Twisted Stick
New Member
Anybody figure out a way around the Tren cough? I have read Bill Roberts article/post on this and have tried to keep the outside of the pin clean of the Tren when removing air but haven't had much luck with the hack.
MESO-Rx
Anabolic Steroids
Tren cough
- Thread starter Twisted Stick
- Start date
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New Member
I just avoid Tren A ; I used Tren E only ... no cough. I've been using only Tren E with Test E in my once a year cycle for five years and never had the cough.
When I got interested in trying Tren I researched it and read you just don't get the cough from Tren E ... and so far, so good
That's over a five year period and many different suppliers.
When I got interested in trying Tren I researched it and read you just don't get the cough from Tren E ... and so far, so good
That's over a five year period and many different suppliers.
1) Use no more than a 50% MIX of Tren and another AAS
2) Inject SLOWLY, over 30 sec (using a 25guage needle is helpful for those in a "hurry")
3) Inject no more than ONE and a HALF cc per pin site
IF you do ALL THREE "Tren cough" resolved, IME!
2) Inject SLOWLY, over 30 sec (using a 25guage needle is helpful for those in a "hurry")
3) Inject no more than ONE and a HALF cc per pin site
IF you do ALL THREE "Tren cough" resolved, IME!
Never once had tren cough. Always used 28 gauge insulin pins with a half mL barrel. Low volume and no sides
viperbluelx
New Member
If pinning more than two compounds, draw the tren up first then your other last. Then there's no tren in the tip of the pin.
I doubt that having any Tren on the pin tip will make any difference since the amount of Tren there is miniscule to that which is contained in the syringe.
Oh p[inning Tren subcutaneously is another means of reducing "Tren cough" and in many instances completely eliminating it!
Oh p[inning Tren subcutaneously is another means of reducing "Tren cough" and in many instances completely eliminating it!
OhNoYo
New Member
Try injecting Trenbolone in deltoids only, instead of gluteals. That lowered that % I got tren cough, but unfortunately didn't resolve it completely.
viperbluelx
New Member
You're probably right. I was told tren in the tip of the pin got into the bloodstream when you nick a vein inserting the pin and that tren hitting the bloodstream causes the cough?
Oh, BULLSHIT!
Goodness think about that one, how else does Tren work on those muscles distant to the injection site if it DOES NOT enter the bloodstream, LOL?
Tren in some way is annoying the pulmonary tree which results in the cough. The rate of injection effecting the cough frequency suggest it's a form of chemical irritant. Perhaps the Tren and it's attached ester is causative ? It is also possible Tren could be forming a weak "dipolar bond" with another endogenous substance, after the ester is cleaved, during transit creating the cough. MY PERSONAL OPINION, once Tren exits the IM injection site it enters the bloodstream where it's ester is rapidly cleaved, (although less likely, it COULD also form a loose "dipolar bond" with some other substance before or after ester dissociation) and providing the concentration is adequate, activates enumerable chemoreceptors simultaneously within the lung parenchyma resulting in the cough. I suspect all of those suggestions I've listed to decrease "Tren cough" are likely to be effective because they lessen ABRUPT alterations in serum concentrations, thus reducing concomitant chemoreceptor activation. This assertion seems reasonably intuitive considering the cough is also reported as more severe and with a higher frequency with acetate compared to enanthate ester. The former ester being more readily removed by "esterase enzymes" exposing the parent anabolic agent allowing synchronous receptor agonism.
I'm curious, OhNoYo, why do you believe Deltoid VS Gluteal injection may lessen the cough, considering my commentary?
Goodness think about that one, how else does Tren work on those muscles distant to the injection site if it DOES NOT enter the bloodstream, LOL?
Tren in some way is annoying the pulmonary tree which results in the cough. The rate of injection effecting the cough frequency suggest it's a form of chemical irritant. Perhaps the Tren and it's attached ester is causative ? It is also possible Tren could be forming a weak "dipolar bond" with another endogenous substance, after the ester is cleaved, during transit creating the cough. MY PERSONAL OPINION, once Tren exits the IM injection site it enters the bloodstream where it's ester is rapidly cleaved, (although less likely, it COULD also form a loose "dipolar bond" with some other substance before or after ester dissociation) and providing the concentration is adequate, activates enumerable chemoreceptors simultaneously within the lung parenchyma resulting in the cough. I suspect all of those suggestions I've listed to decrease "Tren cough" are likely to be effective because they lessen ABRUPT alterations in serum concentrations, thus reducing concomitant chemoreceptor activation. This assertion seems reasonably intuitive considering the cough is also reported as more severe and with a higher frequency with acetate compared to enanthate ester. The former ester being more readily removed by "esterase enzymes" exposing the parent anabolic agent allowing synchronous receptor agonism.
I'm curious, OhNoYo, why do you believe Deltoid VS Gluteal injection may lessen the cough, considering my commentary?
viperbluelx
New Member
It's my understanding tren cough usually starts with a metallic taste in the back of your throat and most get it right after pulling the pin out. If the nicked vein theory is BS then why can guys pin tren daily for 10-weeks yet only get the cough randomly when pinning and not every pin?
