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

[anzel]

Good discussion guys!

 

[drricz]

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.

A few corrections there,

1. In normal human males, this is how the normal biotransformation goes.
Cholesterol -->progesterone-->17alpha hydroxyprogesterone -->androstenedione -->testosterone (extra)which acted upon by aromatase converts to e2.
This e2 binds to the estrogen receptors on the pituitary which makes the pituitary think tht thrs extra progesterone and brings down the endogenous testosterone levels by altering the fsh n LH levels.
So technically progesterone does cconvert to estradiol.

But

Tren is an altered progestin (resistant to aromatase enzyme and 5alpha reductase) so there's absolutely no way its gna transform into Estrogen or DHT as u said

2. high Prolactin levels cn cause gynecomastia by making the lobular type tissues proliferate, it causes lactation and the body itself has a mechanism whn prolactin levels get high it automatically produces a negative feedback inhibition by altering dopamine receptors and bring prolactin to normal by being an antagonist to estradiol..

but here in trens case whr we add exogenous testosterone in higher doses ,normal just wudnt be enough. So an aromatase Inhibitor is necessary..

3. E2-->water retention due to action of angiotensinogen.
Hence AI is really necessary.

4.pCO2 levels aren't elevated, its depressed..And yes most certainly prostaglandins( especially PGE2,TNF alpha) messes with the alveoli and further makes breathing difficult as u said

5. Anastrazole itself is a very potent AI by itself and I've used it before (@ at times 0.25mg and 0.5mg daily when testosterone use was quite high) and had combated d e2 issues efficiently before so adjusting anastrazole levels should do the trick.

6.yes,cholesterol levels can be an issue which constant monitoring is required and adjustments gta be made.. And eating clean certainly matters,,foods with good hdl to ldl profiles..omega3,unsaturated fats frm peanut butter, fish oils etc.

Assuming
1.exogenous testosterone levels r not at whacky levels and with
2.proper use of aromatase inhibitors and
3.caber to deal with prolactin (in those susceptible ones),
this cycle can be made successful I believe.

Tnx a lot halfwit!!

 

[drricz]

For breast tissue formation(i'll include lobular tissues also)
There has to be(synergistic action alryt)
Increased
1. Estrogen
2. Progesterone
3. IGF
4. GH
5. Prolactin (thts whr one starts to lactate)

Prolactin alone cant cause breast tissue development but can cause lobular tissues development, responsible for lactation.

progesterone in males is very less(1ng/ml)
And in females, esp during their mid cycle cn be as high as 20ng/ml..


During pregnancy, their levels rise both estrogen and progesterone significantly but prolactin on the other hand is priming there,not in a significant amount to make any change.
But due to elevated estradiol and progesterone levels,breast tissue proliferation occurs..
But ryt aftr parturition, There is a.sharp fall.in progesterone which leaves a very high level of estrogen which is a prolactin agonist.. And lactation begins.

Ppl might wonder why a pregnant lady example here..
Tren being a progestin and with exogenous testosterone use without proper AI use,tht cn cause estrogen increase..(apart frm those ppl sensitive to progestins.)
This is very much similar to being in a "pregnant woman state"



Heard of witch's milk?
Its when the kid is delivered, upon nipple stimulation, tht newborn kid starts to lactate.. Just a lil.

Cz of?? Yes. prolactin .
Whn in d mothers womb,the placenta produces 3gonadotropins _estrogen and progesterone and one placental gonadotropin -prolactin.
Whn d kid is delivered, there wud be increased prolactin levels and kid starts to lactate upon nipple stimulation.. Eventually prolactin levels decreases and everything is back to normal.

If progesterone and estrogen levels are also high in d kid's circulation, tht along wid high prolactin levels, causes gynecomastia. With milk.
This is very normal and will revert as the hormone levels will rapidly fall back to normal levels.

So it all comes down to this.

Prolactin alone, causes lactation And lobular tissues development.

Added effect of progesterone and estrogen will cause gynecomastia. (there are many other drugs too,but here,its irrelevant)

Bringing in IGF and GH normally produced in the body(or even exogenous)
along with progesterone, estrogen and prolactin will make men develop gynecomastia.



For tren users, controlling e2 and prolactin levels(esp fr.those sensitive ones) cn be beneficial.