trenbolone acetate 1st cycle200mg/week@50mg eod with testosterone cypionate 125mg/wee

[drricz]

opinions on trenbolone acetate with testosterone cypionate cycle.

This is my 1st ever trenbolone acetate cycle 200mg/week@50mg eod with testosterone cypionate 125mg per week. I wud like to know ur opinion on my cycle, as this is why this forum is for.. To help other members,United by iron.


Just to know,
Im 24yrs old, towards the short side in the
height spectrum (5'8") and currenty 73kg/161lbs @ 15% body fat.
Was a long distance runner,pretty skinny 4yrs ago at a measly 48kg/106lbs @arnd 10% body fat.
Lifting weights for the past 4 years. Diet has been pretty solid.

Did 2 cycles at 23yrs of age,
1st one being a sustanon 250mg alone cycle for 12weeks which gave me real good gains n most of it I've been able to maintain.. Probably due to a good pct(hcg n tamoxifen/nolvadex), solid diet and exercise.
2nd one was 8months aftr, a dbol and sustanon 250mg(2-3shots/week) and stanozolol towards d end of d cycle n then Pct.

Aftr graduating @23, ive been practicing (im a dental surgeon) for a year now alongside lifting.


I Currently have in my possession, both 100mg/ml (10ml) of trenbolone acetate and testosterone cypionate 250mg/ml from alpha pharma.

Here's my idea on hw im gna do this cycle as for a lean BULK .

Week 1-6: 50mg tren ace eod wid t-cyp 125mg/week ( for normal physiological functioning,very much like Hormone Replacement Therapy ) with cabergoline 0.25mg E3D (I.e 0.5mg cabergoline /week)

Week 6-8 : 500mg/week test cyp(250mg twice per week) [with anastrazole 0.25mg ED]

Week 8-10: 250mg/week [with anastrazole 0.25mg ED]

21days after last shot,
Week 1-2 Tamoxifen 20mg ED
Week 2-3 Tamoxifen 10mg ED

Hcg was purposely left out, as this I feel is a very short period of time(both for tren as well as test) to knock out my HPTA..

My questions are:

As for a novice in tren ace cycle,does this look good?

Should I be taking anastrazole from the day I last shot test cyp for the next 12days(assuming its t 1/2 is 12days) so whtever test circulating in my body doesnt aromatize?? And then move on wid d pct of tamoxifen /nolva for d nxt 21days??Thnx.


Regards,
Richard.

 

[3J]

if i were you id wait on the tren till your 5th cycle.. go with another compound right now

 

[tbonexl]

Your test cyp dose is all over the place! It doesn't work like that at all. If you want to run 500mgs, do it from beginning of cycle to the end. Tapering dose especially with a long ester does nothing at all. Test cyp takes 4-6+ weeks to kick in. Running it the way you have planned is no good. Your tren dose isn't worth doing either.

I suspect you only have one vial of each and your trying to make a cycle of it. Not going to work. Get atleast one more vial if not 2 of test cyp and run it @ 500mgs for 12+ weeks. Shelf the tren and maybe opt for deca instead or npp...

 

[tbonexl]

Your test cyp dose is all over the place! It doesn't work like that at all. If you want to run 500mgs, do it from beginning of cycle to the end. Tapering dose especially with a long ester does nothing at all. Test cyp takes 4-6+ weeks to kick in. Running it the way you have planned is no good. Your tren dose isn't worth doing either.

I suspect you only have one vial of each and your trying to make a cycle of it. Not going to work. Get atleast one more vial if not 2 of test cyp and run it @ 500mgs for 12+ weeks. Shelf the tren and maybe opt for deca instead or npp...

 

[SJC]

Bumping your dose to 500mg for week 6-8 is pointless. If your also going to run only a 10 week cycle I would strongly recommend Test Prop.

Not knowing the amount to dose your AI is a noob question. If you don't know you AI dosing then you aren't ready to run Tren.

Running Caber also isn't USUALLY necessary if your AI dosing is on point. Generally that is what give you the prolactin issues. I guess it wouldn't hurt though.

