is ALSO why Trenbolone's side effects are reported to be far more pronounced when running it in a high Estrogen environment as a result of stacking Tren with high doses of an aromatizable compound, such as Testosterone (rather than keeping Testosterone at a TRT dose). The whole issue of Prolactin and what causes it to rise up and down is a dodgy one and varies between individuals as well.

Even in William Llewellyn's Anabolics book, he states:

Trenbolone is not aromatized by the body, and is not measurably estrogenic. It is of note, however, that this steroid displays significant binding affinity for the progesterone receptor (slightly stronger than progesterone itself). The side effects associated with progesterone are similar to those of estrogen including negative feedback inhibition of testosterone production and enhanced rate of fat storage. Progesterone also augments the stimulatory effect of estrogens on mammary tissue growth. There appears to be a strong synergy between these two hormones here, such that gynecomastia might even occur with the help of progestins, without excessive estrogen levels. The use of an anti-estrogen, which inhibits the estrogenic component of this disorder, is often sufficient to mitigate gynecomastia caused by progestational anabolic /androgenic steroids . Note that progestational side effects are more common when trenbolone is being taken with other aromatizable steroids.

As far as it goes with gyno... Gyno is also such a complex issue and the mechanism behind which it forms has so many different pathways. The causation is very complex, and its precise specifics are largely unknown, and a number of agents including estrogens, progestins, GH, IGF -1, and prolactin may be involved. However, most authorities believe that a decreased (T+DHT)/E ratio is central to the development of gyno, and that blocking the effects of estrogen, or increasing T + DHT levels, is central to amending the problem. Prolactin is not a central issue, but it is one of the contributing factors should other necessary functions be set in place. There are many different factors in the overall complex mechanism that produces gyno. Therefore, if you can eliminate one or more of the gears in the machine that is responsible for the formation of gyno, you can effectively have a high chance of stopping, blocking, and preventing it.

I hope I have helped you to understand these things better.

Your cycle and PCT looks fine. You know i'm going to suggest pinning EOD if you absolutely possibly can. 3x per week just doesn't cut it. But that's my only critique of your cycle. I'd also reccomend using Aromasin instead of Arimidex , but if availability is an issue then Arimidex is passable.

[lance1337]

Thank you really much. That definitely helped me out and cleared up a lot of things to me!

[Tp911]

quick question, currently on almost same cycle as lance, first week did get a couple of the tren sides such as the insomnia, night sweats and tren cough a couple of times but there after it went away, so I know the tren isnt bunk.
im on week 3 already of a 6wk cycle and just wondering is it a smart idea to bump up my dose from 120mg tren EOD to 160-200mg EOD or 75mg to 100mg ED if im not noticing any sides at all now?

[Atomini]

quick question, currently on almost same cycle as lance, first week did get a couple of the tren sides such as the insomnia, night sweats and tren cough a couple of times but there after it went away, so I know the tren isnt bunk.
im on week 3 already of a 6wk cycle and just wondering is it a smart idea to bump up my dose from 120mg tren EOD to 160-200mg EOD or 75mg to 100mg ED if im not noticing any sides at all now?

You can try, but why would you? If your gains are satisfactory, why bump doses up and then risk worse side effects? Sometimes doing things like this will result in sides suddenly hitting you like a hammer. Remember that Trenbolone is very powerful - you don't need much for great results, so why attempt to push it? It sounds like you've found your sweet spot where you're not experiencing any sides and are having great gains so why bother moving away from that?

[bascat]

Hello Atomini. Thanks again for the amazing collection of well considered data and responses- I am certain you have saved a lot of guys from making some terrible decisions when using Tren .

I am putting together a cycle much like the one described by Oubowtie06 above with the only exception being the use of B6 at around 200mg 2x daily for prolactin control, but have the following questions:

- If running Tren Ace, what is your preferred ester of test to run with it? I have both Prop and Enanthate available. My thoughts were that with the Ace ester being short, running Test E would lead to quite a differential in active levels between the two compounds for the first week or two while the test E builds in the system.
- Should the test be discontinued at the same time as the Tren regardless of the ester, or run for a couple of additional weeks after the Tren is discontinued?
- How long after either test E or test Prop would you typically wait before starting the PCT (are the transitions the same as they would be for any other cycle involving test)?

