The #1 Cortisol Blocker
- 06-08-2008, 04:11 PM
- 06-09-2008, 05:41 PM
Let’s stay on the topic here…
I said DHEA metabolites lower testosterone production and I provided proof of this. DHEA metabolites are in your product, so the burden of proof is on you my friend. Do you have any research to suggest that DHEA metabolites do not lower total testosterone? (free testosterone has nothing to do with testosterone production)
BTW, I never bashed anything or mentioned any products; I only posted research about DHEA metabolites, and why PS is superior.
- 06-09-2008, 05:46 PM
You are right, soy derived PS is slightly chemically different than bovine derided PS, but soy derived PS has been proven to provide all the same benefit. In fact, virtually all studies done in the last 8 years have been with soy derived PS because of the BSE scare. If you’re interested in reading more about this, this is a good review –
Phospholipids and sports performance.
R Jager, et al.
J Int Soc Sports Nutr, Jan 2007; 4: 5
06-09-2008, 05:49 PM
Here are a couple specific studies that review PS and the testosterone:cortisol ratio -
HORMONAL EFFECTS OF PHOSPHATIDYLSERINE DURING 2-WKS OF WEIGHT TRAINING
[Annual Meeting Abstracts]
Fahey, T. D.; Pearl, M.
California State University, Chico
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
The hormonal and perceptive effects of phosphatidylserine administration during two weeks of weight training-induced over-training.
Fayey TD, et al.
Biol Sport 1998, 15(2): 135-144
06-09-2008, 11:24 PM
06-09-2008, 11:29 PM
Oh shut the f*** up.
He didn't burn anyone, nor did we need to be "shut down". Anabolic Minds is not about "burning" and "shutting down" people, its about intelligent discussion, why don't you read around a little bit.
I know I'll get negged for this, but give me a break, no reason to be an a**hole.
06-09-2008, 11:41 PM
Phospholipids and sports performance.
Jäger R, Purpura M, Kingsley M.
Increnovo LLC, 2138 E Lafayette Pl, Milwaukee, WI 53202, USA. email@example.com.
ABSTRACT: Phospholipids are essential components of all biological membranes. Phosphatidylcholine (PC) and Phosphatidylserine (PS) are Phosphatidyl-phospholipids that are required for normal cellular structure and function. The participation in physical activity often challenges a variety of physiological systems; consequently, the ability to maintain normal cellular function during activity can determine sporting performance. The participation in prolonged intense exercise has been shown to reduce circulatory choline concentrations in some individuals. As choline is a pre-cursor to the neurotransmitter Acetylcholine, this finding has encouraged researchers to investigate the hypothesis that supplementation with PC (or choline salts) could enhance sporting performance. Although the available data that evaluates the effects of PC supplementation on performance are equivocal, acute oral supplementation with PC (~0.2 g PC per kg body mass) has been demonstrated to improve performance in a variety of sporting activities where exercise has depleted circulatory choline concentrations. Short term oral supplementation with soy-derived PS (S-PS) has been reported to attenuate circulating cortisol concentrations, improve perceived well-being, and reduce perceived muscle soreness after exercise. More recently, short term oral supplementation (750 mg per day of S-PS for 10 days) has been demonstrated to improve exercise capacity during high intensity cycling and tended to increase performance during intermittent running. Although more research is warranted to determine minimum dietary Phospholipid requirements for optimal sporting performance, these findings suggest that some participants might benefit from dietary interventions that increase the intakes of PC and PS.
PMID: 17908342 [PubMed - in process]
This study gave no numbers, and one of the dosages it cited was .2 grams of PC per kg of body mass, which is an incredibly high dosage.
Do you have the full text?
Since the above study cites running and cycling it's only fair to compare their findings to this one:
Phosphatidylserine supplementation and recovery following downhill running.
Kingsley MI, Kilduff LP, McEneny J, Dietzig RE, Benton D.
