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**dinoiii** · 12-31-2007, 01:01 PM

This is a reprint of a series of posts from DA from Nov 2006 - based on a reccurence of questions though in email, I have opted to have this one reappear.

Quote:

Originally Posted by RisingAgainst

I was curious about the chemical properties of this, ie. what it does, how it works, safe/unsafe, and the ability to take other things with it? Thanks in advance.

**dinoiii** · 12-31-2007, 01:02 PM

My response to the RA question above was as follows:

Ok, ok - lets do the ole chalk talk!

This time, our subject of debate suggested by Rising Againts (you will hence forth be referred to as "RA" in my posts!

): the phytoestrogen derivatives of daidzen, a major phytoestrogenic component extracted from soy.

Ipriflavone (7-isopropoxyisoflavone) is a synthetic derivative of the phytoestrogen daidzen, and 5-methyl-7-methoxyisoflavone ("methoxy") is a derivative of ipriflavone. The existing research indicates that their pharmacological properties are similar, although methoxy is more potent.

So, how we can recap this for easy retention, I have put together the following SUMMARY for your ease:

SOY --> daidzen --> Ipriflavone (7-isopropoxyisoflavone) --> Methoxy-flavone (5-methyl-7-methoxyisoflavone)

Are we all up to par?

So, how the hell did this thing break into the sports supplement industry? The "powers that be" issued Methoxy a patent in the 1970s as an anabolic agent [Hungarian company filed patent in 1977 as an animal feed additive - hehe, the year dinoiii was born - GEESH!!!]. In 1980, it was picked up by the cattle industry suggested to increase lean muscle. Livestock producers flocked by the millions to get ahold of this agent that obviously, if worked as suggested, would produce them significant profits.

There were a couple random (not necessarily well-controlled) studies that demonstrated an increase in protein utilization and one in particular cited IN THE PATENT that reported 4.4-6.6 pounds of "lean" muscle (note the round figures) gained after 3 weeks! These findings were .... perhaps needless to say NEVER ABLE TO BE REPLICATED!!!

But the more exciting results were the potential for anti-catabolic properties when these compounds showed increased calcium, phosphorus, potassium, and perhaps most importantly in the world of body composition, nitrogen retention.

But hold the horn! Results were seen with dosing parameters NOT NECESSARILY used in subsequent trials (the average dosing mimics that of ecdy products (I have talked about this one in the past, but will offer more later) - approaching 1 to 2 grams to get minimal efficacy)....this is UNACCEPTABLE. One POSITIVE side effect to come from the replicated trials were the lowering of LDL and total cholesterol....of course it would do this though....it has pro-estrogenic properties...recall its derivation.

Ipriflavone (its essential predecessor) held up a bit better in human trials, however, it was later found out that its effect was seen on bone mass and it was suggested to be used for osteoporosis and effectively works as a minimal adjunct should you find this an issue (or anyone who is of the current baby boom population, et al)...and perhaps there is a place in bodybuilders with significant bone disorders, but again dosing efficacy likley requires 600mg MINIMALLY coupled with calcium and likely again closer to 1 gram to see true benefit through time.

So what the hell happened Dana?

They broke into the sports supplement sector with vry sketchy rationale and many users subsequently found out why they are hard to use. EAS put out a product Methoxy Factor with close to the right dosage of ideal product, however screwed up the organic solvent data to produce the extract that was used way back when dinoiii was ripped from the womb (and I mean this literally, dinoiii was a C-section baby - there would be NO vaginal delivery for me, I was even picky then dammit!

). This extract issue shows up all over the place and seperates who knows the science and who doesn't as far as copanies simply throwing conglomerates together with bells and whistles. Take Tongkat Ali (Eurycoma) for instance, this is the most well-described, yet most poorly extracted item in the industry today. Anyway...I digress on this point.

Syntrax had a couple of Ipriflavone/Methoxy products that too petered out for the same rationale. But hell, when the former science gurus of Syntrax messed up their Ethers in the prohormone department - there was a time frame they prooved to be nothing more than talk versus efficacy - producing (btw, for those reading, I am NOT speaking of the current company condition! All sorts of personnel changes have been made since the late 1990s...please do NOT misread my words. I have no idea what is being done there today.)

