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USPlabs Conducts Study with Indigo Biosciences: Penn State Researchers
Old 01-22-2009, 03:35 PM   #1
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Intro and basic explaination by Mulletsoldier

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Originally Posted by Mulletsoldier
The following was a study conducted at Indigo Biosciences, by Penn State University researchers, written by BA Sherf, Ph.D and approved by J. Vanden Heuvel, Ph.D to validate one of the major claims [and benefits] surrounding PRIME?s efficacy: A lack of suppressive hormonal action. While "hormonal suppression" is almost exclusively represented as sex-steroidal, suppressive can refer to other endocrine functions such as GR [glucocorticoid receptor] antagonism. GR expression is ubiquitous: Appearing in almost every cell-type in the human body, the agonism and antagonism [and resultant effects on gene regulation] of the GR has a wide array of physiological consequences; ranging from sex-function to the immune system. As a result, this particular endeavor was undertaken to determine whether or not GR antagonism was occurring, and to what degree, to ensure that no hormonal action was occurring.

Fortunately for the consumer, this Penn State Study is the first step in a thorough legitimization process that USPlabs is embarking on with PRIME; it (the Penn State study) will be accompanied by an objective trial of sorts (The Staley Report), where trainees were selected away from mainstream boards (and the associated biases ? positive or negative) and thoroughly recorded their progress under Charles Staley; it will also be accompanied by the release of the Beta Tester's blood abstracts which, along with this particular study, will display no cyto-toxicity and no suppression of endogenous hormones.

Simply, we are objectively validating what we know to be subjectively successful, through unaffiliated, and independent means. While detractors will no doubt detract - merely on a new tangent - upon seeing this study, we feel it important to communicate the uniqueness of the actions we are currently undertaking. The expense and bureaucracy involved in securing studies such as this one from respectable and recognized Universities is enormous; and this is exactly why we [as an industry and consumer] seldom see them surface. While University studies such as this one are often utilized as objective research, they are very seldom conducted for the company itself; however, in the case of PRIME, realizing a lack of objective data to validate consumer feedback, we thought it was only necessary. Fortunately for the consumer, that process has only begun, and not ended, here: The results in respects to GR Antagonism came back negative, as we had hoped;however, as a company we are diligent in our desire to positively illuminate the exact MoA [method of action] of USPlabs PRIME.

However, in that light, we must remember that many products we commonly use today do not have validated MOAs; much in the fashion we have done here, simply their safety and efficacy need be validated for them to be produced en masse. For example, Minoxidil (Rogaine), one of the most effective and the widest-selling hair treatment products available, does not have a proven MOA. Much like PRIME, there are several postulates (one being the mediation of the NO pathway, despite the fact no cGMP-specific action has been proven) but none proven. Does this in any way invalidate the massive body of anecdotal feedback surrounding Minoxidil? Of course not: Despite the lack of MOA for Minoxidil, it is still regarded as the ?first-line-of-defense? for uncomplicated hair loss.

Even Acetaminophen - a compound so engrained in popular culture and medicine, your spell-checker recognizes it - has no verified specific MoA. While it has been elucidated that Acetaminophen lowers levels of Prostaglandin E2, the exact mechanism [Mechanism of Action] through which this is accomplished has not been elucidated. As PGE is a product of the commonly inhibited COX [cyclo-oxygenase, in forms I and II] pathway, Acetaminophen?s exact effect on COX [if any is occurring] is unknown and debatable. This point, then, cannot be stressed enough in regards to the actions USPlabs is currently undertaking: We are seeking to provide for PRIME what has not been provided for the widest-selling analgesic available. Why USPlabs is being subjected to a standard not subjected to a compound each person reading this has ingested remains a mystery ? this being said, we do intend to live up to even the most veracious of detractors in regards to our attempts to validate and legitimize PRIME.

In conclusion, we realize two things: a) that PRIME is a contemptuous topic as of late and; b) that this product, as efficacious as it may be, needs some external validation to dissuade some of the negativity surrounding it. We are going through these great lengths ? funding University Studies, in-depth trials and blood tests and expending massive amounts of capital and energy to do so? to address both of these things at the same time. Simply put, a ?scam company? would not do anything of this scope or magnitude for an ineffective product; we know PRIME works, we simply want to know how, and want YOU to know how.
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Old 01-22-2009, 03:37 PM   #2
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Further explanation by Strategicmove

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Originally Posted by Strategicmove
Following up on Mulletsoldier's post, I would like to add further perspective to the motivation behind the Penn Study. Initial beta-tester feedback on an earlier (beta) version of PRIME was overwhelmingly positive and consistent in the elucidation of the results (cumulative dramatic improvement in strength and endurance, favourable body recomposition, increased libido, truncated post-exercise recovery, and so on) from PRIME beta. A combination of these consistent beta reviews coupled with subsequent favourable reviews of PRIME further fuelled our excitement and led us to investigate various possible mechanisms of action (MoAs) that PRIME may act through. After blood tests showed neither an up-regulation nor a suppression of endogenous hormone production, we decided to investigate whether or not PRIME may act via a glucocorticoid-receptor mechanism. Our a priori expectation was that it does not, implying the absence of a hormonal action by PRIME. The Penn State study showed that PRIME does not act via glucocorticoid antagonism, in line with our a priori postulate. So, what are the implications of the outcome of the Penn State Study? In order to answer this question fairly and completely, we may want to take a step back and consider the background. First of all, sponsoring a study of this type, not only reflects a deep confidence and commitment on the part of a supplement company to a particular product or compound that it considers novel, but also requires significant commitment of resources to the project. Many readers may agree that no company would make this move, if it lacked confidence in its innovation. Second, it was necessary to commit resources to understanding PRIME's mechanism of action (MoA), to not only validate the favourable reviews that countless users have reported, but also to respond to the legitimate inquiry of others with respect to the specific or approximate mechanisms through which PRIME exerts its effects. Our conviction that the positive results reported by many users were not delusional, coupled with the fact that we also have an interest in understanding the full potential of our novel compound, via understanding its biosynthesis, provided further motivation to expose PRIME to rigorous scientific scrutiny. As it turned out, professional laboratory analysis confirmed that PRIME's pathway is non-hormonal, matching our expectations.

