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raybravo
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Re: Re: Re: Biggest Bodybuilding Myths

Posted by: jboldman
Prepare yourself for the suffering!

jb

what even gives u the idea that i'm going to be enjoying the effects of pgf-2 ?? lol , was just planning to do a max androgen protocol and ive been on for a while now , lol , so i guess ive fallen to the myth that i might need to upregulate my receptors again .....


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iced
 iced
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Posted by: bjjfighter
How bout the myth that drinking winny is just as effective as IM.?

i think the difference is minmal at best.


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Nandi
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quote:


Raybravo, I think you need to stop listening to that Rea guy

I was wondering who was responsible for the idea that pgf2-alpha increases AR density. So this is an L Rea "theory"? Do you guys have a link to a post where he elaborates on this?


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mystery_meat
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Posted by: bjjfighter
How bout the myth that drinking winny is just as effective as IM.?

I think this will answer your question... The two are not even close in terms of eficiency...

quote:


The effect of Stanozolol on 15nitrogen retention in the dog.

Olson ME, Morck DW, Quinn KB.

Animal Health Unit and Gastrointestinal Sciences, University of Calgary, Alberta.

The objective of the study was to determine the influence of either oral or intramuscular administration of stanozolol on nitrogen retention in dogs by using a non-invasive 15N-amino acid tracer technique. Ten healthy, intact, adult male sled dogs received either stanozolol tablets, 2 mg/dog PO, q12h, for 25 days (Group 1, n = 5) or an intramuscular injection of 25 mg of stanozolol on Days 7, 14, 21, and 28 (Group 2, n = 5). A 15N amino acid (5.27 mmol) was infused intravenously into each dog on Day 0 (before stanozolol treatment) and on Day 31 (after stanozolol treatment). Urine was collected by catheterization from each animal 3 times daily for 3 consecutive days. The 15N-urea enrichment in urine was determined by high-resolution mass spectrometry and the total amount of urea in the urine was determined. Both oral and injectable stanozolol resulted in significant (P < 0.05) increases in amino acid nitrogen retention compared to pretreatment values. Oral stanozolol increased nitrogen retention from 29.2 +/- 8.2% to 50.3 +/- 9.2%, while stanozolol injection increased nitrogen retention from 26.6 +/- 9.9% to 67.0 +/- 7.5%. The response to intramuscular administration was significantly greater than the response to the oral dosing regime. Stanozolol increases amino acid nitrogen retention in dogs, as has been previously observed in rats. This action of stanozolol may be beneficial in dogs under stress of surgical trauma and chronic disease.


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Blade
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Posted by: Nandi12
I was wondering who was responsible for the idea that pgf2-alpha increases AR density. So this is an L Rea "theory"? Do you guys have a link to a post where he elaborates on this?

Yeah, in a Q&A; on Meso

Exerpt: "The full body circulation of liver produced IGF-1 is full body effectual. This means that the extra IGF-! from oral stanozolol administration has an effect on the entire musculature as does the AAS itself. Unfortunately within a period of about 2 weeks this effect decreases significantly due to an adaptive response in the liver that shuts down the extra growth goodies and a decrease in IGF-1 receptor site sensitivity results as well due to various other hormone actuated events (Action/Reaction Factors). Less IGF-1 production and less receptor sensitivity means less muscle growth and poor chemical synergy.

Site specific administration of an injectable preparation of stanozolol has full body effects due to AAS induced androgenic and anabolic activity but only significant "localized" MGF, PGF-2, IGF-1 and IGF-2. MGF increases IGF-1 receptor sensitivity, PGF-2 increases androgen receptor count and sensitivity, and the localized IGF-1 production acts synergistically with the AAS. Oh, did I mention that the IGF-2 initiates an increase in vascular tissue growth for better nutrient supply?

Day 1-10 & 21-30 25-50mg 2xd (orally)
Day 11-20 & 31-40 50-75mg 2xd (site specifically)

Since stanozolol is a derivative of DHT (dihydrotestosterone) the occurrence of premature balding has been noted in individuals who are predisposed to MPB when administering this drug. For the same reason real stanozolol does not convert to estrogens and has a lesser degree of HPTA inhibition and the effects last for a shorter period post-cycle. However due to the peripheral nervous system and the presence of an abnormally high degree of androgenic activity some " shrunken nuts syndrome" can occur with prolonged use. "

Also, you might like to review his views on thyroid hormones


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Nandi
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Thanks, Blade. Or maybe not...


