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The Arachidonic Acid Help Guide

Anyone heard of "iEnhanced" ArA? Seems like a good price, but I have never heard of this company.

Before everyone tells me not to risk it, use xf/xgels ect; I am using xgels already. Just curious and looking for opinions.
 

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Audioph1x said:
Anyone heard of "iEnhanced" ArA? Seems like a good price, but I have never heard of this company.

Before everyone tells me not to risk it, use xf/xgels ect; I am using xgels already. Just curious and looking for opinions.
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Considering you have no idea what % ara is in there (label jus says "arachidonic acid 350mg") I wouldn't buy it. It's a powder so chances are it's like 5-10% which would make it useless at the doses suggested.
 
booneman77 said:
Considering you have no idea what % ara is in there (label jus says "arachidonic acid 350mg") I wouldn't buy it. It's a powder so chances are it's like 5-10% which would make it useless at the doses suggested.
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Yup. With a powder you would have to take like 30 of those pills lmoa
 
booneman77 said:
Considering you have no idea what % ara is in there (label jus says "arachidonic acid 350mg") I wouldn't buy it. It's a powder so chances are it's like 5-10% which would make it useless at the doses suggested.
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Thanks man. Figured if it were any good, it would have been discussed here.
 
While running ABE+ARA+Tr1umph, is it okay to supplement with vitamin D+calcium tabs preworkout also? or is vitamin D preworkout + ara a bad idea?
 
Okay so this is my second time using ARA, the first time I did 1.5g pre workout but this time in just trying 1g, should that still be effective at ~200lbs?

Also, should I just take them 30-45 minutes pre workout with my OL Tr1umph? And if I've eaten within 1 hour of that time should I just take them with my warm up sets? So basically I should not eat about 1.5-2 hours before my workout, otherwise take it with warm ups?
 
rascal14 said:
Okay so this is my second time using ARA, the first time I did 1.5g pre workout but this time in just trying 1g, should that still be effective at ~200lbs?

Also, should I just take them 30-45 minutes pre workout with my OL Tr1umph? And if I've eaten within 1 hour of that time should I just take them with my warm up sets? So basically I should not eat about 1.5-2 hours before my workout, otherwise take it with warm ups?
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You'll know in a couple weeks if 1g is sufficient. I typically start there during the saturation period and around week 3 bump as needed if I'm not seeing the pumps/strength I expected. Its more personal than by body weight as some need more and some less depending on absorption.

30-45min pre if fasted is optimal, otherwise after warmups if fed.

you pretty much got it.
 
Zariph said:
While running ABE+ARA+Tr1umph, is it okay to supplement with vitamin D+calcium tabs preworkout also? or is vitamin D preworkout + ara a bad idea?
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Sorry, missed this one. You should be good to go with that protocol.
 
Will be giving ArA another go in about 3-4 weeks.
 
kbayne said:
May be OOS as of now I believe.
mw1
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Yes we should have it back in stock in a couple weeks . We changed the labels and it took a little longer to finalize than we expected which caused us to lose our spot in production.
 
I know one website that still shows it in stock. Not board sponsors though so I dunno if I can mention it here so I'll refrain for now
 
mw1 said:
Yes we should have it back in stock in a couple weeks . We changed the labels and it took a little longer to finalize than we expected which caused us to lose our spot in production.
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i was told the same by a rep at FB 6 weeks ago =(
 
ArA pumps are nice n deep like. Fukc. This thread is making me want to hit the 24hr gym just so I can dose my XGELS again lol.
 
Audioph1x said:
Yes sir. Would you be able to use xgels alongside a joint support or would it still be too much?
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You can. Just need to dose away from ArA. Which you shouldn't be dosing joint products close to training sessions anyways.
 
kbayne said:
You can. Just need to dose away from ArA. Which you shouldn't be dosing joint products close to training sessions anyways.
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Sorry, should have been clear. I was asking Misfit28 personally due to joint issues and concerns he had expressed.

But I appreciate it brother. You think 6 hours apart to dose EFAs should suffice?
 