Apologies in advance if the answers to some or all of these questions have been posted before.

[Atomini]

Hello Atomini. Thanks again for the amazing collection of well considered data and responses- I am certain you have saved a lot of guys from making some terrible decisions when using Tren .

I am putting together a cycle much like the one described by Oubowtie06 above with the only exception being the use of B6 at around 200mg 2x daily for prolactin control, but have the following questions:

- If running Tren Ace, what is your preferred ester of test to run with it? I have both Prop and Enanthate available. My thoughts were that with the Ace ester being short, running Test E would lead to quite a differential in active levels between the two compounds for the first week or two while the test E builds in the system.
- Should the test be discontinued at the same time as the Tren regardless of the ester, or run for a couple of additional weeks after the Tren is discontinued?
- How long after either test E or test Prop would you typically wait before starting the PCT (are the transitions the same as they would be for any other cycle involving test)?

Apologies in advance if the answers to some or all of these questions have been posted before.

1. You are correct in your assessment. Tren Ace generally goes well with Test Prop due to the similarities in half-lives, which create ease of injection timing. This is not to say that you can't use Enanthate with Acetate or something, but its just more convenient.
2. Test and Tren can and should be discontinued at the same time. Prolonging one over the other simply serves to increase the time on cycle, and prevent HPTA recovery the longer something is run. Terminate both at the same time, and your cycle ends quicker, and you can start PCT sooner and get your body back to normal quicker.
3. Following the termination of Test E, the user should wait 2 weeks before starting PCT so as to ensure the body is totally clear of any hormones by that point. FOllowing termination of Test Prop, the user should wait about 6 or 7 days before starting PCT.

[kronik420]

1. You are correct in your assessment. Tren Ace generally goes well with Test Prop due to the similarities in half-lives, which create ease of injection timing. This is not to say that you can't use Enanthate with Acetate or something, but its just more convenient.
2. Test and Tren can and should be discontinued at the same time. Prolonging one over the other simply serves to increase the time on cycle, and prevent HPTA recovery the longer something is run. Terminate both at the same time, and your cycle ends quicker, and you can start PCT sooner and get your body back to normal quicker.
3. Following the termination of Test E, the user should wait 2 weeks before starting PCT so as to ensure the body is totally clear of any hormones by that point. FOllowing termination of Test Prop, the user should wait about 6 or 7 days before starting PCT.

your the 1st one to say this.. everyone else says 3 days..... why's that?

[Atomini]

your the 1st one to say this.. everyone else says 3 days..... why's that?

Testosterone Propionate 's half life is 48 hours, which is 2 days. By the 3rd day, do you REALLY think that all of the hormone is gone from the body? Especially after having run it for weeks upon weeks for a full cycle, whereby the hormone levels have consistently built up over those weeks?

[>Good Luck<]

Testosterone Propionate's half life is 48 hours, which is 2 days. By the 3rd day, do you REALLY think that all of the hormone is gone from the body? Especially after having run it for weeks upon weeks for a full cycle, whereby the hormone levels have consistently built up over those weeks?

Would this not affect the pct start times for ALL esters if this were the case? How come nobody else came up with this? Hmm..

[bascat]

Thanks Atomini- just as I suspected.

As far as Tren Ace is concerned, given that I can't obtain prolactin inhibitors and will be using B6, if the worst happened and any prolactin sides surfaced, would discontinuing the tren typically be enough to head things off given the short half life, or does the prolactin remain high regardless? I am hoping that using the B6 for prolactin and Adex to control estrogen coupled with the low test dose will keep everything under control, but as you have said, everyone reacts differently.

[Atomini]

Bascat,

The issue of prolactin is extremely complex (scroll up above to see my giant post) whereby sometimes increased prolactin isn't the issue. Many times prolactin levels can remain low, but high circulating levels of Estrogen can increase the prolactin receptor sensitivity. If you do start experiencing any prolactin effects, immediately take an AI with a prolactin antagonist. If that's not possible, halting administration of all drugs does help, but you will have to bare it out as everything clears from your system.