So, what now? By showing that PRIME acts other than via a glucocorticoid-receptor antagonism, the Penn State Study does not suggest in any manner that PRIME is ineffective; rather, it implies that the mechanism of action lies elsewhere.

As is well-known the absence of a well-described and known mechanism of action relating to any particular agent, is neither a necessary nor a sufficient condition for its efficacy. On the contrary. Drug-discovery or drug-development programmes are known to be littered with cases of powerful compounds with unknown mechanisms of action. In a related fashion, it is not uncommon in those programmes to identify a mismatch between an agent?s postulated in vivo MoA and its in vitro MoA. A couple of examples may suffice. Take the antibacterial compound, hexachlorophene, whose in vivo MoA turned out to diverge from its expected MoA from in vitro biochemical data. Furthermore, in HIV-research, there are various compounds that are known to have bioactivity against HIV, but with unknown MoAs. These compounds are the subject of promising drug-development programmes. For perspective, typically, inhibition of the HIV virus occurs via the well-known MoA, reverse transcriptase (the HIV virus relies on the so-called transfer RNA for its replication. Inhibiting the virus? affinity for tRNA is a preferred anti-viral pathway). As it turns out, certain novel agents have shown promise in the inhibition of the HIV virus while plotting an unknown MoA. Furthermore, (natural) lignans are known to include compounds with antiviral and antineoplastic properties. These include podophyllotoxin, and etoposide and teniposide, two of podophyllotoxin?s semi-synthetic derivatives. Podophyllotoxin?s antiviral MoA is known to be via its inhibition of microtubule assembly in the mitotic apparatus, leading to a blockage of cell division. However, although etoposide and teniposide are included in many cancer chemotherapy protocols, they are known to have a completely different MoA (inhibition of DNA topoisomerase II); while other podophyllotoxin analogues (weak topoisomerase II inhibitors), also used in chemotherapy protocols, do not have a known MoA! Another example: Tyloindices, isolated from a plant from India, were known to be one of the most potent anti-tumor compounds ever screened at the National Institute of Cancer. Yet, their MoA was unknown! To continue, Chagas? disease is a well-known social and health challenge in Latin America. Caused by epimastigotes cultures of Trypanosoma cruzi, it afflicts millions in Latin America. A novel compound, 5-nitro-2-thienyl-malononitrile, was accidentally derived in the process of an unsuccessful attempt to obtain new 3,5-diamino-4-(5'-nitroarylidene)-4H-thiadiazine 1,1-dioxide derivatives. Although, the MoA of 5-nitro-2-thienyl-malononitrile was unknown, it still demonstrated significant anti-Trypanosoma cruzi activity. And so on. Examples abound of compounds without a known MoA, yet demonstrate significantly favourable pharmacological activity. So, is PRIME necessarily ineffective because its MoA has not been uniquely determined? Are users delusional when they report tangible results from PRIME supplementation, just because PRIME's MoA is still undetermined? My response would be a resounding "NO"! Most would admit that agents possessing a potent bioactivity, but with an unknown mechanism of action, are in fact highly sought-after in drug-development circles, as they may embed considerable potential in the activation of key pharmacological pathways.

We would like you to consider the commissioning of this Penn State Study as a demonstration of our confidence in our product. Beyond this, we would also like you to consider this Penn State Study as a validation of our original postulate about PRIME's non-hormonal action, further advancing our confidence in, and passion for, PRIME.

Thank you very much for supporting USPLabs!
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Old 01-22-2009, 03:46 PM   #3
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MEGAUPLOAD.COM, study available for download
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Old 01-23-2009, 06:38 AM   #4
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impressive study! looks to me like the claims USP has on prime are just what the supplement is supposed to do,, looking more and more like a great supplement,, i myself have not tried it, but i may give it a run.
thanks for the info bro..
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Old 01-23-2009, 12:14 PM   #5
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Quote:
Originally Posted by mikeh40+ View Post
impressive study! looks to me like the claims USP has on prime are just what the supplement is supposed to do,, looking more and more like a great supplement,, i myself have not tried it, but i may give it a run.
thanks for the info bro..
Thanks buddy...
Let me know if you have any questions!
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Old 02-20-2009, 10:45 PM   #6
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Looks like USPlabs is really starting to make a run at the big boys of the supplement world.
 
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Old 02-22-2009, 10:52 PM   #7
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Quote:
Originally Posted by GRAVESY079 View Post
Looks like USPlabs is really starting to make a run at the big boys of the supplement world.
haha thanks buddy...

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Old 06-01-2009, 10:03 AM   #8
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WHAT are you talking about??
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