OVerall, because this is methoxy and this is a stream-of-conscious response about my own industry times, et al....I will try and sum it all up. For muscle-building ---- ehhhh, some efficacy BUT lacks cost efficiency! Cholesterol-reduction effects and potential anti-catabolic effects....maybe - but the dosing is out of this world and it comes back to the damn cost efficiency argument...it isn't - your money is better spent elsewhere. Oh yeah...this is a moot point if people don't know how to properly extract it and 95% of the industry I would bet do NOT! No, this is NOT a foolish comment on my behalf...but the rationale for the current state of affairs - separate those that preach science versus those that talk business...the industry has BOTH...simply BE CAREFUL ... one of those buyer beware things...

Ipriflavone may have better efficacy in the long-run, but again, cost efficiency is tainted. I would say ... if there is an issue with bone disease, osteroporosis or otherwise...if other avenues have been exhausted and recurrent fractures or something are a situation of concern...then sure, give it a try...the bone research is solid for things with pro-estrogenic components....nahhhh, you won't grow breasts either guys...so don't take my estrogen comments wrong either.

Overall, they are rather safe...if you are going to try them...there SHOULD BE A REDUCTION IN DOSING IF YOU HAVE ANY KIDNEY ISSUES, otherwise...dose em high and cross your fingers. But when the dust settles and you make very little, if any gains, don't say I didn't warn ya...but send some of the money you have to apparently invest in such products dinoiii's way.

Hope this answers the question on this end... We'll discuss ecdy products in turn ... I have spoken about them in the past so I will try and give you a link....

Hang on a sec...

**dinoiii** · 12-31-2007, 01:03 PM

I have re-read a lot of the threads on this subject...they tend to get people upset so I figured, I would cut and paste some pertencies:

Quote:

Originally Posted by dinoiii

Personal preference:

minimum 200-400mg up to three times a day MINIMUM (unfortunately, some have reported some GI side effects in response to this kind of dosing protocol). When approached to potentially try this, I offered the retort that I didn't feel qty. of ingredient was accurate and would have to follow dosing parameters I set up.

there has been some chatter about the absence of an ecdysterone receptor in humans and I do NOT doubt this fact, but I would likely offer an alternative mechanism of action in humans as statistically significant cholesterol modification, et al. have been noted. Bottom Line: further research needs to be done, especially on its cholesterol-lowering effects and its potential (if any) for alternative ergogenic benefits.

Quote:

Originally Posted by dinoiii

First...much of the data is unfortunately in need of translation from overseas - I think the only promising research to exist comes from Russia and the translations are very difficult (when compared in 1988 to methandrostenelone, the dosing parameters for ecdysterone were ridiculously high, greater than what I suggest...and the researchers concluded superior anabolic properties and voila it was translated as 40mg...huh?). A PubMed serach will yield you ZERO results about the wonders of this compound (although there is one thing out of research from people at Purdue but it doesn't NOT give dosing suggestions). Many people somehow assume anything coming from the Western world exists in excess and this is simply NOT true.

Second...our next translation is how to equate the schistosome research into what it may mean for humans prior to our testing dose. Phytoecdysterones equal 200 in number. Typically, they are C27, C28, or C29 compounds. We "extract" them from plants unto which they are in like Pfaffia glomerata where it is thought they exert a protective effect from insects in order to use them in the supplementation process. But our main sources remain Brazilian Ginseng and Russian Leuzea. Now, you are talking an "extraction" process that ensures enough active (call it the 20-hydroecdysone or what have you...research has been FAR from conclusive).

Third, we will look at in vitros:
with glucose metabolism, the HepG2 cell line has been studied on glucose metabolism...here your "point of diminishing returns" was noted not by the individual - remember, we are talking in vitro...but by the glucose concentration relative to the cell line (i.e. - I think it was 5.5 mmol/L glucose and then the effect disappeared somewhere in the 20+mmol/L tally). This actually would translate into volume of distribution and suggest that in vivo limitations would be set forth by all sorts of things at least in the glucose metabolism realm. Now you ramp up the cell lines and viola...we have our extrapolation of what it would take approximately based on human liver size (i.e. - hepatocyte cell lines).

In vivos:
What about our rodent friends:
Yes, in fact 10-20mg was in fact the dose equivalency found in that research in rats out of Uzbekistan - some say 5mg, but this is NOT the case -and extrapolation would be multipled by a minimum of 10 to gather proper dosing parameters in humans (I'd bet it still volume of distribution related to vary...hence, my suggestion of 200-400 --> has this part been studies...nope, but nor has your suggestion or the ones in the ads).

Back in 2004, we uncovered some enzymes (novel EPPase, et al) to be involved in formation of metabolites we knew about since 2001. The main metabolite through this process is called deoxyecdysone and one can only now start thinking about saturation levels of substrate, etc... and how the heck to translate this data (which I believe to come Greece, but you'd have to check me on that one).

