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I'm on Phosphatidic acid Ya'll

kissdadookie said:
Dr. Stout has suggested that regular soy lecithin is good to go as your PA source. The Fearn lecithin granules seems to be the way to go as the PA (amongst other phospholipids) have been standardized to a high content in that product. It's like $8 for 30 days.
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Are you gays saying this fearn Lecithin granules are a real good and cheap source of phosphatidic acid and all those New supps around PA are totally overpriced then?
 
Royd The Noyd said:
Were stout and wilson saying this when Chemi Nutra was funding their research?
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Nobody asked back then.

The actual study doesn't mention Mediator either iirc or what sort of PA apart from that which comes from soy appears to be vastly superior for mTOR to egg PA, most likely due to being unsaturated and thus having a different molecular structure to that of egg PA (referenced in the study, in the section with the cell culture mTOR chart and discussions section).

Stout was also smart enough to not mention bulk soy lecithin as a source when people asked what was the best source for PA on the tnation Q&A thread for Micro-PA. So it appears that people didn't really think about lecithin until recently when TheScience brought it up. Granted you mentioned it first asfaik on your podcast episode on the topic.
 
Scitec dropping a PA product.
 
This sounds like a ridiculous question...but how do you buy scitec products? Listed on their site are all their products but no ability to buy them. What am I missing?
 
Akagami said:
Any annedoctal accounts from people stacking ARA and PA on a bulk?
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ArA provided me with some expected strength gains and DOMS whilst PA has consistently kept my muscles fuller (this is my 3rd ArA run, I have not experienced ArA pumps ever personally).

Run one or the other for the first time to assess what is going what if both things are new to you.
 
NewAgeMayan said:
Yeah, funny you should mention that, I read it earlier on...very illuminating thread.
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Btw, just so you have some context. What Stout and Wilson were saying in the Q&A thread was prior to Wilson having done the study on sedentary people. The sedentary people study was never published but funded by ChemiNutra, it's obvious why it never made it to publication.

If you read the ChemiNutra Mediator patent as well as the discussion section of the published Tampa study, it is pointed out that they were hoping that PA would have mTOR effect on sedentary people so that it can hopefully be used as part of treatment for muscle wasting conditions. This was their hypothesis initially prior to them having completed the sedentary people study, based on how endogenous PA worked (intracellular). So the dosing on non-training days suggestions was likely based on their assumptions at the time that the supplemental PA may possibly work the way endogenous PA works by being incorporated into the cell membranes. This initial assumption however did not pan out in real world en vivo study.

It would be interesting to see if this failed sedentary people PA study had anything to do with the ChemiNutra patent having been nulled, or if it was due to infringing on previous art/work.
 
People who undertake resistance training are not sedentary though, correct? Sedentary people do not have the same MPS requirements as trainees, even when those trainees are having a day off? It seems to me that dosing PA on off days would still be beneficial in terms of maximising levels and MPS, no?

Also, there can be a difference between something being anti-catabolic, and something being pro-anabolic?
 
NewAgeMayan said:
People who undertake resistance training are not sedentary though, correct? Sedentary people do not have the same MPS requirements as trainees, even when those trainees are having a day off? It seems to me that dosing PA on off days would still be beneficial in terms of maximising levels and MPS, no?

Also, there can be a difference between something being anti-catabolic, and something being pro-anabolic?
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Their theory on using it on off days to increase mTOR to enhance recovery is based on the theory that the PA will act at the intracellular level. At the time they did the Tampa strength training study, they have not yet done the sedentary people study (as the Tampa strength training with PA study even notes that sedentary people/muscle wasting should be investigated, implying they didn't have the en vivo data for that yet). They were still assuming that the PA may have the endogenous PA effect.

Think about how PA typically works. It actually doesn't need physical stimuli to act on mTOR (that was mentioned in the Q&A thread as well). It's a signaler and also attaches itself to mTOR. Based on that assumption of how PA works, it makes sense to take it at other times outside of the period in which physical stimuli is present (exercise), assuming that the PA would make its way to a significant degree into the phosopholipids pool of cells. Thus why the sedentary people study is of importance here, going by what is understood of how endogenous PA works, the sedentary subjects should have demonstrated increased anabolism from PA supplementation. Alas, they did not.