 

[e92]

Running Caber also isn't USUALLY necessary if your AI dosing is on point. Generally that is what give you the prolactin issues. I guess it wouldn't hurt though.

such a common myth. i know plenty of guys, including myself, who have had their e2 ON POINT while running tren (not hard to do when you're on 200mg test prop a week) and still had high prolactin. thank god nothing happened to me but yeah.. if i ever do run tren i will always use it with caber.

anyway, whats the point of ramping up your test? that doesnt make sense. if anything you should lower your test to 125 so you hold less water while u get shredded on tren (if that is your goal). and honestly i wouldnt even bother using tren @ 175mg a week its kind of a waste IMO

 

[drricz]

if i were you id wait on the tren till your 5th cycle.. go with another compound right now

5th cycle Why? Is thr a certain number of cycles with othr 19-nor AAS to be done prior to a tren ace cycle so as to make the body prepared for such a potent drug? Thnx

 

[drricz]

Your test cyp dose is all over the place! It doesn't work like that at all. If you want to run 500mgs, do it from beginning of cycle to the end. Tapering dose especially with a long ester does nothing at all. Test cyp takes 4-6+ weeks to kick in. Running it the way you have planned is no good. Your tren dose isn't worth doing either.

I suspect you only have one vial of each and your trying to make a cycle of it. Not going to work. Get atleast one more vial if not 2 of test cyp and run it @ 500mgs for 12+ weeks. Shelf the tren and maybe opt for deca instead or npp...

Yes brother, got a vial of tren ace and t cyp.
Tren dose of 200mg for the 1st time ever isn't worth it? (given tren is 5x potent thn test,wudnt it be an equivalent of a 1000mg of test?)

N yes, I nw get the point as to why t cyp 500mg/week bumped up fr a coupla weeks doesn't make sense.

If u were in my shoes, how wud u plan this cycle??(with tren ace preferably)

Thnx

 

[drricz]

such a common myth. i know plenty of guys, including myself, who have had their e2 ON POINT while running tren (not hard to do when you're on 200mg test prop a week) and still had high prolactin. thank god nothing happened to me but yeah.. if i ever do run tren i will always use it with caber.

anyway, whats the point of ramping up your test? that doesnt make sense. if anything you should lower your test to 125 so you hold less water while u get shredded on tren (if that is your goal). and honestly i wouldnt even bother using tren @ 175mg a week its kind of a waste IMO

Yeah im nt gna take a risk wid d prolactin here,I dnt wna squeeze out milk fr my proteins aftr workouts..cabergoline it is.I feel its NECESSARY. And tren is 200mg per week @50mg eod n not 175mg/week wonder whr u saw tht..

n no,test cyp levels r planned to be kept at 125mg per week/TRT as long as im on tren..

I planned on ramping up d test ryt aftr tren but nw yeah I got a clear picture as to why tht doesn't look good only fr a few weeks tht is..
Thnx

 

[drricz]

Bumping your dose to 500mg for week 6-8 is pointless. If your also going to run only a 10 week cycle I would strongly recommend Test Prop.

Not knowing the amount to dose your AI is a noob question. If you don't know you AI dosing then you aren't ready to run Tren.

Running Caber also isn't USUALLY necessary if your AI dosing is on point. Generally that is what give you the prolactin issues. I guess it wouldn't hurt though.

Then I guess knowing the AI dosing makes me ready fr a tren cycle ryt? Afterall, knowing proper dosing is wht makes a proper n effective cycle ryt.
Instead of stating thts bad thts not how to do it,tell how to do it..ryt?

And yes,I also feel now tht test 6-8week bumped up dose doesnt make sense.prop makes a whole lot sense,given cyp is a long chained ester.
Thnx

 

[halfwit]

such a common myth. i know plenty of guys, including myself, who have had their e2 ON POINT while running tren (not hard to do when you're on 200mg test prop a week) and still had high prolactin. thank god nothing happened to me but yeah.. if i ever do run tren i will always use it with caber.

anyway, whats the point of ramping up your test? that doesnt make sense. if anything you should lower your test to 125 so you hold less water while u get shredded on tren (if that is your goal). and honestly i wouldnt even bother using tren @ 175mg a week its kind of a waste IMO

Not a myth, you're the exception to the rule. Hyperprolactinemia *usually* relies on estradiol to escalate as estradiol in high doses impacts dopamine - which is the antagonist to prolactin. Some folks however are sensitive to progestins, and do need a dopamine agonist off the bat. This is why it's good to have caber/prami on hand while you figure out if you are susceptible, or choose an incorrect dose for your AI.

