I'd like to see these studies as well
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.
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
Here are a couple specific studies that review PS and the testosterone:cortisol ratio -
HORMONAL EFFECTS OF PHOSPHATIDYLSERINE DURING 2-WKS OF INTENSE 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
burn!!! I was waiting for you to shut them down!
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.
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.
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)
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.
Common guys, were here for good info lets keep it clean
Question about effective dose: Is the effective dose 800 mg of 50% PS or is it twice that or 800 mg of pure PS?
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.
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.
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.