So IF you take the result of the sedentary people study along with Tampa's cell culture data AND previous cell culture data, it would become evident that the way supplemental PA works is that it will have the mTOR effects we are looking for WHEN it is available in circulation in your body (serum) around periods of physical stress (exercise) because that is the window in which PLA2 is present at the extracellular level (due to sufficient physical stress placed on cells, leakage basically).

Thus what Stout and Wilson were talking about 9+ months ago, that was when they did not have the results from the sedentary people study and thus assuming that PA supplementation may have significant intracellular activity to stimulate mTOR. Thus going by that logic, when you take it on off days and if it made it into cells to a significant degree, it should keep you more anabolic.

Another thing to note, notice what Stout was talking about when he talks about keeping serum levels high with PA around workout time. The reason this is suggested, again, is based on PLA2 being present at the extra cellular level to convert the PA to LPA. This is also likely why Wilson and Stout suggests higher PA doses may be better, because you now have more of it circulating giving you a higher percentage of PA converting to LPA.

PA is also not anti-catabolic. It's pro-anabolic in terms of what it does at the intracellular level as it is a signaler for mTOR (anabolism). Exogenous PA however is indirectly anabolic, it's actually providing the substrate for LPA, LPA engages ERK and that leads down in a cascade in which it will stimulate mTOR.

Leucine is also directly anabolic, it is indirectly anti-catabolic. The anti-catabolic activity is actually due to the increase in insulin. Insulin is anti-catabolic, leucine increases insulin release. Just an interesting tidbit for you there.

Also. note De__eB:

Saw your message. I did read the Tampa study thoroughly. Please note in that study they mentioned that investigation of PA's anabolic effects for the use of muscle wasting/sedentary populations should be conducted. At the time that Tampa strength training study was done, they did not have the data on sedentary subjects yet. Their theory on how it may work on sedentary subjects is actually based on the assumption that PA may make it into cell phospholipid pools. That did not pan out in the sedentary subjects study, which was never published since it was funded by ChemiNutra and one of their main bullet points in their patent (obviously it was never published because it didn't work, thus throwing the theory out the window at least for now, and it obviously doesn't look good for ChemiNutra to have a study disprove one of their talking points for Mediator, I'm guessing ChemiNutra owns the study and decides to publish it or not? or it may be that it's under peer review? this was months back that Wilson mentioned it on a podcast somewhere).
 
NewAgeMayan said:
lol dookie, i like how you read a rhetorical question as an oppurtunity to display your knowledge
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Nah, I've been following up with what you have been posting on the other board. Seems to be some confusion in regards to not fully understanding what Stout was talking about in the Q and A thread you were reading. Without the context, it would appear confusing and make it look like Stout and Wilson don't know what they are talking about. Thus I pointed out how the info on that thread preceeded the data that Wilson eventually ended up with for the sedentary people study.

Not trying to display super knowledge or anything. I'm just very obviously wordy :P I also like being detailed. Terrible flaws, I know.
 
ill have to come back to this later, but im really struggling to see how, in this context, the appropriate parallels can be drawn between sedentary people (and those with muscle wasting conditions) and resistance trainees...im not convinced wilson/stout would backtrack on that q and a, and even if they did, id question their reasoning to do so
 
NewAgeMayan said:
ill have to come back to this later, but im really struggling to see how, in this context, the appropriate parallels can be drawn between sedentary people (and those with muscle wasting conditions) and resistance trainees...im not convinced wilson/stout would backtrack on that q and a, and even if they did, id question their reasoning to do so
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If you look at how intracellular PA works, you will see why. intracellular PA engages mTOR independently from physical stimulus (exercise). The reason why physical stimulus is needed for intracellular PA is because the physical stimulus causes the PC in the phospholipids pool of cells to be converted to PA.

The idea of increasing intracellular PA is so that the PC -> PA step can be bypassed. So theoretically if you can increase PA in cells, it should increase anabolism independent of exercise (thus it's application for muscle wasting).