OP: The reason why the 5th or later cycle is recommended is that you simply don't have enough experience yet to know how to dose AAS correctly, manage estradiol, and know what to do if things go poorly.

There isn't really a physiological reason (other than perhaps not really needing AAS due to diet deficiencies) for this - other than keeping one's cool when tren plays with your mind IME.

My .02c

 

[drricz]

Not a myth, you're the exception to the rule. Hyperprolactinemia *usually* relies on estradiol to escalate as estradiol in high doses impacts dopamine - which is the antagonist to prolactin. Some folks however are sensitive to progestins, and do need a dopamine agonist off the bat. This is why it's good to have caber/prami on hand while you figure out if you are susceptible, or choose an incorrect dose for your AI.

PROGESTIN levels--->ups PROLACTIN --->breast tissue proliferation (extra ESTROGEN makes it even worse for men and the added benefit of tren with GROWTH HORMONE ,these r d hormones necessary for human breast tissue growth) gynecomastia cn be a huge concern..


yes,the relationship between prolactin and estrogen hasn't been clearly understood as of now, but as per textbooks,its highly likely that high prolactin levels inhibits the production of othr hormones like exogenous testosterone in males and estrogen in females .

Normally, both men and women have small amounts of prolactin in their blood. Produced by the ant.pituitary in response to binding of stimulating factors on its receptors, Prolactin levels are depressed by other hormones called prolactin inhibiting factors (PIFs), such as dopamine. These are the "supporters " of dopamine (agonist) which binds to the receptors in the pituitary and tricks it into not producing prolactin. Agonists being bromocriptine and cabergoline.


High prolactin levels interfere with the normal production of other hormones, such as estrogen and progesterone.

In men, high prolactin levels can cause galactorrhea /milking tits, inability to have an erection during sex, reduced desire for sex, and infertility. A man with untreated hyperprolactinemia may make less sperm or no sperm at all.

Moral of the story,

cabergoline is a yes.
AI is necessary whn test levels r above physiological doses.

So I can assume that ex*****ant amounts of testosterone isnt logical or advisable when on trenbolone .. Which I feel is a waste.of precious extra testosterone flowing unnecessarily in d body when only TRT does r required. And let tren do its job.

 

[halfwit]

PROGESTIN levels--->ups PROLACTIN --->breast tissue proliferation (extra ESTROGEN makes it even worse for men and the added benefit of tren with GROWTH HORMONE ,these r d hormones necessary for human breast tissue growth) gynecomastia cn be a huge concern..


yes,the relationship between prolactin and estrogen hasn't been clearly understood as of now, but as per textbooks,its highly likely that high prolactin levels inhibits the production of othr hormones like exogenous testosterone in males and estrogen in females .

Normally, both men and women have small amounts of prolactin in their blood. Produced by the ant.pituitary in response to binding of stimulating factors on its receptors, Prolactin levels are depressed by other hormones called prolactin inhibiting factors (PIFs), such as dopamine. These are the "supporters " of dopamine (agonist) which binds to the receptors in the pituitary and tricks it into not producing prolactin. Agonists being bromocriptine and cabergoline.


High prolactin levels interfere with the normal production of other hormones, such as estrogen and progesterone.

In men, high prolactin levels can cause galactorrhea /milking tits, inability to have an erection during sex, reduced desire for sex, and infertility. A man with untreated hyperprolactinemia may make less sperm or no sperm at all.

Moral of the story,

cabergoline is a yes.
AI is necessary whn test levels r above physiological doses.

So I can assume that ex*****ant amounts of testosterone isnt logical or advisable when on trenbolone .. Which I feel is a waste.of precious extra testosterone flowing unnecessarily in d body when only TRT does r required. And let tren do its job.

