Tren . What do you guys personally notice/get from it

[IMT staff]

activity

 

[IMT staff]

I see your sneeky advertizing tactics now

Don't worry its good for everyone. We need more dialogue, activity breeds activity

Cheers

 

[THE-DET-OAK]

I don't agree. Most of the magic is tied the androgens and the elevated thyroid functions. I've seen the elevated side for progesterone when no other compound were present. Its long been my hypothesis that to experience elevator progesterone you had to have elevated estrogen. For the first 10 years around here progesterone was avoided by blocking the estrogen. It was done very effectively or so we thought. times were different we have access to lab test that we didn't in the past.

EXACLTY! So this is my point, if Tren doesn't aromatize then how does PRL go up? Obviously they are taking another aromatizing compound. Because if Tren doesn't convert then it cannot directly or indirectly stimulate PRL.

SO thats what I am saying it is nothing like nandrolone.

 

[Dreaded Pirate Roberts]

EXACLTY! So this is my point, if Tren doesn't aromatize then how does PRL go up? Obviously they are taking another aromatizing compound. Because if Tren doesn't convert then it cannot directly or indirectly stimulate PRL.

SO thats what I am saying it is nothing like nandrolone.

I don't know if we can go that far this is the most intelegent conversation in a while. I will invite some old timers with a backround in pharmacology and chemistry to weigh in.

 

[halfwit]

EXACLTY! So this is my point, if Tren doesn't aromatize then how does PRL go up? Obviously they are taking another aromatizing compound. Because if Tren doesn't convert then it cannot directly or indirectly stimulate PRL.

SO thats what I am saying it is nothing like nandrolone.

Yes, it's due to an aromatizing agent being present MOST of the time.

SO let's start with the pieces and see if I can't put this together to help understand how this works a bit better.

For starters, prolactin is a hormone that is primarily controlled by one other hormone - dopamine. I'll link the educational paper in a minute as it becomes more relevant to the quotes below:

Decreased dopamine or PIF release or transport or interference with dopamine binding. Commonly used drugs such as phenothiazines, tranquilizers, opiates (B enkephalin and morphine), reserpine derivatives, amphetamines, estrogens (BCP) can interfere with dopamine metabolism and result in galactorrhea. Numerous drugs interfere with dopamine secretion (Table 1). The same principles utilized in the management of pituitary microadenomas or hyperplasia can be applied in these situations. If discontinuation of the drugs is feasible, resolution of hyperprolactinemia is uniformly prompt. Stress, trauma, surgery, and marathon running can reduce hypothalamic dopamine release. Galactorrhea can also occur after pituitary stalk section or with a hypothalamic or pituitary condition blocking dopamine transport (Tables 1 and 2).

This snippet also lends credence to how the well known issue with tren decreasing thyroid may also play a role..

Elevated TRH, which acts as an enhancer of prolactin release. TSH is the most sensitive method to evaluate for hypothyroidism. Occasionally, patients with hypothyroidism exhibit hyperprolactinemia with remarkable pituitary enlargement due to thyrotroph hyperplasia. These patients respond to thyroid replacement with reduction in pituitary enlargement and normalization of prolactin levels (34).

The bolded establishes WHY prolactin elevates; now I just need to tie in how prolactin becomes such an issue while on a progestin (19-nors). While tren and deca act slightly different, it should be noted that deca (as an aromatizing agent) has the ability to increase prolactin by itself, without any help.

Source.

Next, we need to define exactly what progestins are. We read about them all the time, and know that tren/nandrolone belong to this class of hormones - but I think the community could use a definition.

Progestins are synthetic progestogens that have progestogenic effects similar to those of progesterone. The two most common uses of progestins are for hormonal contraception (either alone or with an estrogen), and to prevent endometrial hyperplasia from unopposed estrogen in hormone replacement therapy.

Forgive the use of Wikipedia, but it was an easy reference to cite.