Also note, I'm not claiming that this is de facto and must be it, but going by the information currently available, it appears that PA supplementation works at the extracellular level and why Stout thinks so as well, along with Wilson. Of course no researcher in their right mind will say it's conclusive one way or another, that's not how science works. We can however say that it's likely to be this or that based on going through the information presently available to us.
 
kissdadookie said:
If you look at how INTRACELLULAR PA works, you will see why. INTRACELLULAR PA engages mTOR independently from physical stimulus (exercise). The reason why physical stimulus is needed for intracellular PA is because the physical stimulus causes the PC in the phospholipids pool of cells to be converted to PA.

The idea of increasing intracellular PA is so that the PC -> PA step can be bypassed. So theoretically if you can increase PA in cells, it should increase anabolism independent of exercise (thus it's application for muscle wasting).
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I know for sure i am taking my PA everyday ;)
 
Danes said:
I know for sure i am taking my PA everyday ;)
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I am as well. I'm using the expensive stuff too, haven't moved on to the SL yet :P Covering my bases of course, just in case it does something. Then again, I only have 1 day off from the gym per week.
 
kissdadookie said:
I am as well. I'm using the expensive stuff too, haven't moved on to the SL yet :P Covering my bases of course, just in case it does something. Then again, I only have 1 day off from the gym per week.
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I am waiting on Optima SL.. but right now i am doing like you , using the expensive stuff :) i do workout just 4 days per week but i do take PA everyday
 
Danes said:
I am waiting on Optima SL.. but right now i am doing like you , using the expensive stuff :)
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Yup. Ha ha ha. I will be trying Fearn in a few months, seems like the best one for bulk SL.

NewAgeMayan :

Interesting enough, the study Quadzilla99 posted on the other board also appears to show PA working via ERK (which again is at the extracellular level):

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Btw. 3 weeks in for Ara, Magnitropin and PA. (Week 1 of Ara, 3 RD for mag, and been on pa for 10 now) and I'm up 3.5 lbs since adding mag

Muscle fullness and pumps are stupid. Ara pumps are brutal with Magnitropin
 
Lol I don't refer Magnitropin to an epi product whatsoever. Its the vegetable side dish for the whole meal IMO (damn good analogy)
 
I allways gain weight.on PA even without adding more calories. Glycogen retention like u said KDD ..

But seriously,
To all of you who want to try PA , dont be affraid to increase the dosage.
Like i said before. 750mg PA was nothing to brag of but 1.5g and 2g was the thing!

Increased apetitte
Pumps
Musclefullness
Weightgain
Strength gain
Size

So if you dont feel anything from 750mg of PA, it would not hurt increasing the dosage
 
Swolbraham said:
Lol I don't refer Magnitropin to an epi product whatsoever. Its the vegetable side dish for the whole meal IMO (damn good analogy)
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Might give it a try... playing with laxogenin right now. One thing it is doing for certain, lowered my stim tolerance because the usual stim dosages these past few days feels like a little too much. So it's doing something that Humanofort did for me when I used the Humanofort for a few months.
 
kissdadookie said:
Might give it a try... playing with laxogenin right now. One thing it is doing for certain, lowered my stim tolerance because the usual stim dosages these past few days feels like a little too much. So it's doing something that Humanofort did for me when I used the Humanofort for a few months.
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Laxo is really amazing adaptogen which is damn good stack to other adaptogens such as ecdysteroids but pretty much good to stack with everything
 
kissdadookie said:
If you look at how intracellular PA works, you will see why. intracellular PA engages mTOR independently from physical stimulus (exercise). The reason why physical stimulus is needed for intracellular PA is because the physical stimulus causes the PC in the phospholipids pool of cells to be converted to PA.
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So you're saying it works independently of physical stimulus, and then saying that physical stimulus is needed?

The idea of increasing intracellular PA is so that the PC -> PA step can be bypassed. So theoretically if you can increase PA in cells, it should increase anabolism independent of exercise (thus it's application for muscle wasting).
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You have a fundamental misunderstanding of phospholipid metabolism, storage, accumulation, and release.

Also note, I'm not claiming that this is de facto and must be it, but going by the information currently available, it appears that PA supplementation works at the extracellular level and why Stout thinks so as well, along with Wilson. Of course no researcher in their right mind will say it's conclusive one way or another, that's not how science works. We can however say that it's likely to be this or that based on going through the information presently available to us.
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No, you can't say that's likely to be the primary way it works. The data does not support that.
 
