AAS, Cortisol, Phosphatidylserine, stretch marks

[pudzian2]

Doc,

I know that I have brought this up with you before, however after a little more research and thinking I have the following thoughts in my head and I would like you professional opinion.

My last carefully planned and monitored AAS cycle ended in late February. It was essentially 18 weeks of Test enanthate and Bold Undec. I finished with 3 weeks of superdrol which was a very negative experience for me-i didnt respond well to it....

ANYWAY THE POINT IS.

I ONLY noticed stretch marks at the conclusion of the cycle. If I can remember correctly it only took place once the esters cleared up.

this leads me to believe that the post cycle cortisol rebound had something to do with the stretch marks. I have read articles stating that increased corticosteroid production (namely cortisol) can cause stretch marks in those who are otherwise not prone to them. ( I have never had a stretch mark in my life prior)

Now, I did use 17b-triol (Retain 2 from AnabolicXtreme) which supposedly blocks cortisol at the receptor. (I actually DID NOT use this product right away as I was using Dermacrine Sustain....So basically the cortisol rebound that WAS present leads me to think it had soemthing to do with the stretch marks.

as for the future: I will be using a receptor blocker like retain 2 only in PCT, but I was considering using Phosphatidylserine at a moderate to low dose while Training naturally and even when on a cycle of AAS.

the problem: Some say that PS (phosphatidylserine) will compete with the AAS at the receptor...(this was from a bro on another board not a doctor or a study of any sort) HOWEVER, from my research PS was noted to decrease CIRCULATING cortisol which leads me to think it modulates the release of cortisol and NOT its actions at the receptor.

Obviously cortisol is necessary and important to normal healthy function however since I am a student, have many business venture, and a competitive bodybuilder living in a stressfull world, I would think that a healthy dose of PS would benefit someone like me year round if not on some form of cyclical regime...


Questions to you:

-Do you think that using something like PS DURING a cycle would be a bad idea?

-What would be a good way to incorporate it into my lifestyle (dosage and if you suggest cycling it, in what fashion?)

I had the following Idea:

250-500mg PS while ON AAS.

Upon cessation of AAS administration (starting a few days prior to PCT), increase to 800-1000mg PS and ramp down for the full length of PCT, until a dose of 250mg or so is achieved which should be safe enough to run for the rest of my OFF time (which equates to any time im not using AAS and thus more than half of the year )

[swolloniron]

i'm curious to the reply as well

[dinoiii]

Originally Posted by pudzian2

Doc,

I know that I have brought this up with you before, however after a little more research and thinking I have the following thoughts in my head and I would like you professional opinion.

My last carefully planned and monitored AAS cycle ended in late February. It was essentially 18 weeks of Test enanthate and Bold Undec. I finished with 3 weeks of superdrol which was a very negative experience for me-i didnt respond well to it....

ANYWAY THE POINT IS.

I ONLY noticed stretch marks at the conclusion of the cycle. If I can remember correctly it only took place once the esters cleared up.

this leads me to believe that the post cycle cortisol rebound had something to do with the stretch marks. I have read articles stating that increased corticosteroid production (namely cortisol) can cause stretch marks in those who are otherwise not prone to them. ( I have never had a stretch mark in my life prior)

I am probably more inclined to suggest that rapid growth potentially associated with your cycle is responsible for the stretch marks rather than a state of overt hypERcortisolism. Though I am unsure what kind of gains (strength, hypertrophy, et al) were seen here.

On cycle, many steroids actually have anti-catabolic effects through the glucocorticoid receptor, which kind of in their own right keeps cortiosl in check. There is additionally crossover feedback systems that lend to lowcortisol into the frist 2 weeks of post-cycle - all of which I have discussed in depth either on this forum or in my writings from the past, which should be readily available.

Now, I did use 17b-triol (Retain 2 from AnabolicXtreme) which supposedly blocks cortisol at the receptor. (I actually DID NOT use this product right away as I was using Dermacrine Sustain....So basically the cortisol rebound that WAS present leads me to think it had soemthing to do with the stretch marks.

"Did not use it right away" means?

If this was not right away as in the first two weeks post-cycle, that is actually better supported if any support lends credence at all for cortisol control into post-cycle AT ALL.

as for the future: I will be using a receptor blocker like retain 2 only in PCT, but I was considering using Phosphatidylserine at a moderate to low dose while Training naturally and even when on a cycle of AAS.

PS is another item I have discussed at length in the past. The problem is that much of the bovine-offered PS was what presented the original anti-cort effects...it is unclear in the current state of mad-cow scare that the soy-based kind has the same positive effects on cortisol levels (mind you, a mg-tally that is usually cost-prohibitive in this regard - 800mg per day).

