EQ and 1-test

[Big Cat HH]

My theory still wouldn't fly then, because I was referring to shoulders and arms, two areas not particularly rich in adipose tissue.

 

[pa1ad]

ANd it still works better than the oral. What does that tell you ?

Wait a minute, what am I saying. Fuck that, you liar. You tried to trick me. I didn't use water. I used ethanol. Read my post next time. So no problem. You were confusing me. I was thinking "why can't alcohol mix with alcohol ?"

Do you make this stuff up as you go along just so you can discredit me, so you wouldn't have to admit I was right ?

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You said you used 60% ethanol which means it contained 40% water. You are confused I agree

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Then everybody in this frigging industry is a threat but you. My info is a lot more accurate than what most companies are spreading, and when people come to me its with questions about products and claims. I would say that's a substantial improvement listening to me over Muscletech, SDI, VPX, SAN and a whole host of other firms.

And for the record, I'm not coming on these boards and "saying my stuff". I stated an opinion, a theory and had the politeness to add a question mark at the end for you to fill in any mistakes I might have made. There is only one person here who spreads his words like they were gospel, and that's you ...


Its not so much that you are stubborn and rude that bothers me (I am the same way most of the time), its that you seem to operate under the largest scale of hypocrisy I have ever seen in my life.

BTW, love the way you only answer questions you can rebut. I take it you concede the other points ? [/B]

Please review exactly what points you wish to address. You are all over the place on this thread so I don't even know what you are referring to. I will gladly pick you apart one issue at a time if you just make a list for me

 

[Big Cat HH]

You said you used 60% ethanol which means it contained 40% water. You are confused I agree

Not as bright as you look huh ? 60% of the solution. As in 60% ethanol SD40, same stuff you use, 30% IPM and 10% Octyl. Go check the back post.

Please review exactly what points you wish to address. You are all over the place on this thread so I don't even know what you are referring to. I will gladly pick you apart one issue at a time if you just make a list for me

Thank you. I'll have to go back and reread the back posts myself before I find them all, but you can start on this one, i'll edit the post as I find them :

1.Is there any proof to rebut my findings that 1AD is better as a transdermal than as an oral ?

2.Where is this 10-20% number on transdermals coming from, and what sort of carrier are you basing it on ? I find it a hard number to swallow because that would mean oral 4AD, Nor-diol, 5AA, and so forth would be very, very weak at that to see a 5 to 6-fold increase in results on similar doses.

3. I quote : 40-80 mg of a steroid a day is alot of steroid. 4-AD does not have to be super potent to have a discernable effect at this daily dosage. Is there any viable evidence that says 4AD has intrinsic activity ?

4.Straight facts only : IS there evidence of a higher conversion rate of 4AD in other tissues, and in any regard, wouldn't anything lower than 100% conversion completely rebut your theory of getting 40-80 mg of an active androgen in the blood ?

5.Again, just the facts please : Do you have any serious proof that the hepatic breakdown numbers are less than those of the urinary excretion study (as you indicated) and if so, why are both Ergopharm and Molecular nutrition using these excretion studies to document the oral bio-availability of their product ?

I leave it at that for now, if you could give me a straight answer on those I would very much appreciate it. Thanx.

 

[pa1ad]

Not as bright as you look huh ? 60% of the solution. As in 60% ethanol SD40, same stuff you use, 30% IPM and 10% Octyl. Go check the back post.
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I SEE I MISINTERPRETED WHAT YOU SAID THEN

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Thank you. I'll have to go back and reread the back posts myself before I find them all, but you can start on this one, i'll edit the post as I find them :

1.Is there any proof to rebut my findings that 1AD is better as a transdermal than as an oral ?

------------

NO BUT I MADE 50 BOTTLES OF A PROTOTYPE FORMULA AND HAD OVER A DOZEN PEOPLE TRY IT OUT AND MY FEEDBACK INDICATED THAT IT WAS NOT AS GOOD. I WILL PROBABLY COME OUT WITH A 1-AD SPRAY ANYWAY SO PEOPLE HAVE THE OPTION. ENOUGH ABOUT THIS ALREADY

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2.Where is this 10-20% number on transdermals coming from, and what sort of carrier are you basing it on ? I find it a hard number to swallow because that would mean oral 4AD, Nor-diol, 5AA, and so forth would be very, very weak at that to see a 5 to 6-fold increase in results on similar doses.

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IT IS COMING FROM THE RESEARCH ON TRANSDERMAL ABSORPTION OF STEROIDS THAT IS IN YOUR UNIVERSITY LIBRARY. THIS INCLUDES THE INSERT DATA ON ANDRO GEL WHICH HAS IPM IN IT. SO ACCEPT THE FACTS, OK?

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3. I quote : 40-80 mg of a steroid a day is alot of steroid. 4-AD does not have to be super potent to have a discernable effect at this daily dosage. Is there any viable evidence that says 4AD has intrinsic activity ?

-------------

4-AD EITHER ACTS AS JUST A PROHORMONE, OR AS AN ACTIVE HORMONE AND PROHORMONE. I WENT THROUGH THIS BEFORE

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4.Straight facts only : IS there evidence of a higher conversion rate of 4AD in other tissues, and in any regard, wouldn't anything lower than 100% conversion completely rebut your theory of getting 40-80 mg of an active androgen in the blood ?