De__eB said:
So you're saying it works independently of physical stimulus, and then saying that physical stimulus is needed?



You have a fundamental misunderstanding of phospholipid metabolism, storage, accumulation, and release.



No, you can't say that's likely to be the primary way it works. The data does not support that.
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I'm saying endogenous PA is produced when there is physical stimulus. Not that physical stimulus is needed for it to work. Look at the process for endogenous PA. It's PC -> PA when there is physical stimulus. PA is produced from PC endogenously.

The data actually does support what I'm suggesting. Twice. Thrice even if you count the unpublished sedentary subjects study. Four times if you count the hair growth study (which again, operates through the ERK pathway).

Previously, PA and how it works was essentially understood to be something that happens at the intracellular level. There was a later PA study in which they intended to go more in depth to see how PA works exactly at the cellular level. What they found was that the PA didn't do anything. It was odd. Later in that study they narrowed it down to the exogenous PA actually working at the extracellular level by converting to LPA. They found this out by inhbiting ERK to see what the PA would do, the PA didn't stimulate mTOR. Thus they learned that the exogenous PA actually worked on mTOR via ERK signalling, this is something that LPA is doing, which is how they eventually figured out that the PA was converting to LPA and then the LPA was activating ERK. This is confirmed again with the Tampa strength training and PA study, it's in the cell culture data (figure 1). As you can see in that chart, PS, PA, and LPA all activated mTOR similarly. Why does PS work? Because PS -> LPA by PLA2.

Read the Tampa strength training and PA study carefully. They mentioned intracellular PA and how that worked by also mentioning that it is how endogenous PA works. Not how supplemental PA works, though the possibility is of course there if supplemental PA accumulates to a significant degree in the phospholipids pool of the cells. It is due to this notion in which they suspected that supplemental PA may be a good candidate as a muscle wasting treatment (thus the study on sedentary people), however that did not pan out as planned.

Also look at the data for egg derived PA. It didn't work as well for stimulating mTOR. Why is that? Because it tends to get absorbed into cells as part of the PL pool (Stout notes this in the Q and A thread).
 
kissdadookie said:
I'm saying endogenous PA is produced when there is physical stimulus. Not that physical stimulus is needed for it to work. Look at the process for endogenous PA. It's PC -> PA when there is physical stimulus. PA is produced from PC endogenously.

The data actually does support what I'm suggesting. Twice. Thrice even if you count the unpublished sedentary subjects study. Four times if you count the hair growth study (which again, operates through the ERK pathway).

Previously, PA and how it works was essentially understood to be something that happens at the intracellular level. There was a later PA study in which they intended to go more in depth to see how PA works exactly at the cellular level. What they found was that the PA didn't do anything. It was odd. Later in that study they narrowed it down to the exogenous PA actually working at the extracellular level by converting to LPA. They found this out by inhbiting ERK to see what the PA would do, the PA didn't stimulate mTOR. Thus they learned that the exogenous PA actually worked on mTOR via ERK signalling, this is something that LPA is doing, which is how they eventually figured out that the PA was converting to LPA and then the LPA was activating ERK. This is confirmed again with the Tampa strength training and PA study, it's in the cell culture data (figure 1). As you can see in that chart, PS, PA, and LPA all activated mTOR similarly. Why does PS work? Because PS -> LPA by PLA2.

Read the Tampa strength training and PA study carefully. They mentioned intracellular PA and how that worked by also mentioning that it is how endogenous PA works. Not how supplemental PA works, though the possibility is of course there if supplemental PA accumulates to a significant degree in the phospholipids pool of the cells. It is due to this notion in which they suspected that supplemental PA may be a good candidate as a muscle wasting treatment (thus the study on sedentary people), however that did not pan out as planned.

Also look at the data for egg derived PA. It didn't work as well for stimulating mTOR. Why is that? Because it tends to get absorbed into cells as part of the PL pool (Stout notes this in the Q and A thread).
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Obviously that's why when Hornberger hypothesized that PA functioned through ERK-independent mechanisms, and treated subjects with exogenous PA and an ERK-inhibitor, the exogenous PA still induced mTOR, right?
 