University of Wales Swansea, Singleton Park, Swansea, United Kingdom. M.I.C.Kingsley@Swansea.ac.uk
PURPOSE: This study investigated the effects of 750 mg of soybean-derived phosphatidylserine (S-PtdSer), administered daily for 7 d prior to a bout of eccentric exercise and for 2d following exercise, on delayed onset of muscle soreness and markers of muscle damage, inflammation, and oxidative stress that followed prolonged downhill running. METHODS: Following preliminary testing and a familiarization session, eight recreationally active males repeated an individualized downhill run at -16.5% for 51.0 +/- 1.5 min at 8.7 +/- 0.3 km x h(-1) on four occasions (trials 1-4). Trials 1 and 37 were presupplementation control trials. After trials 1 and 3 the subjects received, in a double-blind and crossover fashion, either S-PtdSer or a glucose polymer placebo. Trials 2 and 3 were separated by a 4-wk washout period. Venous blood, perceived soreness ratings, and feeling states were assessed prior to exercise, after exercise, and at 24 and 48 h after exercise during each trial. RESULTS: Downhill running led to elevations in perceived soreness (P < 0.05), creatine kinase activities (P < 0.001), myoglobin concentrations (P < 0.001), interleukin-6 (IL-6) concentrations (P < 0.001), and lipid hydroperoxide concentrations (P < 0.01). However, supplementation did not significantly attenuate these responses. CONCLUSION: These results suggest that supplementation with 750 mg x d(-1) S-PtdSer for 10 d does not afford additional protection against delayed onset of muscle soreness and markers of muscle damage, inflammation, and oxidative stress that follow prolonged downhill running.
06-10-2008, 02:20 AM
BTW, I do have the full text. I can send you the full text if you PM with your email.
As far as the second study, the male subjects may not have been stressed enough to notice an ergonomic improvement from PS, or perhaps the methodology was not precise enough to pick up on a significant difference. Either way, the majority of the research on PS shows a positive effect, I think you found 1 of the 2 studies that showed PS having no ergonomic benefit. (over a dozen studies show a positive effect)
06-10-2008, 03:23 AM
06-10-2008, 05:05 AM
06-10-2008, 02:16 PM
There is no burden of proof for me because there isnt a SINGLE study to show that 7OH or 5AT are suppressive. The burden of proof is on you.
Free testosterone has everything to do with it. You can have an extremely high total test number and it will do absolutely nothing for strength, body comp, recovery etc etc. Besides the fact that total testosterone flucuates all day long.
You bashed my product when you posted this false statement:
05-05-2008 11:26 PM
Primordial Perf Quote:
"Originally Posted by StanChampion
So this product is supposed to be superior to the Lean-X/Activate stack I am currently using? Replace the LX with this?"
"Yes, especially for PCT when supporting natural testosterone production is most important."
You have no science to show that PS would be better over LX, ever, much less PCT.
You ref. this study in your write up and it does not involve any other metabolite of DHEA other then 7OXO and it is delivered by transdermal application. The study provides no conclusion or even questions 7OH or 5AT. This study provides nothing to supprot your claims against 7OH or 5AT or even oral 7OXO for that matter.
Effects of Transdermal Application of 7-oxo-DHEA on the Levels of Steroid Hormones, Gonadotropins and Lipids in Healthy Men.
You also ref this study which only tests transdermal 7OXO. It doesnt suggest in anyway that oral use of 7OH or 5AT would be suppressive in anyway. Your original post is BULL**** and you have no evidence to suggest anything other then people should not use TRANSDERMAL 7OXO during PCT.
06-10-2008, 02:19 PM
06-10-2008, 03:15 PM
06-10-2008, 03:26 PM
06-10-2008, 07:49 PM
Question about effective dose: Is the effective dose 800 mg of 50% PS or is it twice that or 800 mg of pure PS?
06-10-2008, 08:15 PM
Perhaps you didn’t read the full text of the studies I posted. 7OH was the primary active metabolite from the transdermal 7-oxo DHEA administration. 7OH goes up and testosterone, LH and FSH goes down. My original hypothesis still remains – “7-oxo DHEA metabolites lower testosterone”
Based on your above response, it appears you aren’t aware of the connection between 7OH, 5AT and 7-oxo. Let me drive it home for you.