This is not to eliminate the potential for other alternative ergogenic effects (although most are suggested by vested-interest studies), however - as far as anti-cort...probably not.

the problem: Some say that PS (phosphatidylserine) will compete with the AAS at the receptor...(this was from a bro on another board not a doctor or a study of any sort) HOWEVER, from my research PS was noted to decrease CIRCULATING cortisol which leads me to think it modulates the release of cortisol and NOT its actions at the receptor.

I don't believe the combo to have ever been studied (at least not to my knowledge), so anything suggested is hypothesized at best. My personal view: PS seems to only decrease cortisol levels when they are elevated and does not seem to decrease cortisol levels below normal (again, recall that I suggested from numerous lab reports that cortisol is DECREASED on cycle). Decreasing cortisol levels or suppression of cortisol production is not desired in many instances as it may cause adverse effects such as a decrease in reaction time to wounds and healing mechanisms in the body. I am, as a result, inclined to say "no."

Obviously cortisol is necessary and important to normal healthy function however since I am a student, have many business venture, and a competitive bodybuilder living in a stressfull world, I would think that a healthy dose of PS would benefit someone like me year round if not on some form of cyclical regime...

Perhaps, but I would be inclined to suggest something a bit more prudent.

On-Cycle: Ramp-down fashion accounting for early non-adaptive feedback mileu to the HPAA as well as the likelihood most prematurely increase training volume, et al...

Post-Cycle: Weeks 1-2: No anti-corts...Week 3: probably some evidence to suggest the potential for rebound and probably more directly issued with longer cycles.

Questions to you:

-Do you think that using something like PS DURING a cycle would be a bad idea?

I think you could use them in the early-go, but should ramp off them as above to account for HPAA crossover pathways.

-What would be a good way to incorporate it into my lifestyle (dosage and if you suggest cycling it, in what fashion?)

I had the following Idea:

250-500mg PS while ON AAS.

No evidence to suggest such a dose would have cortisol-inhibiting properties. The dose that has been studied is 800mg (2-400mg doses) to have any sort of precipitous advantage, IF one at all is to be had.

Upon cessation of AAS administration (starting a few days prior to PCT), increase to 800-1000mg PS and ramp down for the full length of PCT, until a dose of 250mg or so is achieved which should be safe enough to run for the rest of my OFF time (which equates to any time im not using AAS and thus more than half of the year )

Again, as above, pick up with 800mg (unsure that it wouldn't be dose-limited after that as there is no true data). Personally, I would "ramp down" in accordance with training adaptations (i.e. - decreased volume, etc...).



Does what I have said make sense?

great discussion concept.


D_

[pudzian2]

Originally Posted by dinoiii

I am probably more inclined to suggest that rapid growth potentially associated with your cycle is responsible for the stretch marks rather than a state of overt hypERcortisolism. Though I am unsure what kind of gains (strength, hypertrophy, et al) were seen here.

On cycle, many steroids actually have anti-catabolic effects through the glucocorticoid receptor, which kind of in their own right keeps cortiosl in check. There is additionally crossover feedback systems that lend to lowcortisol into the frist 2 weeks of post-cycle - all of which I have discussed in depth either on this forum or in my writings from the past, which should be readily available.




"Did not use it right away" means?

If this was not right away as in the first two weeks post-cycle, that is actually better supported if any support lends credence at all for cortisol control into post-cycle AT ALL.




PS is another item I have discussed at length in the past. The problem is that much of the bovine-offered PS was what presented the original anti-cort effects...it is unclear in the current state of mad-cow scare that the soy-based kind has the same positive effects on cortisol levels (mind you, a mg-tally that is usually cost-prohibitive in this regard - 800mg per day).

This is not to eliminate the potential for other alternative ergogenic effects (although most are suggested by vested-interest studies), however - as far as anti-cort...probably not.





I don't believe the combo to have ever been studied (at least not to my knowledge), so anything suggested is hypothesized at best. My personal view: PS seems to only decrease cortisol levels when they are elevated and does not seem to decrease cortisol levels below normal (again, recall that I suggested from numerous lab reports that cortisol is DECREASED on cycle). Decreasing cortisol levels or suppression of cortisol production is not desired in many instances as it may cause adverse effects such as a decrease in reaction time to wounds and healing mechanisms in the body. I am, as a result, inclined to say "no."





Perhaps, but I would be inclined to suggest something a bit more prudent.