Oh dear, I was ready to go to bed - but I have to make some corrections here:

1. Prolactin most certainly DOES impact testosterone (endogenous) values. I'm assuming you meant endogenous, as exogenous hormones can't be necessarily controlled by the HPTA. Effects of hyperprolactinemia on testosterone production in rat Leydig cells. - PubMed - NCBI
Yes, that's a study on rats, but I wanted to give an easy read. If you really want one on humans, here you go:
Relationship Between Testosterone and Erectile Dysfunction

2. Progestins are a CLASS of hormones, not the root cause of prolactin elevation. Estradiol most certainly can impact prolactin (Effects of estradiol and prolactin on incertohypothalamic dopaminergic neurons in the male rat. - PubMed - NCBI) in humans (yes, here's a human study showing estradiol can increase PRL: Effects of progesterone administration on follicle-stimulating hormone and prolactin release in estrogen treated eugonadal adult men. - PubMed - NCBI), and in fact - progesterone has a double purpose with gonadotropic hormones. It can agonize prolactin, but reduce estradiol Effect of estrogens and progesterone on gonadotropin and prolactin release in a patient with androgen insensitivity. - PubMed - NCBI.

FYI: Guess what hormone estradiol is an agonist for? If you guessed progesterone, you would be correct! Effect of estrogen agonists and antagonists on induction of progesterone receptor in a rat hypothalamic cell line. - PubMed - NCBI If you want a human study, feel free to have a look through Google, I'm too tired to dig one up.

3. What do you think bromocriptine and cabergoline do? (let's not forget pramipexole too) If you guessed, dopamine agonist, which increases dopamine to antagonize prolactin, you'd be correct again!
Clinical pharmacokinetics of cabergoline. - PubMed - NCBI

Look, I can appreciate a healthy debate, but you just started learning about this stuff, while I've been spending the last several years. If I'm wrong, I'm always more than happy to admit it - as it means I still have an opportunity to learn something new.

I get that you want to be proactive, but as dopamine agonists do carry not only potential side effects - but are also habit forming. I used to have the same philosophy in fact, but when looking at the bigger picture (overall health) - why add more drugs than need be?

As far as a TRT dose of testosterone, that's fine as it does make estradiol control easier. Do not put too much faith into thinking that having physiological levels of testosterone will preclude you from needing an AI though. You still should be getting a blood test to verify at about 5 weeks in, when serum levels have stabilized.

I do want to point out that if your logic behind "wasting testosterone" while on tren has anything to do with receptors; you fail to recognize the fact that not only do androgen receptors have a rather short life cycle, but the human body will create more to accommodate the detection of excess androgens seeking a receptor to bind to.

If your thought process about high testosterone is simply one regarding estradiol, I can assure you from experience that estradiol is easily controlled through diligence and experimentation with aromatase inhibitors. There isn't any wasted hormone, I assure you.

You're still not ready for trenbolone in my opinion, but feel free to take the dive if you feel the need to do so. (it's not really the same as injecting 5x the same volume as testosterone by the way - that's just a reference to determine anabolic effects in rat muscle tissue that we often use to compare compounds.)

 

[drricz]

Oh dear, I was ready to go to bed - but I have to make some corrections here:

1. Prolactin most certainly DOES impact testosterone (endogenous) values. I'm assuming you meant endogenous, as exogenous hormones can't be necessarily controlled by the HPTA. Effects of hyperprolactinemia on testosterone production in rat Leydig cells. - PubMed - NCBI
Yes, that's a study on rats, but I wanted to give an easy read. If you really want one on humans, here you go:
Relationship Between Testosterone and Erectile Dysfunction

2. Progestins are a CLASS of hormones, not the root cause of prolactin elevation. Estradiol most certainly can impact prolactin (Effects of estradiol and prolactin on incertohypothalamic dopaminergic neurons in the male rat. - PubMed - NCBI) in humans (yes, here's a human study showing estradiol can increase PRL: Effects of progesterone administration on follicle-stimulating hormone and prolactin release in estrogen treated eugonadal adult men. - PubMed - NCBI), and in fact - progesterone has a double purpose with gonadotropic hormones. It can agonize prolactin, but reduce estradiol Effect of estrogens and progesterone on gonadotropin and prolactin release in a patient with androgen insensitivity. - PubMed - NCBI.