Yep 6 hours is what I'd suggest to someone looking to dose both daily
 
mPGES-1 Inhitibtion

Hi,

Long time fan of this thread on Arachidonic Acid. Due to the fact I do not have more than 50 posts I cannot link to anything relevant, I've just included DOIs for the papers.

Also forgive me if this has been disucssed in depth previously here, I did attempt to search through the discussion first.

Following a the recent suppversity article on NSAID use in older subjects, I noticed an image detailing that PGE2 pathway leads to muscle atrophy. The image itself is actually from a slightyly older article (Effects of prostaglandins and COX-inhibiting drugs on skeletal muscle adaptations to exercise [doi: 10.1152/japplphysiol.00061.2013]).

Especially interesting is the quote - "Arachidonic acid supplementation increased muscle production of both PGs, but about twice as much PGE2 was synthesized compared with PGF2α"

So naturally I took a closer look at the affects of PGE2 on muscle (Prostaglandin E2 induces transcription of skeletal muscle mass regulators interleukin-6 and muscle RING finger-1 in humans. [doi: 10.1016/j.plefa.2013.02.004]]) and it looks like it is rather detrimental in terms of muscle hypertrophy.
So presumably if the PGE2 pathway is blocked then it should lead to further PGF2a production during exercise, leading to a better result with Arachidonic Acid.

I then took a look at what natural PGE2 synthase inhibitors exist (Identification and development of mPGES-1 inhibitors: where we are at? [doi: 10.4155/fmc.11.136]) most of which seem to be synthetic and the natural ones that do exist also exert an effect on COX (i.e. Curcumin, EGCG).

After a few more interesting papers and dead ends I came across Carnosic Acid (Carnosol and Carnosic Acids from Salvia officinalis Inhibit Microsomal Prostaglandin E2 Synthase-1 [doi: 10.1124/jpet.112.193847]).
The important part being
"Carnosic acid, but not carnosol, inhibited PGE2 biosynthesis in a physiologically relevant human whole-blood assay at low micromolar concentrations that can be achieved in vivo after oral administration. Neither the biosynthesis of other prostanoids than PGE2 nor the activity of cell-free COX-1 or COX-2 was markedly affected, suggesting a preferred interference with mPGES-1 underlying the suppression of cellular PGE2 biosynthesis."

It also appears to have good bioavilaibty (Carnosic acid [doi: 10.1016/j.phytochem.2014.12.026]) and is present in Rosemary. So it should be easy enough to extract, however Rosemary does contain other phytochemicals that likely would inihibit COX (i.e. Ursolic Acid) so a relatively high purity extract would be the way to go.

From what I can see mPGES-1 inhibitors are being actively researched now because they have been implicated in being used for rheumatoid arthritis. This may also suggest that inhibiting this pathway may also aid those who experience joint pain when using ArA.

Regards
Arctek
 
Arc said:
Hi,

Long time fan of this thread on Arachidonic Acid. Due to the fact I do not have more than 50 posts I cannot link to anything relevant, I've just included DOIs for the papers.

Also forgive me if this has been disucssed in depth previously here, I did attempt to search through the discussion first.

Following a the recent suppversity article on NSAID use in older subjects, I noticed an image detailing that PGE2 pathway leads to muscle atrophy. The image itself is actually from a slightyly older article (Effects of prostaglandins and COX-inhibiting drugs on skeletal muscle adaptations to exercise [doi: 10.1152/japplphysiol.00061.2013]).

Especially interesting is the quote - "Arachidonic acid supplementation increased muscle production of both PGs, but about twice as much PGE2 was synthesized compared with PGF2α"

So naturally I took a closer look at the affects of PGE2 on muscle (Prostaglandin E2 induces transcription of skeletal muscle mass regulators interleukin-6 and muscle RING finger-1 in humans. [doi: 10.1016/j.plefa.2013.02.004]]) and it looks like it is rather detrimental in terms of muscle hypertrophy.
So presumably if the PGE2 pathway is blocked then it should lead to further PGF2a production during exercise, leading to a better result with Arachidonic Acid.

I then took a look at what natural PGE2 synthase inhibitors exist (Identification and development of mPGES-1 inhibitors: where we are at? [doi: 10.4155/fmc.11.136]) most of which seem to be synthetic and the natural ones that do exist also exert an effect on COX (i.e. Curcumin, EGCG).