On-Cycle: Ramp-down fashion accounting for early non-adaptive feedback mileu to the HPAA as well as the likelihood most prematurely increase training volume, et al...

Post-Cycle: Weeks 1-2: No anti-corts...Week 3: probably some evidence to suggest the potential for rebound and probably more directly issued with longer cycles.




I think you could use them in the early-go, but should ramp off them as above to account for HPAA crossover pathways.




No evidence to suggest such a dose would have cortisol-inhibiting properties. The dose that has been studied is 800mg (2-400mg doses) to have any sort of precipitous advantage, IF one at all is to be had.





Again, as above, pick up with 800mg (unsure that it wouldn't be dose-limited after that as there is no true data). Personally, I would "ramp down" in accordance with training adaptations (i.e. - decreased volume, etc...).



Does what I have said make sense?

great discussion concept.


D_

Wow doc, Thanks for the in-depth answer.

Well lets recap everything you said. I understand that the soy derivative hasn't been studied or proven to do the same thing, but it's worth a shot. I think primordialperformance is pushing a relatively cost effective new PS product for cortisol reduction and associated ergogenic effects. I did email him about the bovine-soy dilemma and he replied that although there arent as many studies, all the studies his website references for the product have used the SOY derivative.... so apparently there is still some supportive data.

Now, I think PS would have a pretty decent application to longer cycles which we can get into if you wish, however my question was more directed to apply PS to my shorter cycling methods (28 day 'burst' cycles). Would your recommendations still apply?

As far as your dosing suggestion (800mg is the minimum recommend dose to yeild any results cortisol-wise). So:

Begin a cycle with 800mg ED, and as the cycle progresses into the weeks or ( days in my case) prior to PCT, rampd down the dose in accordance with ramping down the volume of training to promote less of a catabolic response to training? The purpose of ramping the PS down is to allow for the natural feedback mechanisms/reactions that keep cortisol low during the first two weeks of PCT, Then begin at 800mg again and ramp down until the end of PCT? (please correct me if I am understanding you wrong).

Would you suggest using somethign like PS in accordance with a receptor binding cotisol blocker like 17b-triol? (retain 2 etc)? or do you feel iffy on the studies (or lack thereof) suggesting PS reduces cortisol production as apposed to blocking it at the receptor?

Does the 1-2 week low cortisol period post cycle depend on the compounds used and their characteristics/actions in the body (aromatization, modes of action etc) or is it just generally applied to a suppressed HPTA regardless?

(if the goal of these short cycles that I do is minimal endogenous disruption would messing with cortisol do more harm then good)?

I agree this is an interesting discussion topic. Thanks for the replies doc.

[dinoiii]

Originally Posted by pudzian2

Well lets recap everything you said. I understand that the soy derivative hasn't been studied or proven to do the same thing, but it's worth a shot. I think primordialperformance is pushing a relatively cost effective new PS product for cortisol reduction and associated ergogenic effects. I did email him about the bovine-soy dilemma and he replied that although there arent as many studies, all the studies his website references for the product have used the SOY derivative.... so apparently there is still some supportive data.

This is incorrect. I just referenced the studies you speak of and they do NOT all implore soy-based product. In fact, it looks as though just one that was from a highly vested interest group at the ACSM meeting offered any levels of significance on only a 2-week trial which certainly would be suggested as far from conclusive.

This is NOT to admit that there aren't soy-based studies out there and some encouraging, just not in the cortisol-department and one could question rationale for employment.

Now, I think PS would have a pretty decent application to longer cycles which we can get into if you wish, however my question was more directed to apply PS to my shorter cycling methods (28 day 'burst' cycles). Would your recommendations still apply?

My apologies as you said you had issues after "x" weeks (implied months) on Test E. That said, suppression rather than length is the issue in that case. If true suppression is felt, then my rules above apply. You are getting Anti-cort by many PH/PS/DeS/AAS through action mediated by the glucocorticoid receptor; concurrent employment makes little sense.

Most post-cycle regimes are dictated by a hypOcortisol (hypOadrenal) state about 2.5 weeks into PCT and as such my standard recommendation is maintained at about 2 weeks to offset said effects should they occur.

As far as your dosing suggestion (800mg is the minimum recommend dose to yeild any results cortisol-wise). So:

Begin a cycle with 800mg ED, and as the cycle progresses into the weeks or ( days in my case) prior to PCT, rampd down the dose in accordance with ramping down the volume of training to promote less of a catabolic response to training? The purpose of ramping the PS down is to allow for the natural feedback mechanisms/reactions that keep cortisol low during the first two weeks of PCT, Then begin at 800mg again and ramp down until the end of PCT? (please correct me if I am understanding you wrong).