FYI: Guess what hormone estradiol is an agonist for? If you guessed progesterone, you would be correct! Effect of estrogen agonists and antagonists on induction of progesterone receptor in a rat hypothalamic cell line. - PubMed - NCBI If you want a human study, feel free to have a look through Google, I'm too tired to dig one up.

3. What do you think bromocriptine and cabergoline do? (let's not forget pramipexole too) If you guessed, dopamine agonist, which increases dopamine to antagonize prolactin, you'd be correct again!
Clinical pharmacokinetics of cabergoline. - PubMed - NCBI

Look, I can appreciate a healthy debate, but you just started learning about this stuff, while I've been spending the last several years. If I'm wrong, I'm always more than happy to admit it - as it means I still have an opportunity to learn something new.

I get that you want to be proactive, but as dopamine agonists do carry not only potential side effects - but are also habit forming. I used to have the same philosophy in fact, but when looking at the bigger picture (overall health) - why add more drugs than need be?

As far as a TRT dose of testosterone, that's fine as it does make estradiol control easier. Do not put too much faith into thinking that having physiological levels of testosterone will preclude you from needing an AI though. You still should be getting a blood test to verify at about 5 weeks in, when serum levels have stabilized.

I do want to point out that if your logic behind "wasting testosterone" while on tren has anything to do with receptors; you fail to recognize the fact that not only do androgen receptors have a rather short life cycle, but the human body will create more to accommodate the detection of excess androgens seeking a receptor to bind to.

If your thought process about high testosterone is simply one regarding estradiol, I can assure you from experience that estradiol is easily controlled through diligence and experimentation with aromatase inhibitors. There isn't any wasted hormone, I assure you.

You're still not ready for trenbolone in my opinion, but feel free to take the dive if you feel the need to do so. (it's not really the same as injecting 5x the same volume as testosterone by the way - that's just a reference to determine anabolic effects in rat muscle tissue that we often use to compare compounds.)

Omg ur right!! I meant endogenous! Not exogenous!! My bad!

Yes,the purpose of discussion is to have a solution ryt otherwise it would be considered an argument

Yeah progestins aren't the ONLY cause of hyperprolactinemia, there are many others..even a few antipsychotic drugs, cardiac drugs even some antihistamines are known to create hyperprolactinemia n gyno. ***128514;

There's this mechanism called negative feedback inhibition to maintain homeostasis Within the body..

hence prolactin being d antagonist for estradiol (normal physiological example for this is women cant have kids while lactating cz prolactin stops e2 production )

and dopamine being d prolactin antagonist and so n so..

And yes you certainly are right abt this endocrinology related topic, based on my experience in medical school(4yrs)and(2yrs in dental school,irrelevant here though) I cn definitely say ur very knowledgeable in this area.

But then human studies on trenbolone has never been done and thts a major drawback as many do use it---for competitions and for recreational purpose. And studying such cases aren't very methodological from our point of view due to its very limitations and the results cn Be very inconclusive ..

Hence my knowledge in this special case is limited n im tryin to know more abt this drug.

Haha yes ur right,dopamine agonists causes psychological dependence but tht has been reported among ppl who use it in the long term,not for a mere 5- 6 weeks. Tht too 2tabs /week tht requires a lot more dosage n frequency brother

Very interesting topic,

Thnx a lot

 

[drricz]

Hyperprolactinemia *usually* relies on estradiol to escalate as estradiol in high doses impacts dopamine - which is the antagonist to prolactin. Some folks however are sensitive to "progestins"(?), and do need a dopamine agonist off the bat. This is why it's good to have caber/prami on hand while you figure out if you are susceptible, or choose an incorrect dose for your AI.

