Very serious ARA question (not joking)

[b8audis4]

Hello I am looking to cut down but maintain lean muscle mass, I am 5'8 184 lbs and about 17 percent body fat. I have cut from 215 lbs but I have lost a lot of muscle and strength on the way.
My friend has given me the 50 day supply of X factor advanced and i very much would like to use it.. But I know it is a inflammatory product and i had astmah in the past when I was very younger i would like to know if it would be safe to take it now. Don't know if this product inflames internal organs as well as muscles

 

[b8audis4]

Any one have any expirence or knowledge of ARA being an inflammatory on internal organs???

 

[b8audis4]

No one ?��really wanted some
Info so I can take this

 

[Kickstart7]

Shoot a PM to Jiigzz

 

[mr.cooper69]

Arachidonic acid, through the cyclooxygenase pathway, will prevent formation of the plug involved in primary blood clotting. In the endothelium it will prevent platelet aggregation. As far as people being able to recognize organ inflammatory response, what you do mean? I am pretty sure none of us are able to notice a slight inflammatory response, or at least I am not aware of anyone with x-ray vision. As far as the asthma goes, you should be fine if you do not continue to suffer symptoms of asthma. When you have adolescent asthma I believe it would be fairly rare to have the issue resurface from dietary intake, however I am not 100% on that. If any other biomedicine/ biochem fellas would like to chime in it would be a learning opportunity for many on here.

Incorrect, ArA is also metabolized via COX-1, to produce TxA2 and its chief effect is actually clotting, not bleeding (hence why NSAIDs, aka non-selective COX inhibitors, lead to bleeding).

 

[Jiigzz]

Hello I am looking to cut down but maintain lean muscle mass, I am 5'8 184 lbs and about 17 percent body fat. I have cut from 215 lbs but I have lost a lot of muscle and strength on the way.
My friend has given me the 50 day supply of X factor advanced and i very much would like to use it.. But I know it is a inflammatory product and i had astmah in the past when I was very younger i would like to know if it would be safe to take it now. Don't know if this product inflames internal organs as well as muscles

I dont tend to recommend a product use IF there is a chance you could worsen your current state however with Ara its very individualistic. Some people get enhanced inflammation and some people wont. At least none they feel.

IMO you can give it a try (bearing in mind Ara is pro-asthmatic) and cease its use should things not go to plan. Taking a high dose of fish oil should help get rid of the Ara for you

 

[brundel]

Google is your friend.

 

[Jiigzz]

Jiigzz, if someone were to be affected adversely from AA with regards to pro-asthmatic response, how long would it be with supplementation where an effect could be noticed as I am unaware of the speed of metabolism? I appreciate the knowledge if you have more on this.

Also, would supplementation of Mega Gamma-Linolenic Acid aide the pro-inflammatory reduction with regards to the asthmatic effect, as it supports healthy production of pge-1 and Pge-1 is effective against histamine related bronchoconstriction. If I remember correctly histamine can induce aa release.

I woyldnt have a clue to specifics as to when you would notice the effect, but absorption occurs very rapidly after administration. I doubt very highly you would notice within a week but who knows.

Either of the w3s will aid in reduction as they both work against AA to reduce net inflammation through competitive inhibition, displacement and counter action. I wouldnt advise using GLA alongside AA unless you needed too

 

[furion]

This is a tricky question-
Different arachidonic acid metabolites can act as both bronchodilators (PGe2 PGi2) and bronchoconstrictors (PGd2 and Leukotrienes)
As asthma hypersensitivity responses and precipitants are variable and sometimes idiosyncratic- it would be difficult to determine your response.
Have you ever suffered asthma symptoms after taking an NSAID anti-inflammatory such as ibuprofen or diclofenac? If so I would err on the side of caution and potentially take a small dose of AA (maybe 250mg) and keep your reliever puffer handy.
You could also use a mast cell stabilising puffer such as nedocromil or sodium cromoglycate prior to taking the AA and exercising- in theory this should mitigate the release of the bronchoconstrictive metabolites in the airways- however once again I would try this with a smaller dose first.

 

[Jiigzz]

This is a tricky question-
Different arachidonic acid metabolites can act as both bronchodilators (PGe2 PGi2) and bronchoconstrictors (PGd2 and Leukotrienes)
As asthma hypersensitivity responses and precipitants are variable and sometimes idiosyncratic- it would be difficult to determine your response.
Have you ever suffered asthma symptoms after taking an NSAID anti-inflammatory such as ibuprofen or diclofenac? If so I would err on the side of caution and potentially take a small dose of AA (maybe 250mg) and keep your reliever puffer handy.
You could also use a mast cell stabilising puffer such as nedocromil or sodium cromoglycate prior to taking the AA and exercising- in theory this should mitigate the release of the bronchoconstrictive metabolites in the airways- however once again I would try this with a smaller dose first.

Strong first post welcome

 

[mr.cooper69]

Actions of AA are on page 6. https://www.google.com/url?sa=t&rct=j&q=&esrc=s&********web&cd=8&cad=rja&uact=8&ved=0CFQQFjAH&url=http%3A%2F%2Fwww2.courses.vcu.edu%2Fptxed%2Fm2%2Fpowerpoint%2Fdownload%2FWelch%2520AA%2520Cascade.PDF&ei=NFjSVKCUGYekNrnfgUA&usg=AFQjCNGunQppOjqF4mr5E63uCDVVh9-NTA&sig2=E7dcoPihnUA-fcYAFr_7cw&bvm=bv.85076809,d.eXY you only spoke of one branch of action. Next time before you call out incorrect, know your pathways completely please...

