Company Opposes Banning of 3 Prohormones
- 08-24-2008, 07:17 PM
Company Opposes Banning of 3 Prohormones
Supplement Consultants put up some counter points to Boldione and Estra 4,9 Dione being scheduled. I guess DMT is a lost cause... I got an email about it. Here it is
For purposes of this comment, we review only the claims that boldione, and 19-nor- 4,9(10)-androstadienedione satisfy the requirements of chemical and pharmacological relationship to testosterone. As indicated in the proposed rule, the scientific literature regarding desoxymethyltestosterone appears sufficient to satisfy all four requirements. Thus, Supplement Consultants takes no position toward this substance. However, such is not the case for boldione nor 19-nor-4,9(10)-androstadienedione. Instead, the proposed rule is based solely upon two studies sponsored by the DEA. Thus, these studies must be evaluated critically for conclusive results to determine whether the substances identified herein completely satisfy the aforementioned requirements.
I. The Drug Enforcement Administration has failed to show that boldione and 19-nor-4,9(10)- androstadienedione are chemically related to testosterone.
Both boldione and 19-nor-4,9(10)-androstadienedione are distinctly different from testosterone in that each lacks C-17 Beta Hydroxyl, which is present in testosterone. Although, the DEA proposes that ?[t]he human body would be expected to metabolize the ketone group at carbon 17 into a hydroxyl group that is present on testosterone,? no authority is cited for such claim. Moreover, the DEA?s proposition that the substance will likely produce anabolic effects inappropriately blurs the line between the requirement to show a chemical relationship with the requirement to show a pharmacological relationship. Looking at the chemical relationship requirement in a vacuum, the absence of the C-17 Beta Hydroxyl in both of these substances indicates that the two are not chemically related to testosterone because the carbon is necessary for full androgen receptor activation and, consequently, anabolic effects. Even assuming that it were appropriate to look at the pharmacological relationship to determine whether the body indeed metabolizes the substance in such a manner, the studies sponsored by the DEA fail to provide any conclusive evidence of anabolic effects. When analyzing the data from these studies, it is evident that the DEA?s expectation does not come to fruition and that the absence of C-17 Beta Hydroxyl is determinative.
The DEA must show a stronger chemical relationship between the substances and testosterone that it has presented in its proposed rule. Any similarity in the chemical structure combined with a mere possibility of further metabolization in the human body is not sufficient analysis to satisfy this preliminary requirement in order to schedule a substance as an anabolic steroid. Such superficial analysis could lead to absurd conclusions. For example, one could argue that cholesterol should be added to the list of anabolic steroids. It is common knowledge that cholesterol can metabolize into testosterone because of its chemical structure. First, cholesterol is converted to pregnenolone. Pregnenolone is then converted into17a-hiydroxyprengnenolone. Subsequently 17a-hidroxyprengnenolone converts into DHEA. DHEA then converts into androstenedione, which converts into testosterone. Of course the point of this example is not to advocate that the scheduling of cholesterol as an anabolic steroid. Rather, it should be clear that there must be a strong chemical relationship in order to preclude classifying substances as ?anabolic steroids? when they are missing the component responsible for producing anabolic effects. The DEA must avoid the slippery slope logic of lumping everything into the category of an anabolic steroid precursor.
II. The Drug Enforcement Administration has failed to show that boldione and 19-nor-4,9(10)- androstadienedione are pharmacologically related to testosterone.
To satisfy the requirement that the substances are pharmacologically related to testosterone, the DEA must show that the substances produce anabolic and androgenic effects within the body. The proposed rule briefly interprets ?pharmacologically related to testosterone? to mean that the substances ?produce similar biological effects.? Of course, this proposed standard is too vague. What biological effects are required? What degree of biological effect is sufficient? The DEA?s interpretation could easily be satisfied by thousands of substances that are clearly not anabolic steroids. Instead the appropriate standard, as apparent from the studies sponsored by the DEA, is whether the substances produce anabolic and androgenic effects within the body.
In determining whether the DEA has satisfied this requirement, it is important to remember that the DEA has already admitted that ?the published literature contained insufficient pharmacological data to determine whether boldione and 19-nor-4,9(10)-androstadienedione were pharmacologically related to testosterone.? Instead, the attempt to satisfy this requirement is based solely upon two studies sponsored by the DEA. Two studies drawing conclusions consistent with the specific aim of agency sponsoring the studies is insufficient scientific justification and indicia of reliability to serve as the basis of scheduling the substances herein as controlled substances. If the Department of Justice insists upon relying solely upon these two studies, the studies must conclusively show that the substances produce both anabolic and androgenic effects within the body. Otherwise, the DEA has failed to show that the substances are pharmacologically related to testosterone.
A. The Pharmacological Analysis of Boldione and 19-Nor-4,9(10)-Androstadienedione for Androgenic Activity Using C3H10T1/a Stem Cells does not show a pharmacological relationship.
The study is tainted because the sample is not random. The study indicates that ?[o]nly sub populations that displayed stable myogenic differentiation were used in the subsequent experiments for testing the compounds.? This selection was unnecessary based upon the fact that the cells were obtained from the ATCC and were subcultured according to protocol. Thus, the experiment is called into doubt. It cannot be certain whether these cells both differentiate and de-differentiate. Thus, it is not possibly to adequately assess promotion of myotubial formation in order to determine whether the substances produce anabolic effects.
This study cannot be relied upon to determine wither the androgenic or the anabolic activity of either substance. In order to draw the conclusion that the substances are androgenic, the study relies upon an assumption that mere binding to an androgen receptor and translocation to the nucleus is sufficient to show androgenic activity. However, this is merely a preliminary step in the process of producing an androgenic effect. In order to conclude that there is androgenic effect, the androgen must also bind to the specific sites on the nucleus and binding to those sites must release the expected RNA transcripts.