Sensitive to prolactin u mean..then dopamine agonists aka prolactin antagonists helps. (cabergoline /pramipexole /bromocriptine)

 

[halfwit]

Sensitive to prolactin u mean..then dopamine agonists aka prolactin antagonists helps. (cabergoline /pramipexole /bromocriptine)

Well, as progestins can elevate progesterone - a hypersensitivity to their method of action would create a sharp rise in prolactin. I personally started tren with a ridiculous amount of pramipexole, tried it the second time without - found that I had sides (erectile dysfunction comes far earlier than lactation), and slowly caught on to the correlation between hyperprolactinemia and elevated estradiol. Now, I keep a dopamine agonist in the fridge, and simply make sure estradiol stays in optimal range.

This is what SJC was referring to, as it is often sufficient to manage ONLY estradiol - as it is often the largest catalyst in issues from AAS use. Some folks, as E92 pointed out, just aren't as lucky.

There are some studies, but they rare (re: trenbolone studies) as parabolan was pulled from human use shortly after it was released. Tren hex is the non-trade name for parabolan.

Re: Caber habit formation; as a fresh grad, you should know it's serum concentrations that matter - not dosing frequency. Time length is a factor, but some of us are genetically predisposed to such behavior. I'm not saying one pill will cause issues, but 5 weeks (should be the entire length of exposure to the progestin) is certainly long enough for those disposed.

 

[golfer34]

Just so I have this clear.....as long as your estrogen is at an optimal level then there is not a need for caber?......correct?

 

[halfwit]

Just so I have this clear.....as long as your estrogen is at an optimal level then there is not a need for caber?......correct?

If you're not sensitive to the effects of a progestin like tren/nandrolone, correct. If you're not so lucky, it is needed.

 

[drricz]

Well, as progestins can elevate progesterone - a hypersensitivity to their method of action would create a sharp rise in prolactin. I personally started tren with a ridiculous amount of pramipexole, tried it the second time without - found that I had sides (erectile dysfunction comes far earlier than lactation), and slowly caught on to the correlation between hyperprolactinemia and elevated estradiol. Now, I keep a dopamine agonist in the fridge, and simply make sure estradiol stays in optimal range.

This is what SJC was referring to, as it is often sufficient to manage ONLY estradiol - as it is often the largest catalyst in issues from AAS use. Some folks, as E92 pointed out, just aren't as lucky.

There are some studies, but they rare (re: trenbolone studies) as parabolan was pulled from human use shortly after it was released. Tren hex is the non-trade name for parabolan.

Re: Caber habit formation; as a fresh grad, you should know it's serum concentrations that matter - not dosing frequency. Time length is a factor, but some of us are genetically predisposed to such behavior. I'm not saying one pill will cause issues, but 5 weeks (should be the entire length of exposure to the progestin) is certainly long enough for those disposed.

Halfwit thnx a lot! I just had to go brush up my theory and I think this is how stuff works. I believe this is why tren shuts down endogenous testosterone and causes gynecomastia with hyperprolactinemia.


See,progestins are drugs tht mimics/similar to the function of progesterone. Like, trenbolone. Which is a progestin derivative.


Now,going back to the very basics.

In (non hormonally altered) males aka normal healthy males ,
Testosterone is produced from cholesterol And in between, there r many steps. I'll simplify


Im givin a basic explanation of progesterone/progestins. (not specifying tren now,later)

step 1.
PROGESTERONE is CREATED from CHOLESTEROL

Given,we're administering progestins alryt.

Step 2.
This Progesterone is converted to 17 alpha hydroxyprogesterone which is converted to ANDROSTENEDIONE. Part of this is also converted to E1 and E3.(both derivatives of estrogen only)

Step 3. This ANDROSTENEDIONE is converted to TESTOSTERONE,
a part of which in the presence of 5-alpha reductase is converted into DHT.

Step4. excess TESTOSTERONE gets converted to estradiol (E2) by the action of aromatase.


Normally, if thrs extra testosterone, it gets converted to estradiol by aromatase and this estradiol is sensed by the pituitary and tells d testes to stop testosterone production by decreased LH levels. Once balance has been achieved, Testosterone production commences.