[DurdenTyler]

Good read, read it more than 5 times. good work

Can I get away without pram/caber at 150mg tren a eod, 35mg prop eod? Also Can i run this cycle for 10 weeks? How should i use adex at .25 eod, is it even necessary?

thanks man

[Atomini]

I advise always running Caber or Prami regardless. If you want to try without it, go ahead... but just be aware of the risks. At 35mg EOD prop, there's no need for an AI but it is a good idea to keep it on hand just in case.

[DurdenTyler]

I advise always running Caber or Prami regardless. If you want to try without it, go ahead... but just be aware of the risks. At 35mg EOD prop, there's no need for an AI but it is a good idea to keep it on hand just in case.

What dose would you recommend for liquid pram? Its taken orally right? Can i run the same tren amount for 10 weeks, or am i risking myself?

thanks

[Atomini]

What dose would you recommend for liquid pram? Its taken orally right? Can i run the same tren amount for 10 weeks, or am i risking myself?

thanks

Please read the FAQ. All the answers you seek are already there.

Q: Prolactin antagonists like Prami and Caber help prevent gyno and tren-dick? How do I use them?

Cabergoline can be used at 1mg per week, as it has a very long half life, approximately 7-14 days. Pramiprexole should be dosed at 0.5mg per day for the first few days, and then increase to 1mg thereafter. Nausea has been reported when increasing the dose too fast or too much. If you experience nausea, bring it down a notch. I think everyone will be different with the nausea effect. With that being said, 1-2mg per day is even considered a low dosage. Patients who are perscribed Prami are commonly perscribed 3 or 4mg per day too! Take prami before bed, as it apparently gives you excellent deep sleep and can make you drowsy and sleepy if taken during the day. Apparently it can knock you out cold. Prami is a very new compound, there is still data being collected on it. It seems to carry a couple side effects that Caber does not have. Nausea and drowsiness. I have personally not yet used Prami.

[Rv8G30]

Theres a stack I can get that is tren , test prop, masteron all 50mg each. I think its all together one vial. Does this sound right? Would eod injection of this make sense? Do you think gains would be good or is there a better way to go? Did a test e cycle went well no sides. Cutting for a few months naturally then going to try something for a lean bulk.

[Atomini]

Theres a stack I can get that is tren, test prop, masteron all 50mg each. I think its all together one vial. Does this sound right? Would eod injection of this make sense? Do you think gains would be good or is there a better way to go? Did a test e cycle went well no sides. Cutting for a few months naturally then going to try something for a lean bulk.

Scroll up above or go back in the thread a bit, there's a guy who posted the exact same question as you I think. EOD shots should be just fine with something like that. Gains from something like that should be good, provided nutrition is spot on.

[mockery]

have you ever nailed a good balance of tren test and estrogen? specifically speaking sex drive and libdo? Im a machine 24/7 , my gf hates it now haha, and its so bad the other night i think i tore the fascia off the abdominal wall from going all out during sex. could be a hernia... im a a idiot and wont go see a doctor. This cycle of tren, had me crying alot, but the libido is amazing, ill take crying like a bitch over limp dick... i dropped prami, and cut back adex ALOT. all i know is i feel like a tren god, no insomnia, no limp dick, get night sweats maybe once a week. and rage has been replaced with being horny. and strength is great in the gym. Its like i can keep adding more and more but at the same time i can feel joints and tendons screaming, but the muscle says **** it lets get there!!

Almost think my tren isnt tren, but with that being said what ever it is.. its bloody better then tren lol.

[Atomini]

LOL why are you crying on cycle?

And you should definitely get your abdomen checked at the doctor if you think you got a hernia from going at it too hard during sex. Hernias can be serious, and if left unchecked can cause other issues especially if training in the gym and such.

I've never had libido issues on Trenbolone . Always had a far higher than normal libido even when running TRT doses of Testosterone . It definitely sounds like you've got some solid Tren from what you've told me. How many mg per week are you using?

[mockery]

350-400 ace weekly

[mockery]

i think the last time i got tren from a different brand it was teh estrogen fina pellets. hence why i am experiencing something a lot different then my last tren cycle.

