What are your thoughts on Eric (LG) claim that ecdysterone is NOT orally active and is rapidly cleared by the liver? LG claims their Sublingual delivery method is more efficient and by dozing sublingually it will bypass the liver and deliver the ecdysterone directly to the muscles.
In your opinion is there any truth to this?
Also their ecdy appears to be standardized to - HydroxyPropyl Beta Cyclodextrin, 20-Hydroxy-ecdysterone & 6-Keto Diosgenin, is this along the same lines of what you were saying by "over" standardization?
Thanks for your input
First and foremost, I think the world of the work Eric/LG did on exposing the UV vs. HPLC 20-H fiasco. They certainly did their homework, and it showed. If you dig deep enough, this issue actually came up/was also encountered and discussed by Chuck Rudolph (Scivation), with respect to their "Anagen" product. Believe this product has since been dis-continued...
Listen closely at 34:30 concerning UV vs. HPLC...
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You'll note that while Scivation feels strongly you need only extract for 20H and it matters not what genus it comes from....this appears to have been based on their discussion with a Russian researcher's comments, via email correspondence. You may also have picked up on the fact, that he was using a 50% Rhaponticum Carthamoides Extract - to obtain favorable results.
Hmmm... wonder if the other 50% of the material from Lueza/Maral Root (synonyms for RCE) contributed? "Maral" btw, is the Russian word for "deer", in the region of Siberia RC was originally discovered.
There is much confusion though, even in this interview where he cites "THOUSANDS" of ecdysterones. To be clear, there are 454 known ecdysterones to date, per this outstanding resource:
Invalid Link Removed. Regardless, he gave an otherwise solid interview, citing much overlooked properties that companies are missing the boat on (i.e. its glucose disposal properties - superb).
Now, with respect to Ecdysterone not being orally active, I'm afraid I'd have to disagree. I'm not doing so to be combative, but consider the following, from LaFont's 2003 Paper in
Insect Science - "Practical uses for ecdysteroids in mammals including humans: an update" Lafont R.
and Dinan L.
"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 intraperitoneal injection of 750 µg of this compound.
So we see here in a
HUMAN, oral dosing results in the compound making it into plasma/circulation. If it didn't, they wouldn't have been able to pick anything up on the radio-immuneassay - and therefore wouldn't have been able to gauge half life. In terms of Ecdysterone being orally administered to livestock, furry rodents of all sorts - it's done all the time. Dissolving in apricot resin tends to be a favorite, when administering to rats. Also, there's a veterinary preparation (2 actually), one of which is added to animal feed (BCL PHYTO - anabolic) and a related product (BIOINFUSION - injectible, moreso to deal with sickness/parasites). I'm being respectful here - I see no evidence Ecdy is
NOT orally active.
I do agree with LG, in the respect that oral isn't optimal for all Ecdy's. 100% agreement in fact, that 20-H is a waste orally (in humans) for performance enhancement. The goal of bypassing the liver though, is but one company's/person's strategy. In fact, oral Ecdysterone benefits the liver tremendously. For example, from the same paper...
Ecdysteroids stimulate hepatic functions: 20E accelerates recovery after hepatitis induced by heliotrine treatment (Syrov et al., 1981b). 20E and other ecdysteroids (turkesterone, cyasterone) administered ( 1 0 mg / k g ) t o r a t s wi t h h e p a t i t i s i n d u c e d b y s u b c u t a n e o u s i n j e c t i o n o f c a r b o n t e t r a c h l o r i d e p r e v e n t it s hepatotoxic action (Syrov et al., 1992).
Moreover, a pretreatment with 20E (5 mg/kg) for one week will reduce the effects of a subsequent heliotrine treatment (Badal’yants et al., 1996)...."
HPBCD is the correct cyclodextrin complex (if you're interested in going that route). But yes, when referring to isolating TRUE ecdysterones from a given genus (20-H, Cyasterone, Rubrosterone etc.), that's where I feel many are going awry. Each time, XYZ company thought for sure they had found the "active", responsible for the plethora of Ecdy's benefits. Subsequent to each attempt, the test of time bore out that the magic never fully materialized. What then, may explain the broad range of RCE's beneficial effects? Incorporation into the cell membrane, via the PI3K-AKT pathway (IMO).
And why do I believe this? You need look no further than fish oil, it's same broad range of benefits and how it "builds" into your cell membrane's structure.
In the Blueprint, we also know what else juices this pathway - and how to leverage it, in order to radically accelerate muscle growth. It rains PR's on The BP forums every day, and that's no accident...
The sapogenin analogs (often erroneously referred to/painted with a broad brush) and referred to generically as "6-keto diosgenin", are another story....