But u see,the problem here is we're administering a progestin based AAS .(lets assume quite a big dose alryt)

Increased dosage of progesterone, suppresses LH levels which brings down testosterone levels to a hault.

This means, quite hard on the testicles..

And see,

Progestins at high doses, without an aromatase inhibitor like anastrazole (see step 4) converts to E2 and further suppresses the LH, credits to the HPTA.


And at high serum levels of estradiol, as halfwit said, it messes up with the dopamine mechanism and prolactin is released by the ant.pituitary.

Ppl who r sensitive now begin to develop breast tissue and lactate.(synergistic action of prolactin, estradiol and progesterone)

Aaand,Prolactin increase means in a normal male, decreased endogenous testosterone, and a flaccid penis--though tht has another mechanism and not cz of suppressed testosterone levels)



But it should be remembered, tren is an altered 19nor AAS.
Trenbolone is totally resistant to the aromatase enzyme (which is the enzyme that is responsible for the conversion of aromatizable androgens into Estrogen). Therefore, Trenbolone holds zero Estrogenic activity as it cannot convert into Estrogen in any amount. Trenbolone also is completely resistant to the 5-alpha reductase enzyme, which is the enzyme responsible for the reduction of Testosterone into the Dihydrotestosterone (DHT).

So how to fix,
1. Stop taking the progestin /tren which wud be a no.

Or
2. Aromatase inhibitors -anastrazole 0.25mg a day along with exogenous testosterone in "decent" doses and nt letting E2 levels out of control, TRT dose should be safe I suppose.
+
3.cabergoline 0.5mg per week.
Or bromocriptine or pramipexole.. As the prolactin antagonist.
(better safe than sorry ryt) . And tht too depends on the individual, as many folks here mentioned.


Since tren is a progestin, it will continue to elicit properties of progesterone and with proper use of an AI,exogenous testosterone and caber,,estrogen conversion is out of the question.

so the progesterone (tren) properties would be (im stating whats relevant here,apart frm the many othr uses) in the short term.

1. Thermogenesis (would explain the sweats) (and in females,this is why they have an elevated temperature during ovulation than males)
2. Lipolysis (increased expenditure of energy from fat cells)
3. Partial pr. Of CO2 is decreased, which means, the blood is slightly more alkaline. (a mild respiratory alkalosis) --tht wud explain why ppl are gassed out during aerobic activities. (a similar to being hyperventilation)
3. Increased blood pressure -Aldosterone is retained, which is a hormone tht increases blood pressure usually due to physiological response.
4.Muscle cramps could possibly occur as progestins causes natriuresis( natri-natrium/sodium in d urine) and Na+/K+ is d triggering factor for muscle contraction..


In short, I cn conclude a proper knowledge abt the drug being used and decent dosing and a reasonabe duration along with adequate precautions can in fact be beneficial for the bodybuilding community rather than dng a few more cycles to understand more abt trenbolone (pre-requisite: gta do test based AAS before).. one needs to know how to properly use them and reap the gains,which requires more in depth research abt the drug.
Long term use can be highly detrimental to the organs though ,hence use with caution.

 

[halfwit]

Halfwit thnx a lot! I just had to go brush up my theory and I think this is how stuff works. I believe this is why tren shuts down endogenous testosterone and causes gynecomastia with hyperprolactinemia.


See,progestins are drugs tht mimics/similar to the function of progesterone. Like, trenbolone. Which is a progestin derivative.


Now,going back to the very basics.

In (non hormonally altered) males aka normal healthy males ,
Testosterone is produced from cholesterol And in between, there r many steps. I'll simplify

step 1.
PROGESTERONE is CREATED from CHOLESTEROL

Step 2.
This Progesterone is converted to 17 alpha hydroxyprogesterone which is converted to ANDROSTENEDIONE. Part of this is also converted to E1 and E3.(both derivatives of estrogen only)

Step 3. This ANDROSTENEDIONE is converted to TESTOSTERONE,
a part of which in the presence of 5-alpha reductase is converted into DHT.

Step4. excess TESTOSTERONE gets converted to estradiol (E2) by the action of aromatase.