Here is a quote from your LX product write up about 7OH –
“Neither of the two isomers of 7-OH can convert to androgens or estrogens but appear instead to convert between each other and another DHEA metabolite called 7-oxo-DHEA5”
And another quote about 5AT –
“5-AT, the first new ingredient in Lean Xtreme, is another interesting compound. Like 7-OH, it is a metabolite of DHEA.”
Case in point, these 7-oxo derived hormones are generally synonymous in action.
Just for fairness, here is a study on oral 7-oxo DHEA. Again, you see a drop in testosterone. (significant 8% drop)
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.
If you have research showing that 7-oxo derived ingredients don’t lower testosterone, feel free to post it. Otherwise, you have no reason to call BS until you bring something to the table.
06-10-2008, 08:16 PM
06-10-2008, 11:31 PM
06-10-2008, 11:38 PM
LOL! Seriously? You sure you want to bring up that study?
Despite an 8% decrease in total testosterone in
the blood of 7-oxo-DHEA-treated subjects (p <
0.01), both statistical methods disclosed that there
was a significant (14.4%, p < 0.01) increase of free
testosterone from day 0 (26.7 [1.3] pg/mL, mean [and
standard deviation]) to day 56 (30.8 [1.9] pg/mL) in
subjects treated with 3β-acetyl-7-oxo-DHEA.
06-11-2008, 12:13 AM
Besides, the topic here isn’t about increasing free testosterone. It’s about increasing production of testosterone (total T) and avoiding inhibition of the HPTA – something you can’t avoid with the DHEA metabolites.
06-11-2008, 12:25 AM
I would trade an 8% decrease in total T for an 14% increase in free T any day....
Just thought I'd point that out since you failed to leave that important part out from your "abstract". An 8% drop in total T would suck without the increase in free T.
06-11-2008, 12:37 AM
When Testosterone levels are low (ie, during PCT) you dont want further inhibition of the HPTA. An increase in Total T is what you should be looking for, not a supplement to "free up" your non-existent T levels.
06-11-2008, 03:36 PM
In these studies it was shown that oral use of 7OXO did not induce any anabolic or androgenic response and that body chemistry was unchanged when compared to placebo.
This has been proven by the patent holder (Humantecs) and can be found all over their website (humaneticscorp.com), which is why it is legal to use it in naturally tested events.
Lardy, H. et al (1998) "Ergosteroids 3 II: Biologically active metabolites and synthetic derivatives of dehydroepiandrosterone" steroids 63: 158-65.
Lardy, H. "Dehydroepiandrosterone and ergosteroids affect energy expenditure", in Health Promotion and Aging, R. Watson, ed. Harwood Acad. Pub. 1999. pp. 33-42. Zenk, J. Living Longer In The Boomer Age. NY: Advanced Research Press, 1998.
But just incase those weren’t enough, I pulled some more.
In this study the researchers tested DHEA and its metabolites for their androgenic actions. It was shown that DHEA-S, 7alpha-OH-DHEA, 7beta-OH-DHEA, and 7-oxo-DHEA had NO androgenic activity.
J Steroid Biochem Mol Biol. 2006 Apr;99(1):50-8. Epub 2006 Mar 9.
Dehydroepiandrosterone and its metabolites: differential effects on androgen receptor trafficking and transcriptional activity.Mo Q, Lu SF, Simon NG.
These results provide the first systematic comparison of the (i) androgenic activity of DHEA and its sulfated and hydroxylated metabolites, (ii) relative androgenicity of DHEA itself vs. the established androgens Adione and Adiol, and (iii) ability of DHEA and its major metabolites to promote AR-GFP intracellular trafficking. In addition to partitioning DHEA and its metabolites into compounds with (DHEA, Adione, Adiol) and without (DHEA-S, 7alpha-OH-DHEA, 7beta-OH-DHEA, and 7-oxo-DHEA) androgenic activity, the findings improve our understanding of the intracellular processes mediating the genomic effects of DHEA through AR.
This study confirmed what the other studies had already found out, no AR transcription by 7-oxo-dhea.
Proc Natl Acad Sci U S A. 1998 Sep 15;95(19):11083-8.
Delta5-androstenediol is a natural hormone with androgenic activity in human prostate cancer cells.