Nope, this is what is what I was in fact suggesting.

Would you suggest using somethign like PS in accordance with a receptor binding cotisol blocker like 17b-triol? (retain 2 etc)? or do you feel iffy on the studies (or lack thereof) suggesting PS reduces cortisol production as apposed to blocking it at the receptor?

17b-triol (or AET for short as I reference it in accordance with science literature) has VERY poor oral bioavailability. I actually don't care for AET through oral route, though TD admin may be interesting if a group like PP puts one out.

There biggest selling point appears that 7-oxo (keto) DHEA has potential to impart action on the HPTA however, which would already suggest an anti-AET run. But - in labs we have run in clinical trial, this suggestion appears to be false as well. Both 7-oxo and/or other metabolites do NOT apper to impart precipitous influence on the HPTA at all.

As for PS, like I said above, it only seems to impart actions while cortisol is high rather than kept in check. I would be inclined to think that alone stands as grounds for hypothesis to suggest it does more than merely act at the receptor, because if the opposite were true, you'd likely see some life-threatening suggestion in creation of hypOadrenal states. That said, you should NOT view cortisol as bad as you seem to - that is marketing; trust me - cortisol has its place in the endocrinologic mileu.

Does the 1-2 week low cortisol period post cycle depend on the compounds used and their characteristics/actions in the body (aromatization, modes of action etc) or is it just generally applied to a suppressed HPTA regardless?

In our lab reports, it actually appears almost independent of the compounds used believe it or not.

(if the goal of these short cycles that I do is minimal endogenous disruption would messing with cortisol do more harm then good)?

It very well could, which has drawn solid contention with my heavy writing on this topic for years. As you see, cortisol is one of those things that has been so misrepresented in marketing campaigns...it is almost unfortunate.



D_

[pudzian2]

Originally Posted by dinoiii

This is incorrect. I just referenced the studies you speak of and they do NOT all implore soy-based product. In fact, it looks as though just one that was from a highly vested interest group at the ACSM meeting offered any levels of significance on only a 2-week trial which certainly would be suggested as far from conclusive.

This is NOT to admit that there aren't soy-based studies out there and some encouraging, just not in the cortisol-department and one could question rationale for employment.





My apologies as you said you had issues after "x" weeks (implied months) on Test E. That said, suppression rather than length is the issue in that case. If true suppression is felt, then my rules above apply. You are getting Anti-cort by many PH/PS/DeS/AAS through action mediated by the glucocorticoid receptor; concurrent employment makes little sense.

Most post-cycle regimes are dictated by a hypOcortisol (hypOadrenal) state about 2.5 weeks into PCT and as such my standard recommendation is maintained at about 2 weeks to offset said effects should they occur.





Nope, this is what is what I was in fact suggesting.





17b-triol (or AET for short as I reference it in accordance with science literature) has VERY poor oral bioavailability. I actually don't care for AET through oral route, though TD admin may be interesting if a group like PP puts one out.

There biggest selling point appears that 7-oxo (keto) DHEA has potential to impart action on the HPTA however, which would already suggest an anti-AET run. But - in labs we have run in clinical trial, this suggestion appears to be false as well. Both 7-oxo and/or other metabolites do NOT apper to impart precipitous influence on the HPTA at all.

As for PS, like I said above, it only seems to impart actions while cortisol is high rather than kept in check. I would be inclined to think that alone stands as grounds for hypothesis to suggest it does more than merely act at the receptor, because if the opposite were true, you'd likely see some life-threatening suggestion in creation of hypOadrenal states. That said, you should NOT view cortisol as bad as you seem to - that is marketing; trust me - cortisol has its place in the endocrinologic mileu.




In our lab reports, it actually appears almost independent of the compounds used believe it or not.





It very well could, which has drawn solid contention with my heavy writing on this topic for years. As you see, cortisol is one of those things that has been so misrepresented in marketing campaigns...it is almost unfortunate.



D_

I didn't actually take a look at all of those references on PP's site. I suppose he was blowing a little steam when saying ALL his studies were soy-derived.

I really dont view cortisol as bad, I just seek knowledge so as to control it, as not doing so MAY have detrimental actions on muscle growth after a cycle (as you said after about 2 weeks).

I agree that there is a lot of misconception about cortisol, just as there is about estrogen (good vs bad).

Conclusively, I suppose a transdermal 17-keto DHEA or a PS regime would nicely compliment the latter portion of post cycle therapy.