Normally, if thrs extra testosterone, it gets converted to estradiol by aromatase and this estradiol is sensed by the pituitary and tells d testes to stop testosterone production by decreased LH levels. Once balance has been achieved, Testosterone production commences.




But u see,the problem here is we're administering tren, a progestin.(lets assume quite a big dose alryt)

Increased dosage of progesterone, suppresses LH levels which brings down testosterone levels to a hault.

This is why I believe trenbolone goes hard on the testicles.

And u see,
Progestins at high doses, without an aromatase inhibitor like anastrazole (see step 4) converts to E2 and further suppresses the LH, credits to the HPTA.


And at high serum levels of estradiol, as halfwit said, it messes up with the dopamine mechanism and prolactin is released by the ant.pituitary.

Ppl who r sensitive now begin to develop breast tissue and lactate.(synergistic action of prolactin, estradiol and progesterone)

Aaand,Prolactin increase means in a normal male, decreased endogenous testosterone, implies a flaccid penis.literally.

So how to fix,
1. Stop taking the progestin /tren which wud be a no.

Or
2. Aromatase inhibitors -anastrazole 0.25mg a day along with exogenous testosterone, TRT dose should be safe I suppose.
+
3.cabergoline 0.5mg per week.
Or bromocriptine or pramipexole..
(better safe than sorry ryt) . And tht too depends on the individual, as many folks here mentioned.

In short, I cn conclude a proper knowledge abt the drug being used and decent dosing and a reasonabe duration along with adequate precautions can in fact be beneficial for the bodybuilding community rather than dng a few more cycles to understand more abt tre.. one needs to know how to properly use them and reap the gains,which requires more in depth research abt the drug.
Long term use can be highly detrimental to the organs though ,hence use with caution.

You're close. I have to head off in a few, so I don't have the time to hit every point - but here's the major ones, and why waiting until later is beneficial for you.

1. Progesterone doesn't convert to estradiol. It's just an agonist, that can tell the hypothalamus that more estradiol is needed. The funny thing is that while the negative feedback loop is engaged (you're correct in that progesterone can signal this too), only the call for more aromatization is sent - LH remains turned off as exogenous androgens themselves trigger the feedback loop. Assuming that there is only tren involved, the amount of estradiol created will actually be quite small, and likely not enough to cause gynecomastia.

2. Prolactin cannot create gynecomastia. Only estradiol or a select few drugs can. This is why 19-nors are often a great compliment or a DHT derivative, as they do not add to the estradiol equation in and of themselves. Prolactin just allows for the breast tissue to lactate, as mentioned.

3. Trenbolone is a special progestin in that it has nutrient partitioning capabilities. Lipolysis is more of a function of this than a thermogenic property - this also means that it can potentially cause cholesterol issues. Tren causes sweats (the leading theory anyway) due to a sympathetic nervous system reaction. It's most noticeable at night, because this is when circadian rhythms dictate our state - which is interrupted by tren.

Loss of ability with cardio has been attributed more to the prostaglandin issues wrecking havoc with alveoli in the lungs, although co2 isn't a terrible guess. I have never seen it elevated in blood testing though. Most AAS does (at higher doses) have this effect (among others) in aldosterone, which I agree, is a part of the blood pressure problem. However, estradiol control is usually the culprit, as elevated e2 causes water retention - > hypertension.

In conclusion, the reason why you're being advised to wait isn't because of your lack of pharmacokinetics or understanding how the HPTA works. It's because tren has a very serious impact on mental stability. Add this to the unique issues that progestins can bring to the table - and you have a recipe for disaster. Knowing how you react on nandrolone first, for example, will help prepare you for some of what tren can bring to the table. Having the ability to inject oneself with a degree of proficiency will also come from experience - which is vitally important to keep from panicking when you first experience "Tren cough". There are just so many things that tren can do, it's really in everyone's best interests to experiment with other compounds, build up some experience (for instance, do you KNOW how much AI you would need for your test dose?) and then you should try trenbolone.

Tren is a fantastic hormone; but if it's not treated with respect, it will very certainly ruin your day.