Tren cough

[DireWolf13]

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 Jim very informative. I will try these

 

[Dr JIM]

Three other options not included are
1) Use Enanthate rather than
the Acetate ester
2) Use a muscle group with lower blood flow. The order of INCREASING blood flow, unless recently exercised;
Deltoids < Quads (mid lateral region) < Gluteus medius < Gluteus Maximus
3) Avoid muscle groups which have been "exercised" in the past 24 hours
3) If all that fails, which hasn't been reported (to me) to occur this far sub-q injections WILL NOT!

 

[leoclaw79]

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?

There's less blood flow to the shoulders than to the glutes!

 

[Dr JIM]

Correct, which is why the question was parsed, according to MY post, as an effort to elicit pharmacodynamic insight.

 

[Dr JIM]

After reviewing you post once again OKOHNO it's clear your comprehension of human hemodynamics and neurologic reflex mechanisms is limited. For instance if you injected Tren (or any other AAS) into a site far removed from your lung, the foot for example, how long would it take to reach the pulmonary circulation once it enters the blood stream ......seconds........ and if that substance was a noxious chemical and significantly stimulated the pulmonary chemoreceptors such that a cough REFLEX was elicited how much time would lapse (having to pass through the afferent and efferent neural pathways) before the cough occured....seconds! All these physiologic processes combined would require NO MORE THAN FIVE SECONDS which it why the Tren cough often begins BEFORE the injection is finished and that DOES MAKE "SENSE", and is completely compatible with my earlier description and explaination of the "Tren cough", which you rebutted even though you apparently were not cognizant of the physiologic processes involved (which doesn't make sense)! I believe I've made painstaking efforts to express my theory and will await your exposition on why you believe "prostaglandins" may be causative.

 

[PillarofBalance]

If I feel it coming on I stick my head in the freezer and take slow shallow breaths thru the nose. Works for me

 

[MR10X]

I have done 4 cycles with Tren A which i made from the pellets,so it is very real. I always mixed it with Test,sometime E and some times Prop depending on where i was in my cycle,and EQ at 1 cc each. I always injected in my glutes slowly,sometimes i would get the metal taste and 1 time i got a minor cough.
My son also did the same as i gave him the shots and he got the metal taste quite a few times and one took his breath away but no cough. It seems people react diffent to tren and some get the cough and some dont,i definately believe doing the shot slowly helps.

 

[viperbluelx]

Prostaglandins

 

[Dr JIM]

Prostaglandins and Tren what data, NOT, but rather another BLOG hypothesis which is inconsistent with known physiologic processes. Additionally although someone read "Wiki" prior to scripting the post, no effort was made to attempting correlate their "theory" with diseases therapeutics relative to prostaglandins.
For instance, if prostaglandins were the mechanism responsible for the TREN COUGH why are their primary physiologic effects, bronchial smooth muscle constriction and or vasodilation NOT observed or reported during the cough!
Another example, although prostaglandins are responsible for the bronchial smooth muscle constriction in cases of reactive airway disease, yet comparatively, the cough stimulus or allergy in RAD is exogenous entering through the airways NOT the bloodstream (as is the case with Tren). Interestingly a direct hematogenous entry point is also noted in certain instances of anaphylaxis, such as a "wasp sting", (which does not explain the etiology either since NO PRIOR EXPOSURE is required for the cough to occur). Moreover corticosteroids (which decrease cycloxygenase and lipooxygenase by inhibiting arachidonic acid production) although quite effective in a variety of prostaglandin mediated disorder such as asthma, COPD, atopic dematitis etc, have no effect on reducing the Tren cough based on my observation of patients whom developed the Tren cough in spite of concurrent systemic glucocorticoid use!

 

[viperbluelx]

I'm curious what your opinion is for what happened to me. I was 12 days in pinning 100mg tren ace eod and my chest got tighter every day, more a tightening of my airway I think. It felt exactly like the exercise induced asthma I had as a teen but the feeling was constant. This was not something mild it was scary. I had to take ephedrine just to breath good and never had the cough. I was supposed to pin last night but I skipped it and this morning I was totally back to normal.

 

[viperbluelx]

I used my sons nebulizer with albuterol last night and I got some noticeable relief.

 

[MR10X]

This is from another forum:
I used to extract and purify the parent compound of the pellets. I also never ever bought premade from pellets as why would I trust that to someone else that I had no control or any knowledge of their process. LOL Other than the very first conversions I always used a crystallization as the final process. This way all I ever had was about as close are you could get to pure tren outside a real lab.
Even to this day I push all AAS thru .22 mic filters just to be safe. Only the AAS I get directly from my pharmacy does not go thru a filter. Take only a bit of time and adds little to over all costs.

Trenbolones possible connection to breathing difficulties and spastic cough from bronchial contractions and spasms. Here is the basic processes that could be the connection of tren to these specific issues.

The effects of trenbolone fat burning qualities in theory in part via prostaglandin formation. 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 across membranes, modulate synaptic transmission, induce sleep, mediate lipid release, and regulate metabolism is various tissue.

Prostaglandins are synthesized from arachidonate(Lipoxygenase which catalyze the dioxygenation of polyunsaturated fatty acids) in the cell membrane by the action of phospholipase A2. 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.