[Trying-Hard]

Atomini,

I know you don't advocate posting cycle advice for a 1st time tren user, so I am going to generate one myself based on all of your advice in this thread and ask you if you approve 100%..=) If you think there is anything that can be changed for the better, please advise.

wk 1-8: 25mg prop eod
wk 1-8: 75mg tren a eod
wk 1-8: 1mg caber/wk
wk 9: PCT

Adex on hand. I know you are more of a Aromasin fan
(but most likely will not use the AI- depends on BW results on week 4)

How is it looking??

Cheers!

[Atomini]

IF someone is going to dive into the deep end and use Trenbolone in their very first ever cycle, then I would approve of that cycle layout. With this being said, however, I do not approve of Trenbolone use for a first ever cycle lol.

[Atomini]

Oops, I didn't realize that you meant first-time Tren user as opposed to first time ever AAS user. In this case, I agree 100% that is the perfect Trenbolone beginner cycle!

[Trying-Hard]

Oops, I didn't realize that you meant first-time Tren user as opposed to first time ever AAS user. In this case, I agree 100% that is the perfect Trenbolone beginner cycle!

Thanks brother.

[zacheryah]

Hey Atomini

I decided the first week of november to give your "trenbolone as primary anabolic " idea a try. Ive had 4 other tren cycles before and was very happy about them.
So far it has been quite the succes. I'm training for strenght, and the increase in both power and mass is very noticable.

My current schema was

800 mg trenbolone enathate, each week, all 10 weeks
250mg sustanon , each week, all 10 weeks
40mg dianabol (for kick), each day, first 4 weeks

Halfway currently and increased 1rm for squat and deadlift with 50 kilograms, and bench with 20 kilograms.

usually in tren cycles i experience a slight dropback in power when going off the dianabol, but havent noticed anything yet.
Furthermore, 250mg testosterone blend works just fine for keeping normal sexual functions.


Only problem i currently encounter, is anorgasmia, caused by elevated levels op prolactine, because in my country i cant get cabergoline, wich is kinda frustrating.

I'm only halfway, but allready my gains are far superior then any cycle i did before. I wonder where what improvement i'll have made when i ended it.

Thanks for the great info !

[Atomini]

Hey Atomini

I decided the first week of november to give your "trenbolone as primary anabolic " idea a try. Ive had 4 other tren cycles before and was very happy about them.
So far it has been quite the succes. I'm training for strenght, and the increase in both power and mass is very noticable.

My current schema was

800 mg trenbolone enathate, each week, all 10 weeks
250mg sustanon , each week, all 10 weeks
40mg dianabol (for kick), each day, first 4 weeks

Halfway currently and increased 1rm for squat and deadlift with 50 kilograms, and bench with 20 kilograms.

usually in tren cycles i experience a slight dropback in power when going off the dianabol, but havent noticed anything yet.
Furthermore, 250mg testosterone blend works just fine for keeping normal sexual functions.


Only problem i currently encounter, is anorgasmia, caused by elevated levels op prolactine, because in my country i cant get cabergoline, wich is kinda frustrating.

I'm only halfway, but allready my gains are far superior then any cycle i did before. I wonder where what improvement i'll have made when i ended it.

Thanks for the great info !

Excellent, great feedback and I am very pleased to hear your positive results!

In response to your anorgasmia issue, if you can't get a hold of Pramipexole or Cabergoline in your country, you can try vitamin B6. Look back through this thread or do a search function in this thread and you'll find the dosing guidelines for vitamin B6 to control prolactin and the studies conducted with it. I believe 600mg per day (split into two separate doses). The only issue with B6 is that excessive doses for prolonged periods can cause nerve damage and other problems in the body, this is why B6 for prolactin is not always my first advice for people. It's usually no big concern when using it at this dose for Prolactin control, but it is something everyone should be aware of.

[zacheryah]

Excellent, great feedback and I am very pleased to hear your positive results!

In response to your anorgasmia issue, if you can't get a hold of Pramipexole or Cabergoline in your country, you can try vitamin B6. Look back through this thread or do a search function in this thread and you'll find the dosing guidelines for vitamin B6 to control prolactin and the studies conducted with it. I believe 600mg per day (split into two separate doses). The only issue with B6 is that excessive doses for prolonged periods can cause nerve damage and other problems in the body, this is why B6 for prolactin is not always my first advice for people. It's usually no big concern when using it at this dose for Prolactin control, but it is something everyone should be aware of.