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raybravo
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he also mentions it in his book :
this is what he says "some had also used site injections of prostaglandin for 2 weeks before the beginning of AAS or prohormone site injection protocols . this created a dramatic upregulation and sensitivity of androgen receptor sites . "


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Nandi
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Ever since I first heard that claim I've looked far and wide for any research to support it. What a bizarre thing to just make up out of the blue, but I sure as hell can't find a shred of supporting evidence.


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Nandi
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I'm wondering if this is the train of logic he is following.

PGF2-alpha is believed to exert its antiadipogenic effect by blocking the peroxisome proliferator-activated receptor gamma (PPAR) nuclear hormone receptor

See fig 4. So PGF2-alpha inactivates PPAR-gamma.

On the other hand, ligands for PPAR-gamma, like troglitazone, exert an antiandrogenic effect by possibly either inhibiting coactivators or stimulating corepressors of the activated AR

So Rea could be making the logical jump that since PPAR agonists are antiandrogenic, PPAR antagonists like PGF2-alpha are androgenic by stimulating AR signaling. This is a big leap, and it also has nothing to do with AR upregulation (increase in density).
In fact, the second study specifically noted that troglitazone, the PPAR agonist, did NOT downregulate the AR. So there would be no reason to think that PGF2-alpha would UPREGULATE the AR.


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Blade
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This is just an example of his several leaps of faith and outright flaws in logic. When confronted with these inconsistencies (I see Raybravo has posted some questions at his forum), he either evades the question or doesn't answer it at all. Not only is he responsible for sustaining a lot of these BB myths you mentioned, but he even contributes with some of his own...


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Fonz
 Fonz
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Posted by: Nandi12
I'm wondering if this is the train of logic he is following.

PGF2-alpha is believed to exert its antiadipogenic effect by blocking the peroxisome proliferator-activated receptor gamma (PPAR) nuclear hormone receptor

See fig 4. So PGF2-alpha inactivates PPAR-gamma.

On the other hand, ligands for PPAR-gamma, like troglitazone, exert an antiandrogenic effect by possibly either inhibiting coactivators or stimulating corepressors of the activated AR

So Rea could be making the logical jump that since PPAR agonists are antiandrogenic, PPAR antagonists like PGF2-alpha are androgenic by stimulating AR signaling. This is a big leap, and it also has nothing to do with AR upregulation (increase in density).
In fact, the second study specifically noted that troglitazone, the PPAR agonist, did NOT downregulate the AR. So there would be no reason to think that PGF2-alpha would UPREGULATE the AR.

I think he is basing his assumption on Dharkhams old prostaglandin article.

Basically, the addition of PgF2A to a cycle of AAS causes a vast decrease in the time to reach muscular hypertrophy.

So, Dharkham speculated that the less AAS would be needed if PgF2A was used in a cycle.....as opposed if pgF2A was not used.

Real world results correlate with what Dharkham speculated......BB'ers who were on AAS cycles that incorporated Pgf2A had to decrease the amount of AAS they were on b/c the pumps were just becoming too painful.

However, the science is lagging behind real world results. We know very little about the anabolic effects of prostaglandins.

I still don't get were he gets prostaglandins up-regulate the AR's though. IMO prostaglandins exert their anabolic effects through non-AR mechanisms. But again, the science here is not very clear cut.

Classic case of not enough scientific information. We're playing the assumption game.

Fonz

If I want to add flavor to my cooking. . . . . . . I just burn it

There is NO such thing as over training just under EATING. ~ Trey Brewer


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iced
 iced
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I had a friend try pgf2, he said the injection pain was horrible, forget about a real job if you try to inject 5x a day, he was in the bathroom more than anything. He couldnt work out that muscle for two-three days he injected in. Sure it may theoretically work, but who gives a damn if you hurt bad and cant leave the bathroom.