De__eB said:
Obviously that's why when Hornberger hypothesized that PA functioned through ERK-independent mechanisms, and treated subjects with exogenous PA and an ERK-inhibitor, the exogenous PA still induced mTOR, right?
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From Tampa study:

"It is interesting to note that the endogenously produced PA can directly bind to, and activate, mTOR signaling which, in-turn, can promote an increase in protein synthesis. These effects appear to be independent of the PI3K and ERK signaling pathways [14,20]. However, exogenous PA can also be hydrolyzed to LPA, which binds to the LPA family of G-protein-coupled receptors. The binding of LPA to these receptors results in a cascade of events which stimulate the ERK signaling pathway and also increase PLD activity within the cell [15]. The result is a dual mediated increase in mTOR signaling via increased PA content within the cell as well as via the activation of the ERK signaling pathway [15]. Thus through the activation of multiple pathways, supplementing with PA could result in greater rates of MPS than RT alone and might explain why we observed a greater increase in skeletal muscle accretion when supplementing with PA."

They make a distinction between endogenously produced PA have the ERK and Pl3K indpependent effect on mTOR. Keyword endogenously produced. Then they end that paragraph with noting how when you have resistance training + PA supplementation, you can now hit multiple pathways with PA supplementation. How? Because you are endogenously producing PA (PC -> PA, this occurs when there's mechanical stress) which acts on mTOR independent of Pl3K and ERK whilst you have your exogenous source of PA acting through ERK by hydrolyzing to LPA. That is how they are theorizing how training + PA supplementation is working, you have that extra activation of mTOR via ERK. You're already producing a good amount of PA at the intracellular level. If anything, it makes sense to try to increase PC levels in cell PL pools (something that was actually specifically brought up in the Q and A thread), but as Wilson pointed out, PC is highly regulated and it does not appear that supplementing with PC would significantly increase PC levels in the cell PL pools.
 
You forgot to bold the part of the sentence where they say that the PA supplementation is working through multiple pathways.

--

You also completely failed to address the fact that Hornberger; who has a dozen publications on phosphatidic acid, explicitly tested exogenous phosphatidic acid combined with an ERK inhibitor, to determine that the mTOR effect of exogenous PA is ERK-independent.
 
De__eB said:
You forgot to bold the part of the sentence where they say that the PA supplementation is working through multiple pathways.

--

You also completely failed to address the fact that Hornberger; who has a dozen publications on phosphatidic acid, explicitly tested exogenous phosphatidic acid combined with an ERK inhibitor, to determine that the mTOR effect of exogenous PA is ERK-independent.
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Both of these studies are more recent, and both test exogenous PA with an ERK inhibitor and find that it is ERK-independent

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Oh, and in case you aren't confused enough by the myriad of enzymes involved, suddenly, a 3rd enzyme appears jealous of the attention ERK and PLD have been getting:

DGKZ wants in on the party: Invalid Link Removed

But wait, there's more!

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---

I suggest reading the content at lipidlibrary, and all of the recommended reading you can find there.
 
Also, and again, from the study you keep on citing ad nauseam:

It has also been shown that exogenous sources of PA can promote the activation of mTOR signaling, yet the effects of exogenous PA appear to be driven through multiple mechanisms.
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De__eB said:
Both of these studies are more recent, and both test exogenous PA with an ERK inhibitor and find that it is ERK-independent

Invalid Link Removed
Invalid Link Removed

Oh, and in case you aren't confused enough by the myriad of enzymes involved, suddenly, a 3rd enzyme appears jealous of the attention ERK and PLD have been getting:

DGKZ wants in on the party: Invalid Link Removed

But wait, there's more!

Invalid Link Removed

---

I suggest reading the content at lipidlibrary, and all of the recommended reading you can find there.
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Will be reading :D

Btw, the ERK blocking one above, that appears to be seeing if ERK is involved with endogenous PAs effect on mTOR. That's an intracellular level mechanism. ERK dependent activation from PA is actually indirect and at the extracellular level. There is a distinction.
 
kissdadookie said:
Will be reading :D

Btw, the ERK blocking one above, that appears to be seeing if ERK is involved with endogenous PAs effect on mTOR. That's an intracellular level mechanism. ERK dependent activation from PA is actually indirect and at the extracellular level. There is a distinction.
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What?

