Hindered gains from Thistle

**taiotosh7** · 06-12-2006, 04:40 PM

So far I have yet to see any documented proof that milk thistle actually hinders gains and prevents an aas from working 100%. Was this thought just conjured up by human logic through the knowledge that we have of aas and thistle??? Where did this idea come from? Does anybody know? I would like to know?

**guest589745** · 06-12-2006, 05:49 PM

I have never hear of it effecting gains. How would it?

**fLgAtOr** · 06-12-2006, 05:58 PM

There is a study that I need someone to makle sense of...I be back...

**stuball** · 06-12-2006, 06:00 PM

Originally Posted by taiotosh7

So far I have yet to see any documented proof that milk thistle actually hinders gains and prevents an aas from working 100%. Was this thought just conjured up by human logic through the knowledge that we have of aas and thistle??? Where did this idea come from? Does anybody know? I would like to know?

Ive been hearing that a lot lately, And thats a great question, read a thread before that there is milk thistle without silymarin ( not sure if that spelled right ) and that the silymarin hinders gains, but the milk thistle i have is mostly silymarin, i really dont know what to think half the time..Do it dont do it ???

**taiotosh7** · 06-12-2006, 06:01 PM

I hear about it all the time on this board how someone is either unsure that it hinders gains or ones claiming that it will for sure. I hear that thistle hinders protein synthesis therefore hindering gains.....I hear that thistle helps to assist the liver in breaking down the 17aa of pills therefore a smaller amount goes in the bloodstream......I wanna hear some more!

**fLgAtOr** · 06-12-2006, 06:01 PM

I found this on another board...But I need some help making sense of it.

Silybin inactivates cytochromes P450 3A4 and 2C9 and inhibits major hepatic glucuronosyltransferases.

Sridar C, Goosen TC, Kent UM, Williams JA, Hollenberg PF.

Department of Pharmacology, The University of Michigan, Ann Arbor, MI 48109, USA.

Silybin, a major constituent of the milk thistle, is used to treat several liver disorders. Silybin inactivated purified, recombinant cytochromes P450 (P450) 3A4 and 2C9 in a mechanism-based manner. The inactivations were time-, concentration-, and NADPH-dependent. The inactivation of the 7-benzyloxy-4-(trifluoromethyl-)coumarin O-debenzylation activity (P450 3A4) was characterized by a K(I) of 32 microM, a k(inact) of 0.06 min(-1), and a t(1/2) of 14 min. Testosterone metabolism to 6-beta-hydroxytestosterone (P450 3A4) was also inactivated with a K(I) of 166 microM, a k(inact) of 0.08 min(-1), and a t(1/2) of 9 min. The 7-ethoxy-4-(trifluoromethyl)coumarin O-deethylation activity of purified human P450 2C9 was inactivated with a K(I) of 5 microM, a k(inact) of 0.14 min(-1), and a t(1/2) of 7 min. Parallel loss of heme was observed with both P450s. Activity of both P450 enzymes was not recovered after removal of silybin either by dialysis or by spin gel filtration. In addition, silybin inhibited the glucuronidation of 7-hydroxy-4-trifluoromethylcoumarin catalyzed by recombinant hepatic UDP-glucuronosyltransferases (UGTs) 1A1, 1A6, 1A9, 2B7, and 2B15, with IC(50) values of 1.4 microM, 28 microM, 20 microM, 92 microM, and 75 microM, respectively. Silybin was a potent inhibitor of UGT1A1 and was 14- and 20-fold more selective for UGT1A1 than for UGT1A9 and UGT1A6, respectively. Thus, careful administration of silybin with drugs primarily cleared by P450s 3A4 or 2C9 is advised, since drug-drug interactions cannot be excluded. The clinical significance of in vitro UGT1A1 inhibition is unknown.

**stuball** · 06-12-2006, 06:06 PM

Originally Posted by fLgAtOr

I found this on another board...But I need some help making sense of it.

Silybin inactivates cytochromes P450 3A4 and 2C9 and inhibits major hepatic glucuronosyltransferases.

Sridar C, Goosen TC, Kent UM, Williams JA, Hollenberg PF.

Department of Pharmacology, The University of Michigan, Ann Arbor, MI 48109, USA.