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Nandi
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quote:


I still don't get were he gets prostaglandins up-regulate the AR's though


This is my problem as well. There is actually quite a bit of research on the anabolic effects of prostaglandins, much of it suggesting that PGF potentiates the anabolic effects of insulin, and controls the rate of protein turnover in muscle. Here is one example

Biochem Biophys Res Commun 1983 Nov 15;116(3):1084-90 Related Articles, Links

The possible involvement of prostaglandin F2 alpha in the stimulation of muscle protein synthesis by insulin.

Reeds PJ, Palmer RM.

The addition of insulin (8 ng/ml) in vitro to muscles from fasted rabbits increased protein synthesis (+80%) to a value similar to that found in muscles from fed donors. The addition of either indomethacin or meclofenamate completely blocked this effect of insulin. Muscles from fasted rabbits released less prostaglandin (PG)F2 alpha into the medium and the presence of insulin increased and indomethacin and meclofenamate reduced PGF2 alpha release. Other conditions (work load and leucocyte pyrogen) which increase protein synthesis in muscle also stimulate PGF2 alpha release. As both arachidonic acid and PGF2 alpha in themselves increase protein synthesis we suggest that accelerated phospholipolysis and PG synthesis have a general role in the control of muscle protein turnover.


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Dante
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Bill Llewellyn of Molecular Nutrition is soon to release his X-Factor product, consisting of Arachidonic Acid.

There was a good debate about this on Avant, with Bill, Par, Patrick and Elzi Volk ("Labrat") participating. I can post the link, if anyone cares, as it gets into the role of prostaglandins and such.


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Fonz
 Fonz
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Posted by: Dante
Bill Llewellyn of Molecular Nutrition is soon to release his X-Factor product, consisting of Arachidonic Acid.

There was a good debate about this on Avant, with Bill, Par, Patrick and Elzi Volk ("Labrat") participating. I can post the link, if anyone cares, as it gets into the role of prostaglandins and such.

I'll say exactly what I said on A's board. I think this product will bomb.

First some background:

Arachidonic acid is an essential, unsaturated, 20 carbon fatty acid that humans use to synthesize regulatory molecules such as prostaglandins and thromboxanes.

Arachidonic acid is metabolized by one of two enzyme pathways into various prostaglandins (by cyclooxygenase) or leukotrienes (by lipooxygenase). Both prostaglandins and leucotrienes are highly pro-inflammatory, bronchospastic and vasodilatory.

There are 2 hypothetical problems:

#1

AA is the precursor to the prostaglandins. OK.
Both the good(Series 1 or Pgf2A) and the bad(Series 2 PGE2)
However, prostaglandins are ALWAYS produced at a 1:1 ratio.
So, according to Llewellyn, the addition of exogeneous AA will increase prostaglandin production. OK.....but that increase will be at a 1:1 ratio no matter what(He whoever is betting it will be more PGf2A than PGE2...thats a BIG assumption). ALSO however, leukotrienes WILL ALSO be increased.....these are very pro-inflammatory. This is NOT a good thing.

#2 The conversion of AA to prostaglandins and leukotrienes is also ENZYMATIC. Therefore it is rate-limited. Doesn't matter how much AA you take, only a certain portion will be used for prostaglandin production and leukotriene production for a certain period of time. Your body has only so many enzymes. The un-used AA will simply be excreted.

What he needs to do to prove this stuff works is:

1. Run a controlled trial w/ people that can be trusted.

Its failry easy to prove if his AA product will work. If you do raise prostaglandin production(the good PgF2A), your body temperature will go up. This can be measured with an accurate digital thermomemter.

I have done this with a substance that in theory reduced PGE2 production...therefore shifting the normal 1:1 prostaglandin ratio more to the good prostaglandin side(Pgf2A)....and guess what?
My temperature went up. Which makes perfect sense.

If his AA product does indeed work.......it shouldn't be too hard to prove. All you need is a digital thermometer and a weeks time to find out the dosing schedule due to the enzymatic rate-limiting factor.

Thats just my opinion.

In fact...I think his product COULD work...if he added a certain fat to it.......

If I want to add flavor to my cooking. . . . . . . I just burn it

There is NO such thing as over training just under EATING. ~ Trey Brewer


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