M&M members,

Cortisol can catabolize muscle and testicular tissue leading to smaller muscles and lower testosterone levels. That’s why it’s desirable to suppress, or at least control cortisol levels. The most important time to guard you body against the effects of cortisol is during PCT when Testosterone levels are low, and cortisol can easily dominate and wreck havoc on the body. (Testosterone is a primary antagonist of cortisol)

Many cortisol blocking supplements on the market include one of the many DHEA metabolites such as 7-keto DHEA (7-oxo DHEA), 7-beta DHEA or androstenetriol. Short term studies have shown that these pro-hormone based cortisol blockers can lower LH & FSH thus inhibiting natural testosterone production. (1,2) While these may be useful supplements during a cycle, they should be avoided for PCT.

Phosphatidylserine (PS) is a ‘non-hormonal’ cortisol blocker that can effectively lower cortisol levels. Rather than lowering testosterone production, PS can actually increase testosterone production. (3,4) PS works by reducing CRH and ACTH release from the pituitary, thus reducing cortisol release from the adrenal glands.

Unfortunately PS has been prohibitively expensive, until now. In order to bring you the most affordable PS on the net, we are offering a month’s supply of PS (800mg/day) for only 47.99 – AKA EndoAmp.

Plus…

- Take an additional 10% off with the code SPONSOR10!

And…

- Get free 2-3 day priority shipping when you spend over $100!

Thank you loyal Primordial fans!

-Pp



1. Effects of Transdermal Application of 7-oxo-DHEA on the Levels of Steroid Hormones, Gonadotropins and Lipids in Healthy Men.
J Sulcova, et al.
Institute of Endocrinology 50: 9-18, 2001

2. Delayed effects of short-term transdermal application of 7-oxo-dehydroepiandrosterone on its metabolites, some hormonal steroids and relevant proteohormones in healthy male volunteers
Jarmila Sulcova, et al.
Institute of Endoacrinology 43 (2):221-227 2005

3. HORMONAL EFFECTS OF PHOSPHATIDYLSERINE DURING 2-WKS OF INTENSE WEIGHT TRAINING [Annual Meeting Abstracts]
Fahey, T. D.; Pearl, M.
California State University, Chico


4. Blunting by chronic phosphatidylserine administration of the stress-induced activation of the hypothalamo-pituitary-adrenal axis in healthy men.
Monteleone et al.
Eur J Clin Pharmacol 1992, 42(4):385-388

Using this stuff right now. I've been mixing it into my shakes.

Quick question - does splitting the dose up offer any benefit? I'm taking half a dose upon waking and half a dose 4 hours later (since cortisol is supposed to be higher around these two times). Also, what about taking an additional dose or half dose around workout time?

I like to take my full dose after my workout in my protein shake.

I dont think spliting the dose would make much difference. Once it absorbs from the digestive track it probably stores in the body for quite a while.

-Pp

Why haven't I seen these studies before? this is really bad and I don't get it.

This is what laways baffled me with exogenous 7-oxo but I was too lazy to heck it out. once it inhibits b-hsd-11 it gets reduced to 7-oh, and than what? if its not cleared it will flow around in your system actually promoting the bad b-hsd back

worst of all, if there is 11-bhsd in your skin than it alraedy arrives in your blood as 7-oh, stuck there like that actually doing the opposite of what you wnat.

getting info from spook and Par at this stage though is not something to bet on.

How do you like it...?

Liorrh, I was thinking about home-brewing some FL7, but after looking at those studies I'm kind of hesitant now...


It's hard to say... PS hasn't ever been one of those things I can "feel", but it does seem like I'm recovering better. I'd like to see what effect it has on my waistline, but that will take a while.

thats wicked expensive, I can get transD 7-oxo for like 20 bone. Going to read the study now.

Gotcha. Thanks!

do you have access to the full text?

Here's first one..

Click to view attachment

Edit: Here's #2..

Click to view attachment

would rep if we did that on this site..thanks apparently my school does not grant me access to pubmed

just skimmed both of them, that sucks.