Additional: Gadzhieva, R.M. et al. (1995) A comparative study of the anabolic action of acdystn, leveton and Prime Plus, preparations of plant origin. Eksp Klin Farmakol Sep-Oct 58 Dosing Parameters: 40mg/kg body weight (again, volume of distribution). No ill effects (i.e. - Lethal dose) up to 800mg - minor GI sides beyond this, which is what I said.

Quote:

Originally Posted by dinoiii

Dosages of that study were roughly as follows, but the translation lags:

5 MG/KG X Your Weight = Dosage:
In Kilograms: 5 mg X 70 kg = 350

[citation: Chermnykh NS ; Shimanovski¨i NL ; Shutko GV ; Syrov VN
Farmakol Toksikol, 51(6):57-60 1988]

These "well-trained" athletes the study quotes were larger than 70kg, but the above is simply an example to mimic the average person considered "prototype." Mind you, this is 350mg PER DOSE. Best dosing parameters remain multiple per day...up to three based on half life w/o an actual receptor et al. (see below) which was determined later on.

This study is usually followed up by the following "rat" study:

Anabolic activity of phytoecdysone-ecdysterone isolated from Rhaponticum carthamoides.

Author:
Syrov VN ; Kurmukov AG
Farmakol Toksikol, 39(6):690-3 1976 Nov-Dec

Abstract:
Introduction of phytiexdizone-exdisterone (0.5 mg/100 g) [but keep in mind volume of distribution for humans when extrapolating rat data] to rats for 7 days is shown to be attended by an accelerated body weight gain and also by a rising weight of the liver, heart, kidneys and musculus tibialis anterior. In these organs the total amount of protein increases. All of the above-stated changes are more marked when the substance is given to growing rats (70--80 g). In experiments on castrated sexually immature rats the androgenic action of exdisterone, unlike that of methandrostenolone, is not demonstrable.

What's more - as I stated: Ecdysteroids are rapidly eliminated requiring multiple daily dosing (up to gram tallies and this is even if the poorly-controlled Russian studies can be translated from insects, rats, and quail to humans!).

In the case of humans, two different studies have been performed. Simon and Koolman (1989) analysed the pharmacokinetics of E and 20E (given orally, 0.2 mg/kg b.w.) to a male volunteer, by monitoring with a radioimmunoassay the subsequent plasma and urine titres. This gave an effective half-time (EHT) of elimination of 4 hours for E and 9 hours for 20E. In lambs, EHT for 20E was shown to depend strongly on the mode of administration, with values of 0.4, 0.2 and 2 hours after oral, intravenous and intramuscular administration, respectively (Simon and Koolman, 1989). The method used did not allow the detection of metabolites, if present. The half-life seems shorter in smaller mammals, with reported values of 8.15 min for 20E in mice (Dzukharova et al., 1987). More recently, Albanese et al. (2000) found a plasma half-life of 48 min for ponA in mice after intra-peritoneal injection of 750 µg of this compound.

Both urinary and faecal routes seem to be used for the elimination of the administered molecules. In mice, the faecal route was found to be the major one by Hikino et al. (1972 - 2 different studies) and Lafont et al. (1988), although Dzukharova et al. (1987) found that faecal and urinary routes were equally important. Such a question can be easily assessed only by the use of radiolabelled molecules, but no data are available for humans. Kinetic studies in mice showed that ecdysteroids were taken up by the liver and then excreted into the gut via the bile (Hikino et al,1972 - 2 different studies; Lafont et al., 1988).

Granted sheep and pig data show nitrogen retention and the like stallion at very small doses, but metabolic processing and volume of distribution is MUCH different than humans - perhaps this is the source of confusion.

The problem is to start going above 600mg, you start talking some GI discomfort.

Right Hook · 03-15-2008, 02:36 PM

Was the post just above strictly referring to ecdy?

Can you by chance reference the below study? I'm looking at one but not sure its the same study and it shows an increase in LBM:

Quote:

There were a couple random (not necessarily well-controlled) studies that demonstrated an increase in protein utilization and one in particular cited IN THE PATENT that reported 4.4-6.6 pounds of "lean" muscle (note the round figures) gained after 3 weeks!

.....

Quote:

approaching 1 to 2 grams to get minimal efficacy)....this is UNACCEPTABLE.

How so? In terms of price or what? Prices have dropped significantly I believe.

I'll go grab that study now...