So, we've established that estradiol and decreased thyroid output can diminish dopamine - which is an antagonist to prolactin. Now how does progesterone (or more specifically progesterone mimetics) play into this?

This is where it gets interesting. According to this study (animals, but mammals, and I'll look for a better one in a minute) BOTH estradiol AND progesterone are needed to significantly induce prolactin response.

E alone had little effect on serum prolactin levels, but E+P significantly increased prolactin as compared with ovariectomized controls. The BE levels increased with E treatment and remained elevated with E+P treatment in MBH and POA. The BE content was stimulated in DMH and MB by E+P treatment and not with E alone.

Source

This next quote adds information that I was unaware of, but I feel is relevant:

As a matter of fact, one study conducted on female lambs involved the administration of Trenbolone along with Estradiol (E2) and another group of lambs with Estradiol-only, which resulted in the expected effect of Prolactin increases as a result of Estradiol, but the Trenbolone + E2 group experienced an anti-Estrogen effect from Trenbolone, preventing the mammary stimulus of Estrogen[1]. This is hardly surprising, considering it is common knowledge that androgens can and do decrease the number of Prolactin receptors in the body as well[2] (especially strong androgens such as Trenbolone).

So tren being such a powerful androgen works against us? Whoa. Source

Another effect that plays into this is how progestins can actually INCREASE the sensitivity of estrogen receptors. Oddly, this is something that progesterone itself doesn't do, but as progestins are structurally different, it's an unwanted effect as they're derivatives.

Bleh, I was digging for a good link to substantiate the last paragraph, but I'm being told by the warden... Errrrrrrrrr.. wife, that it's dinner time. Hopefully that's enough to draw some solid connections and shed some light on the topic at hand.

 

[THE-DET-OAK]

Right.....but Tren doesn't actually have any progesterone attributes, so it is pretty much labeled incorrectly. A progestin is just a synthetic progesterone. I don't think we can say a steroid that has a 100 less affinity to the PGR proves that it has progesterone like affects at all. If it were truly a progestin, wouldn't it have to have AT LEAST the same affinity to PGR as a progesterone?

Next you mention how Tren needs estradiol to cause prolactin to go up, the problem with that is Tren may have nothing to do with that at all. It could be all estrogen.

The other argument is that progestin activity actually stimulates PRL production. This is why its a problem on Deca, but with Tren it cant be an issue because it has next to no affinity to PGR.

So we are right back at square one, unfortunately I don't see anything in the above post that is contradicting to saying Tren is completely different than nandrolone.

100x less affinity is a lot. I want to say nandrolone has 3 times (trouble recalling I know its more) the affinity as progesterone.

I truly think this info started so long ago and no one ever questioned it because there are no human studies. But vet studies prove the low affinity to PGR.

I will think about some more and do some more digging tomorrow.

 

[halfwit]

I have to put a little one to bed, but I do believe that the chief metabolite of trenbolone has a very high affinity with the PGR. Let's see what you can find; I think it's called 17B-trenbolone or something along those lines.

 

[THE-DET-OAK]

Thats what I thought too until I read bill roberts explanation.

It does not in practice invalidate what I wrote though, although it might merit a statement of possibly being a very weak progestin, so weak that -- given its strong affinity -- its effect in vivo could well be to reduce the effect of endogenous progesterone, replacing it with much less activity of its own, for no net effect at all or even a reduction in net effect.

Or if there is some net increase despite this displacement, it's hard to see how it could be significant, as the potency is so low.

It's important to realize that the graph shown is on a logarithmic scale. Thus, being shifted a little to the right means being exponentially less potent.

Specifically, eyeballing the thing it appears that the EC50 of THG is about 10 to the negative 9.5 molar, or about 0.3 nanomolar; that of progesterone is about 10 to the negative 8.5 molar, or about 3 nanomolar; and that of trenbolone is about 10 to the negative 6.5 molar, or about 300 nanomolar.