As did I, it seems that (especially Ironic after ordering a product with 7-oh-dhea in it just a day or so ago) one does not want to be taking these forms of DHEA. The worst part, really, is that none of them found changes in cortisol at all. Only decreases in Test/E2. Furthermore, it seems that only 7-oxo partially competes for 11b-HSD1 in the cortisone reduction, whereas 7-oh actually competes (stongly I might add) with the oxidation of cortisol. In effect preventing its deactivation! (see: Here & Here)

I recall the 11-OXO writeup mentions the problem WRT 7-OH. Major bummer.

Ab-Solved seems to work very well, though, so local application of 7-Keto seems to be ok.

DHEA derivates are good at antagonizing cortisol directly at the receptor, thus blunting its catabolic action. We have 7-keto in our DermaTherm which can be beneficial in extreme calorie deprivation, especially when stacked with some anabolic pro-hormone or AAS.

It’s just not a cortisol blocker that should be used for PCT.

-Pp

I'll limit discussion to 7-keto/7-oxo because 7-oh is pretty clearly a bad idea.

I browsed your citations for the DermaTherm writeup on your site and found no sources for that claim. I'd be grateful if you could show me some evidence of 7-oxo interacting with the corticoid receptor.

In light of this new evidence, I fail to see how 7-oxo could have any use sans androgens, whether that be in PCT or just in day to day use (or in dieting).

I pulled these reffs from the product write up. You should find what you need here -

7 beta-OH-DHEA counteracts dexamethasone induced suppression of primary immune response in murine spleenocytes. Sterzl, I., Hampl, R., Sterzl, J., Votruba, J., and Starka, L. (1999). J. Ster. Biochem. Mol. Biol. 71, 133–137.

Glucocorticoids inhibit interconversion of 7-hydroxy and 7-oxo metabolites of dehydroepiandrosterone: a role for 11beta-hydroxysteroid dehydrogenases? B Robinzon, KK Michael, SL Ripp, SJ Winters, and RA Prough Arch Biochem Biophys, Apr 2003; 412(2): 251-8.

Pregnenolone and dehydroepiandrosterone as precursors of native 7-hydroxylated metabolites which increase the immune response in mice. R Morfin and G Courchay J Steroid Biochem Mol Biol, Jul 1994; 50(1-2): 91-100.

-Pp

"The mechanism(s) through which 7-hydroxylated metabolites of DHEA act is unknown. We have studied the effect of 7α-OH-DHEA on early stages of dexamethasone action in vitro. Likewise DHEA, 7α-OH-DHEA did not compete for glucocorticoid receptors in rat hepatocytes, either influenced the activation of glucocorticoid–glucocorticoid receptor complex or its binding to DNA-cellulose in cell-free system."



These ones dont even have a single instance of receptor or receptors anywhere in either the papers.

And actually after looking in the references of the first study you provided me with, I came across this rather illuminating study:



It seems that there is no receptor activation or antagonism, but rather the (unverified) possibility that the Glucocorticoid Receptor Complex is being modified outside the nucleus which lessens the binding affinity of glucocorticoids like dexamthasone to the receptor complex. This is an interesting (possible) effect, but not quite the one you described.

I find it interesting, however, that no reduction in dexamethasone binding occured in the cells when they were still clustered together, like they are in vivo. You have to be careful when it comes to issolated studies on rat/mouse tissue because its not in vivo human tissue (and its known, for example, that human 11b-HSD1 acts differently than others).

It is not supposed to reduce Cortisol. lets step back a bit.

Cortisol is circulating as inactive cortisone and is activated by 11-HSD1. the amount of this enzyme in the cell decides the amount of cortisol activity. now 7-oxo takes care of this enzyme. But, if its only by competition (i.e being a substrate instead of cortisone) than, blood levels of 7-oh, which is the reduced result will rise continuously, preventing inactivation of cortisol in other tissues. for VAT it does not matter as there is plenty more of the reducing 11b-HSD1 than the 2 isoform. but in other tissues where 11-HSD2 is suppose to be inactivating cortiosl mainly the liver, cortisol will not be deactivated, wrecking havoc on HPA feedback. I suspect it will wreck havoc, in one form or another on your testes causing leydig cell atrophy, and that is why you get the lower T.