I did my first run with tren a recently. I found that if I hit a blood vessel IE it bled a little when I pulled the pin out, I was much more likely to get a little cough.
I never got the metallic taste, or serious coughing.... And I have asthma too. All I really got was a heavy feeling in my chest, I'd take a few deep breaths and it would subside eventually. For me it was by FAR the least of the sides I encountered from tren.
I never got the metallic taste, or serious coughing.... And I have asthma too. All I really got was a heavy feeling in my chest, I'd take a few deep breaths and it would subside eventually. For me it was by FAR the least of the sides I encountered from tren.
tanuki
New Member
Might be the short ester. I get this tightness in my chest occasionally with test prop. A feeling of grasping for air and not getting enough. Then again its much rarer in my experience to get cough with powder than pellets.
On the plus side the cough means your supplier isn't ripping you off. I never got the night sweats and was worried.
On the plus side the cough means your supplier isn't ripping you off. I never got the night sweats and was worried.
Oh I've heard plenty of stories about Tren cough but I'm reasonably convinced the primary factor is an ABRUPT increase in Tren levels above baseline. Every mate whom has followed my 4-5 suggestion has the problem resolved , IME.
Well at least they don't mention it anymore suggesting their satisfied with the outcome.
Well at least they don't mention it anymore suggesting their satisfied with the outcome.
Twisted Stick
New Member
1) Use no more than a 50% MIX of Tren and another AAS
2) Inject SLOWLY, over 30 sec (using a 25guage needle is helpful for those in a "hurry")
3) Inject no more than ONE and a HALF cc per pin site
IF you do ALL THREE "Tren cough" resolved, IME!
Thanks DR. J. I did what you recommended with great results.:tiphat
4) And if that doesn't work subcutaneous injections will!
OhNoYo
New Member
Oh, BULLSHIT!
Goodness think about that one, how else does Tren work on those muscles distant to the injection site if it DOES NOT enter the bloodstream, LOL?
Tren in some way is annoying the pulmonary tree which results in the cough. The rate of injection effecting the cough frequency suggest it's a form of chemical irritant. Perhaps the Tren and it's attached ester is causative ? It is also possible Tren could be forming a weak "dipolar bond" with another endogenous substance, after the ester is cleaved, during transit creating the cough. MY PERSONAL OPINION, once Tren exits the IM injection site it enters the bloodstream where it's ester is rapidly cleaved, (although less likely, it COULD also form a loose "dipolar bond" with some other substance before or after ester dissociation) and providing the concentration is adequate, activates enumerable chemoreceptors simultaneously within the lung parenchyma resulting in the cough. I suspect all of those suggestions I've listed to decrease "Tren cough" are likely to be effective because they lessen ABRUPT alterations in serum concentrations, thus reducing concomitant chemoreceptor activation. This assertion seems reasonably intuitive considering the cough is also reported as more severe and with a higher frequency with acetate compared to enanthate ester. The former ester being more readily removed by "esterase enzymes" exposing the parent anabolic agent allowing synchronous receptor agonism.
I'm curious, OhNoYo, why do you believe Deltoid VS Gluteal injection may lessen the cough, considering my commentary?
Easy, experience. Read these two threads below if you are interested...
https://thinksteroids.com/community/threads/134287608
https://thinksteroids.com/community/threads/134289602
Meathead27 has had the same problem as I, provided here: https://thinksteroids.com/community/threads/134288845
The glute vs delt deal with trenbolone acetate isn't just something I made up, as others have told me they have had the same problem.
Now, I will break down your post to show you why some of it doesn't make any sense.
" Tren in some way is annoying the pulmonary tree which results in the cough. The rate of injection effecting the cough frequency suggest it's a form of chemical irritant. Perhaps the Tren and it's attached ester is causative ?"
Trenbolone isn't exclusive in causing this cough (read other highlighted posts above), as it has occurred with other AAS, it just appears that trenbolone acetate causes the most frequency & intensity of symptoms. Also, Idk what you mean being a chemical irritant. One would suspect if it is that quick of a chemical irritant to the lungs, then injecting IM would cause other irritation (e.g. skin) too, and may even result in anaphylaxis, but I've never heard of anyone going into anaphylaxis from trenbolone. Regardless, injecting fast or slow (unless as in slow you took hours), it would still irritate the lungs, and if it was irritating the lungs, then it would more than likely result in pulmonary damage, and there is no link that I know of between lung damage & trenbolone use.
" It is also possible Tren could be forming a weak "dipolar bond" with another endogenous substance, after the ester is cleaved, during transit creating the cough."
This makes no sense whatsoever and Idk how you came up with this idea. Any chemist or biochemist will tell you the same thing.
"Goodness think about that one, how else does Tren work on those muscles distant to the injection site if it DOES NOT enter the bloodstream, LOL?"
Trenbolone Cough (at least the cough I am referring to) comes up very quickly, in mere seconds to a couple minutes at most, and only lasts a few minutes. The compound being discussed isn't trenbolone base, it has an ester which prolongs half-life, and even if it was base, "work on those muscles distant to the injection site..." still wouldn't matter (see my comment below this one).