After a few more interesting papers and dead ends I came across Carnosic Acid (Carnosol and Carnosic Acids from Salvia officinalis Inhibit Microsomal Prostaglandin E2 Synthase-1 [doi: 10.1124/jpet.112.193847]).
The important part being
"Carnosic acid, but not carnosol, inhibited PGE2 biosynthesis in a physiologically relevant human whole-blood assay at low micromolar concentrations that can be achieved in vivo after oral administration. Neither the biosynthesis of other prostanoids than PGE2 nor the activity of cell-free COX-1 or COX-2 was markedly affected, suggesting a preferred interference with mPGES-1 underlying the suppression of cellular PGE2 biosynthesis."

It also appears to have good bioavilaibty (Carnosic acid [doi: 10.1016/j.phytochem.2014.12.026]) and is present in Rosemary. So it should be easy enough to extract, however Rosemary does contain other phytochemicals that likely would inihibit COX (i.e. Ursolic Acid) so a relatively high purity extract would be the way to go.

From what I can see mPGES-1 inhibitors are being actively researched now because they have been implicated in being used for rheumatoid arthritis. This may also suggest that inhibiting this pathway may also aid those who experience joint pain when using ArA.

Regards
Arctek
Click to expand...

I'm not too sure you comprehended the information you have read. As far as I understand- PGE2 is actually desired metabolite and you certain wouldn't want to restrict the AA metabolism to it. Most of the preliminary research that assessed inflammatory cascades as a mediator of muscle cell hypertrophy (using NSAIDs) first specifically identified PGE2 as a primary responsible prostanoid.
The discriminate mechanism of PGE2 as anabolic metabolite of AA has been described. It is proposed that it acts in a sort of secondary paracrine fashion by acting as a chemotaxic agent for macrophages which ultimately infiltrate the muscle cell and locally secrete myokines and cytokines responsible for the muscle cell regeneration.
Additionally, bio-converted PGE2 is most likely to be responsible for the vasodynamic effects (which are consistently reported through anecdote) through its direct action on the endothelium and induction of nitric oxide synthase.
 
furion said:
I'm not too sure you comprehended the information you have read. As far as I understand- PGE2 is actually desired metabolite and you certain wouldn't want to restrict the AA metabolism to it. Most of the preliminary research that assessed inflammatory cascades as a mediator of muscle cell hypertrophy (using NSAIDs) first specifically identified PGE2 as a primary responsible prostanoid.
The discriminate mechanism of PGE2 as anabolic metabolite of AA has been described. It is proposed that it acts in a sort of secondary paracrine fashion by acting as a chemotaxic agent for macrophages which ultimately infiltrate the muscle cell and locally secrete myokines and cytokines responsible for the muscle cell regeneration.
Additionally, bio-converted PGE2 is most likely to be responsible for the vasodynamic effects (which are consistently reported through anecdote) through its direct action on the endothelium and induction of nitric oxide synthase.
Click to expand...

Maybe I am reading it wrong? But from my reading its the PGF2a pathway - via PI3K/ERK/mTor[SUP]1[/SUP] that is the desired one and that the PGE2 pathway is not because it increases protein degradation[SUP]2[/SUP] likely via IL-6/MuRF-1[SUP]3[/SUP].

Which is why the recent studies on COX inhibition in older individuals is theorised to lead to increased hypertrophy as PGE2 is upgregulated in older populations:
"Specifically, the COX inhibitor appeared to reduce the negative effects of PGE2 on protein synthesis and degradation, working through established myokines and other cellular regulators of protein turnover"[SUP]4[/SUP]

If you are able to point out any papers that shows PGE2 having anabolic effects in muscle, it would be much appreciated as from my initial reading of the literature I couldn't see this.