The questions are:
1. how does the body remove the 7-oh from circulation? the 2nd study seems to show it just does not or VERY slowly. I need to look at my liver references and stuff, long time till I checked that. It seems that re-oxidizing capabilities of liver and kidney are poor. but I do not trust this study.

2. Does 7oxo inhibit the 1 isoform by other mechanism like reduce mrna expression?

Matt Cahill's stance
http://forum.bodybuilding.com/showthread.php?t=107030111

Sledge? has nothing new to offer in that thread.

If the blood test distinguishes between Cortisol and Cortisone, then yes, in my opinion the Cortisol levels should be lower, and the Cortisone levels should be higher (a proportion would be a good way of representing this).

I don't disagree with the rest of what you say, but I think that the data is all suggesting that it shouldnt be used, dispite DS's claims that their blood tests showed no difference.

they are interchangeable in the literature.

Wow,

So what's causing the positive feedback from LX and Reduce XT, even in PCT?

I have a bottle of LX in my stash but now I may just chunk it.

Well that at least saves the possibility that the 7-oxo is having some effect on cortisol interconversion...

The research about DHEA’s metabolites antagonizing cortisol at the receptor (or perhaps ameliorating its action as you pointed out) was research I was doing about 2 years ago, with much of my notes inaccessible now.

At any rate, perhaps this reff may provide more insight to the action of DHEA’s metabolites with anti-glucocorticoid activity (Atriol, rather than the 7-oxygenated metabolites) >

In vitro potentiation of lymphocyte activation by dehydroepiandrosterone, androstenediol, and androstenetriol
DA Padgett and RM Loria
J. Immunol., Aug 1994; 153: 1544 - 1552.

-Pp

If that is true, I would expect that when used on cycle or for an extended period of time there would be some nasty cort rebound side effects upon cessation. If you've been running on cycle that would be the last thing you'd want during PCT.

It almost wouldn't be worth bothering with on cycle IMO.

I was pointing out that there are some effects outside of the steroidogenic enzyme inhibition with DHEA’s metabolites. There may not be a direct receptor block on cortisol, but certainly a modification of its effects (similar to the action of meny AAS).

-Pp

Is the ps cattle or soy derived?
Most tests used the cattle derived form, which is largely unavailable Im told.

Yes, our PS is soy derived.

Most all the studies that have been done in the last decade have been with soy derived PS. In fact 95% of the reffs used in our product write up are studies from soy derived PS. Its basically the standard now ever since the BSE scare and banning of bovine derived PS.

-Pp

Really?

DS introduced this 7OH to the supplement world and spent a lot of time and money for that development. DS is no longer in the business of helping other companies rip off our ideas. Bloodwork is for inhouse use only and will not be posted.

Delivery method is definitely relavant when you understand how these metabolites work and where they work. 7OH does its work in the liver. 7oxo is used in a transdermal to skip the liver. If you read the following study (1) youll see that oral use of 7oxo showed no changes in hormonal concentrations.

What you need to understand is that the use of transdermal 7oxo is not the same as oral use of 7oxo or 7oh. Based on the studies we have you should not use transdermal 7OXO during PCT. Beyond that I dont know what else you are looking for.

(1)Safety and pharmacokinetic study with escalating doses of 3-acetyl-7-oxo-dehydroepiandrosterone in healthy male volunteers.

Davidson M, Marwah A, Sawchuk RJ, Maki K, Marwah P, Weeks C, Lardy H.

Chicago Center for Clinical Research, Ill, USA.