The results indicated that exogenous PA was sufficient to induce signaling through both ERK and mTOR, however, inhibition of ERK with UO126 did not prevent the ability of PA to induce mTOR signaling...Similar to the results observed with exogenous PA, inhibiting ERK with UO126 did not prevent the ability of MS to induce mTOR signaling.
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Furthermore, we determined that mechanical stimulation induced these mTOR-dependent events, and protein synthesis, through an ERK-independent mechanism. Similar to mechanical stimulation, exogenous PA also induced mTOR-dependent signaling via an ERK-independent mechanism
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De_eB, for the sake of the layman...will it prove beneficial for resistance trainees to dose PA/soy lecithin on days off? Will it stimulate protein synthesis moreso than if you didnt dose on days off?
 
NewAgeMayan said:
De_eB, for the sake of the layman...will it prove beneficial for resistance trainees to dose PA/soy lecithin on days off? Will it stimulate protein synthesis moreso than if you didnt dose on days off?
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Also De_eB is the best way to dose the soy lecithin granules at 1 tablespoon/twice a day & 7 hours apart?
 
De__eB said:
Also, and again, from the study you keep on citing ad nauseam:
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Read that entire paragraph in context. They hypothesize that it may be through multiple mechanisms if the PA actually makes it into the PL pool of cells based on the data for how PA acts at the intracellular level. That's the condition that needs to be met it would appear since the data they are basing that off of is based on endogenously produced PA. Also keep in mind this Tampa study was prior to the later sedentary subjects study. This study, keep in mind, was a first phase for ChemiNutra essentially. If you read the ChemiNutra patent, they were hoping that supplemental PA would increase PA content in PL pools thus leading to increased intracellular PA effects on mTOR and thus they hoped they could use it for muscle wasting conditions (thus they used the sedentary subjects in the later study which bared no gains unfortunately).
 
kissdadookie said:
Read that entire paragraph in context. They hypothesize that it may be through multiple mechanisms if the PA actually makes it into the PL pool of cells based on the data for how PA acts at the intracellular level. That's the condition that needs to be met it would appear since the data they are basing that off of is based on endogenously produced PA. Also keep in mind this Tampa study was prior to the later sedentary subjects study. This study, keep in mind, was a first phase for ChemiNutra essentially. If you read the ChemiNutra patent, they were hoping that supplemental PA would increase PA content in PL pools thus leading to increased intracellular PA effects on mTOR and thus they hoped they could use it for muscle wasting conditions (thus they used the sedentary subjects in the later study which bared no gains unfortunately).
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The ERK-pathway isn't MS dependent though, so if the effects were primarily ERK-related, the sedentary subjects study would have shown gains. The fact that they didn't lends MORE credence towards the effects being intracellular primary and PA primary, not ERK-primary and LPA primary.

Also, you're missing the entire point.

The fact that you should be taking it pre-workout has nothing to do with whether its effects are intra/extracellular and everything to do with at what point in time you can most effectively deliver phospholipids to skeletal muscle.
 
NewAgeMayan said:
De_eb, for the sake of the layman, will it prove beneficial for resistance trainees to dose PA/soy lecithin on days off? Will it stimulate protein synthesis moreso than if you didnt dose on days off?
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Think about it, when can you shuttle phospholipids into cell membranes, and skeletal muscle most effectively?

(Hint: Consider the maximizing arachidonic acid absorption thread)

When exercising!

This has nothing to do with whether its effects are intra/extracellular, and everything to do with the fact that you want this supplement to be going into skeletal muscle cell membranes, and not <anywhere else>.

koi1214 said:
Also De_eB is the best way to dose the soy lecithin granules at 1 tablespoon/twice a day & 7 hours apart?
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I would take one large dose, pre-workout, with ArA, because synergy.
 
De__eB said:
Think about it, when can you shuttle phospholipids into cell membranes, and skeletal muscle most effectively?

(Hint: Consider the maximizing arachidonic acid absorption thread)

When exercising!

This has nothing to do with whether its effects are intra/extracellular, and everything to do with the fact that you want this supplement to be going into skeletal muscle cell membranes, and not <anywhere else>.



I would take one large dose, pre-workout, with ArA, because synergy.
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This makes an interesting fasted training protocol.

I'm guessing insulin has the same effect on PA as does ARA?
 
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