" MY PERSONAL OPINION, once Tren exits the IM injection site it enters the bloodstream where it's ester is rapidly cleaved, (although less likely, it COULD also form a loose "dipolar bond" with some other substance before or after ester dissociation) and providing the concentration is adequate, activates enumerable chemoreceptors simultaneously within the lung parenchyma resulting in the cough. I suspect all of those suggestions I've listed to decrease "Tren cough" are likely to be effective because they lessen ABRUPT alterations in serum concentrations, thus reducing concomitant chemoreceptor activation. This assertion seems reasonably intuitive considering the cough is also reported as more severe and with a higher frequency with acetate compared to enanthate ester. The former ester being more readily removed by "esterase enzymes" exposing the parent anabolic agent allowing synchronous receptor agonism."
I hope you're not stating here that tren cough occurs due to AR activation from trenbolone. This makes no sense whatsoever. First off, if that were the case, people would have the cough consistenly while on-cycle. Secondly, as I briefly hinted upon earlier, tren cough happens very quickly, but the way AR work in regards to binding, translocation, gene expression regulation, dissocation, etc, these and the other many processes that go with it take hours, not nearly how long it takes for tren cough to run its course. So your explanation and the abrupt increase in serum concentrations make no sense and the chemoreceptor part didn't make much sense anyway. I will admit though that trenbolone enanthate isn't a big culprit with the tren cough, I thought this may be due to maybe cuz it is known to be raw powder and tren ace coming from pellets sometimes (so possibly being contaminated), but I know of tren cough occurring with both acetate raw powder & pellet formulations. Plus I'm with you on injecting slowly, as I could always have that "metallic taste" in my mouth, I knew to slow or even stop the injection, cuz if I keep going, tren cough was gonna get me!
Unfortunately though, maybe no 1 will know how this cough & horrible symptoms occur, as it is really all speculation by our part, as no peer-reviewed literature, as far as I know, has published a study on the MOA. My best bet is that it may have to do with some type of prostaglandin activation, as these act extremely quickly in the body, but this is really just a guess on my part. If one would think if it was some type of allergic hypersensitivity, it would very most likey occur with every injection, and if anaphylaxis did occur then there is a mortality rate with that, but I've never heard of any1 dying from "tren cough", so I think this can be thrown out as a possible option.
Please provide a summary why my comments "don't make sense" oh and incidentally the AAS cough IS ALMOST ENTIRELY EXCLUSIVE TO TREN!
I don't know what the connection threads are there to demonstrate, people are different duh. The deltoids should and do make a difference because the perfusion is lower compared to the glutes. Moreover the abrupt absorption of Tren is eliminated when administered subq, try it and see if ya get the cough......NOPE. I never said or implied the cough was an IgE mediated "allergic reaction" (absurd) which may be activating the lung CHEMORECEPTORS, but a chemical reaction since this also occurs with ACE inhibitors and is a relatively common side effect of that anti hypertensive ,,look it up fella! If you've got a better means of explaining the cough, post it, I'm all ears. Also post how to reduce the cough since what I've suggested WORKS!
Oh and incidentally my undergraduate degree was chemistry and the relatively weak dipolar bonds are quite common physiologically especially in enzymatic reactions. Even though it don't believe this is the causative mechanism as I STATED it's not implausible.
Apparently you are not aware attaching varied esters increased the half life PRIMARILY by keeping the anabolic well contained within MUSCLE. Because once the anabolic is reseased into the bloodstream the enzyme esterase separates the ester from the AAS allowing the anabolic to enter the cell or attach to the androgen receptor (NEITHER OF WHICH CAN HAPPEN UNTIL THE ESTER IS REMOVED)! This may indeed account for the the higher incidence of Tren cough with acetate compared to enanthate because the acetate is cleaved much faster than enanthate once they enter the blood stream, which occurs to some extent in every IM injection.
You apparently are also not aware the lungs contain various receptors juxtaposed between the capillary bed and the bronchial epithelium, thus they can be activated by external chemicals (smoke) or internal chemicals such as ACE inhibitors or in this instance Tren! I was referring to the pulmonary chemoreceptors NOT the androgen receptors activation as Tren passed through the lung, since the latter are obviously quite limited there.
Apparently you are not aware attaching varied esters increased the half life PRIMARILY by keeping the anabolic well contained within MUSCLE. Because once the anabolic is reseased into the bloodstream the enzyme esterase separates the ester from the AAS allowing the anabolic to enter the cell or attach to the androgen receptor (NEITHER OF WHICH CAN HAPPEN UNTIL THE ESTER IS REMOVED)! This may indeed account for the the higher incidence of Tren cough with acetate compared to enanthate because the acetate is cleaved much faster than enanthate once they enter the blood stream, which occurs to some extent in every IM injection.
You apparently are also not aware the lungs contain various receptors juxtaposed between the capillary bed and the bronchial epithelium, thus they can be activated by external chemicals (smoke) or internal chemicals such as ACE inhibitors or in this instance Tren! I was referring to the pulmonary chemoreceptors NOT the androgen receptors activation as Tren passed through the lung, since the latter are obviously quite limited there.