Even if the assumption were accepted, the significance of any androgenic activity is devastatingly insignificant. Figure 1 indicates that A1 and E1 were ten times as concentrated as DHT, yet DHT was still more potent in inducing the AR translocation. More specifically the concentration levels for both substances were 100 nM, yet they were fairly comparable to the potency of translocation of the androgen receptor as the control. Most astonishing is the fact that DHT was concentrated ten-fold and only doubled the control. Certainly there needs to be a threshold for how potent the concentration must be in determining the androgenic effect when the DEA attempts to establish a pharmacological relationship. This would certainly be a case where the threshold has been crossed and the relationship too small to satisfy such a requirement.
B. The Analysis of Androgenic and Anabolic Activities of 1,4-Androstadien-3,17-Dione (Boldione) and 19-Nor-4,9(10)-Androstadenedione in Male Sprague Dawley Rats does not show a pharmacological relationship.
The DEA argues that this study satisfies the requirement to show a pharmacological relationship between boldione and testosterone based upon the claim that boldione prevented atrophy of the ventral prostate, seminal vesical, and levator ani in castrated male rats. Thus, the DEA concludes that boldione produces androgenic and anabolic effects within the body. However, a critical review of the study paints a much different picture. The study does not indicate any significant increase in androgenic or anabolic activity.
The study does not credibly show anabolic effects in the body. Figure 2 of the study illustrates that the rats that were implanted with empty silastic capsules gained approximately 90g. The study clearly shows that 19-Nor-4,9(10)-Androstadenedione is not anabolic. There was very little weight gain by the rats implanted with the substance. In fact the rats implanted with 19-Nor-4,9(10)-Androstadenedione gained only approximately 15g! Likewise, the study shows no anabolic activity for the castrated rats implanted with boldione. These rats did not gain a significant amount greater than the castrated sham. As the study concludes, ?[g]rowth and final body weight was not effect (sic) by administration of 1,4-androstadien,3,17-dione.? How can the DEA propose to classify these substances as anabolic steroids without showing them to actually be anabolic? The only potential claim for muscle growth to indicate anabolic activity is an overreliance upon an increase in the levator ani muscle. This muscle is not present in humans and should not serve as the basis to show anabolic effects in humans, especially in light of insufficient scientific literature.
Moreover, the study does not show that the substances have androgenic activity. In fact the study specifically states that ?[t]he direct androgenic and anabolic activity of 1,4-androstadien-3,17-dione in sham operated rats is less clear.? Actually, the test results contradict themselves for both substances, especially when evaluating androgenic activity. The study indicates an increase in testosterone. However, when looking at Table 3, it is apparent that the intact rats implanted with boldione had a decrease in hormonal levels. This, flies directly in the face of the conclusion that the substances are androgenic. The study does provide evidence suggesting that 9-Nor-4,9(10)-Androstadenedione androgenic activity based upon increased hormonal levels of the rats. However, the severely limited weight gain in these rats suggests a problem with the population and the results are therefore unreliable. To argue that either of these substances are androgenic is a stretch beyond reason.
The DEA has failed to satisfy all four statutory requirements in order to classify boldione and 9-Nor-4,9(10)-Androstadenedione as schedule III anabolic ateroids under the Controlled Substances Act. The only evidence proffered to evaluate whether these substances are chemically and pharmacologically related to testosterone are two studies that were sponsored by the DEA itself. Upon critical review of the studies, it is apparent that the DEA has failed to satisfy the requirements stated herein. Without such a showing, the DEA has not satisfied its burden and there is no grant of rulemaking authority to permit the scheduling of these substances.
- 08-24-2008, 07:18 PM
Glad to see someone fighting back!
08-24-2008, 07:20 PM
08-25-2008, 01:19 AM
08-25-2008, 01:31 AM
Interesting info. I'm somewhat confused by their argument of the missing the hydroxl at c17 though as all 'PH's' have a keto instead - even all the previously banned PH's like 1AD and 4AD. The Keto alteration that PH's have still allows binding to the androgen receptor like with test through conversion to the hydroxyl.
08-25-2008, 08:42 AM
08-25-2008, 02:54 PM
08-25-2008, 05:10 PM
I hope this stand works, and I hope those tards back off. I wont be able to enjoy the good products in the future
08-25-2008, 05:42 PM
I 100% completely hope the ban doesn't happen, and I'm all for individual choice. I'm just slightly pessimistic since the US Gov't always gets their way regardless. But my point above is even if these compounds don't 'directly' have anabolic properties - once they're ingested they convert to anabolic hormones.
08-25-2008, 05:47 PM
Well argued...let's hope it has traction.
No reason previous bans cannot be overturned by establishing precedent with THIS one.
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08-25-2008, 05:50 PM
08-27-2008, 07:13 PM
I am going to beg this guy to start an association. I am just too busy with all of our bull****, but a real association where ALL of the money goes to fight for supplement freedom.
08-27-2008, 07:27 PM
08-28-2008, 09:12 AM
No reason that they can't but I am not sure the mechanism for this. Someone should write this guy and ask him.
08-28-2008, 09:44 AM
08-28-2008, 11:22 AM
You have to consider that if this ban were overtuned through legal procedings than any future legal procedings would likely be held in the same level (or higher [appeals, sup., etc]) court in the same jurisdiction where precedent is not necessarily binding.
08-28-2008, 09:50 PM
I doubt we will ever see a reversal of something that is scheduled...take a look at pot. We have had now 3 standing presidents that publicly admitted to smoking pot...yet it is still illegal? Come now... If one can still govern the country after...OH MY GOD...smoking pot... should it really be something punishable by 25 years in prison in some states?
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