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There is a method of prostaglandin production whereby prostaglandins made from one pathway in particular happen to dictate some muscle constriction as well as platlet aggregation, while the other method of production dictates bronchial constriction, and this could possibly be the means by which Tren Acetate causes that vicious cough. The reason why though this is speculation the enanthate version doesn't cause this rapid rise in prostaglandins is because of its more steady release, and my body's ability to gradually acclimatize itself to this. If you look at the graphs in the Minto studies (in the Deca profile), you'll see that the rise and rapid peak in blood plasma levels afforded by short esters are profoundly higher than those provided with longer esters, and it's my belief that the enanthate ester provides a lower peak level and less rapid rise in prostaglandin levels, especially the ones which dictate that second form of prostaglandin release which causes bronchial constriction. I feel that this bronchial constriction never really leaves you while you use any form of Tren, and this is what causes the shortness of breath experienced by many athletes on Tren.