Blockade of ArA metabolism creates a bleeding diasthesis (see ANY NSAID) because ArA is prothrombotic. Yes, it is metabolized to anti-platelet prostanoids as well, BUT THE DOMINANT PATHWAY IN HUMANS is for thrombosis. This is the difference between knowing biochemistry and knowing human physiology. You likely have only learned one side of the coin in any appreciable detail

 

[mr.cooper69]

Basically, ARA is the primary fatty acid responsible for inflammation in muscle tissue. This 20-carbon omega-6 fatty acid resides in the cell membranes of our muscles, known as the sarcolemma. When your muscles are damaged by lifting weights, certain enzymes flock toward the affected area and "free" the ARA from the membrane.

When this happens, the freed ARA gets broken down and used to create small localized hormones called prostaglandins, which more directly cause the inflammation and pain we feel post-training. That may sound negative, but on the flip side, these inflammatory mediators also signal the body's repairing response in muscle tissue. Additionally, they play a critical role in increasing the amount of nuclei in our muscle cells, ultimately boosting muscle protein synthesis.

Prostaglandins have two derivatives: prostacyclins and thromboxanes. Prostacyclins are powerful locally acting vasodilators and inhibit the aggregation of blood platelets. Through their role in vasodilation, prostacyclins are also involved in inflammation. Prostacyclins are synthesized in the walls of blood vessels and serves the physiological function of preventing needless clot formation. Prostacyclins are responsible for regulating the contraction of smooth muscle tissue

Without the necessary local vasodilation the clotting factors serve no purpose for muscle swell/ repair/ growth.

No. Again, just no.

There are THREE metabolites: thromboxanes, leukotrienes, and prostaglandins. Thromboxanes are not a kind of prostaglandin. And prostaCYCLIN is just PGI2, not a whole category. You are correct about myonuclear accretion.

All in all, you have the knowledge, but it looks like you need to brush up a bit.

 

[mr.cooper69]

This is a tricky question-
Different arachidonic acid metabolites can act as both bronchodilators (PGe2 PGi2) and bronchoconstrictors (PGd2 and Leukotrienes)
As asthma hypersensitivity responses and precipitants are variable and sometimes idiosyncratic- it would be difficult to determine your response.
Have you ever suffered asthma symptoms after taking an NSAID anti-inflammatory such as ibuprofen or diclofenac? If so I would err on the side of caution and potentially take a small dose of AA (maybe 250mg) and keep your reliever puffer handy.
You could also use a mast cell stabilising puffer such as nedocromil or sodium cromoglycate prior to taking the AA and exercising- in theory this should mitigate the release of the bronchoconstrictive metabolites in the airways- however once again I would try this with a smaller dose first.

Someone is either in med school or a doctor

 

[heavylifter33]

I'll start popping the corn.

 

[mr.cooper69]

I was not speaking as to a singular primary function as you can see in my original post. Glad to see that you are knowledgeable and prefer to throw accusations around before politely explaining knowledge that you already have attained. Thank you for your concern and am glad to have you explain with capital letters allowing me to read in a larger format. Don't yell too much with your keyboard, I can't hear it. So you discredit all other pathways as to one primary pathway. That is like saying there are no other side effects from metabolism of a certain compound. Pure silliness my friend. No need to be heated about anything.

Do not assume anything, you have no idea of the vast expanse of my knowledge....

I have no reason to shine brighter for a single person whom I do not know, nor care to know.

I appreciate your clarification Mr. Cooper69. I also applaud your ignorance.

My post really wasn't heated at all and I'm attempting to be objective. On the flip side, your post here is loaded with negative remarks.

I wouldn't go around saying things like this though:

you have no idea of the vast expanse of my knowledge....

Just poor form to the outside reader

 

[mr.cooper69]

Eicosanoids: prostaglandins, thromboxanes, leukotrienes. My bad as to the confusion I should have noted that Eicosanoids. Yes I have been away from this world for quite some time because I was too busy taking care of dying people. My bad.... appreciate your knowledge, just not your literature.

There really isn't any ill intent with my posts. Capital letters are for emphasis of key points

 

[heavylifter33]

Well that was a waste of popcorn.

 

[Jiigzz]

I was not speaking as to a singular primary function as you can see in my original post. Glad to see that you are knowledgeable and prefer to throw accusations around before politely explaining knowledge that you already have attained. Thank you for your concern and am glad to have you explain with capital letters allowing me to read in a larger format. Don't yell too much with your keyboard, I can't hear it. So you discredit all other pathways as to one primary pathway. That is like saying there are no other side effects from metabolism of a certain compound. Pure silliness my friend. No need to be heated about anything.

Do not assume anything, you have no idea of the vast expanse of my knowledge....

I have no reason to shine brighter for a single person whom I do not know, nor care to know.

I appreciate your clarification Mr. Cooper69. I also applaud your ignorance.

Mr.cooper meant no ill, that I can assure you. Unfortunately correction in any form can come across as arrogance, however he is simply explaining how it works. In terms of biochemistry, pharmacology and other related matters he is one of the forums most respected members.

He does get a bit of flak for correcting/ debating but id much prefer he did as this is how we learn/ can offer up opposing views.