Regards
Arc

1 Prostaglandin F2α stimulates PI3K/ERK/mTOR signaling and skeletal myotube hypertrophy [doiI: 10.1152/ajpcell.00549.2009]
2 Arachidonic Acid, Prostaglandin E, and F2a Influence Rates of Protein Turnover in Skeletal and Cardiac Muscle
3 Prostaglandin E2 induces transcription of skeletal muscle mass regulators interleukin-6 and muscle RING finger-1 in humans. [doi: 10.1016/j.plefa.2013.02.004
4 COX Inhibitor Influence on Skeletal Muscle Fiber Size and Metabolic Adaptations to Resistance Exercise in Older Adults
 
Arc said:
Maybe I am reading it wrong? But from my reading its the PGF2a pathway - via PI3K/ERK/mTor[SUP]1[/SUP] that is the desired one and that the PGE2 pathway is not because it increases protein degradation[SUP]2[/SUP] likely via IL-6/MuRF-1[SUP]3[/SUP].

Which is why the recent studies on COX inhibition in older individuals is theorised to lead to increased hypertrophy as PGE2 is upgregulated in older populations:
"Specifically, the COX inhibitor appeared to reduce the negative effects of PGE2 on protein synthesis and degradation, working through established myokines and other cellular regulators of protein turnover"[SUP]4[/SUP]

If you are able to point out any papers that shows PGE2 having anabolic effects in muscle, it would be much appreciated as from my initial reading of the literature I couldn't see this.

Regards
Arc

1 Prostaglandin F2α stimulates PI3K/ERK/mTOR signaling and skeletal myotube hypertrophy [doiI: 10.1152/ajpcell.00549.2009]
2 Arachidonic Acid, Prostaglandin E, and F2a Influence Rates of Protein Turnover in Skeletal and Cardiac Muscle
3 Prostaglandin E2 induces transcription of skeletal muscle mass regulators interleukin-6 and muscle RING finger-1 in humans. [doi: 10.1016/j.plefa.2013.02.004
4 COX Inhibitor Influence on Skeletal Muscle Fiber Size and Metabolic Adaptations to Resistance Exercise in Older Adults
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There are a few papers on this- but these are probably the most deeming.

As far I understand the theory behind the potential ergogenic/anabolic action of supplemental ARA is to influence the hormetic response of muscle inflammation. As such I'm not too sure whether extrapolating data using older adults as the models would be universally applicable to the populations that actually use it.

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This paper is probably the most comprehensive in terms of describing some of the muscle cell inflammatory hormetic/adaptive mechanisms.
 
How long does it take you guys to notice joint issues? I never did before but I'm three days in and my joints have been achy the past couple days. I'm not sure if it's the ARA or something else.
 
rascal14 said:
How long does it take you guys to notice joint issues? I never did before but I'm three days in and my joints have been achy the past couple days. I'm not sure if it's the ARA or something else.
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That's way too soon to notice anything. Typically it's two weeks or so for saturation to occur that you will begin seeing much of anything.

That said, I don't see joint issues until the last few days, if at all, on a 50day run. And usually only if I've been pushing the weights higher than normal.
 
booneman77 said:
That's way too soon to notice anything. Typically it's two weeks or so for saturation to occur that you will begin seeing much of anything.

That said, I don't see joint issues until the last few days, if at all, on a 50day run. And usually only if I've been pushing the weights higher than normal.
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I figured, I just haven't had any issues in a while and as soon as I started they came up! It must be the weather, lol
 
Zariph said:
almost finished my first bottle of ara 1g every wourkout day and dont feel anything, guess I should up my next bottle to 1.5g
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Not everyone will notice DOMS with ArA.

But IMO, 1.5 grams will yield greater results.
 
I may use this again to bulk with, I used it previously for a 50 day run 5 on 2 off for 10 weeks and found i maintained all strength and even gained 5 pounds during my PCT from an 8 week cycle of halodrol @ 100mg per day and trenavar @ 90mg per day. My calories were slightly below maintenance which i feel held back the effectiveness.
 
paul56778 said:
I may use this again to bulk with, I used it previously for a 50 day run 5 on 2 off for 10 weeks and found i maintained all strength and even gained 5 pounds during my PCT from an 8 week cycle of halodrol @ 100mg per day and trenavar @ 90mg per day. My calories were slightly below maintenance which i feel held back the effectiveness.
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It's good for just about everything, but I like it during a bulk. The last heavy rep for a double/triple is getting a little easier each day. I say go for it if you can find it.
 
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