Miyamoto H, Yeh S, Lardy H, Messing E, Chang C.
George Whipple Laboratory for Cancer Research, Department of Pathology, University of Rochester Medical Center, 601 Elmwood Avenue, Box 626, Rochester, NY 14642, USA.
It is known that androst-5-ene-3beta,17beta-diol (Adiol), a precursor of testosterone (T), can activate estrogen target genes. The androgenic activity of Adiol itself, however, is poorly understood. Using a transient transfection assay, we here demonstrate in human prostate cancer cells that Adiol can activate androgen receptor (AR) target genes in the presence of AR, and that AR coactivator ARA70 can further enhance this Adiol-induced AR transcriptional activity. In contrast to this finding, an active metabolite of dehydroepiandrosterone, 7-oxo-dehydroepiandrosterone, does not activate AR target gene in the absence or presence of ARA70.
Although the study you posted showed what was “statistically significant” drop of total testosterone for that study, the drop itself is not significant because of the natural highs and lows of test production in the body. The following studies demonstrate the difference between those through the day as well as those differences between young and old (this study will be refd in my next post).
Circadian variation in testosterone, sex hormone-binding globulin, and calculated non-sex hormone-binding globulin bound testosterone in healthy young and elderly men
S. R. Plymate, J. S. Tenover and W. J. Bremner
Department of Clinical Investigation, Madigan Army Medical Center, Tacoma, WA 98431-5454.
Clin Endocrinol (Oxf). 1993 Aug;39(2):163-71.
Circadian variation in serum free and non-SHBG-bound testosterone in normal men: measurements, and simulation using a mass action model.
Cooke RR, McIntosh JE, McIntosh RP.
There is also an interesting study done which shows that testosterone production can be boosted just by knowledge of a sports event or testing.
So as I stated earlier, you are wrong.
06-11-2008, 03:43 PM
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06-11-2008, 03:55 PM
There are dozens of studies showing free testosterone is the bioactive form of testosterone, it is not something which has been overated by the supplement industry.
"Only about 2 percent of the total testosterone in the plasma of men is free or nonprotein bound; about 1 percent in women. In most men and women, more than 50 percent of total circulating testosterone is bound to sex hormone-binding globulin (SHBG), and most of the rest is bound to albumin. It is only the free or nonprotein bound testosterone which is the hormonally active form, able to interact with cellular hormone receptors. SHBG-bound testosterone is not readily available for intracellular complex formation because of SHBG's high binding affinity for testosterone."
"Testosterone-bound SHBG is considered biologically inactive. SHBG levels are sensitive to changes in estrogen and testosterone. Thus conditions which affect SHBG will directly affect the serum levels and biological activity."
For PCT you want an increase in total testosterone, free testosterone, control of estrogen, control of cortisol, increases in lean mass, decreases in fat mass and prevention of fat accumulation. All of the above is done by LX and is backed by science, which is why it is leaps and bounds better then PS.
06-11-2008, 03:57 PM
It can which is why an AI with DHEA doesnt provide any additional benefit then what an AI alone would provide. You would need to block 5ADs action on the estrogen receptor.
06-11-2008, 04:03 PM
This is a very informative thread, I'm going to come back to this.
Cortisol isnt really a hormone you want elevated during PCT at all. It brings a host of negatives. The most important (I believe) is its ability to lower LH and GnRH to some extent.
06-11-2008, 04:05 PM
06-11-2008, 05:02 PM
Nobody is questioning the fact that these DHEA metabolites don’t activate the AR. They don’t have to activate the AR to suppress the HPTA. That’s where your logic is wrong -- you assume that since they have no “anabolic or androgenic” action that they don’t influence the HPTA. They do suppress the HPTA, and the research clearly shows it. (It could even be argued that these metabolites are anti-androgens, since they cause a sharp rise in epitestosterone, the anti-androgen)
At any rate, you still haven’t addressed the original issue. Do you have any research showing that these ingredients don’t suppress the HPTA?
06-11-2008, 05:22 PM
If you want to debate the endocrinologic relationship and importance of free-test and total-test, feel free to start a new thread. This isnt the place.
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