OBJECTIVES: To evaluate the safety and pharmacokinetics of 3-acetyl-7-oxo-DHEA (3beta-acetoxyandrost-5-ene-7,17-dione) given orally. DESIGN: A randomized, double blind, placebo-controlled, escalating dose study. SETTING: The Chicago Center for Clinical Research. PARTICIPANTS: Twenty-two healthy men. STUDY METHOD: The participants received placebo (n = 6) or 3-acetyl-7-oxo-DHEA (n = 16) at 50 mg/d for 7 days followed by a 7-day washout; 100 mg/d for 7 days followed by a 7-day washout; and 200 mg/d for 28 days. OUTCOME MEASURES: Safety parameters, evaluated at each dose level, included measurement of total testosterone, free testosterone, dihydrotestosterone, estradiol, cortisol, thyroxin and insulin levels. Analyses for 7-oxo-DHEA-3beta-sulfate (DHEA-S), the only detectable metabolic product of the administered steroid, were conducted on plasma drawn from all subjects at 0.25, 0.5, 1, 2, 4, 6 and 12 hours after the final 100 mg dose of 3beta-acetyl-7-oxo-DHEA. RESULTS: There were no differences in the clinical laboratory values or in reported minor adverse experiences, between treatment and placebo groups. In general, blood hormone concentrations were unaffected by the treatment with 3beta-acetyl-7-oxo-DHEA and remained within the normal range. No changes in vital signs, blood chemistry or urinalysis occurred during treatment with 3beta-acetyl-7-oxo-DHEA compared to placebo. The administered steroid was not detected in the blood but was rapidly converted to 7-oxo-DHEA-S, the concentrations of which were proportional to dose. This steroid sulfate did not accumulate; plasma concentrations 12 hours after the 3beta-acetyl-7-oxo-DHEA dose at 7 and 28 days on the 200 mg/d dose were 15.8 and 16.3 microg/L respectively. The mean time to peak plasma level of 7-oxo-DHEA-S was 2.2 hours; the mean half life was 2.17 hours. The apparent clearance averaged 172 L/h, and the apparent mean volume of distribution was 540 L. CONCLUSION: These results indicate that 3beta-acetyl-7-oxo-DHEA is safe and well tolerated in normal healthy men at doses up to 200 mg/d for 4 weeks.
===========================================

Our research indicates it is not complete inhibition, but more competitive inhibition of 11betaHSD1 -- 7-alpha OH uses it to convert to 7-keto, and 7-keto uses it to convert back to 7-alpha OH (and 7-beta OH). Since cortisone uses the enzyme to convert to cortisol, the net result is lowered concentrations of cortisol.

While on the subject of those pondering the drop in testosterone, there was another study performed, seemingly to establish whether there was any toxicity issues (http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum) that show an estradiol reduction of 8%, cortisol reduction 7.7%, and (surprisingly) free testosterone INCREASE of around 15%.

And there is another study that was mentioned in an article by David Tolson saying that there was no change in testosterone or estradiol levels and only T3 was increased (J Ex Physiology online. 1999 2(4). Double-Blind Study Evaluating the Effects of Exercise Plus 3-Acetyl-7-oxo-dehydroepiandrosterone on Body Composition and Endocrine System in Overweight Adults. Colker CM, Torina GC, Swain MA, Kalman DS.)
===========================================

I don't need bloodwork, more looking at science talk and references.



7-oh+liver=7-oxo+more cortisol/cortisone in liver-->less HPA activation

7-oxo+peripherial tissues(Vat/skin/kidney)=7-OH+less cortisol/cortisone in those tissues-->VAT more sensitive to catecholamines. PS large quantities of VAT than it will act like oral 7-oh(lots of reduced 7-dhea will go to the liver)

but something is wrong with the results here. the studies you posted about oral 7-oxo are irrelevant. the two texts attached above show a clear problem. if circulation 7-oh does not clear, and the consequences are some weird loop on the HPA and testes, than your product will suffer from the same problems.

I don't know if to trust this research, but this is a big flag and no results show otherwise. I do remember good research on transdermal 7-oxo but can't find it.

So, why don't you recommend trans 7-oxo in PCT and you do recommend oral 7-oh?

I dont recommend either one for PCT. I recommend LX for fatloss and lean muscle gains. The reason to not use transdermal 7oxo during pct would be because of the only 2 studies show lowered test.

How are they irrelevant?

Also youre missing a step. 7aOH-7OXO-7bOH.

no' I'm saying they are very relevant. just asking the avant guys WTF. so you are saying this extra step is the difference between trans 7-oxo and oral 7a-oh

I will check that.