So in other words, it was found about 100 times less potent than progesterone itself. (Much less potent because a much higher concentration was required for given degree of effect.)

Also this was in yeast cells transfected with human receptors. which may not necessarily correspond with what happens in humans or in human or mammalian cells, but quite likely does have reasonable correlation.

In contrast, as the affinity for the bovine progesterone receptor has been shown to be actually greater than the affinity of progesterone itself, the overall situation may be that trenbolone readily displaces progesterone, but is only 1/100th or so as potent. Thus potentially giving LESS progestagenic effect, if progesterone is present, due to displacing but itself being far less potent ~ Bill Roberts

Institut fr Physiologie, Research Center for Milk and Food Weihenstephan, Technical University Munich, Germany.

For the steroidal growth promoters trenbolone acetate (TBA) and melengestrol acetate (MGA) neither the complete spectrum of biological activities nor the potential endocrine disrupting activity of their excreted metabolites in the environment is fully understood. The potency of these substances in [3H]dihydrotestosterone ([3H]-DHT) displacement from the recombinant human androgen receptor (rhAR) and from human sex-hormone binding globulin (hSHBG) was evaluated. In addition, the potency for [3H]-ORG2058 displacement from the bovine uterine progestin receptor (bPR) was tested. For comparison, different anabolics and synthetic hormones were also tested for their binding affinities. For 17beta-trenbolone (17beta-TbOH), the active compound after TBA administration, an affinity the rhAR similar to dihydrotestosterone (DHT) and a slightly higher affinity to the bPR than progesterone were demonstrated.

 

[THE-DET-OAK]

OH I forgot about this one Just for more info:

Trenbolone has a high affinity ligand for the androgen receptor (Bauer, 2000; Wilson, 2002). In the Hershberger assay (in vivo), trenbolone is as potent as testosterone propionate in tissues that lack 5{alpha}-reductase but less effective at increasing weight of tissues with this enzyme (Wilson, 2002). The anabolic effect of trenbolone acetate, which is 8-10 times stronger than that of testosterone propionate (Neumann, 1976), is based on androgenic and antiglucocorticoid activity (Meyer, 1985; Danhaive, 1986).

 

[soldier74]

damn guys, i think my IQ went up a couple points after reading this thread!!
Great conversation. From now on, anyone that asks about tren, we should just direct them to this thread;-)

 

[halfwit]

The only problem with what Roberts is saying is that it's not only yeast (outside a system) and he's looking at the molarity of the hormone in comparison to progesterone. I don't think (this is reeeeally stretching my couple semesters of Chem) a comparison can be drawn like that as a progestin, by definition, will only mimic a substance - not necessarily replace or assume the role of it beyond the target substance.

I'll look some more later this evening too.

 

[THE-DET-OAK]

I agree sir But its all we got to go on lol Thats what makes it so interesting I think

 

[Dreaded Pirate Roberts]

I see the boss has been posting using this account again. I will see if I can offer anything to the thread.

I do see one statement that is incorrect so far. TSH is not the most sensitive means of measurement for thyroid hormones. The dr who set the TSH as the standard no longer supports it because of the negitive feedback loop and the coralation between t3,t4 and t2 much like the need to have a totall testosterone level free testosterone tested to fully understand the activity of the thyroid. Any test or study that draws conclusion to the thyroid activity based on TSH should be questioned. The standard has not been changed although the dialisis method has been recommded for over 10 years by Dr Tennant. ( I'm hypo and I happend to sit in of a presentation by Dr Tennant at a conference a few years ago)

In fact the effect that Tren has on the thyroid is the increased uptake of and processing of the thyroid hormones resulting in a elevated metabolism. This is a strong contributing factor in the body re - composition effects experenced by users. The fat loss and striations in musculature.