Silybin, a major constituent of the milk thistle, is used to treat several liver disorders. Silybin inactivated purified, recombinant cytochromes P450 (P450) 3A4 and 2C9 in a mechanism-based manner. The inactivations were time-, concentration-, and NADPH-dependent. The inactivation of the 7-benzyloxy-4-(trifluoromethyl-)coumarin O-debenzylation activity (P450 3A4) was characterized by a K(I) of 32 microM, a k(inact) of 0.06 min(-1), and a t(1/2) of 14 min. Testosterone metabolism to 6-beta-hydroxytestosterone (P450 3A4) was also inactivated with a K(I) of 166 microM, a k(inact) of 0.08 min(-1), and a t(1/2) of 9 min. The 7-ethoxy-4-(trifluoromethyl)coumarin O-deethylation activity of purified human P450 2C9 was inactivated with a K(I) of 5 microM, a k(inact) of 0.14 min(-1), and a t(1/2) of 7 min. Parallel loss of heme was observed with both P450s. Activity of both P450 enzymes was not recovered after removal of silybin either by dialysis or by spin gel filtration. In addition, silybin inhibited the glucuronidation of 7-hydroxy-4-trifluoromethylcoumarin catalyzed by recombinant hepatic UDP-glucuronosyltransferases (UGTs) 1A1, 1A6, 1A9, 2B7, and 2B15, with IC(50) values of 1.4 microM, 28 microM, 20 microM, 92 microM, and 75 microM, respectively. Silybin was a potent inhibitor of UGT1A1 and was 14- and 20-fold more selective for UGT1A1 than for UGT1A9 and UGT1A6, respectively. Thus, careful administration of silybin with drugs primarily cleared by P450s 3A4 or 2C9 is advised, since drug-drug interactions cannot be excluded. The clinical significance of in vitro UGT1A1 inhibition is unknown.

You gotta be fvckin with me, someone make sence of that ???

**fLgAtOr** · 06-12-2006, 06:07 PM

HAHAH....I was hoping there were some chem guys around...

I'm gonna try to get some more info...

**taiotosh7** · 06-12-2006, 06:10 PM

Originally Posted by stuball

Ive been hearing that a lot lately, And thats a great question, read a thread before that there is milk thistle without silymarin ( not sure if that spelled right ) and that the silymarin hinders gains, but the milk thistle i have is mostly silymarin, i really dont know what to think half the time..Do it dont do it ???

I could be wrong but I believe that the silymarin is what gives the proper liver function and detox properties. If you consume the whole milk thisle plant (seeds, leaves, stems, everything) you get a certain amount of silymarin in it. If you compare it to weed, as we all know the thc is what gives the sedative and increased appetite properties which are in the buds, not the entire plant. So the extracted silymarin FROM the thistle is what gives the herb it's value........so milk thistle without silymarin is like marijuana without thc.......or kind of like odouls beer!

**stuball** · 06-12-2006, 06:19 PM

Originally Posted by taiotosh7

I could be wrong but I believe that the silymarin is what gives the proper liver function and detox properties. If you consume the whole milk thisle plant (seeds, leaves, stems, everything) you get a certain amount of silymarin in it. If you compare it to weed, as we all know the thc is what gives the sedative and increased appetite properties which are in the buds, not the entire plant. So the extracted silymarin FROM the thistle is what gives the herb it's value

Wow thc, i remember that as a teenager, and thats 25 years ago, so your sayin that they could eliminate the silymarin, witch saves the liver ??? That thc is really kickin in now im fvckin lost !!

**guest589745** · 06-12-2006, 06:21 PM

I dont understand that at all.

**Liftnainez** · 06-12-2006, 06:27 PM

what is the final conclusion about the milk thistle effecting gains while on? anybody know??

**stuball** · 06-12-2006, 06:31 PM

Originally Posted by Liftnainez

what is the final conclusion about the milk thistle effecting gains while on? anybody know??

Thats gonna be the question of the day, we need someone that could explain this, not just people's experence ... This is a tough one..

**TheDfromGC** · 06-12-2006, 06:34 PM

i heard that it somehow gets to certain receptors and can slow down gains from orals at least. was gonna use it as a filler for var but somebody said that, not sure if its true or not

**stuball** · 06-12-2006, 06:47 PM

Dont want to change the subject, but i hear the same thing about nolvadex , some people take it through out the cycle some just wait till pct because it can hinder gains ...

**guest589745** · 06-12-2006, 06:49 PM

Originally Posted by stuball

Dont want to change the subject, but i hear the same thing about nolvadex, some people take it through out the cycle some just wait till pct because it can hinder gains ...

Completely different. And not true.

**Natty99** · 06-12-2006, 06:53 PM

I hate O'douls

**stuball** · 06-12-2006, 06:57 PM

Originally Posted by Skullsmasher

Completely different. And not true.

I will search it but thats what i recall reading.. but i will make that another thread...

**statuZ** · 06-12-2006, 07:08 PM

BUMP for an answer. I aswell read that taking Milk thistle reduces igf-1 levels. Im not sure if this is any significant amount, and dont take my word for it. I can recall reading something like this on AM.

