Quote Originally Posted by marcus300 View Post
Many years ago me and a friend discussed and researched why tren A seems to produce the cough far more than tren E, we came up with few reasons why but there was one what we debated alot over. There are two systems the body use's for circulation, systematic and pulmonary. The pulmonary takes the deoxygenated blood back to the lungs for oxgenation, when we inject part of the injection will be taken up into the capillarys where it heads back to the heart out of the left atrium to the lungs and are expelled co2 and waste products in this case BA. Tren A dissassociates with BA far more easily than other hormones or ester's ie enan,hex. Inject slowly this will slow down the solution hitting the lungs instead of hitting it all in one lump, Always aspirate you could hit a vein and then the hormone and solvents (BA) will hit pulmonary circulation far faster and you are likely to cough your head
Indeed.

Tren cough is also thought to be related to prostaglandin metabolization.

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 controll tissue metabolization, so fat burning is a luxerry of either pathway of formation. It's the pathway from which they are constructed that dictates tren cough. 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)

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