Tren- Fat burning and "fina cough" both from prostaglandin metabolization

It's been widely disussed of Trens fat burning properties through 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.
So below, a brief dicription of prostoglandins and their role in fat burning, "fina cough", and why a person going through Tren administration can experience it's fat burning effects without the dreaded "Cough"

The term prostaglandin comes from the word-Prostate. The first prostoglandins were first dicovered in semen about the mid 1930's and it was thought that prostaglandins were made from the prostate. Since this time, it has been dicovered that most prostaglandins are not even constructed in the prostate.

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 "fina 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)


Refs:
Cackatoo Press
Columbia Encyclopedia 6th Edition
Science Daily Magazine

great info...awesome post bro..

Interesting...Good Post.

nice read

Very interesting read Pheedno.

Would it be safe to assume that by increasing the production of prostaglandins in the cyclooxygenase pathway and decreasing the production in the lipoxygenase pathway, that the anabolic/angdrogeninc effects of the tren could be increased while at the same time decreasing some of the side effects like the shortness of breath, fina-cough, and the congested feelings? This is interesting. I would like to see if there would be a way to change how these prostaglandins are produced.

As a second thought, maybe that is what THG is designed to do.

-moto

5-Lipoxygenase inhibitors are used in some asthma medsbut I don't know much on specific meds mechanism of action, and if effects through the cyclooxygenase are a possiblity


asprin and Ibuprofen are prostaglandin inhibitors as well, but, of the cyclooxygenase pathway.

Now that you mention it, I have heard that about aspirin and ibuprofen. I have inquired ebfore about the use of asthma drugs or inhalers in combating the breathing-related sides of fina, but was quickly advised to not try anything like this by the resident docs. I would still be curious to see if any other asthma treatment options would eb effective in reducing this particular type of prostaglandins.

-moto

Thanks Pheedno. Interesting stuff.

"Leukotrienes are made in leukocytes and macrophages via the lipoxygenase pathway. They are potent constrictors of the bronchial airways."


You wouldn't want a 5-Lipoxygenase inhibitors, you'd want a Leukotriene modifier.

http://asthma.nationaljewish.org/tre...eukotriene.php

http://asthma.about.com/library/weekly/aa062298.htm

http://www.familyallergy.com/therapy/leukotriene.asp

Thanks for the links Pheedno. I'm going to look into this more. There is nothing worse than not being able to breath while in the middle of a fina cycle.

-moto

let me get this straight, its specifically the constriction of the bronchioles that causes the cough? so it activates the same mechanism the lungs use to remove foreign particle?

I'm asthmatic and have some unconverted tren. Obviously I am concerned about tren cough so did a bit of research:

Series 1 & 3 prostaglandins (the “Good”) and Series 2 prostaglandins (the “Bad”). Obviously the 'bad' series 2 is what is going on. Here are the series 2 symptoms.

Increased vasoconstriction
Increased pain
Decreased endurance
Immune system suppression
Decreased oxygen flow
Increases cellular proliferation
Creates platelet aggregation (clotting)
Constricts airways
Increases inflammation

I don't know about some of these but do know that if you get yourself an albuterol inhaler and take a few puffs prior to injection it will help as it is used to prevent and treat wheezing, difficulty breathing and chest tightness Albuterol inhalation aerosol is also used to prevent breathing difficulties during exercise. Albuterol is in a class of medications called bronchodilators. It works by relaxing and opening air passages to the lungs to make breathing easier.