**mwolffey** · 06-12-2006, 07:24 PM

imo, and no i dont have studies, but if it does hinder gains, it so f'n small that it could probably be barely measured...jmo, but save your liver or take some risks...your choice

**brutesinme** · 06-12-2006, 10:10 PM

Cytochrome P450 denote a large. related groups of enzymes. 3a4 is involved in testosterone metabolism, as is cyp2c9. This suggests that supplementing with thistle may affect your gains, however, on an 17aa cycles I'd personally rather be safe than sorry. To each their own however.

**brutesinme** · 06-12-2006, 10:12 PM

my mistake, 3a4 IS involved in test. metabolism, but 2c9 may not be, i can't find out for sure, i'll keep looking

**fLgAtOr** · 06-12-2006, 10:42 PM

Thanks dude... Appreciate the help.

**brutesinme** · 06-12-2006, 11:28 PM

here you go
cytochrome p450 2c9
-primary metabolism of most NSAIDS,
-s warfarin (have no idea what this is),
-phenytoin
Inhibited by:
fluconazole (and i guess by milk thistle)

**taiotosh7** · 06-13-2006, 10:53 AM

Originally Posted by stuball

Wow thc, i remember that as a teenager, and thats 25 years ago, so your sayin that they could eliminate the silymarin, witch saves the liver ??? That thc is really kickin in now im fvckin lost !!

No man they have nothing to do with each other. I was trying to make a simple example of the plant name (milk thistle) to the chemical name (silymarin) that gives the plant value, or worth....sorry to confuse you

**taiotosh7** · 06-13-2006, 11:08 AM

From what I have gathered (which is from nothing proven) my human logic tells me this: a 17aa is so the drug can make it past the liver without being completely destroyed to pass on through the bloodstream. This obviously makes the liver work harder to break down the 17aa and over time will weaken the liver. Since the thistle works to help cleanse and strenthen the liver it would be breaking down the 17aa at full power therefore more would be broken down and less would be absorbed.........like wolffey said if it does hinder gains, it so f'n small that it could probably be barely measured...but save your liver or take some risks...your choice

**mwolffey** · 06-13-2006, 02:10 PM

Originally Posted by taiotosh7

From what I have gathered (which is from nothing proven) my human logic tells me this: a 17aa is so the drug can make it past the liver without being completely destroyed to pass on through the bloodstream. This obviously makes the liver work harder to break down the 17aa and over time will weaken the liver. Since the thistle works to help cleanse and strenthen the liver it would be breaking down the 17aa at full power therefore more would be broken down and less would be absorbed.........like wolffey said if it does hinder gains, it so f'n small that it could probably be barely measured...but save your liver or take some risks...your choice

amen brother

**Swifto** · 06-13-2006, 02:13 PM

Originally Posted by fLgAtOr

I found this on another board...But I need some help making sense of it.

Silybin inactivates cytochromes P450 3A4 and 2C9 and inhibits major hepatic glucuronosyltransferases.

Sridar C, Goosen TC, Kent UM, Williams JA, Hollenberg PF.

Department of Pharmacology, The University of Michigan, Ann Arbor, MI 48109, USA.

Silybin, a major constituent of the milk thistle, is used to treat several liver disorders. Silybin inactivated purified, recombinant cytochromes P450 (P450) 3A4 and 2C9 in a mechanism-based manner. The inactivations were time-, concentration-, and NADPH-dependent. The inactivation of the 7-benzyloxy-4-(trifluoromethyl-)coumarin O-debenzylation activity (P450 3A4) was characterized by a K(I) of 32 microM, a k(inact) of 0.06 min(-1), and a t(1/2) of 14 min. Testosterone metabolism to 6-beta-hydroxytestosterone (P450 3A4) was also inactivated with a K(I) of 166 microM, a k(inact) of 0.08 min(-1), and a t(1/2) of 9 min. The 7-ethoxy-4-(trifluoromethyl)coumarin O-deethylation activity of purified human P450 2C9 was inactivated with a K(I) of 5 microM, a k(inact) of 0.14 min(-1), and a t(1/2) of 7 min. Parallel loss of heme was observed with both P450s. Activity of both P450 enzymes was not recovered after removal of silybin either by dialysis or by spin gel filtration. In addition, silybin inhibited the glucuronidation of 7-hydroxy-4-trifluoromethylcoumarin catalyzed by recombinant hepatic UDP-glucuronosyltransferases (UGTs) 1A1, 1A6, 1A9, 2B7, and 2B15, with IC(50) values of 1.4 microM, 28 microM, 20 microM, 92 microM, and 75 microM, respectively. Silybin was a potent inhibitor of UGT1A1 and was 14- and 20-fold more selective for UGT1A1 than for UGT1A9 and UGT1A6, respectively. Thus, careful administration of silybin with drugs primarily cleared by P450s 3A4 or 2C9 is advised, since drug-drug interactions cannot be excluded. The clinical significance of in vitro UGT1A1 inhibition is unknown.

Jeez.....

My only suggestion is to email, Anthony Roberts (Hooker).