Oh sorry I didnt get that. Im also saying that trans 7OXO can not be compared to oral 7OXO or oral 7OH. Handpicking certain studies can paint an entirely different picture then when you review all relevant data. Besides the fact there a major issues with both of the trans studies.

Sldge,

Do you have the full text of this study?

-Pp

Click to view attachment

The study showed a statistically significant 8% drop in total Testosterone in the 7-oxo group. It would be interesting to see more detail, but the study only measured hormones at the pre and post therapy points – 56 days apart.

I think we are in agreeance that DHEA metabolites are not ideal for PCT cortisol reduction, however I believe they do have their place in a cutting cycle.

-Pp

nos, thanks for the study.

The same study also showed an increase in free test by 14% and a decrease of cortisol by 7.7%. With just a small drop in Total Test but a corresponding drop in Estrogen and knowing that the values return to baseline quickly there is no reason to think you couldnt use this during PCT. Now if you used anything else that might slightly raise total test (ie forskolin, etc), which everyone uses during PCT, then you would easily off set the slight drop in just Total Test and it would be fine for PCT. You would have an increase in Total T, Free T, a reduction of cortisol and a decrease in Estrogen. What else would you want during PCT?

The values return to baseline quickly? I was under the impression that what all these negative studies were saying was that there are longterm destabilizations of the gonadal hormones in response to 7-oxo administration. What say you?

My main point is that PS is a superior cortisol blocker. It raises total testosterone, rather than reduce it and this is more conducive to PCT. This is the reason we don’t suggest our DermaTherm for PCT.

-Pp

I used LX post-pct with little results....anecdotal completely of course.




Something with similar action that doesnt decrease total test.

The transdermal 7oxo studies do not apply to oral 7OH use.




You do understand that Total Test flucuates up and down throughout the day.




LX Increases Total Test, Increases Free Test, Decreases Estrogen, Decreases Cortisol, increases lean muscle and burns fat. But then again it was never made for PCT to begin with nor does it contain 7OXO.

Yes, I’m well aware of how the HPTA functions. Thank you.

7-oxo is synonymous to 7-aOH as far as I’m concerned. I see the same trend with transdermal 7-oxo and oral 7-oxo administration – sex steroid reduction and cortisol reduction – just to a lesser extent with oral administration. My original point to this thread still stands.

-Pp

I'm about to be super bro-tastic, but I do believe anecdotal feedback has some merit. I have seen quite a bit from LX, out of all of it I think I saw one guy report a slight decrease in libido. Results were pretty great all around, loss of fat, gain of muscle. Maybe 7-OH alone could cause some of the aforementioned problems, but coupled with forskolin + 5-AT these 'problems' no longer exist.

I guess what I'm getting at is I would like to see some product testing of Endo-Amp by itself.

Sure, I bet LX is a great product. Improvements in body composition are quite normal when administering anti-catabolic steroid hormones, just as we’ve seen with our DermaTherm.

On the other hand, if you’re looking for a non-hormone based cortisol blocker that will support natural testosterone production rather than hinder it then I believe PS is superior choice.

-Pp

I wonder why the avant labs reps, who's former product and credit is being shot to pieces here are staying numb.

I'm pretty sure I saw an abstract that indicated that the cortisol effect from soy PS is not comparable or not present. I can dig it up but I'm sure people here have seen it too?

I'd rather not try my hand at something thats above my level, but I don't see how it is getting shot to pieces. As far as I can tell FL7 was not marketed as a PCT prodcut, and Primordial themselves has a systemmic carrier with 7-oxo. If Par wanted to talk about old FL7 thats cool, but I am avant research and FL7 is not made anymore anyway. Perhaps you could get a dermabolics rep in here for 7-cort.

did you even bother to read the abstracts? Lowers T, E, doubles SHBG, does not clear for 100 days raises blood levels of 7-oh which is contrary to what you wnat if it works by the mechanism they suggested. .. what is good about that, PCT or not? anyway even if it is good I need to know this thing when I use a product