Oh allright, i'll try that instead then. Should i use it for the remaining 5+2 weeks, or less considering the sides ?


One thing i wanted to add about results from the cycle :

Acnee, still relatively low. got a cycle support with N-acetyl cysteinne and silymarin ready just in case.
Bloodpressure : since i train with 350mg asperine, not a real issue.
heath generation : Its freezing point temperature here, yet i have no problems running around in kneehigh shorts and a sweater/jacket. when i exert myself, i get a very warm feeling in my cheecks,who turn red in the progress. I consider it to be a good side effect.
Irritation : wel its a little higher then on 600mg, but to be honest, since this is the 4th time tren , its something i got used to.

and

Recovery : this is amazing. twice i have an injury to a rotator cuff, that hurted pretty bad troughout the day, but twice it got healed completely in 6 days time. as in no pain and no powerloss when 3rm benchpressing. I remember in an offperiod 1 year ago, i had the same injuries, and it took weeks to heal properly.

[Jonnyg419]

AR-R doesn't seem to have Caber anymore, any other research supply companies that you would recommend?

[Atomini]

AR-R doesn't seem to have Caber anymore, any other research supply companies that you would recommend?

AR-R never had Caber to begin with. It's also against forum rules to give out, exchange, and discuss other research chem sources on the open forum.

[Jonnyg419]

ooh my bad Atomini, I didn't know that applied to research chems

[RyanGreg]

A few questions Atomini.

1 - I don't yet have my prami is it ok to start tren and start the prami the following week (its on the way to me now) so should be here within a few days time. Will start ASAP it arrives....

2 - If I notice possible gyno sides from too much estrogen is it wise to increase aromasin dose? Currently on 12.5mg ED.... I know some people jump to letro but can I just increase my aromasin dosage (if need be).

[bascat]

Excellent, great feedback and I am very pleased to hear your positive results!

In response to your anorgasmia issue, if you can't get a hold of Pramipexole or Cabergoline in your country, you can try vitamin B6. Look back through this thread or do a search function in this thread and you'll find the dosing guidelines for vitamin B6 to control prolactin and the studies conducted with it. I believe 600mg per day (split into two separate doses). The only issue with B6 is that excessive doses for prolonged periods can cause nerve damage and other problems in the body, this is why B6 for prolactin is not always my first advice for people. It's usually no big concern when using it at this dose for Prolactin control, but it is something everyone should be aware of.

Take a look at this link
muscle-health-fitness.com/prolactin-inhibitor.html

This is a superb rundown on the use of B6 and notes that certain types of B6 are ineffective in lowering prolactin- specifically Pyrodoxine Hydrochloride (which is the basis of many B6 supplements). The use of P5P instead is supposed to eliminate any issues with potential nerve damage from high doses.

[Atomini]

A few questions Atomini.

1 - I don't yet have my prami is it ok to start tren and start the prami the following week (its on the way to me now) so should be here within a few days time. Will start ASAP it arrives....

2 - If I notice possible gyno sides from too much estrogen is it wise to increase aromasin dose? Currently on 12.5mg ED.... I know some people jump to letro but can I just increase my aromasin dosage (if need be).

1 - Never start any cycle without having everything you need in your possession. Sure, you can go ahead and start while something is on its way but you'll look like an idiot if something happens within the first week (or if your item's arrival is delayed in the mail for whatever reason, and now you've started your cycle and start to lactate from Prolactin - you're screwed). It is common sense to wait to have everything before you start, and there are many horror stories you can easily find on this forum of people too impatient to wait before ALL of their ancillaries arrive.

2. Yes, it is actually the preferred protocol to increase your AI dose rather than start a new AI if you get gyno symptoms. Aromasin is a pretty strong AI, so increasing to a full 25mg ED dose if gyno symptoms appear is a good way to control estrogen in order to take care of the gyno.

[Jonnyg419]

Kind of a broad question but if using Test E and Tren A together, would you have to wait until the forth week of Test use before starting the Tren due to the difference in esters?