 

[DinoTexas]

After six weeks I've now developed a full time cough (just the past two days). I have no allergy issues or congestion, only a cough which feels to me is related to the Tren Ace. The cough doesn't come directly after injecting, I'm literally coughing all day at the moment - not terrible but definitely not normal either. I had three more weeks planned at 100 EOD. If it were you, would you dial back the dose to 75 eod or stop the cycle?

 

[darkwing86]

right now im running 140mg eod . aiming for around 500mg per week . started wednesday . so fun should start kicking in real soon haha

 

[Megatron28]

After six weeks I've now developed a full time cough (just the past two days). I have no allergy issues or congestion, only a cough which feels to me is related to the Tren Ace. The cough doesn't come directly after injecting, I'm literally coughing all day at the moment - not terrible but definitely not normal either. I had three more weeks planned at 100 EOD. If it were you, would you dial back the dose to 75 eod or stop the cycle?

The cough and the tren don't sound related to me.

 

[SoHo]

what do i get from tren? everything, because tren is the ultimate. lowers bodyfat, tighter midsection, vascularity, crazy strength, crazy sex drive (if you fucking run caber with it). i even grow on tren while eating at a caloric deficit on a daily basis. it even makes you better looking (your face).

i've run tren twice in the past, both times i built my way up to 700mg a week which is fucking insane because it drove me insane eventually. i just started tren again yesterday, this time at 350mg a week which i think i wont go past. when i was injecting 100mg of tren every single day i was so mentally unstable and irrational.

i think 700mg of TEST per week is a pretty high dose.. and tren is what like 5 times more anabolic and androgenic than test? for those who havent used it try to imagine what that does to your body and mind. i dont want that anymore. now i have a solid job and a serious girlfriend, and im afraid to lose those things just to look that much more ripped. im realizing that a little bit of gear goes a long way.

 

[cbburrr]

Great discussion guys. most of it is over my head, I think I'll have to read it a few more times.

 

[cbburrr]

As far as the impact on kidney function from tren, is it all related to dehydration?

 

[THE-DET-OAK]

It could be related to a rise in prostaglandins.

Also a few posts up thats what your cough could be.

Hypothetically if one were to take such a hormone, drinking water and adding singulair may help.

Trens causes rises in IGF and Prostaglandins. While IGF is a fairly well known substance in the bodybuilding world today, prostaglandins are fairly unknown in terms of formation and roles in the body.

Prostaglandins are made by two different pathways(Cyclooxygenase and Lipoxygenase), and considering prostaglandins are a group of about 20 lipid cells, they have contrary function; responsible for stimulating as well as alleviating inflammation(Inflammation stimulation is the rapid metabolism of them expelled through the bronchials), regulate blood flow to particular organs, control ion transport acrossmembranes, modulate synaptic transmission, induce sleep, mediate lipidrelease, and regulate metabolism is various tissue.

Cyclooxygenase and lipoxygenase pathways, compete with one another to form prostaglandins(as well as thromboxane or leukotriene-leukotriene being a bronchial stimulator). In the cyclooxygenase pathway, the prostaglandins D, E and F plus thromboxane and prostacyclin are made.

Thromboxanes are made in platelets and cause constriction of vascular smooth muscle and platelet aggregation Leukotrienes are made in leukocytes and macrophages via the lipoxygenase pathway. They are potent constrictors of the bronchial airways. They are also important in inflammation and hypersensitivity reactions as they increase vascular permeability.

Because trenbolone causes the rate of production of prostaglandins to rise, the corresponding rise in Leukotrienes causes inflammation in the lungs such as wheezing and shortness of breath.

Singulair (Montelukast), a common allergy medication, is a Leukotriene Modifier. It blocks the Leukotriene receptors in your lungs, eliminating trenbolone sides such as wheezing and shortness of breath.

Put simply, taking Singulair, or certain other Leukotriene modifiers will block the tren effects on cardio.

I do not suggest any therapeutic programs that are not monitored closely by a physician.

Thanks