Being that prostaglandins from either pathway, are still fatty acids of a group, they mediate lipid release and control tissue metabolization, so fat burning is a luxury of either pathway of formation. . As prostaglandins made from the Cyclooxygenase pathway dictate muscle constriction and platlet aggregation, and the Lipoxygenase pathway dictates bronchial constriction(the main form of expulsion)

Now one possibility to how this ends up at the effect of decrease lung performance. Trenbolone causes the rate of production of prostaglandins to rise.

Leukotrienes are synthesized in the cell from arachidonic acid by 5-lipoxygenase. The catalytic mechanism involves the insertion of an oxygen moiety at a specific position in the arachidonic acid backbone.

The lipoxygenase pathway is active in leukocytes, including mast cells, eosinophils, neutrophils, monocytes, and basophils. When such cells are activated, arachidonic acid is liberated from cell membrane phospholipids by phospholipase A2, and donated by the 5-lipoxygenase-activating protein (FLAP) to 5-lipoxygenase.

5-Lipoxygenase (5-LO) uses FLAP to convert arachidonic acid into 5-hydroperoxyeicosatetraenoic acid (5-HPETE), which spontaneously reduces to 5-hydroxyeicosatetraenoic acid (5-HETE). The enzyme 5-LO acts again on 5-HETE to convert it into leukotriene A4 (LTA4), an unstable epoxide.

Leukotrienes cause allergy symptom in the lungs such as wheezing and shortness of breath. They also as stated above cause the contraction of smooth muscles one being the brochi (bronchial passage ways). This is what is responsible for continued bronchial constriction in asthma. They also indirectly release histamines.

The other possibilities is the correlation of the Cyclooxygenase pathways. Many recognize this by its acronym COX1 COX2 (like heard of COX inhibitors such as the infamous VIOX) They can casue inflammation. If this is targeted in the lungs there could not be the possibility of lung tissue inflammation.


So there you have a few possibilites on the processes as they may have a effect on breathing and even the infamous tren cough.



References:

Color Atlas of Pathophysiology 2010 By Stefan Silbernagl, Florian Lang

 

[OhNoYo]

This is from another forum:
I used to extract and purify the parent compound of the pellets. I also never ever bought premade from pellets as why would I trust that to someone else that I had no control or any knowledge of their process. LOL Other than the very first conversions I always used a crystallization as the final process. This way all I ever had was about as close are you could get to pure tren outside a real lab.
Even to this day I push all AAS thru .22 mic filters just to be safe. Only the AAS I get directly from my pharmacy does not go thru a filter. Take only a bit of time and adds little to over all costs.

Trenbolones possible connection to breathing difficulties and spastic cough from bronchial contractions and spasms. Here is the basic processes that could be the connection of tren to these specific issues.

The effects of trenbolone fat burning qualities in theory in part via prostaglandin formation. 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 across membranes, modulate synaptic transmission, induce sleep, mediate lipid release, and regulate metabolism is various tissue.

Prostaglandins are synthesized from arachidonate(Lipoxygenase which catalyze the dioxygenation of polyunsaturated fatty acids) in the cell membrane by the action of phospholipase A2. 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.

Being that prostaglandins from either pathway, are still fatty acids of a group, they mediate lipid release and control tissue metabolization, so fat burning is a luxury of either pathway of formation. . As prostaglandins made from the Cyclooxygenase pathway dictate muscle constriction and platlet aggregation, and the Lipoxygenase pathway dictates bronchial constriction(the main form of expulsion)

Now one possibility to how this ends up at the effect of decrease lung performance. Trenbolone causes the rate of production of prostaglandins to rise.

Leukotrienes are synthesized in the cell from arachidonic acid by 5-lipoxygenase. The catalytic mechanism involves the insertion of an oxygen moiety at a specific position in the arachidonic acid backbone.

The lipoxygenase pathway is active in leukocytes, including mast cells, eosinophils, neutrophils, monocytes, and basophils. When such cells are activated, arachidonic acid is liberated from cell membrane phospholipids by phospholipase A2, and donated by the 5-lipoxygenase-activating protein (FLAP) to 5-lipoxygenase.

5-Lipoxygenase (5-LO) uses FLAP to convert arachidonic acid into 5-hydroperoxyeicosatetraenoic acid (5-HPETE), which spontaneously reduces to 5-hydroxyeicosatetraenoic acid (5-HETE). The enzyme 5-LO acts again on 5-HETE to convert it into leukotriene A4 (LTA4), an unstable epoxide.

Leukotrienes cause allergy symptom in the lungs such as wheezing and shortness of breath. They also as stated above cause the contraction of smooth muscles one being the brochi (bronchial passage ways). This is what is responsible for continued bronchial constriction in asthma. They also indirectly release histamines.

The other possibilities is the correlation of the Cyclooxygenase pathways. Many recognize this by its acronym COX1 COX2 (like heard of COX inhibitors such as the infamous VIOX) They can casue inflammation. If this is targeted in the lungs there could not be the possibility of lung tissue inflammation.


So there you have a few possibilites on the processes as they may have a effect on breathing and even the infamous tren cough.



References:

Color Atlas of Pathophysiology 2010 By Stefan Silbernagl, Florian Lang

Looks like I may have been right all along, Jim...
From now on, please keep an open mind, Sir.