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I DID NOT SAY ACTIVE ANDROGEN. GUESS WHAT, ANADROL IS NOT AN ACTIVE ANDROGEN. I SAID STEROID

THERE IS NO EVIDENCE OF HIGHER 4-AD CONVERSION IN OTHER TISSUES BUT IT IS WELL KNOWN THAT ENZYME LEVELS VARY TREMENDOUSLY THROUGHOUT THE BODY. I HAVE DONE 1000 TIMES THE RESEARCH THAT YOU HAVE DONE ON THESE SUBJECTS BTW

------------------


5.Again, just the facts please : Do you have any serious proof that the hepatic breakdown numbers are less than those of the urinary excretion study (as you indicated) and if so, why are both Ergopharm and Molecular nutrition using these excretion studies to document the oral bio-availability of their product ?


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YOU KNOW WHAT? I CAN EXPLAIN THIS TO YOU BUT YOU WOULD NOT UNDERSTAND IT. SO THERE

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I leave it at that for now, if you could give me a straight answer on those I would very much appreciate it. Thanx.

------------

WHY DON'T YOU GET THROUGH COLLEGE AND STUDY SOME SCIENCE FIRST?

 

[Big Cat HH]

Wow, I'll take that as "No Big cat, I can't give you a straight answer", and draw my conclusions from that. Thanx for giving it a shot though.

 

[Big Cat HH]

IT IS COMING FROM THE RESEARCH ON TRANSDERMAL ABSORPTION OF STEROIDS THAT IS IN YOUR UNIVERSITY LIBRARY. THIS INCLUDES THE INSERT DATA ON ANDRO GEL

Ok, sorry, i couldn't let this go. But you are referring to the standard ethanol/IPM mix. You forget there are other and better transdermal enhancers. So it could account for our differences in opinion. The addition of octyl salicylate to my mix may have accounted for the better results then.

Although I still have to contest that even norandro-spray would be near the top end of your 10-20% range.

 

[pa1ad]

Ok, sorry, i couldn't let this go. But you are referring to the standard ethanol/IPM mix. You forget there are other and better transdermal enhancers. So it could account for our differences in opinion. The addition of octyl salicylate to my mix may have accounted for the better results then.

Although I still have to contest that even norandro-spray would be near the top end of your 10-20% range.

The addition of octyl salicylate is not gonna do a whole heck of alot

 

[pa1ad]

Wow, I'll take that as "No Big cat, I can't give you a straight answer", and draw my conclusions from that. Thanx for giving it a shot though.

Actually your question made no sense to me. I am not sure what you were even referring to.

What I recall vaguely is that you quoted a percentage of steroid recovered from urine as an indication of bioavailablity. Urinary metabolites are not a good indication of bioavailability - if they were then you would have to determine that testosterone injections have very little bioavailability since very little testosterone shows up in the urine

In the case of the 1-androstenes however you can make a case by comparing the percentage of 17beta hydroxyl metabolites that are recovered in the urine versus those recovered from other prohromones. What you find is that a significantly greater amount is recovered. This indicates that more of the 1-androstenes are converting to active hormone, therefore the RELATIVE bioavailability must be greater. You cannot get a real number for the bioavailability from urinary metabolites of course, that can only be determined from blood sampling. A clinical study of blood hormone responses from 1-AD in humans is about to be completed. I will share the information so that other companies that don't do a damn thing but copy the innovators that actually fund research can use it to promote their knock offs

So are you ever gonna do a clinical study to support the claims you are making such as that your topical has magical properties that give it bioavailability over 20%? Or are you just gonna use your wonderful anecdotal methods of shoulder swelling as verification?

Just busting your balls.....

 

[Big Cat HH]

So basically the urinary excretion shows an arbitrary comparison between prohormones based on both availability and conversion ? Wouldn't that mean that its possible that the 1-double bond doesn't do anything against hepatic breakdown but just assures a better conversion ? That too is a likely explanation.

As for sharing the data, there aren't a whole lot of people you can depend on for reliable information. Those of us who actually read the research will still see who sponsored it.

So are you ever gonna do a clinical study to support the claims you are making such as that your topical has magical properties that give it bioavailability over 20%? Or are you just gonna use your wonderful anecdotal methods of shoulder swelling as verification?

You know, that's not a half bad idea for a first published study. You sponsoring ?

Just busting your balls.....

Fair enough, I deserved it

 

[pa1ad]

So basically the urinary excretion shows an arbitrary comparison between prohormones based on both availability and conversion ? Wouldn't that mean that its possible that the 1-double bond doesn't do anything against hepatic breakdown but just assures a better conversion ? That too is a likely explanation.

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The phenomenon specifically that is observed with 1-androstenes is a decrease in excretion of 17-keto steroids (inactive) and increased excretion of 17beta-hydroxyl steroids. This is either due to a shift in the 17beta-HSD equilibrium towards the formation of hydroxyl steroids, or to an inhibition of excretion of the hydroxyl steroids. Or maybe a combination of both. I dunno, for practical purposes it doesn't really matter what the mechanism is as long as the net result is that more 17beta-hydroxyl is formed.

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As for sharing the data, there aren't a whole lot of people you can depend on for reliable information. Those of us who actually read the research will still see who sponsored it.

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Yeah I know